DISEASE IN CAPTIVE WILD MAMMALS AND BIRDS
INCIDENCE, DESCRIPTION, COMPARISON
BY
HERBERT FOX, M.D.
PATHOLOGIST TO THE ZOOLOGICAL SOCIETY OF PHILADELPHIA, DIRECTOR OF THE
WILLIAM PEPPER CLINICAL LABORATORY, UNIVERSITY OF PENNSYLVANIA
WITH A FOREWORD BY
CHARLES B. PENROSE, M.D.
PRESIDENT OF THE ZOOLOGICAL SOCIETY OF PHILADELPHIA
[Illustration: ZOOLOGICAL SOCIETY OF PHILADELPHIA. INCORPORATED 1859]
PHILADELPHIA, LONDON & CHICAGO
J. B. LIPPINCOTT COMPANY
COPYRIGHT, 1923, BY HERBERT FOX
THIS BOOK
IS DEDICATED TO
CHARLES BINGHAM PENROSE, M.D., PH.D., LL.D.
IN GRATEFUL APPRECIATION OF HIS FRIENDSHIP
AND OF HIS GUIDANCE AND ENCOURAGEMENT
IN ALL MATTERS PERTAINING
TO THIS LABORATORY.
CONTENTS
PAGE
FOREWORD—DR. CHARLES B. PENROSE 1
SECTION
I. INTRODUCTION 17
Zoological Classification
Numerical List of Autopsies Upon Which the Work is
Based.
II. DISEASES OF THE HEART 48
III. DISEASES OF THE BLOOD VESSELS 66
IV. DISEASES OF THE BLOOD AND BONE MARROW 83
V. DISEASES OF THE LYMPHATIC TISSUES INCLUDING SPLEEN 114
VI. DISEASES OF THE RESPIRATORY TRACT 134
VII. DISEASES OF THE ALIMENTARY TRACT
The Tube Proper 166
The Liver 222
The Pancreas 244
The Peritoneum 260
VIII. DISEASES OF THE URINARY TRACT 263
The Kidney
IX. DISEASES OF THE FEMALE REPRODUCTIVE ORGANS 287
X. DISEASES OF THE MALE REPRODUCTIVE ORGANS 313
XI. DISEASES OF THE DUCTLESS GLANDS.
The Thyroid 316
The Thymus 336
The Suprarenal 336
XII. DISEASES OF THE SKELETON AND ITS JOINTS 343
XIII. DISEASES OF THE CENTRAL NERVOUS SYSTEM AND SPECIAL SENSES 372
The Eye 402
XIV. CONSTITUTIONAL DISEASES 410
XV. THE RELATION OF DIET TO DISEASE BY E. P. CORSON-WHITE,
M.D. 415
XVI. NEOPLASMS 462
XVII. THE INFECTIOUS DISEASES.
Tuberculosis 483
Mycosis 558
Streptothricosis 567
Miscellaneous Infections 596
XVIII. ANIMAL PARASITES, THEIR INCIDENCE AND SIGNIFICANCE, BY F.
D. WEIDMAN, M.D. 614
LIST OF TABLES
PAGE
1. The incidence of degenerative and inflammatory changes in the
heart 51
2. The incidence of hypertrophy and dilatation of the heart with
principal associated lesions 57
3. A condensation of the important features of Tables 1 and 2 63
4. The heart-to-body-weight ratios 63
5. The incidence of arteriosclerosis 71
6. The differential percentage of the circulating leucocytes in a
number of different animals 84
7. The various types of splenitis 126
8. The incidence of the various types of bronchitis and of
pulmonary parasites 142
9. The incidence of the various forms of pneumonia 150
10. An analysis of cases of abscess and gangrene of the lung 156
11. The incidence of gastroenterocolitis, its distribution and an
analysis of the causes 182
12. An analysis of the inflammations of the alimentary tract in
Ungulata 196
13. An analysis of the inflammations of the alimentary tract in
Marsupialia 200
14. An analysis of the cases of pancreatitis, the associated
pathology and the details of the anatomy of various orders 252
15. The weight of the thyroid body in relation to body weight 318
16. The incidence of the various enlargements of the thyroid body 326
17. The incidence of cases of degenerative bone disease in the
various orders 357
18. The weight of the brain and the relation of this to the body
weights in 196 animals 388
19. An analysis of pathological conditions in terms of diet 423
20. An analysis of the diets used in the Philadelphia Garden 426
21. The incidence of tumors 464
22. An analysis of the breeding, captivity and visceral
distribution of neoplasms, of tumor-bearing animals 466
23. An analysis of the incidence, character and distribution of
tuberculosis 486
24. The incidence of parasites in the zoological orders 630
25. The incidence of heterakis in pheasants 635
26. The incidence of various parasitic orders and families 636
27. The visceral distribution of parasites 639
28. The occurrence of blood parasites in zoological classes 651
FOREWORD
BY
CHARLES B. PENROSE
The work on which this book is based was begun in November, 1901. From
that date, systematic autopsies were made on animals dying in the
Philadelphia Zoological Garden. Previously autopsies had been made very
rarely and only on animals of especial importance and interest.
Pathological conditions were occasionally noted in animals subjected to
anatomical study. The work was strictly volunteer, for there was no one
on whom the Society had the right to call. Dr. Henry C. Chapman, a
former Director, whose interest was in physiology and comparative
anatomy, made nearly all the autopsies that were made before the
beginning of the present work. In the annual reports from the foundation
of the Garden in 1872, very few such examinations are recorded. In some
reports there are lists of important deaths, but no record of the cause
of death.
This state of things was not peculiar to the Philadelphia Garden. It
existed in every zoological garden in the world. It exists in most of
them to-day. When an animal died it had no interest or value except for
its hide and bones. Rare specimens were sent to the Academy of Natural
Sciences from the Philadelphia Garden. The great majority, however, were
immediately destroyed, and thus during the twenty-nine years from the
foundation of the Garden, preceding this work, there have been lost many
opportunities—some of which will never recur—of increasing our knowledge
of pathology.
This book gives results of the study of animals that have not been
subjected to experimental procedures and conditions, and though their
mode of life has not been that strictly natural to them, yet they have
not been influenced by any of the artificial procedures of the
laboratory which are usually followed in investigations on animals.
Though the object of the work was the pursuit of knowledge for its own
sake, yet results of practical value have followed: hygiene has been
improved; disinfection has been made scientific; epidemics have been
arrested; some diseases, notably tuberculosis in monkeys, and
spiropteriasis in parrots, have been practically eliminated.
The value of the work is recognized by the keepers. Their interest has
increased and their morale has improved. The frequent deaths in a large
collection of animals are discouraging, and a good animal man must have
courage and optimism—traits that are stimulated by the knowledge that
every animal that dies is studied to determine the cause of death, and
to prevent its recurrence.
Some results of this study are to be considered as “raw material,” while
others permit cautious or tentative conclusions. The first include—
visceral weights, incidence of certain lesions like anemia and hepatic
cirrhoses, occurrence of calculi and observations on weak hind quarters,
convulsions and constitutional diseases. The second include—eradication
of tuberculosis and spiropteriasis, the response of the mammalian and
avian heart to strain and disease viruses, the origin of pneumonia in
birds, the genesis of bronchiectasis, the nature of osseous degeneration
with relation to diet and alimentary tract, the comparative anatomy,
physiology and pathology of the female genitalia, the occurrence of
lesions in the thyroid comparable to those in man, the character of
kangaroo disease.
Great praise is due Dr. Herbert Fox and his assistants Drs. F. D.
Weidman and E. P. Corson-White, for the splendid scientific spirit and
thoroughness with which they have done this work, with no adequate
remuneration, except the intangible reward appreciated only by the real
research worker.
It is a mistake to think that all animals in the wild state are healthy.
The healthy wild animals that we see are the survivors, the sick and the
weaklings having died. Undoubtedly diseases are fewer than in captive
animals; but on the other hand wild animals are exposed to dangers to
which captive animals are not exposed—such as lack of care in sickness
and old age, starvation, and attacks of enemies that feed on them. The
maximum longevities in some species are probably in captive animals. It
is doubtful if a wild animal ever reaches the greatest age possible to
it.
Many kinds of parasites have been found in wild animals captured only a
short time before arriving at the Garden, so that they must have existed
in the wild. Thirteen wild cats received from South Carolina within a
few days after capture were infested with intestinal, muscular, and
pulmonary parasites. Several years ago there were received from the
Island of Chincoteague, off the coast of Virginia, a number of native
birds recently captured, all of which had mould disease of the air sacs.
This happened on several occasions, so that it became necessary to
reject all birds from this locality. Among the birds were meadow larks
and cardinals.
Hunters not infrequently kill animals with disease, and if more hunters
knew enough to recognize the disease there would be more recorded cases.
Sick animals are not as likely to be killed by the hunter as healthy
ones, as sick animals seek seclusion and do not move about. In many
localities of the United States white-tailed deer are infested with the
liver-fluke. Trout and other fish in remote mountain streams are found
with tapeworms. Round worms and other parasites infest the white
rhinoceros in the African forest.
In many instances the parasites and the host, when in health, get on
very well together; but when the host weakens the parasites may give him
the finishing stroke.
Though some morbid conditions described in this book are peculiar to
captivity, yet it seems reasonable to assume that many of the diseases
found in captive animals occur also in the wild. Some of the extinct
races of animals may have been wiped out by disease.
Captivity causes numerous physical and mental disarrangements.
Unaccustomed, unnatural and unvaried food, change of climate and
environment, physical and mental degeneration from disuse of muscle and
brain, fear, ennui, nostalgia, lack of the exhilaration of chasing and
being chased, unsatisfied sexual feeling—all react harmfully on the
captive.
No captive animals get their natural food; and though some, like the
carnivora, may get approximately their natural food, yet they do not get
it in the natural way. They have but little variety and may miss
elements important to their well-being. They get only certain cuts—
muscle and bone; they do not get blood, guts and glands. The lion’s meat
is handed to him. He does not tear down his prey; and one result is that
the jaws of the captive-bred lion differ decidedly in shape from the
jaws of the wild-bred lion. He gets his food regularly, with awful
monotony—twelve pounds of meat at 3.30 p.m. day after day; there is no
alternation of feasts and fasts, with consequent change in the balance
of the body reserves.
Some animals, such as caribou, the moose, the black cock, the hoatzin,
the koala, do not long survive captivity, because it is impracticable to
obtain their natural food. Gastrointestinal disease is the commonest
disease of wild animals. Twenty-five per cent. of sick humans in
civilized communities also suffer from it. On the other hand, many
animals become accustomed to the new diet and thrive on it.
Animals also often thrive in a climate very different from that of their
natural habitat. Some animals from warm countries, though kept outside
without any artificial heat, get on very well during the severe weather
of Philadelphia winters, when the temperature often drops to zero
Fahrenheit. For the past two years it has been the custom to put
outdoors all monkeys—of value—that are suspected of having tuberculosis.
The cheap monkeys are killed. The outdoor monkeys are kept in fair sized
cages—five feet square and six feet high—usually singly, though
sometimes two are together. The vervet, the grivet, the leonine macaque,
the yellow baboon, the Hainan gibbon and many others, have not only
survived the climatic conditions but have not succumbed to tuberculosis.
South American monkeys do not stand cold as well as Old World monkeys,
and cannot be kept out in severe winter weather.
The monkeys that are kept indoors during winter have free access to the
outside through swinging doors and they often go out voluntarily in the
coldest weather. The same is true of other animals. A note made several
years ago (February 12, 1914) states: “Temperature last night was 1° F.
At 2 P.M. outside temperature 13° F., in carnivora house 25° F.,
elephant house 38° F., giraffe house 39° F., monkey house 42° F. Two
Bengal tigers were voluntarily outside. Monkeys that have been out all
winter are: two Barbary apes, Hainan gibbon, lion-tailed macaque, yellow
baboon, grivet monkey, pigtailed macaque, and eleven rhesus macaques.
All the animals appeared comfortable.”
The physical condition of the animal and the kind of cold—damp or dry—
have much to do with its ability to stand low temperatures. Monkeys have
passed through very severe winters without damage, and subsequently in a
less severe winter have had frozen fingers, toes or tail.
The size of the cage or pen has not as much effect upon the well-being
of the animal as might be expected. Reptiles, birds and mammals do as
well in cages and pens of medium size as in very large ones. A deer or
antelope in a large enclosure does not use all its domain. It usually
has a favorite corner near the food, water and shelter, and stays there.
Nor has a large enclosure been found perceptibly to diminish mortality
from cage-mates. The stronger will follow the weaker until he gets him,
no matter what the enclosure. Even in the large flying cage for birds it
is necessary to keep out those of a scrappy disposition. From the point
of view of the public small enclosures are more satisfactory.
Mental disease in captive animals offers a fascinating field for study—
now chiefly speculative. Many conditions are present to produce it—all
the conditions that cause prison psychoses in man. And many if not all
the insane and perverted acts of animals have their counterpart in the
human. Masturbation is very common in mammals. Eating of their own
feces, coprophagy, is not infrequent, and is especially notable in one
of the highest types—the Chimpanzee. Perhaps occasionally coprophagy may
be due to some defect in diet. There is no instinctive disgust at
excrement in the lower animals any more than there is in the uneducated
child. Nevertheless, eating feces cannot be healthful, and probably does
not occur in nature; and occurs only in the human with mental disease.
Some of the insane acts of animals if prevalent in the wild would
probably cause the extinction of the race. Such are killing of the young
by the father and by the mother; killing of the female by the male,
usually during rutting time, in some instances reminding one of Sadism
in man. This kind of sexual killing does not often occur in the wild.
The female has a better chance to escape, and the male probably does not
feel so inclined to damage her when he chooses her himself as when she
is chosen for him by his gaoler. When the mother devours her young it is
usually shortly after birth. I have, however, the record of a Jungle cat
(_Felis chaus_) who ate two of her kittens when they were seven weeks
old. Some of the domestic animals devour their young; the sow often does
it, and occasionally the bitch.
Sucking, gnawing and eating parts of itself or of a cage-mate is not
uncommon in a variety of animals. Bears lick their paws until they are
sore; a monkey may gradually gnaw away its tail from the tip to the
body; an ocelot (_Felis chibigonazon_) bit open his scrotum and devoured
his testicle; a Tasmanian devil (_Sarcophilus ursinus_) bit off one of
his front feet at the wrist; a monkey may gradually gnaw away its
fingers; and numerous other self-inflicted mutilations occur. Often
there is a local irritating cause, as skin disease, lice, or freezing.
But in many cases no local cause can be found, as no local cause can be
found for thumb-sucking or nail-biting in the human.
The surgery done by monkeys on their frozen fingers and toes is
interesting. After the flesh has sloughed the monkey bites off the
protruding phalanges, apparently without pain, so that satisfactory
well-covered stumps are made.
Animals often mutilate their cage-mates in an amicable way as
distinguished from fighting. A bear may lick its mate’s ears until the
hair and skin are gone. A monkey may eat its mate’s tail or patches of
its skin, the victim lying placidly while the process goes on. Many
animals are addicted to perverted acts on their own or their mate’s
sexual organs.
It is probable that the phenomena just mentioned are due to confinement,
idleness and ennui, and that they do not often happen in nature where an
animal is kept busy seeking his food, fighting and avoiding his enemies,
attending to his mate or mates, and meeting the various vicissitudes of
his environment.
It should be remembered, however, that the members of a wild species
vary in intelligence and temperament, as humans do. There are morons and
perverts among animals in the wild; but not being coddled by the normal
members of the species, they have a poorer chance than has the subnormal
human of surviving and of transmitting their peculiarities.
Fear, ennui, loneliness and nostalgia, by affecting the minds of captive
animals, react on their physical condition. Some animals have the fear
of man bred in them. The young often show it from time of birth. This is
especially common in animals that have survived for generations in
proximity to man. It is one reason for their survival. The mother and
father may have become tame and gentle in captivity and yet the young
one may be a wild thing from birth. Such fear is sometimes
uncontrollable, an apparently slight cause making the animal dash itself
against the fence of the enclosure. It is not mere speculation to
discuss the physical effects of the emotions on the animal body. It has
been shown that fear, anger, and grief bring about distinct measurable
physical changes. Dr. Corson-White has found that the red corpuscles are
increased by over two million per cubic centimetre in the blood of a cat
frightened by a dog barking at it. The amount of blood sugar is also
increased.
Such observations are suggestive in a consideration of the changes that
may occur in a captive animal subjected to acute and chronic fear.
The monotony of a captive animal’s life is broken only by feeding, the
sight and sounds of others in the same building or nearby, and by
visitors. Many animals show their appreciation and pleasure when
visitors approach, and some of the more intelligent animals, bears and
monkeys and some birds, “show off” apparently to keep the visitors
there. When there is nothing doing, some stand swaying their heads, like
a weaving horse, or pacing the cage, inanely tagging at each turn the
side of the cage with the head or other part of the body—often so
persistently that a sore is produced. Nearly all animals are social and
suffer from loneliness when kept by themselves. This is true even of the
lowly forms. The keeper of the reptile house reported that a giant
tortoise became despondent and refused to eat when his companion, a
leopard tortoise, was taken from him, and that he braced up as soon as
the leopard tortoise was returned. It is not necessary that the
companion be of the same species, or even of the same family. A lion or
a tiger may be satisfied with a little dog for a companion, and there
was an African rhinoceros at the Philadelphia Garden that was very
discontented and unhappy when alone and became perfectly satisfied when
she was given a domestic goat as a cage-mate; and the huge rhinoceros
stood for a good deal of butting and bullying from the goat without
retaliating. A sympathetic keeper may do much to relieve the loneliness
of the animals in his care.
Nostalgia, or homesickness, has been felt by all men. Some have died of
it. The tradition among writers is that it affects young people and
those who have been living nearest to a state of nature. In this country
the American Indian and the negro are affected more than the whites.
Much was written of it after the Franco-Prussian War and the American
Civil War. It is a real condition, capable in extreme cases of causing
death and of so weakening the sufferer as to make him more susceptible
to the invasion of other diseases. At the present day we hear less of it
among civilized people than formerly, perhaps because the conception of
home has been broadened by modern methods of intercommunication. The
wild animal’s conception of home is narrow; he comes directly from it
into an environment where he may see many other animals, but not one of
his own kind. Predisposing causes of nostalgia are stronger with him
than with the human. That home means a great deal to animals is shown by
the migration of birds—the return of the carrier pigeon, and of the lost
dog, and of the swallow, which returns every year to the same nesting
place.
All animals long for the things of nature—open air, earth, grass and
water. They are thrilled when their feet touch the sod. Even the
hippopotamus gambols when he leaves his concrete house and his feet
touch earth and grass.
The face and carriage of many animals cannot express feelings as in the
human, though it is not unreasonable to assume that animals may indicate
feelings by expression understood by their mates, though not understood
or even noticed by man. When they can express it in a human way their
feelings may be read. The dejection of nostalgia is especially shown by
anthropoid apes. Gorillas have been noted for it from the earliest
writers. The orang is prone to it, shows it by his attitude and
expression, and sometimes dies of it.
It is stated in _A Handbook of the Management of Animals in Captivity in
Lower Bengal_, p. 130, that elephants have been observed to shed tears
abundantly if forced to leave their old home and surroundings. How much
other animals who cannot express homesickness may feel it, and how often
it is a cause of unhappiness, depression and predisposition to disease,
it is impossible to say.
Most wild animals in captivity are sterile. The reason is not known. It
shows the profound effect of captivity. It would be difficult to
determine whether the sterility of a mating is the fault of the male or
the female.
There is no apparent rule for sterility. Some families are always
sterile in captivity, others are fertile, even with very unfavorable
surroundings. The deer, horses, hippopotamuses, pigs, goats, sheep and
oxen, are good breeders; while antelopes, rhinoceroses, giraffes,
elephants, are poor breeders. Some members of a family may be good,
others poor. The lion and puma breed fairly well; the tiger, leopard and
jaguar, very poorly. Bears breed well, but the mother usually destroys
her young.
We cannot mate wild animals and birds simply by putting males and
females together in the same cage. Domestic mammals and birds usually
mate under such conditions, but wild ones often refuse. Many mammals and
probably all birds that are not polyandrous or polygamous reserve the
right to select their mates, and if the sexes are put together by man
they may view each other with indifference or with animosity. There are
many males and females of the same species of mammals at the Zoological
Garden that will not consent to live together. A male monkey in a cage
with several females will very often select one female for his mate and
will have nothing to do with the others.
Among monkeys fertility varies greatly. It is not practical to determine
the ratio among the various kinds, as some kinds are much commoner in
zoological collections than others. I think that in general the Old
World monkeys (_Cercopithecidæ_) are better breeders in captivity than
those of the New World (_Cebidæ_). The anthropoid apes are very poor
breeders indeed; of the many gibbons, orangs, and chimpanzees, that for
years have been captive in Europe and America, it is probable that only
the chimpanzee has bred, and that very rarely.
Refusal to mate, sterility, infanticide by father and mother, and sexual
killing keep down reproduction in zoological gardens; and the number of
young ones is a good indication of the character of a garden and of the
provisions made for the happiness, comfort and health of the animals.
With the birds in a zoological garden the conditions for nesting and
laying are not good. Caged birds have no material for a nest, no privacy
and rarely lay an egg. The outdoor water birds and the outdoor upland
birds with natural surroundings, with secluded retreats, lay and hatch
very well. Birds like mammals apparently are indifferent to publicity
when copulating, but seek seclusion for laying and nesting—from maternal
fear for the safety of the young.
The sexual instinct in indoor caged birds in a zoological garden is
dormant. Very few copulate and very few lay eggs; pigeons and Mexican
conures (_Conurus holochlorus_) are exceptions to this general rule.
Probably because the sexual instinct is dormant the males never fight
over the females among perching birds, and very rarely kill each other.
In some species of finches, however, as the chestnut-eared (_gn.
Amadina_), the females fight among themselves if there are not enough
males.
Ovoviviparous reptiles breed more often in captivity than one would
expect; and egg-laying snakes often lay eggs, which of course are only
hatched artificially.
Birds suffer less than mammals from the psychological effect of
captivity. The mental development of a bird is much lower. With few
exceptions, like the ruffed grouse, the bird accepts captivity easily
and becomes tame, though he will not stand being touched. He views his
keeper and visitors with indifference or friendliness. If a bird house
is bright, cheerful and sunny, all the inmates thrive and appear to be
happy. These conditions undoubtedly affect the health of the bird, as is
evidenced by their plumage; bright colors that are lost in a dark and
gloomy house are retained and developed when the house is cheerful and
sunny. There are some birds, however, that never retain their colors in
the captivity of a zoological garden. Among them are the scarlet ibis,
the American flamingo, and the roseate spoonbill. It has been suggested
that the loss of color is due to the lack of something in the diet,
mineral or organic, that the bird gets in its natural habitat. Tame
scarlet ibises living with the chickens about the dwellings of natives
in Venezuela retain their brilliant color. The material of the beautiful
red color on the under surface of the wings of the touracou contains
copper, yet these birds retain this color very well in captivity, even
after several moultings.
The source of the copper has long been uncertain. In nature the birds
are fruiteaters, and their diet in captivity consists of bone meal,
zweibach, corn meal, white potatoes, eggs and carrots—foods that are
usually assumed to contain no copper; and no copper utensils are used in
the preparation of the food. Dr. John Marshall, however, writes me that
all the common cereals contain minute quantities of copper; and Dr. Leon
A. Ryan, _University of Pennsylvania Medical Bulletin_, June, 1907,
states that copper may be found in animal tissues. Dr. E. P. Corson-
White has found traces of copper in the bone meal used at the
Philadelphia Zoological Garden. The copper in the red color of the
touracou’s wing therefore comes from the food.
It is probable that a bright and cheerful bird house does not influence
the color of birds by the direct action of light on the color as much as
indirectly by improving the health and spirits of the birds. Coloration
in birds is a very complicated proposition. It depends upon age, sex,
season, health, light, heat, moisture, mode of life, and food. No one
bird house can combine all the conditions necessary for the retention of
natural colors in every species. The desert species from a habitat of
intense light and dryness require for their color a different
environment from the forest species, from a habitat of shade and
moisture. The suppression of sexual feeling in captive birds may
influence color. In nature the finest colors are attained by mating
birds.
It may be said that all animals—except those of nocturnal habit—have a
feeling of joy and well-being in fine weather and bright surroundings
that reacts favorably on the general health.
The variability of the breeding period induced by captivity in many
animals may be mentioned with sterility. It was shown some years ago in
the Philadelphia Garden by the European brown bear which in one year
gave birth on January 16th, and in the following year on July 25th. It
is another evidence of the profound effect of captivity on the captive
animal. I know of no observations of the effect of captivity on the
period of gestation.
There is considerable mortality among captive animals from killing of
cage-mates. I do not refer to sexual killing, already mentioned, or to
fights over a female. Often males, with no females near, cannot be kept
together; probably sexual jealousy is at the bottom of it. Antelope and
deer are especially inclined to scrap. Even a large enclosure will not
save the weaker male; the stronger follows him with horrible
persistency, sometimes for days, around and around the enclosure, often
at a walk, but always on the offensive, at least during the day; until,
careless from weariness, the weaker is caught unawares and finished by a
horn-thrust in the side.
Both birds and mammals often kill their mates when the mate is sick, or
“down” from injury or disease. All animals hate sickness and death, and
show their dislike by attacking or shunning it. Birds may get on happily
together for months until one becomes sick, and as he crouches in a
corner with ruffled feathers the others pick on him and finish him. The
same is true of mammals, the sick one being horned or tramped to death
by the mate with whom he had formerly been on most friendly terms. The
keeper often reports an animal “killed by its mate,” whereas the mate
has only given the _coup de grace_.
This brutality is not universal. Rarely a parrakeet will stand guard
over his sick and dying mate; and we have seen a ratel—of a ferocious
family—stand guard over and resist the removal of his sick companion.
The diagnosis of disease in wild animals is unsatisfactory; usually
impossible; clinical study as we know it in the human is impossible. We
know that the animal is sick, but not why. A certain group of symptoms
accompanies all diseases—dull, rough coat or feathers, refusal to eat,
weakness in the hind quarters, and finally getting down. They rarely
show symptoms of pain—or at least we cannot read the symptoms. The pain
of acute pancreatitis in man is violent, yet many animals die with it
and we cannot tell that they suffer. Animals do not suffer as much as
the human, and they stand the ravages of disease better than the human.
At autopsy we often wonder how the animal could have lived with the
conditions that are found. A monkey may be apparently well until a few
days before his death, though his lungs and abdominal organs may be a
mass of tubercle. A small red howler monkey (_Alonata seniculus_) was in
apparent good health, playful and lively until twenty-four hours before
his death from acute pancreatitis, though his stomach and intestines
contained fifty-one nematode worms, some of which were eight inches in
length.
As diagnosis is unsatisfactory, so is treatment. Usually all we can do
is to treat symptoms; and by the time disease has advanced to the point
of becoming externally noticeable, it has usually gone beyond the reach
of medical treatment. It must also be remembered that drugs vary very
much in their action in different families of animals. Nux vomica will
not kill the gallinaceous birds of North America, and Tenant says that
in Ceylon the hornbill feeds on the fruit of strychnos nux vomica. The
pigeon is immune to opium. The _Felidæ_ are said to be unusually
susceptible to carbolic acid; veratrum viride is harmless to sheep and
elk, but poisonous to the horse; dogs can take with impunity large
quantities of cyanide of potassium. These statements are true when the
drugs are administered by mouth—the usual way of giving them to wild
animals. The action may be different if the drugs are administered
intravenously or subcutaneously. Variations in effect when they are
administered by mouth are often due to chemical variations in the
digestive secretions. It is probable that the action of cyanide of
potash on dogs depends on the amount of hydrochloric acid in the
digestive tract.
When worms or their eggs are found in the stools vermifuges are used,
and with some animals especially liable to infestation by intestinal
worms, periodic doses of vermifuges are given as a prophylactic.
Turpentine is given to the zebra at fixed intervals for the round worm;
santonin, male fern and areca nut to the carnivora for the various worms
that are so common in the intestinal tracts of these animals.
The work of the Laboratory of Pathology is throwing light on the subject
of diagnosis, and though from the character of the clinical material
diagnosis can never be as satisfactory as in the human, yet we may
fairly hope for improvement. Prophylaxis is our chief reliance, and
always will be.
DISEASE IN CAPTIVE WILD
MAMMALS AND BIRDS
SECTION I
INTRODUCTION
“We have also parks and enclosures of all sorts, of beasts and birds;
which we use not only for view and rareness, but likewise for
dissections and trials, that thereby we may take light what may be
wrought upon the body of man.”
The purpose of a menagerie under the auspices of a zoological society
can scarcely be put into better words than those found in this quotation
from Sir Francis Bacon’s _New Atlantis_. Apt as this description of the
mythical island’s collection may be, it is but a reflection of the
teachings of Plato’s original legend of a perfected community, and the
practical applications of these teachings by Aristotle in his _Anatomy
and Physiology of Animals_. The history of human study shows a constant
investigation of lower forms of life, ever broadening in its scope, ever
more satisfying in its explanation of biologic problems and ever
increasing in value from an economic standpoint.
If, however, all animals are to be subjected to “dissections and trials”
there inevitably will come under observation many specimens presenting
variations from the accepted mean or standard or even from an average
for their kind and therefore approaching what may be called
pathological.
The desire to explain the abnormal has had the effect, during the half
century since Virchow defined cellular pathology and Darwin systematized
the world’s knowledge of comparative biology, of directing attention to
comparative pathology and of stimulating the study of veterinary
medicine. Moreover in the past twenty-five years much work has been done
and many isolated publications have appeared upon the diseases of wild
animals, notably Bland-Sutton’s work, _Evolution and Disease_ (1895), a
thoroughly scientific and most charmingly written book, but rather
elementary in its approach of the subject of pathology, and Wood
Hutchinson’s _Diseases of Animals_, a more or less popularly presented
treatise. I am unaware, however, of any systematic monograph upon the
subject wherein we may find data showing the character of pathology in
the various animal groups or the incidence of the various lesions. The
reports of some zoological gardens contain the result of medical and
pathological data collected for the report period. The publication of
greatest merit and value is that from the Zoological Society of London,
whose huge collection studied by a large official personnel makes it
possible to present valuable data. The New York Zoological Park uses its
material in a similar manner and has been able to explain some of the
knotty problems so frequently met in wild animal collections.
Here at Philadelphia it has been our practice now for twenty years to
perform an autopsy upon every mammal and bird that dies, and upon all of
the large or important reptiles. There is no aquarium connected with the
Garden. The office of the society keeps a record of the arrival and a
general description of every animal so that a brief history of the
specimen is usually available. The keepers are required to observe their
charges regularly and closely and to report any abnormalities to the
officials of the Garden. Somewhat detailed discussions upon signs of
sickness will be given at appropriate places, where also a few remarks
upon treatment will be included, but as this work is not intended to be
a treatise on therapy and since this subject does not differ from that
referable to domesticated animals, little space will be devoted thereto.
Upon death a complete autopsy is performed and the findings are recorded
upon a printed form from which, when the histological, bacteriological
and parasitological studies have been completed, a set of cross index
catalogue cards are typed; these are divided into the principal
diagnoses and determinations. The report of the Zoological Society,
appearing at the end of their fiscal year, February 28th, contains a
résumé of the observations for the year, together with notes of
interesting cases and experimental work.
There have accumulated the records of nearly six thousand autopsies and
upon them as a basis has been founded the following report of the
incidence and nature of pathological manifestations in the various
animal groups, using also as additional data, published reports from
other gardens. The book might be described as a collection of our
studies, parts of which have appeared as separate articles, but most of
which are entirely new, put together with as much connection as the
subject matter will permit. The zoological and pathological literature
has been consulted very extensively, but except for the reports of
zoological societies and the publications of special students, it
usually represents isolated notes by travellers and veterinarians so
that many articles may have been overlooked. Therefore no claim of
perfect completeness of reference is made, the statements resting
chiefly upon our own records. The subject will be approached from the
standpoint of description and incidence, but it is inevitable that
comparisons and contrasts must be noted.
Into the realm of evolution[1] I shall not venture because I appreciate
a lack of adequate preparation for such an attempt, and because, even if
such were not the case, the material at hand is lacking in data upon
fishes, many kinds of reptiles and invertebrates.
A direct and practicable application of these data will be in the
direction of explaining some of the pathological states in domestic
animals and man. There are indeed many disease entities or syndromes in
these groups for which no useful hypothesis has been advanced, while for
others a partial explanation has been offered, usually, however,
inadequate wherewith to form the basis of rational prevention or
therapy. Thus, for example, essential emphysema seems to be limited to
the animals of civilization; on the other hand, the anatomical basis of
exophthalmic goitre may be seen throughout nearly the whole animal
kingdom yet the clinical phenomena belong characteristically to man, and
are occasionally seen atypically in the dog. While it may be impossible
to give a complete comparative anatomy and physiology for each of the
pathological states, the attempt will be made to treat all subjects
analogically through the zoological orders.
The experimental pathologist may find the records of the Garden useful
in his work. For example, he can know that rodents are not prominent
among the orders showing spontaneous arteriosclerosis, but that
nephritis occurs among them in about a quarter of natural deaths; or he
may learn that the Primates have a good cardiac reserve while the
Marsupialia have not. Too often experimental work is not based upon
facts including natural probabilities.
A collection of pathological data such as is presented in the following
pages may be of assistance to veterinarians and managers of zoological
gardens in the diagnosis of sickness in animals, both wild and
domesticated. We do not presume to offer a system of veterinary
medicine, but it is possible to introduce certain objective findings of
practical hygienic and therapeutic value. Such observations are,
however, limited and in our experience at the Philadelphia Garden the
diagnosis of disease in a wild animal, excepting of course those which
are perfectly self-evident, is more often speculation and conjecture
than at all well grounded. It is not uncommon for animals to come to
autopsy presenting a perfect galaxy of abnormalities, yet the closest
antemortem observation failed to reveal unusual conduct or appearance.
On the other hand specimens are frequently opened whose organs fail to
contain any lesions discoverable even by careful study. Dr. Henry
Chapman, sometime prosector to the Society, once made a remark in this
connection—“Why do they die or how can they live so long.” Space is
given to this phase of the observation of wild animals in order to
emphasize the difficulties of interpreting their conditions, but of
course it should be understood that certain data of value may be gained
by close attention to the details of their normal behavior and to
changes which occur indicating that something is wrong.
The naturalist and the trained animal keeper are, in our opinion, better
judges of a wild animal’s condition than is the veterinarian, unless he
be at the same time a zoologist and have long experience with a
menagerie. My own observation of dogs and horses leads me to think that
more acumen is needed to interpret the actions of wild animals since
they seem to have greater natural reserve, and of course in regard to
them there are many more variables since we see fewer specimens of each
species than we know familiarly among domestic varieties. The principal
objects for observation are, as in veterinary medicine, the eyes, the
hair and skin, the mucous surfaces, the droppings, the condition of the
abdomen, the appetite and the desire for water. Physical examination is
limited to tractable beasts and those which can be caught and handled
without danger to the personnel or unusual fright and damage to
themselves. In the interpretations of physical signs in tractable
animals, such as many ungulates and some monkeys, the experience of the
trained veterinarian is of the greatest value, but this fails amongst
carnivores and birds. It might be said that anesthetics could be used
for a thorough examination, but this would be undesirable for a
seriously sick animal and it is, in our experience, none too safe a
procedure although often perfectly practicable. Animals do not like to
be molested much as they may seem to enjoy attention, and when it is
possible it is our practice to avoid handling them.
It might be contended that observations upon diseased states in captive
animals would not represent natural developments, in other words, not
that which occurs in the wild. Such indeed may be true in regard to the
infectious diseases, but since we are imperfectly informed as to the
pathology of the wild state, we are obliged to accept and use the best
substitute at hand. Moreover it seems perfectly fair to consider as
characteristic for an animal or group, the physical and even
physiological expressions of morbid agencies as we know them, even
though the animals be at the time under conditions not natural to them.
It would be perhaps incorrect to say that cirrhosis of the liver occurs
in .6 per cent. of animals in the wild as is the case for our autopsies,
since incorrect food and infections are potent in its causation; on the
other hand, our experience and some few data from naturalists and
pathologists make it conceivable that tumors occur to this number in
native states. The incidence of tumors in wild rodents is quite well
known. Degenerations and fibroses, the result of parasitism, are known
to exist throughout the entire animal kingdom. Further to illustrate how
pathology is distributed in wild life, Plimmer’s experience[2] with 500
rats (_M. decumanus_) might be cited. He found the following: Tubercle 3
times, tape worm cysts 10, Tryp. lewisi 49, empyema 2, tumor of jaw from
old injury 1, pleuritis and hydrothorax 1. Bacteria were found in 71
rats, 40 times in the lungs, 31 times in the spleen; saccharomyces were
found 16 times in the lungs. Dr. W. L. Abbott reports to us personally
that he has repeatedly found coiled exproventricular worms in the wild
specimens he has collected. Not only are we informed of some isolated
and individual pathological states but the existence of epizoötics of
communicable disease among wild life is well authenticated. The simple
citation of the extermination of deer in one section of Colorado by
pleuropneumonia will suffice to illustrate this point. Other examples
are, however, interesting. The occurrence of changes in the jaw bone
almost certainly those of actinomycosis is reported by Blair, the
specimens being shot in the wild and believed never to have been near
civilization. The white-tailed deer of the Swan River Valley in Montana,
are known to be constant carriers of liver-flukes.
It would seem therefore that it is not unfair to use material gathered
from animals under somewhat unnatural conditions as representing the
reaction of the zoological orders to pathogenic agencies. Such
conclusions must however be made very guardedly, for it is probable that
not over ten per cent. of the total number of mammalian and avian
species are to be observed in captivity. Because of the number of orders
and the great variety of genera included in the present study it is
probable nevertheless that the lesions are fairly representative of the
whole animal kingdom.
However, the numbers and percentages given should be read to indicate
the probabilities and should not be interpreted as implying the
mortality relationships since different varieties have differing powers
of resistance to the same pathological state. The margin of safety in
any given group for one or several different disease entities cannot at
present be stated with any degree of precision but this factor is
doubtless very great. The work of physiologists suggests that there is a
reserve power in the human lung sufficient to sustain life until five-
sixths of the functionating organ is useless, and I shall quote a case
of an opossum wherein only one-tenth of the respirable surface seemed to
have remained; we have repeatedly seen both lungs of a monkey apparently
entirely solid. Such physical vital incompatibilities might be
exemplified by many other cases, but when one reviews the physiological
margin of safety, inexplicable and contradictory instances are equally
numerous. I have seen a male deer run a doe against the fence and butt
her, without result, whereas in an apparently similar occurrence the
animal would be dead in a short time. Numerous instances of slight
enteritis of a short stretch of duodenum or ileum have killed, with
almost nothing to be found microscopically, and on many occasions we
have been chagrined in being unable to discover the cause of death. The
capacity of self-healing is a variable one, but seems in direct
proportion to the quietness and seclusion possible for the animal and
inversely to the chance of bacterial infection.
The effect of captivity has been the subject of much speculation. For
the preservation of health it would seem that animals require periods of
rest and activity, thorough elimination, possibly a moderate exercise of
their procreative functions, but most of all, appropriate food obtained
by the physical effort we term chase. All but the very last condition is
supplied in a measure in well managed collections. The degenerating
effect of the absence of chase must be admitted. An interesting and
suggestive example of this was noted by Mr. Jones at the London
Zoological Gardens. He observed the skull of a lion that had been in
captivity thirteen years, in which the canine area of the face and the
part of the skull acting as the insertion for the seizing and holding
muscles had undergone atrophy while the chewing muscles with their bony
bases had remained normal. Numerous examples of disease atrophy are on
record and those of a physical nature must have counterparts in the
realm of physiology. The size to which an animal will attain cannot be
estimated by the examples seen in menageries. Judging by the accounts of
collectors and hunters and upon the more reliable of the moving picture
displays of wild animals in their native haunts, it would seem probable
that under normal conditions of habitat the average size of wild beasts
is considerably in excess of that in park specimens.
The effect of captivity may also be felt in the direction of reduced
resistance to infectious diseases. Brooks, of the New York Park,
expresses the view that captivity increases susceptibility to bacteria
and causes parenchymatous degenerations. In the latter direction it is
interesting to learn that Seligman of London claims to have seen sudden
deaths in wading and struthious birds from myocardial disease, without
valvular or other lesions, for which he holds the enervating effects of
captivity responsible. It is well recognized that a species may be
unusually susceptible to a disease that it has not encountered in its
phylogenic development. Man illustrates this peculiarity very clearly.
Europeans were found exceedingly susceptible to sleeping sickness when
they went first to the part of Africa inhabited by the tsetse fly, and
the American Indians died in hordes when they met the tubercle bacillus
for the first time. Judging by the ravages of tuberculosis in captive
monkeys a similar susceptibility probably explains the matter for there
are no entirely satisfactory records of this disease among them in the
wild state.
In so far as general susceptibility to infection is concerned, it may be
in part due to one of the artificial conditions of captivity, that of
inbreeding. This influence is undoubtedly very great, both by chance in
families, and by intention on the part of dealers as well as the mating
which occurs in menageries. However, it is not known how far inbreeding
may go in the wild state so that one must be very careful about drawing
conclusions in this particular. Several years ago, at the time we
reported the neoplasms found at the Garden, discussion arose as to the
effect of inbreeding, and thereafter some observations were made in this
direction. With the exception of the hyperplasias of the thyroid, not
certainly of neoplastic nature, in a much mixed-up family of wolves, we
could find no evidence that inbreeding was responsible for tumors.
Plimmer and Murray of London, seem to imply that some of their inbred
animals are likely to have tumors; reference to this matter will be made
later in this book. In so far as diseases of the organic systems are
concerning those of the bones seem to be the only ones in which
inbreeding is significant.
The individual resistance will be reduced of course by the unsanitary
surroundings incident to trapping, shipping and storage, but this need
not affect the figures or pathological tendencies of classes or orders.
The effect of captivity is felt in another way. A very large percentage
of wild life perishes during the first weeks or months after its
capture, and in gardens the heaviest mortality occurs among the recent
arrivals. The London Garden figures that from thirty-three per cent. to
fifty per cent. of their total mortality is in animals that have not
been in the garden six months and that die because they are not yet
accustomed to their new surroundings. It seems to us, both from an
academic and a practical standpoint, that this is a long time and should
afford ample opportunity for the garden to study the specimen and for
the specimen to become acclimated. These early deaths are perhaps to be
ascribed in large part to failure of acclimatization but many are
doubtless the result of infection acquired in the wild, in transit while
in the hold of vessels, at quarantine, or in trains, or at the
establishments of dealers. We have seen a few deaths which have followed
behavior that might be likened to homesickness. Perhaps the age at
arrival has an influence upon the morbidity and mortality of wild
animals, for it is easily conceivable that the young and the very old
might adapt themselves to new surroundings with much less readiness than
the sturdy middle-aged adult. The age of animals upon arrival is very
rarely known, and can only be recorded as “young,” “fully developed,”
and “old.” This will have an effect upon statistics and when possible is
noted in the text, but this is not practicable to the extent we desire.
The meaning of “young,” “adult,” and “old” is not the same throughout
the animal orders nor even within orders.
Mitchell[3] has attempted to gain concrete ideas of the expectancy of
life among animals by analyzing the records of the London Gardens. This
gentleman bases his figures upon known ages and the length of time in
captivity, from a combination of which data the specific viability and
the potential longevity may be estimated. Such results, he admits, can
only be approximate and they show within classes and orders, a decided
lack of uniformity. The terms “specific” and “potential” longevity,
coined by Sir Ray Lankester, apply, for the first, to the average length
of life as it is affected by external conditions and those incident to
procreation, while, if an animal be under ideal conditions it will
attain the potential longevity which is longer than the former. These
considerations have a biological and economic importance, while a
knowledge of the pathology shown by the various groups may help to
explain these durations of life. Contrariwise figures of the expected
longevity may assist us in evaluating youth and senility in the causes
of death but can hardly affect the comparative nature of the lesion.
A résumé of Mitchell’s studies indicates that the higher apes have a
potential longevity and a hardihood much less than man but still upwards
of thirty years. As one investigates lower in monkeys, life periods
become shorter, while in the next order, Lemures, the length of life
rises. Carnivora have a reasonably good vitality, their potential
periods varying from ten years in the foxes to thirty-three years in
bears. Insect eating animals are short lived, three years being a
maximum. The Bat family shows great variations, the greatest life being
not over seventeen years. The Rodentia have long lives compared to their
sizes—twenty years in porcupines, fifteen years in squirrels, thirteen
in marmots, nine in agoutis and capybaras, and three in dormice (which
is also about the maximum for the rat). Hyraces live four years on the
average. Proboscidea, although reputed to live to great age, probably
rarely live a half century and may be said to have an expectancy of
twenty to thirty years. Perissodactyla (horses, tapirs and rhinoceroses)
while they may live half a century, have an average life of between
fifteen and thirty years. The closely related Artiodactyla fall into two
groups, a first comprising antelopes, sheep, goats and deer which rarely
exceed seventeen years, and a second consisting of cattle, camels and
giraffes, which vary in expectancy from eighteen to thirty years. The
smaller members of the Ungulata have in relation to size a relatively
greater viability, the ruminants, however, having on the whole a low
viability. Marsupials vary from a maximum of seven years in the opossum
to eighteen in the wombats, but none of this group has a good viability.
The Aves as a class or if compared according to dietary requirements,
have longer potential ages and better viability than mammals. Passerine
birds average twenty years and many live to sixty, while the Picariæ
approach the former figure but do not have such good viability. Psittaci
and Striges may live a half century but the resistance of the latter is
much reduced by any unfavorable surroundings. The raptatory birds live
fifty years, but their viability is variable. Herodiones have a maximum
expectancy of thirty years and good resistance, while their relatives,
Steganopodes, may live fifty years, and Odontoglossæ have a good
viability, up to twenty years. Anserine birds may live to be fifty, and,
unless conditions are quite unfavorable, have a good resistance. Columbæ
may under good conditions live to be fifty. Gallinaceous birds may only
be expected to survive twenty years, a figure also given for Fulicariæ.
Alectorides may live up to fifty years. Limicolæ, though they do not
thrive in captivity, may live thirty years. Impennes live poorly under
artificial conditions, the greatest record being twelve years, a figure
also holding for Crypturi. Struthiones, if the conditions be right, may
live fifty years.
Because of the variable specific longevities, it is frequently difficult
to decide when an animal is senile. Man is said to be as old as his
arteries, and his span of life nowadays is in the neighborhood of half a
century. Parrots exhibit lesions of the vascular system comparable to
the arteriocapillary fibrosis of human beings, and their expected
longevity is about the same or a little greater. From a study of our
cases of this lesion in parrots it can be said to appear quite early in
life and not to lead to organic disease as it is alleged to do in man.
It is, however, interesting to note that in those animals which are
supposed to have the longest specific lives—elephants, snakes, anserine
and raptatory birds, parrots—there is relatively low mortality and fewer
infectious diseases are encountered. The last part of this statement
should be qualified by stating that anserine birds and parrots are quite
susceptible to mycoses, in all probability from musty food, which raises
their death rate, but as this is accidental and artificial, it can be
excluded from consideration.
In a rough way there is a direct relationship between the size of an
animal and its longevity, but this is not close enough to be a reliable
guide; whales and elephants live a long time, but so do snakes and
parrots. Within orders this relation of size and expected longevity is
more easily seen but is not absolute. I cannot state, according to my
present studies, that there is an unqualified relationship between the
size and expected longevity of an animal and its pathological lesions.
The immediate surroundings and the management of captive animals have a
very direct and important bearing upon the mortality and perhaps upon
the incidence of morbid processes but probably not upon the character of
the latter. A full knowledge on the part of the personnel of a
zoological society concerning the habits and habitat of every animal in
their keeping is essential, to which must be added a group of interested
keepers. In engaging the last, it should not be forgotten that certain
men have “a way” with animals and that others cannot manage themselves.
The enormous literature at the disposal of the naturalists permits
executive officers to formulate a plan of housing and feeding with fair
accuracy for each kind of animal, but of course it is rarely possible to
obtain in sufficient quantity the natural food (_e.g._, ants for
anteaters). In so far as food is concerned it seems that with a few
exceptions like the one just mentioned, the substitutions made at the
zoological gardens are nearly satisfactory. The elements in which the
captive diet is poor are the inorganic salts and vitamins since Dr.
Corson-White, some of whose work is included in a later chapter, has
shown that for those animals which our statistics indicate as most prone
to have rickets and osteomalacia, the available phosphorus and calcium
are low, and one vitamin was also below the desired quantity. In this
regard, however, I am not at all convinced that diet alone will suffice
to explain these degenerative osseous diseases; I shall take this up
more fully later. Careful inspection of all food should be made and
cleanliness (sifting of cereals, protection of meat from flies, etc.),
is indispensable. The mortality among our carnivora has materially
decreased since the horse meat after butchering was placed in covered
galvanized iron pans. There are many problems of feeding, too numerous
to be covered in a survey of this sort, which must be solved, and it is
a credit to superintendents that this they have studied carefully.
There are two problems in the management of animals upon which much
difference of opinion exists, namely the heating of houses and the
material of which cages are made. It seems to be the practice in many
gardens to keep animals very warm. Dr. Chalmers Mitchell states
unqualifiedly that adult animals do not have to be kept warm, and that
even an equable temperature is not demanded, variations in temperature
having a distinctly stimulating effect. However he maintains that they
should be kept dry and must be supplied with a shelter. This is in
accord with the experience at the Philadelphia Garden, since for many
years we have allowed access to the open air all winter to every animal
that could stand it. A large group of macaques has now lived entirely in
an open “band stand” cage for nine years with a lower mortality than in
the rest of the monkey collection, which is permitted to go indoors some
of the time. Occasionally one in poor health is frozen to death, and
healthy ones may lose fingers, toes, or a part of the tail, but the
general condition is so much improved that they present an attractive
exhibit to visitors. Unless a storm be of great severity, wild animals
are usually indifferent to it although they may seek their shelter. Snow
apparently is no source of fear to them, and many enjoy playing in it.
The general principles of the enclosure should be proper lighting, free
access of air, dryness and shelter in time of storm, the last so
arranged that the sleeping place is well protected. Appropriate
arrangements should be made for nocturnal animals, regardless of their
visibility to visitors, if their preservation is of importance.
The hygiene of communicable disease has influenced everyone to use
concrete and metal for cages. These substances are without doubt most
simply kept clean, but they are heat-conducting and remain cold or damp
longer than wood or the ground. It may be claimed that the latter two
cannot be disinfected so well, but this need not militate against their
use. Wood can be disinfected by sunlight or by mechanical cleaning plus
disinfectants, by a blast lamp and by paint. The ground will disinfect
itself if allowed to lie fallow for a time, or it may be turned over
after sprinkling with lime. It is fair to note that the New York
Zoological Garden reduced their mortality, especially from verminous
pneumonia, by changing some deer herds to concrete paved enclosures; if
that were the only change made the result would be very significant, but
it should not be forgotten that another clean ground range might have
served as well to a herd from which the infected ones had died. My own
observations with guinea-pigs, rabbits, mice and dogs lead me to believe
that they thrive and breed better on wooden floors than on metal or
stone.
I have tried to work out figures to show that more animals die when
housed in enclosures of stone and metal than when upon the earth or on
wood, but the attempt has been unsuccessful chiefly because of the
presence of epidemics and parasites, principally among the birds. The
attempt was further embarrassed because some members of an order are
housed on both floorings. However, there was no great advantage for the
metal and concrete floors even after the epidemic had been discounted.
This Garden does not have a great number of pneumonias, a disease said
to be favored by dampness and cold, but those that occur are chiefly
among the small mammals, on wooden floors and in the large bird house in
cages of concrete and metal. However, the construction of both these
houses permits the visitors to approach very close to the cage, a factor
that doubtless explains the disproportionate incidence of inflammation
of the lungs. In so far as outdoor fowl and ungulate ranges are
concerned, they should be changed frequently under the best conditions
since occasionally one will find groups doing badly until moved.
Moreover the ground becomes contaminated with parasites such as
esophagostomum and heterakis, infestation with which while not very
serious in itself, may lead to fatal infection with bacteria.
The effect of animal parasites upon the morbidity and mortality of wild
beasts and birds in captivity is by no means clear, and Doctor Weidman
and I are inclined to be sceptical, with certain reservations of course,
of their great importance in the death rate. Doctor Weidman has kindly
agreed to contribute a chapter upon the general distribution of
protozoal and metazoal parasites with a summary of their probable
pathogenic importance.
The groups known to have a decided pathological power might be divided
into the toxic, the tumor formers and the mechanically obstructive;
certain parasites have properties placing them in two of these classes.
The first group comprises the hemosporidia and hemogregarines, the
uncinaria and some of the cestodes, forms which produce hemolysis and
hemorrhages with varying grades of anemia. The importance of this group
is shown chiefly among the Aves, in which high grades of anemia are
occasionally met from malarial infections, but cats and dogs or even
herbivores also frequently suffer from hookworm. The tumor-producers are
chiefly echinococcus worms, the cysts of which may grow large enough to
occupy nearly the entire abdomen. A certain grade of anemia and general
ill health accompany this hydatid disease, partly the result of a toxin
and partly by damage to important viscera. Those parasites which
obstruct mechanically do so by their own bulk or by an accompanying
inflammation, incited by them as foreign bodies or by bacteria which
have gained entrance at the irritated point. This is exemplified by the
enormous collection of nematodes sometimes found in reptiles (a pailful
was removed from a python) and by the tightly coiled or tangled thread
and tape worms frequently found in birds. The effect of swelling by the
mucous membrane under the influence of worms is illustrated by the
infestation of the proventricle in parrots. Here spiroptera penetrate
into and under the glandular layer which swells and pours out mucus, the
total mass of nematodes, mucus and tissue obstructing the passage.
Very many animals show parasitic infestation at postmortem, but the
percentage in which they can be said to be principal causes of death is
quite small, while that in which they play a rôle as activator of the
terminal condition is also small but indeterminate. The latter group
comprise, together with the anemias mentioned above, certain forms of
pneumonia, of hepatic and vascular lesions. Inflammations of the lungs
from ascaris and paragonimus are fairly well known; fortunately we have
been troubled less with this than have most gardens, possibly because we
do not have such large herds of herbivora susceptible to it. Hepatic
diseases from flukes, from coccidia and from amœbæ we have always with
us in small numbers, but they are unimportant excepting enterohepatitis,
a condition which appears in nearly all orders. This last disease, be it
purely amœbic as in dysentery of man and monkeys, or like blackhead of
turkeys and chickens or in the forms of quail disease, arrests the
attention at once and evokes a desire to explain the association of
large intestines and liver. Parasitic vascular lesions are relatively
unimportant.
Taking parasitic infestations by and large, there are close similarities
throughout the entire animal kingdom, and the effects produced by a
given genus will be repeated almost exactly in several others. The
pathological pictures of anemia, of hepatic degeneration, of cystic
degeneration, of colonic ulceration or of fibroses are similar in
different hosts, only slight variations in the type of inflammation
being noted, for instance in reptiles and birds as against the mammals.
We have made rather close observations upon the effect of parasites in
the production of neoplasms, incited by Fibiger’s discovery of nematodes
in the rat’s stomach cancer, but, with the possible exception of a
papillomatous growth in the stomach of opossums from the action (?) of
physaloptera, we have been unable to establish such an etiological
relationship. A decision of the importance of parasites in any given
case is not without its difficulty, and we are inclined to reserve
judgment pending further analysis unless the effect of the invaders is
unequivocal. Leiper[4] does not seem to credit animal parasites with a
great effect on the mortality after a specimen has been in the
collection six months since all the intestinal varieties he studied came
from animals dying in that period. On the other hand the forms which
invaded the internal organs and tissues were, in his series, from
specimens resident several years in the garden. He seems to think the
conditions of life at the garden favor the expulsion of intestinal
worms. To what extent some intestinal worms may be commensal remains as
uncertain as the value of certain bacteria in the gut tract. In man
considerable importance has been ascribed to certain fermentative and
putrefactive germs in the maintenance of a reaction unfavorable to
strict pathogens and some observers have looked at them as possessing a
digestive power. In the digestive tract of the animals eating large
quantities of carbohydrate as cellulose, nature provides for its use by
rumination and by supplying a large hind-gut, by which means secondary
mastication and bacterial decomposition of the cellulose capsule insures
its full use. Possibly a similar usefulness may be finally ascribed to
some animal microbes or even larger metozoa.
The rôle of vegetable parasites in the causation of disease among wild
animals seems as undoubted as it is in the human being and the
pathologic results are usually as clear, at least for the entities of
which we have exact data, based upon comparisons with man and domestic
animals.
There seems to be no essential difference among mammals between the
pathological pictures of infectious septicemias, the mucous and serous
membrane inflammations and tuberculosis for example. They are
characterized by fibrinous, purulent or infiltrative inflammations which
may go on to necrosis or repair, by fever, by leucocytosis and by
evidences of resistance—all of these things occurring in a similar way
throughout the class. Of course not all animals are receptive to all
infections since specific racial and generic immunities exist, but the
basic response in terms of pathology is similar. There are no normal
means of judging the susceptibility of wild animals on their native
heath to the important pathogens of civilization, pneumococci,
streptococci, staphylococci, cholera bacilli, the typhocolon group, the
Friedlander group and others, but it is interesting to note that in
captive conditions they evince some receptivity to these germs or their
congeners. The pneumococcus takes a fairly heavy toll in zoological
collections every year and the Friedlander bacillus, not a very common
cause of human pneumonitis, has been seen here and at London.
Among the birds, however, quite distinct differences in some
pathological processes occur, not only from the mammals but also within
the class. As a whole birds do not produce pus as we know it in man,
probably because of the absence from their leucocytes of a protein-
splitting ferment; their leucocyte-producing organs do not seem to
respond as readily to a virus, the place of purulent exudate being taken
by a coagulum or necrosis. The former varies from a clear gelatin-like
material seen upon serous surfaces to a thick mat or mass of coarse but
short fibrinous strands. Necrosis may succeed upon the latter or occur
so promptly as to appear like the original form of degeneration. It is
usually rapid, accompanied by a circumferential congestion but not
associated with active phagocytosis. Giant cell production is variable,
but when developed the appearance is like that of large syncytia.
Hemolysis is not marked in the simple infections but a hyperplasia of
the mononuclear nodes of the liver is the rule. The function of this
nodal increase is not quite clear. It has been always thought that the
scanty bone marrow would supply the necessary erythrocytes, but we have
seen these mononuclear areas full of pale red cells fitted with round
nuclei and without pigment. The fibrin mentioned above does not have the
delicate interweaving that we know in a fibrinous exudate in man. This
is interesting when we consider the composition of the blood and its
coagulation in the Aves. The cell upon which human coagulation seems to
depend, the platelet, is represented in birds by the thrombocyte, which
appears only up to about 50,000 per cubic millimetre. Coagulation time
is relatively short and the resulting clot is firm and irregular.
Perhaps this may have something to do with the nature of an inflammatory
exudate.
The response to infection on the part of birds may to some extent depend
upon differences in anatomy, which are quite distinct, not only from the
mammals within which class the anatomy is more uniform, but also from
one avian order to another. These differences among the birds may be
exemplified by the large foramina between lungs and air sacs in the
water birds, a passage which permits infection, notably mycosis, to
spread from the first to the second. Again the close apposition of the
pancreas to the duodenum over a long stretch permits easy infection of
the former from the latter. Still again the large renal-portal vein in
the gallinaceous birds explains some of the infections of the liver
secondary to intestinal disease. The position of the lungs, deep in the
thorax and fitted into recesses made by the sharp anterior border of the
ribs and overlaid anteriorly by a rather firm air sac wall, makes it
difficult for these organs to expand and therefore renders even a simple
congestion a dangerous thing. The position of the ovary subjects the
shell-less egg to much danger from the intestinal area.
These and many other peculiarities of anatomy affect the pathological
picture in birds. To be sure there are also noteworthy differences among
the Mammalia, notably in the intestinal and genital tracts, but the
pathologic response is not so varied as in the birds. When due allowance
is made for the kind of stomach and absorptive area, apparent
differences can be reconciled. For example, there is little confusion
experienced in comparing acute erosive gastritis or the follicular
enteritis of an omnivorous intestinal tract (man or pig), of a
sacculated stomach and absorptive tract (the marsupial), of a
carnivorous gut (cat) or a herbivorous compound stomach with its long
digestive and water-absorbing surface (cow or camel) and an expansive
muscular organ with a very extensive digestive area (seal). The type of
lesion seems the same, in that inflammation, pus, necrosis, granulation
tissue and cicatrices are comparable throughout the series. The size of
the hind-gut has been taken by Metchnikoff as an indicator of the
possibility of intoxication by degradation products of digestion. He
believes that the capacious colon of herbivora and the short small one
in carnivora explain the relatively greater life in the latter, because
here less stagnation and absorption can take place. A reference to the
expected lengths of life given before hardly substantiates this, and in
our later chapters there will be found no strong indication that animals
with large colons suffer with degenerative visceral changes more than
those with small ones; nay even the reverse may be found true.
In regard to epizoötics the behavior of man and lower animals is similar
except perhaps that during an outbreak a smaller percentage of the
latter give evidence of individual immunity and whole groups are apt to
be carried off. Occasionally hygienic measures stay the ravages, at
other times nothing seems to avail. Fortunately it is sometimes possible
to sacrifice infective specimens and remove contagion. We have had few
serious outbreaks, unless one might call our former heavy infection with
tuberculosis in monkeys an epizoötic. The principal ones were an
unexplained water fowl disease which carried off one hundred and forty-
six birds, an imported epizoötic of quail disease which killed about the
same number, a few cases of blackhead among wild turkeys, and a small
group of cases of amœbic dysentery in monkeys and of thrush in passerine
birds, and a small number of tuberculous pneumonias in snakes.
Pathology may be difficult upon an anatomical basis, but when we engage
to explain functional physiological defects we are surely embarked, with
a poor compass and weak rudder, upon an uncharted sea. One knows, of
course, that all animals require the same amount of food elements per
kilo of body weight, that man eliminates his nitrogen as urea and uric
acid, that monkeys do the same, that most other mammals destroy uric
acid and excrete allantoin, that birds and reptiles form uric acid but
chiefly urates, that there is an adaptation of alimentary tract and
diet, that herbivores have a high threshold for carbohydrates, that
there is a variable quantity of enzyme present in different organs and
in different animals, that vitamins, whatever they may be, are necessary
for the growth of young animals, that hormones exist whereby
correlations of parts are kept normal—but these things, rather than
being learned thoroughly from animals, have merely been substantiated by
comparisons with man. Constitutional diseases so-called, from which the
necessity to investigate much of this physiology originated, are little
known in the wild animal. Many cases of so-called gout have been
encountered and we have seen an instance of diabetes in a fox, but more
extensive experience is needed for definite practical comparisons. This
applies to thyroid and pituitary disorders and to the vague conditions
we have at times been obliged to call marasmus or inanition.
Some attention has been given to the study of diets for the wild
specimens of our Garden, but no systematic observations have been made
or records kept upon purely physiological subjects. Reference will be
made at appropriate places to accepted comparative physiological facts,
but our statistics permit additions to such knowledge only in a limited
manner and in isolated instances. Doctor Corson-White has very ably
summarized the diet, alimentary tract and physiology of the zoological
groups with the pathology as found in our records.
A word might be added here as to the destruction of animals by injury
from fighting and harassment by others in the cage. Fighting doubtless
causes death, especially when males are together, but it is our
experience that in cases of traumatic death search should always be made
to see if the resistance of the dead animal had not been reduced by some
disease. This is well illustrated in birds. Very frequently a specimen
will come to autopsy with its head feathers plucked out, or with a
billthrust in the wing or pelvic region. Such birds are not infrequently
suffering from malaria, or heavy intestinal parasitism or from organic
disease whereby the resistance and self-preservatory power has been
decreased.
The foregoing survey of the approach to our subject reveals the
multiplicity of factors which affect the study of comparative pathology.
No one of them can be entirely omitted, no one is without some effect
upon the origin and expression of disease, and no one is fully
understood. Yet it is to be hoped that a study of our material,
accumulated under routine conditions and uninfluenced by any
experimental procedures, will demonstrate the natural response of
various zoological groups to morbific agencies. Perhaps reactively some
of the modifying conditions may thus be understood. It is also not
unreasonable to expect that alterations observed as natural responses in
a large number of specimens in nearly normal surroundings would serve as
more reliable guides to investigative speculation than would changes in
a few animals under artificial technical experimentation. We hope that
the few facts we have been able to record may afford someone a basis for
further biological studies. It is also to be hoped that something has
been learned which in the end will afford an explanation of the diseases
of man. Too great optimism in this direction should be guarded against
because the human being is indeed an animal _sui generis_ and, from the
standpoint of normal conditions of nature, a wild animal.
The zoological classification found on pages 43–46 was compiled in 1903
by Dr. A. E. Brown on the basis of the British System. With a few
exceptions the computations in the text are made on the basis of
zoological _orders_ since the number of specimens in families is often
too small and the complications of so many different figures would be
confusing. The tables will be found to correspond to the sequence of the
classification. Dr. Corson-White has, however, used for her analysis the
dietary groupings. A carnivore in her chapter implies strictly a meat-
eater, in the rest of the book one of the zoological group Carnivora.
The Laboratory of Comparative Pathology at this Garden speaks for the
earnest desire on the part of the Directors to use the material to its
fullest extent, and I, acting for myself and my associates, wish to
record our appreciation of the facilities offered to us for study, and
for the broad-minded, scientific coöperation the Board has always
displayed. The President, Charles B. Penrose, M.D., Ph.D., LL.D., was
the active originator of the plan whereby this department was started,
and he has given to it continuously the support of his rich experience.
I wish to express for myself the deepest appreciation of his personal
interest in my studies, and assistance which has been constructive and
stimulating. Whether or not this present work prove useful to the extent
that is hoped, the results from the Laboratory are such as to make the
scientific world debtor to this gentleman.
It is a duty, and a pleasant one, to record, though unfortunately in
memoriam, my association with Arthur Erwin Brown, A.M., Sc.D., Ph.D.,
C.M.L.Z.S., for many years the Secretary of the Society and Executive
Officer of the Garden. Doctor Brown as teacher was ever ready to help in
the broad subject of biology, and I am proud to recall that he guided me
also as a friend.
The first director of the Laboratory was Courtland Y. White, A.M., M.D.,
who served from 1901 to 1906, retiring then to accept a position in the
City Laboratory. The foundation of the recording system is still in use
essentially unchanged from his plan, and is a credit to his foresight.
Our clerk and technician, Miss Harriet M. Phelps, has served the Garden
faithfully and well since 1906. The condition of the museum is very much
due to her interest and watchfulness. Thanks and appreciation for her
work are felt by every one, the author most of all. Dr. F. D. Weidman
has been our first assistant since 1911, and his work on parasitology
has been of the greatest value, practically and scientifically. It is to
be hoped that we shall be able to retain him indefinitely. Dr. E. P.
Corson-White has in recent years taken an assistant position with us,
armed for the work with a thorough knowledge of applied organic
chemistry and immunology, and has already obtained useful results.
ZOOLOGICAL CLASSIFICATION
│
MAMMALIA
PLACENTALIA
PRIMATES
_Simiadæ_ Anthropoid apes
_Cercopithecidæ_ Old World monkeys (macaques, baboons).
_Cebidæ_ New World monkeys (capuchins, howlers,
spiders).
_Hapalidæ_ New World monkeys (marmosets).
LEMURES
_Lemuridæ_ Lemurs, Loris, Galagos.
CARNIVORA
_Felidæ_ Cats
_Viverridæ_ Civets, Genets, Paradoxures, Ichneumons.
_Hyænidæ_ Hyena.
_Canidæ_ Dogs, Wolves, Foxes, Jackalls, Etc.
_Mustelidæ_ Marten, Skunk, Weasel, Otter, Badger, Etc.
_Procyonidæ_ Raccoon, Bassaris, Coati, Kinkajou.
_Ursidæ_ Bear.
_Otariidæ_ Eared Seal, Sea Lion.│These are grouped
│separately as suborder,
│PINNIPEDIA, illustrating
│water carnivores.
_Phocidæ_ Common Seal, Walrus. │ „
INSECTIVORA
_Tenrecidæ_ Tenrec.
_Solenodontidæ_ Solenodon.
_Talpidæ_ Moles, Shrews.
_Erinaceidæ_ Hedgehog.
CHIROPTERA
_Pteropodidæ_ Fruit Bats, “flying foxes.”
_Vespertilionidæ_ Common bats.
_Emballonuridæ_ Snouty Bats, Free-tailed Bats.
RODENTIA
_Sciuridæ_ Squirrels, Spermophiles, Marmots.
_Castoridæ_ Beaver.
_Muridæ_ Rats, Mice.
_Geomyidæ_ Pouched Rats, “Gophers.”
_Dipodidæ_ Jumping Mice, Jerboas.
_Heteromyidæ_ Kangaroo Rats.
_Octodontidæ_ Capromys, Coypu.
_Hystricidæ_ Porcupines.
_Chinchillidæ_ Viscacha, Chinchilla.
_Dasyproctidæ_ Agouti, Spotted Cavy.
_Caviidæ_ Guinea-pig, Capybara.
_Leporidæ_ Rabbits, Hare.
PROBOSCIDEA Elephant.
HYDRACOIDEA Cape Hyrax.
UNGULATA
PERISSODACTYLA (odd toed)
_Rhinocerotidæ_ Rhinoceros.
_Tapiridæ_ Tapir.
_Equidæ_ Horse, Ass.
ARTIODACTYLA (even toed)
_Bovidæ_ Oxen, Antelopes, Sheep, Goats.
_Cervidæ_ Deer, Moose, Elk.
_Antilocapridæ_ Prong-horned Antelope.
_Giraffidæ_ Giraffe.
_Tragulidæ_ Chevrotains, Muis Deer.
_Camelidæ_ Camels, Llama.
_Hippopotamidæ_ Hippopotamus.
_Suidæ_ Swine, Warthogs.
_Tayassuidæ_ Peccaries.
SIRENIA Sea-cow, Manatee, Durong.
CETACEA Whales, Porpoises.
EDENTATA
_Bradypodidæ_ Sloths.
_Dasypodidæ_ Armadillo.
_Myrmecophagidæ_ Anteaters.
MARSUPIALIA
MARSUPIALIA
_Didelphyidæ_ Opossums.
_Dasyuridæ_ Dasyures, Tasmanian “Devils.”
_Peramelidæ_ Bandicoots.
_Phascolomyidæ_ Wombat.
_Phalangeridæ_ Phalangers.
_Macropodidæ_ Kangaroo, Wallabies.
MONOTREMATA
MONOTREMATA
_Echidnidæ_ Echidna, Ornithorhynchus.
AVES
PASSERES
_Turdidæ_ Thrushes, Robins, Etc.
_Sylviidæ_ Warblers, Kinglets.
_Paridæ_ Titmouse.
_Troglodytidæ_ Wrens, Mockingbirds, Catbird, Etc.
_Pycnonotidæ_ Bulbul.
_Crateropodidæ_ Babblers, Jay-thrushes.
_Oriolidæ_ Oriole.
_Motacillidæ_ Wagtails.
_Dicruridæ_ Drongos.
_Mniotiltidæ_ Chats, Warblers, “Woodwarblers,” Etc.
_Cœrebidæ_ Sugarbirds.
_Vireonidæ_ Vireos.
_Laniidæ_ Shrikes.
_Ampelidæ_ Waxwing.
_Hirundinidæ_ Martins, Swallows.
_Meliphagidæ_ Honeyeaters.
_Tanagridæ_ Tanagers.
_Ploceidæ_ Weavers, Whydah birds, Waxbills, Finches, Etc.
_Fringillidæ_ Finches, Sparrows, Buntings, Grosbeaks, Etc.
_Icteridæ_ Hangnests, Troupials, Grackles, “Blackbird,”
Etc.
_Sturnidæ_ Starlings, Mynahs.
_Corvidæ_ Crows, Jays, Magpies, Jackdaws.
_Alaudidæ_ Larks.
_Tyrannidæ_ Tyrans.
_Cotingidæ_ Bellbird, Cock-of-the-rock, Etc.
PICARIÆ
_Upupæ_ Hoopæ.
_Trochilidæ_ Hummingbirds.
_Cypselidæ_ Swifts, “Chimney Swallow.”
_Caprimulgidæ_ Night hawk, Whip-poor-will.
_Coraciidæ_ Roller.
HALCYONES
_Alcedinidæ_ Kingfisher.
_Momotidæ_ Motmots.
BUCEROTES
_Bucerotidæ_ Hornbill.
TROGONES
_Trogonidæ_ Trogons.
SCANSORES
_Picidæ_ Woodpeckers.
_Rhamphastidæ_ Toucans.
_Capitonidæ_ Barbets.
COCCYGES
_Cuculidæ_ Cuckoos.
_Musophagidæ_ Touracous.
PSITTACI
_Loriidæ_ Lories, Lorikeets.
_Cacatuidæ_ Cockatoos.
_Psittacidæ_ Macaws, Conures, Amazons, Parrots, Parrakeets.
STRIGES
_Strigidæ_ Barn owl.
_Bubonidæ_ All other owls.
ACCIPITRES
_Falconidæ_ Buzzards, Hawks, Falcons, Eagles, Etc.
_Serpentaridæ_ Secretary Vulture.
_Catharidæ_ Vultures.
COLUMBÆ
_Treronidæ_ Fruit pigeons.
_Columbidæ_ All other pigeons and doves.
PTEROCLETES
_Pteroclidæ_ Sand grouse.
GALLI
_Tetraonidæ_ Grouse, Ptarmigans.
_Phasianidæ_ Pheasants, Fowls, Turkeys, Quail, Etc.
_Cracidæ_ Curassows, Guans, Etc.
_Megapodidæ_ Brush turkey.
HEMIPODII
_Turnicidæ_ Hemipodes.
FULICARIÆ
_Rallidæ_ Rails, Porphyrios, Gallinules, Coots, Etc.
ALECTORIDES
_Aramidæ_ Courlan.
_Eurypygidæ_ Sun bittern.
_Gruidæ_ Cranes.
_Cariamidæ_ Cariama “Crane.”
_Psophiidæ_ Trumpeters.
LIMICOLÆ
_œdicnomidæ_ Thicknees.
_Charadriidæ_ Plovers, Sandpipers, Curlews, Woodcocks, Etc.
_Chionidæ_ Sheathbills.
GAVIÆ
_Lariidæ_ Gulls, Terns.
_Stercorariidæ_ Jaeger Gull.
PYGOPODES
_Colymbidæ_ Loons, Grebs.
_Alcidæ_ Auks, Murrs, Puffins.
IMPENNES
_Spheniscidæ_ Penguins.
STEGANOPODES
_Sulidæ_ Gannets.
_Pelicanidæ_ Pelicans.
_Phalacrocoracidæ_ Cormorants.
_Anhingidæ_ Darter “Water turkeys.”
TUBINARES
_Procellariidæ_ Petrels, Fulmars.
HERODIONES
_Ardeidæ_ Herons, Bitterns, Egrets.
_Ciconiidæ_ Storks, Ibises.
_Plataleiidæ_ Spoonbills.
ODONTOGLOSSÆ
_Phœnicopteridæ_ Flamingoes.
PALAMEDEÆ
_Palamedeidæ_ Screamers.
ANSERES
_Anatidæ_ Swans, Geese, Ducks.
STRUTHIONES
_Apterygidæ_ Kiwis, Apteryx.
_Casuariidæ_ Cassowaries.
_Struthionidæ_ Ostriches.
_Rheidæ_ Rheas.
CRYPTURI
_Tinamidæ_ Tinamous.
_List of Animals subjected to
Autopsy giving the number of
each. These Figures are used to
obtain the percentages quoted
in the Tables and Text._
MAMMALIA
Primates 498
Lemures 86
Carnivora 481
Pinnipedia 20
Insectivora 6
Chiroptera 5
Rodentia 198
Ungulata 365
Proboscidea 3
Hyracoidea 7
Edentata 16
Marsupialia 175
Monotremata 0 1860
————
AVES
Passeres 1355
Picariæ 87
Striges 133
Psittaci 689
Accipitres 196
Columbæ 157
Pterocletes 0
Galli 299
Hemipodii 2
Fulicariæ 35
Alectorides 37
Limicolæ 6
Gaviæ 20
Pygopodes 0
Impennes 5
Steganopodes 21
Tubinares 0
Herodiones 98
Odontoglossæ 6
Palamedes 5
Anseres 317
Struthiones 32
Crypturi 5 3505
———— ————
5365
SECTION II
DISEASES OF THE HEART
The heart is an organ whose duty, throughout the two classes considered
in this study, remains entirely identic, purely a physical one in
driving the blood through the corresponding vascular system. The physics
involved naturally differs between mammals and birds, but energy is
derived from the automatic power lodged in the cardiac musculature.
Whether this be neuromyogenic, as seems to be the case in all mammals,
or purely myogenic, as is probably the case for the birds in which
MacKenzie and Robertson[5] say there is no atrioventricular bundle, the
result is the same, since in both classes there is some continuity of
muscle fibres from auricle to ventricle. The gross anatomy varies little
if any more than the physiology, albeit there is proportionately greater
auricular capacity in the mammals than in the birds, and indeed there
are differences within the classes which cannot now be readily
explained; certain minor variations of valvular arrangement exist, such
as the absence of the membranous light tricuspid in Aves.
When, however, one considers the cardiac power available for various
animals, the subject becomes one of greater breadth and complexity, for
no consistency obtains even within families, since the demand for
cardiac strength will vary more with habits than with zoological
relationships. Thus for example the domestic rabbit has a small heart
volume while the wild hare has a great one. Although, of course, the
size of an organ may not be an absolute measure of its efficiency (a
flea’s leg muscle has relatively greater power than a man’s), yet size
is the only physical gauge one has for estimating nature’s preparation
for expected demand. Perhaps this will be shown later when after
discussing the pathological anatomy of the heart in the wild mammals and
birds, we can study these changes in light of statistics upon the
relative size of the heart.
EXPRESSION OF CARDIAC DISEASE.
The diseases of this organ are known only by their physical effects,
chiefly by causing physical or functional defects in other organs and to
a minor degree by purely physiological irregularities in the heart
itself (tachycardia, arrhythmia). All the latter and most of the former
are subjects discovered by observation during life and unfortunately
cannot be included in the study at hand. Both states are well known to
the veterinarian who diagnoses them with reasonable ease in animals that
can be handled; I saw one case of arrhythmia in a monkey for which no
adequate gross morbid explanation was found postmortem. Some of these
functional abnormalities are certainly caused by myocardial disease and
cardiac failure has occurred among many orders. An interesting
observation was made by Plimmer[6] on several large birds (ostriches,
storks, cassowaries) which apparently died from this condition; at
autopsy he found myocardial degeneration, or epicardial edema or only a
flabby heart. Lack of exercise was held responsible by this observer.
Such cardiac deaths have probably been encountered at this Garden but we
have accounted them to shock, or gastrointestinal disease; this matter
will be discussed on a later page.
CORONARY ARTERY DISEASE.
If a degenerative sclerosis of coronary vessels be the cause of angina
pectoris then perhaps paroxysms of this kind occur, for we have seen
such anatomical changes in the heart of three widely separated varieties
of animals, a Nylghaie, a Hamadryas Baboon, a Macaque, and a Brown
Pelican. The history of these animals does not register anything
resembling the clinical picture of angina pectoris in man, and they did
not come to their death from the arterial changes in the heart alone
since sufficient other pathology also existed.
KINDS OF PATHOLOGICAL CHANGE.
As an introduction to the strict pathology of the heart it might be well
to outline the headings of the scheme upon which it seems desirable to
study the subject. It is hardly profitable to take up seriatim the
ordinary general pathological processes as discussed in systems of
pathology for it is our purpose to show the distribution of basic
aberrations from the normal in terms of zoological position. To this end
one must consider the response of the heart (a) to damaging influences
and (b) to a demand for increased work. In the first group come
degenerations and inflammations, upon which may succeed an incompetency
in the form of dilatation. The response of the normal heart to any
physical demand greater than customary has usually been thought to lie
in the direction of hypertrophy, but on occasion it has seemed to be in
the form of dilatation, especially if the strain has been sudden and
severe. Starling thinks that the primary and normal reaction of the
heart to physical strain is always dilatation. The idea of hypertrophy
must not be confused with an understanding of the relatively large
hearts in animals whose habits demand great cardiac power, for then it
is their norm and might be called “physiological cardiac hyperplasia.” I
shall use the terms “increased muscle bulk” and “increased chamber
space” as preferable to hypertrophy and dilatation; this also focuses
attention upon the two features of an enlarged heart.
DEGENERATIONS AND INFLAMMATIONS.
Degenerative changes in disease are recorded in our system as amyloid,
hyaline, fatty metamorphosis, granular and cloudy degeneration. While
there is perhaps between some of these conditions and true myocarditis a
matter only of degree, the records have been analyzed as filed and
perhaps some lessons can be learned from the responses of the various
zoological orders. In the accompanying Table 1 will be found the
distribution of degenerative and inflammatory lesions through the
zoological orders. The percentages speak for themselves but deserve as
well some consideration from the standpoint of normal heart value; this
will be taken up later after the other lesions have been discussed.
TABLE 1.
_Table Showing Incidence, in the Orders, of Degenerations and Inflammations,
or in Other Words the Response to Infectious and Toxic Agencies._
════════════╤════════╤═══════╤════════╤════════╤════════╤════════╤══════════
Heart of │Degener-│Myocar-│Pericar-│Endocar-│Total[7]│ Cases │Percentage
│ ations │ ditis │ ditis │ ditis │ │followed│in deaths
│ │ │ │ │ │ by │per order
│ │ │ │ │ │dilation│
────────────┼────────┼───────┼────────┼────────┼────────┼────────┼──────────
Primates │ 8│ 12│ 18│ │ 38│ │ 7.6
Lemures │ 1│ │ │ │ 1│ │ 1.2
Carnivora │ 19│ 14│ 11│ 10│ 54│ 5│ 11.
Pinnipedia │ 2│ 1│ │ │ 3│ │ _15._
Rodentia │ 5│ 7│ 6│ │ 16│ │ 8.
Insectivora │ │ │ │ │ │ │
Chiroptera │ │ │ │ │ │ │
Proboscidea │ │ 1│ │ │ 1│ │ _33._
Hyracoidea │ │ │ │ │ │ │
Ungulata │ 3│ 9│ 8│ 2│ 20│ │ 5.4
Edentata │ 2│ 3│ 1│ │ 7│ │ _44._
Marsupialia │ 12│ 5│ 6│ 12│ 33│ │ 19.
Monotremata │ │ │ │ │ │ │
│ │ │ │ │ │ │
Passeres │ 4│ 4│ 9│ 2│ 19│ │ 1.4
Picariæ │ 2│ 1│ 3│ │ │ 6│ 6.7
Striges │ │ │ 1│ │ 1│ │ .8
Psittaci │ 10│ 7│ 7│ │ 24│ │ 3.4
Accipitres │ 2│ 19│ 8│ 7│ 36│ 1│ 18.3
Columbæ │ 2│ 1│ │ │ 3│ │ 2.
Pterocletes │ │ │ │ │ │ │
Galli │ 4│ 10│ 13│ 1│ 28│ 1│ 9.3
Hemipodii │ │ │ │ │ │ │
Fulicariæ │ 2│ │ 1│ │ 3│ │ 8.6
Alectorides │ │ 1│ 1│ │ 2│ │ 5.4
Limicolæ │ │ │ │ │ │ │
Gaviæ │ 1│ 1│ │ │ 2│ │ 10.
Pygopodes │ │ │ │ │ │ │
Impennes │ │ 1│ │ │ 1│ │ 16.
Steganopodes│ │ 1│ 2│ 1│ 4│ │ _20._
Tubinares │ │ │ │ │ │ │
Herodiones │ 1│ │ 1│ 2│ 4│ │ 4.1
Odontoglossæ│ │ │ │ │ │ │
Palamedes │ │ │ │ │ │ │
Anseres │ 16│ 17│ 11│ 6│ 50│ 1│ 15.7
Struthiones │ 2│ 3│ 5│ 1│ 11│ │ _34._
Crypturi │ │ │ │ │ │ │
────────────┼────────┼───────┼────────┼────────┼────────┼────────┼──────────
Total │ 98│ 118│ 112│ 44│ 367│ 8│
════════════╧════════╧═══════╧════════╧════════╧════════╧════════╧══════════
In this and subsequent tables, figures in italics are for small groups
of animals coming to autopsy, usually less than one hundred, and from
which percentages may be misleading. The number of autopsies upon such
groups may be found by consulting the list given on page 47.
ENDOCARDITIS, MYOCARDITIS.
Romberg said in his classical work on the heart that there is always
some form of myocardial disease with endocarditis. The 44 cases of
valvular disease detected at this Garden are 15 of chronic nature, 29 of
acute or subacute character. In the former, the chronic, 9 showed some
grade of muscular involvement, while 21 of the 29 acute cases of
valvular inflammation were accompanied by myocardial damage; the
percentages are 60 for chronic and 72 for acute, a relation that would
be expected if one credit the theory that many valvular inflammations
start at the root of the valves, but, at all events, they indicate that
after the acute stages have passed the myocardial damage may be
repaired.
[Illustration:
FIG. 1.—VEGETATIVE AND ULCERATIVE ENDOCARDITIS OF AORTIC VALVE.
OSTRICH (STRUTHIO AUSTRALIS). ORGANISMS ISOLATED CORRESPONDED
CLOSELY TO BAC. AFANASIEFFICHESTER.
]
The large number of cases of endocarditis among the Carnivora,
Accipitres, Anseres and Marsupialia is noteworthy and can hardly be
explained by other argument than a special vulnerability of this organ
in these groups. However, the unusual number of cases in our only native
marsupial, the opossum, seems worthy of a special note since ten of the
twelve instances in the order Marsupialia affected this particular
animal. When seen these ten cases were acute in five instances, subacute
in three and chronic in two. The Streptococcus pyogenes was isolated in
three of the five acute cases; bacteriology of the others was negative
or not done. All of the acute and one of the subacute cases were
combined with some evidence of general septicemia. The type of lesion
was in no way peculiar, unless the facts that all were vegetative when
acute and markedly deforming when chronic, be noteworthy. In two chronic
aortic cases the valvular orifice was almost closed, yet the left
ventricle could not be considered as greatly hypertrophied and no
dilatation existed. In one acute aortic and mitral case, general
dilatation existed. The mitral was involved nine times, three times
alone, four times with the aortic, once each with the tricuspid and
pulmonary. Once the vegetations were limited to the mural endocardium.
Nine of these animals came from one enclosure over a period of two and a
half years, during which time other opossums died from similar bacterial
infections (pneumonia) despite repeated cleansing of the place. No
unusual number of cases of this or similar kinds occurred elsewhere in
the Garden at this time, but it would seem that we had in this cage a
continued bacterial infection.
UNUSUAL PERICARDIAL CHANGES.
The appearance of a stiff gelatinous exudate in the pericardial sac has
attracted our attention on ten occasions (8 birds, 2 mammals). The
substance seems quite homogeneous and almost entirely acellular. One
specimen became solid on heating and another became turbid when put into
Kaiserling’s fluid. In two cases bacterial cultures were made; nothing
grew. It has not been associated with tuberculosis or tumors nor has any
one pathological lesion more than another appeared to accompany it.
A peculiar lesion occasionally seen in birds is “uratic pericarditis” a
process not infectious at all, according to Plimmer, but due to renal
disease. It has been seen here in association with retention of urates
in the kidney, with gout of birds, and apparently quite independent of
any renal or constitutional disease. Both layers of the sac are pearl
gray or irregularly salted with a whitish granular material so that they
are entirely opaque; occasionally the distribution is spotty. The
deposit does not seem to penetrate the myocardium. There is at times
some involvement of other serosæ, but this is usually much less marked
than around the heart. It does not seem that this of itself should be
fatal, but it has been the most decided pathological factor in some of
the autopsies.
Aside from pericarditic exudates, twenty-one instances of pericardial
effusion have been encountered. They offer little that is peculiar in
etiology, chemistry or cytology, but as there has been some question of
the position of the accumulation of the fluid in human beings, it might
be well to note the position in our material. It is recognized in
veterinary medicine that the cardiac dullness is increased especially to
the right, and that most of the fluid will be on that side and
posteriorly. At our autopsies on mammals this is the position usually
occupied by the fluid, the apex being covered by pericardium, unless the
quantity be great enough to make the sac taut, and this position is
retained whether the animal be laid upon the one side or the other; nor
does the fluid all leave the base of the heart when the body is placed
prone. The crown of the heart is nearly always well covered. In birds,
on the other hand, the fluid occupies the apical part of the sac,
probably due to the fact that this membrane is attached by its tip to
the transverse air sac wall which takes the place of a diaphragm, so
that the tip of the heart is always free and the pericardium of the base
fairly closely applied to the epicardium. This holds good even for the
birds whose cardiac apex is normally attached to the pericardium by a
fibrous band.
HYPERTROPHY AND DILATATION.
The response of the heart to a continued demand upon its working
capacity will, as already indicated, lead to increased muscle bulk or to
larger chamber size. Whether hypertrophy be purely the building of a
bigger engine or be accompanied by, or due to, muscular disease as had
been suggested by certain authors, was a question to which an answer was
hoped, but it would seem that the solution is no nearer than can be
obtained in human pathology. Fifteen of the 34 cases showed some degree
of myocardial damage. Some of the other cases may have been instances of
so-called essential hypertrophy, enlargements due to hard work or to low
grade hidden infection. Aubertin[8] ascribes such cardiac muscle
increase to overwork under the stimulus of intoxication from intestinal
sources or from irregular constitutional functions. For information
concerning this and pathological enlargements one may consult the Table
(2) of Hypertrophies and Dilatations; in advance the method of charting
must be known. Since it is usually impossible to decide what may be the
single important factor in the cardiac disease, all of the accredited
factors have been listed with the hope that the resulting figures would
be significant. Thus an animal may have recorded pericarditis, nephritis
and arteriosclerosis—who shall say which was primary or most potent in
the cardiac change.
Essential hypertrophy is limited to those cases for which there was no
concomitant pathology that might have been responsible for the
overgrowth. There was one in a carnivore (fox) and one in a raptatory
bird (buzzard). Idiopathic dilatations on the other hand are much more
common, but they still bear a relation to the apparent vulnerability of
the heart. Their distribution is as follows: Primates 1, Carnivora 1,
Pinnipedia 1, Ungulata 1, Marsupialia 4, Anseres 1. These may be cases
such as Plimmer described, of cardiac failure, indicated by dilatation,
the result of inactivity. Besides these special instances and the ones
accounted for in the list, there were three acute dilatations apparently
due to shock, two ungulates and one marsupial, probably incidental to
fright when being caught by the keepers.
The association of secondary dilatation with hypertrophy is only evident
in three instances. One case and perhaps the most interesting, is that
in which the principal antecedent pathology was thyroid hyperplasia and
nephritis; the dilatation was perhaps agonal or shortly before the last
struggles. It would seem that all of the dilatations occurred shortly
before death because long standing passive congestions and dropsies of
cardiac origin are exceedingly rare; only one certain case is recorded
(carnivore).
Let us now examine the Table (2) according to orders and then as to
causation. The Primates’ heart is apparently well able to increase in
size in response to increased work, a demand most often made by
pulmonary, pleural and pericardial diseases. Two of these cases occurred
in animals suffering with pulmonary tuberculosis sufficiently extensive
to impede cardiac action while in another case the tuberculous lesion
was mild but a pericarditis existed. When the right hand columns are
inspected it would seem that on occasion dilatation may occur; one of
the tuberculous pulmonary cases had a dilated heart. The slothful lemurs
apparently have no call upon their cardiac mechanism.
Carnivora with their large organ, which, it would seem, should be
prepared for excess work either simply as a reserve or as an inherent
ability to grow, present in about equal numbers, hypertrophy and
dilatation. It is admitted that there are within this order, genera of
differing habits, but analysis of the canidæ, felidæ and ursidæ for
examples, in the first place, offer too few specimens for conclusions
and, secondly, have upon trial actually shown nothing definite, so that
we are forced to use the larger group, the order. It is interesting to
note that long continued infection is in this order the most potent
factor in enlargements of the heart. Four of the ten cases show
myocarditis. Nephritis does not seem very important in relation to
cardiac muscular increase, but occurs with great frequency in
association with dilatation. Three of the cases of hypertrophy were
associated with thyroid disease and two of these showed dilatation as
well. The general causes of chamber distention are more diverse, and we
see associations that do not appear with hypertrophy, namely
arteriosclerosis and diseases of the chest.
TABLE 2.
_Table Showing Incidence per Order of Hypertrophy and Dilatation, and
the Principal Associated Lesions Believed to Have Etiological
Importance._
═════════════╤═════════════════════════════════════════════════
Heart of │ Hypertrophy
─────────────┼─────┬────────┬────────┬────────────────┬────────
„ │Total│Percent.│Valvular│Arteriosclerosis│Diseases
│ │ for │Disease │ │ of
│ │ Order │ │ │Thoracic
│ │ │ │ │ Serosæ
─────────────┼─────┼────────┼────────┼────────────────┼────────
Primates │ 4│ .8│ │ 1│ 3
Lemures │ │ │ │ │
Carnivora │ 10│ 2.1│ 1│ │
Pinnipedia │ │ │ │ │
Rodentia │ │ │ │ │
Insectivora │ │ │ │ │
Chiroptera │ │ │ │ │
Proboscidea │ │ │ │ │
Hyracoidea │ │ │ │ │
Ungulata │ 4│ 1.2│ │ │ 1
Edentata │ │ │ │ │
Marsupialia │ 1│ .6│ 1│ │
Monotremata │ │ │ │ │
Total Mammals│ 19│ │ 2│ 1│ 4
│ │ │ │ │
Passeres │ │ │ │ │
Picariæ │ 1│ 1.1│ │ 1│
Striges │ │ │ │ │
Psittaci │ │ │ │ │
Accipitres │ 8│ 4.1│ │ 4│ 1
Columbæ │ │ │ │ │
Pterocletes │ │ │ │ │
Galli │ 2│ .7│ │ 1│
Hemipodii │ │ │ │ │
Fulicariæ │ │ │ │ │
Limicolæ │ │ │ │ │
Gaviæ │ │ │ │ │
Pygopodes │ │ │ │ │
Impennes │ │ │ │ │
Steganopodes │ │ │ │ │
Tubinares │ │ │ │ │
Herodiones │ │ │ │ │
Odonotoglossæ│ │ │ │ │
Palamedes │ │ │ │ │
Anseres │ 2│ .6│ │ │
Struthiones │ 2│ _6.2_│ │ │ 2
Crypturi │ │ │ │ │
Total Birds │ 15│ │ 0│ 6│ 3
─────────────┼─────┼────────┼────────┼────────────────┼────────
Total │ 34│ │ 2│ 7│ 7
─────────────┴─────┴────────┴────────┴────────────────┴────────
═════════════╤════════════════════════════════════════════════════════
Heart of │ Hypertrophy
─────────────┼─────────┬───────┬─────────┬─────────┬───────┬──────────
„ │Pulmonary│ Renal │ Chronic │ Acute │Thyroid│Myocardial
│ Disease │Disease│Infection│Infection│Disease│ Disease
│ │ │ │ │ │
│ │ │ │ │ │
─────────────┼─────────┼───────┼─────────┼─────────┼───────┼──────────
Primates │ 3│ 1│ 1│ 1│ │
Lemures │ │ │ │ │ │
Carnivora │ │ 2│ 6│ 1│ 3│ 4
Pinnipedia │ │ │ │ │ │
Rodentia │ │ │ │ │ │
Insectivora │ │ │ │ │ │
Chiroptera │ │ │ │ │ │
Proboscidea │ │ │ │ │ │
Hyracoidea │ │ │ │ │ │
Ungulata │ │ 4│ │ │ │ 2
Edentata │ │ │ │ │ │
Marsupialia │ │ 1│ │ │ │ 1
Monotremata │ │ │ │ │ │
Total Mammals│ 3│ 8│ 7│ 2│ 3│ 7
│ │ │ │ │ │
Passeres │ │ │ │ │ │
Picariæ │ │ 1│ │ │ │
Striges │ │ │ │ │ │
Psittaci │ │ │ │ │ │
Accipitres │ │ 3│ 1│ 1│ │ 5
Columbæ │ │ │ │ │ │
Pterocletes │ │ │ │ │ │
Galli │ │ 1│ │ 1│ │ 1
Hemipodii │ │ │ │ │ │
Fulicariæ │ │ │ │ │ │
Limicolæ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │
Pygopodes │ │ │ │ │ │
Impennes │ │ │ │ │ │
Steganopodes │ │ │ │ │ │
Tubinares │ │ │ │ │ │
Herodiones │ │ │ │ │ │
Odonotoglossæ│ │ │ │ │ │
Palamedes │ │ │ │ │ │
Anseres │ │ │ 1│ 1│ │ 1
Struthiones │ │ │ 1│ 1│ │ 1
Crypturi │ │ │ │ │ │
Total Birds │ 0│ 5│ 3│ 4│ 0│ 8
─────────────┼─────────┼───────┼─────────┼─────────┼───────┼──────────
Total │ 3│ 13│ 10│ 6│ 3│ 15
─────────────┴─────────┴───────┴─────────┴─────────┴───────┴──────────
═════════════╤═════╤═══════════════════════════════════════════
Heart of │ │ Dilatation
─────────────┼─────┼────────┬────────┬────────────────┬────────
„ │Total│Percent.│Valvular│Arteriosclerosis│Diseases
│ │ for │Disease │ │ of
│ │ Order │ │ │Thoracic
│ │ │ │ │ Serosæ
─────────────┼─────┼────────┼────────┼────────────────┼────────
Primates │ 4│ .8│ │ 1│
Lemures │ │ │ │ │
Carnivora │ 11│ 2.2│ │ 1│ 2
Pinnipedia │ │ │ │ │
Rodentia │ 8│ 4.2│ │ │
Insectivora │ │ │ │ │
Chiroptera │ │ │ │ │
Proboscidea │ │ │ │ │
Hyracoidea │ │ │ │ │
Ungulata │ 11│ 3.│ │ │ 4
Edentata │ 2│ _12.5_│ │ │
Marsupialia │ 8│ 4.5│ │ │
Monotremata │ │ │ │ │
Total Mammals│ 44│ │ 0│ 2│ 7
│ │ │ │ │
Passeres │ 1│ │ │ │
Picariæ │ │ │ │ │
Striges │ │ │ │ │
Psittaci │ 1│ .1│ │ │
Accipitres │ 1│ .5│ │ │ 1
Columbæ │ │ │ │ │
Pterocletes │ │ │ │ │
Galli │ 2│ .7│ │ 1│ 1
Hemipodii │ │ │ │ │
Fulicariæ │ │ │ │ │
Limicolæ │ │ │ │ │
Gaviæ │ │ │ │ │
Pygopodes │ │ │ │ │
Impennes │ │ │ │ │
Steganopodes │ │ │ │ │
Tubinares │ │ │ │ │
Herodiones │ │ │ │ │
Odonotoglossæ│ │ │ │ │
Palamedes │ │ │ │ │
Anseres │ 5│ 1.5│ │ │ 1
Struthiones │ │ │ │ │
Crypturi │ │ │ │ │
Total Birds │ 10│ │ 0│ 1│ 3
─────────────┼─────┼────────┼────────┼────────────────┼────────
Total │ 54│ │ 0│ 3│ 10
─────────────┴─────┴────────┴────────┴────────────────┴────────
═════════════╤════════════════════════════════════════════════════════
Heart of │ Dilatation
─────────────┼─────────┬───────┬─────────┬─────────┬───────┬──────────
„ │Pulmonary│ Renal │ Chronic │ Acute │Thyroid│Myocardial
│ Disease │Disease│Infection│Infection│Disease│ Disease
│ │ │ │ │ │
│ │ │ │ │ │
─────────────┼─────────┼───────┼─────────┼─────────┼───────┼──────────
Primates │ 1│ │ │ 1│ │ 1
Lemures │ │ │ │ │ │
Carnivora │ 2│ 4│ 1│ 2│ 3│ 2
Pinnipedia │ │ │ │ │ │
Rodentia │ 3│ 2│ 2│ 4│ │
Insectivora │ │ │ │ │ │
Chiroptera │ │ │ │ │ │
Proboscidea │ │ │ │ │ │
Hyracoidea │ │ │ │ │ │
Ungulata │ 1│ 2│ 2│ 2│ │ 1
Edentata │ 1│ │ 1│ │ │ 1
Marsupialia │ 1│ 3│ 2│ 2│ │ 1
Monotremata │ │ │ │ │ │
Total Mammals│ 8│ 12│ 7│ 11│ 3│ 10
│ │ │ │ │ │
Passeres │ │ │ │ 1│ │
Picariæ │ │ │ │ │ │
Striges │ │ │ │ │ │
Psittaci │ 1│ │ │ │ │
Accipitres │ │ │ │ 1│ │ 1
Columbæ │ │ │ │ │ │
Pterocletes │ │ │ │ │ │
Galli │ │ │ │ 1│ │ 1
Hemipodii │ │ │ │ │ │
Fulicariæ │ │ │ │ │ │
Limicolæ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │
Pygopodes │ │ │ │ │ │
Impennes │ │ │ │ │ │
Steganopodes │ │ │ │ │ │
Tubinares │ │ │ │ │ │
Herodiones │ │ │ │ │ │
Odonotoglossæ│ │ │ │ │ │
Palamedes │ │ │ │ │ │
Anseres │ │ 2│ 1│ 2│ │ 1
Struthiones │ │ │ │ │ │
Crypturi │ │ │ │ │ │
Total Birds │ 1│ 2│ 1│ 5│ 0│ 3
─────────────┼─────────┼───────┼─────────┼─────────┼───────┼──────────
Total │ 9│ 14│ 8│ 16│ 3│ 13
─────────────┴─────────┴───────┴─────────┴─────────┴───────┴──────────
For meaning of italics see foot note Table 1.
The rodents seem to have no power to increase muscle bulk, but a
sufficient number of cases of dilatation occur to make one conclude that
this is their method of response to unusual strain. Pulmonary disease,
mostly of infectious nature, and myocardial degenerations are the
principal causes.
The next order to show cardiac enlargement is the Ungulata where
nephritis is the most frequent association with hypertrophy and disease
of the pleura and pericardium with dilatation, or the reverse of the
factor value in the Carnivora. These animals, fairly well prepared for
flight, with moderately large hearts, seem more often to show dilatation
than hypertrophy.
Two Edentata (armadillo) showed dilatation but no hypertrophy.
Marsupials behave somewhat like rodents in that the heart does not seem
to increase muscle bulk, but our records do not explain this clearly. As
already mentioned four cases had no sufficient internal reason for
dilatation, but as one was probably the result of shock three only
remain to be accounted for. Nephritis seemed to exist in all three, but
two of them had kangaroo mycosis of the jaw and a general chronic
infection.
If now our attention be given to the Aves we find the highly specialized
Passeres and Striges not represented and their closely related well-
organized orders Picariæ and Psittaci with only an isolated single case.
This is the more interesting since the last order suffers reasonably
often with arteriosclerosis. Accipitres, the birds of pugnacious habit
and carnivorous diet, seem well able to increase their muscle upon
demand, but do not often suffer dilatation. Vascular and renal diseases
stand out most prominently in the etiology, and one-half of them show
myocardial change. The Galli, which includes both ground and flying
birds, are represented but fail to exhibit any unusual accompanying
disease. Anserine birds apparently have a low power to increase the size
of the heart, but most often allow it to dilate. Struthiones, large
stalking and rapidly travelling birds, apparently have a good margin of
safety in their cardiac mechanism.
SUMMARY OF LESIONS ASSOCIATED WITH HYPERTROPHY AND DILATATION.
Analysis of the associated pathology will reveal that among the mammals,
renal disease, chronic infections and diseases of the thoracic serosa
are most often responsible for hypertrophy, and that something over one-
third of the hearts showed myocardial damage. Among the Aves
arteriosclerosis and renal disease are most important in enlarging the
heart; half of the cases had myocarditis. In so far as dilatation in
mammals is concerned, renal disease and acute infections are decidedly
more important than other influences, even than the next in order—
chronic infections and pulmonary diseases; only one-fifth of the cases
had myocardial disease. Acute infectious disease is the most potent
cause of dilatation in birds; only two of the eight cases had
degeneration of the heart muscle.
COMPARISON OF MAMMALIA AND AVES.
If a comparison of the incidence of increased muscle bulk in the two
classes be made[9] it will be found to occur two and one-half times more
often in mammals, while dilatation occurs nearly ten times more often
among the mammals than among the birds. Hypertrophy is accompanied by
myocardial change in 44 per cent. of the cases, whereas muscular
degeneration was only seen in 24 per cent. of the dilatations; this
change is conspicuously lacking in the Primates, Ungulates and
Marsupials. The usual teaching has been that dilatation, which means
enlargement of chambers and thinning of walls or at least no thickening
thereof, implied an inability on the part of the heart to keep up with
increased demand—a decompensation. If Starling be correct that
dilatation is not a degeneration of pump value but merely one of
adaptations to increased demand, then this method is more characteristic
of mammals than of birds. There is, however, the reserve power to
increase the muscle bulk inherent in the mammalian, not possessed or
needed by the avian heart. The large-hearted class Aves certainly dilate
their blood pump less frequently than mammals and indeed have less
cardiac disease.
An analysis of the incidence of hypertrophy _versus_ dilatation shows
that hypertrophying power resides in the Primates, Accipitres and
Struthiones, their hearts relatively seldom dilatating. Lack of such
power and consequent dilatation resides in Rodentia, Ungulata,
Marsupialia and Anseres. Hypertrophying power lies therefore chiefly in
the heart of average size for its class, dilatation occurring in the
small heart. (See page 63.)
AVIAN HYPERTROPHY.
There is little to be learned from the nature and anatomy of the
hypertrophies and dilatations except perhaps their character among the
birds, in which the physics of the circulation is somewhat peculiar. In
this class both the hypertrophy and distention are predominatingly left-
sided, a state probably explained by the pressure against which the pump
must work in flight because then the lungs and the viscera are somewhat
compressed by the pressure of an excess of air in the pneumatic sacs. At
all events while concentric hypertrophy was mentioned once, it is
difficult to estimate the degree of increase in the right chambers
because they are not uncommonly well filled when diastole occurs at
death. Grober[10] asserts that the normally large heart (or what I have
called “physiological hyperplasia”) shows a “hypertrophy” of the right
ventricle because of the extra work entailed in flying. This is
certainly not the case in the material we have seen under pathological
conditions. Right sided increase might be expected if pulmonary or
serous membrane affections were prominent, but left-sided increase,
following arteriosclerosis and nephritis is the actual finding. The best
examples of concentric hypertrophy are in the dogs with thyroid disease
and the best examples of concentric dilatation in ungulates suffering
shock.
SUMMARY.
The foregoing pathological data can now be summarized by grouping the
facts under the headings of absolute and relative vulnerability of the
heart. By the former is meant the actual number and quality of lesions
in the various orders, but here at once one comes upon the irregularity
of examples of zoological and pathological character, and if one trust
entirely to the percentages, fallacious conclusions might be reached.
Basing judgment upon the incidence of pathological lesions in mammals
and birds, it is evident that the former has greater vulnerability, as
13 is to 6.2. This is noteworthy as we shall learn that the bird has a
larger and apparently better prepared heart than the mammal. Attempts to
discover the order or kind of animal having the greatest or lowest
vulnerability are difficult for the reason given above. Thus, for
instance, Pinnipedia, Proboscidea, Edentata, Gaviæ, Impennes,
Steganopodes, and Struthiones present the highest percentages of cardiac
lesions, but the total specimens examined are so few that these figures
may well be misleading. (See Tables 1 and 2.) If, however, figures mean
anything in such small groups, these are the animals which have the
greatest cardiac vulnerability. They have little in common in regard to
zoological relationships and habits; four of the seven orders are rather
slothful and three are active. It is much better to limit our
observations to those orders from which sufficient examples have been
subjected to autopsy and upon which we have some standards for
comparison in the heart-body weight ratio. It so happens that in the
above seven orders I was unable to obtain any reliable figures of heart
weight. Table 3 is a combination of data from Tables 1 and 2 for the
principal orders from which we have enough material (at least one
hundred autopsies) and for which it is possible to obtain as comparative
standards figures indicating the weight of the normal heart in kilograms
of body weight; Table 4 gives these ratios for normal hearts. The
information about the weights was obtained from some of our own figures
and the references given in the footnote.[11] There are no extensive
data upon weights and measures in exact terms, such as body weight, so
that we are limited to the numbers quoted in parentheses besides the
orders in the table. The ratios might be modified slightly by a greater
number of examples, but they show certain things by comparison of the
classes; in a rough manner the heart ratios correspond to the pathology.
TABLE 3.
_Table Containing a Condensation of the Two Foregoing Tables and
Showing Figures for Degenerations, Hypertrophy and Dilatations for
Orders Having the Largest Number of Autopsies._
═════════════════╤═════════════════╤═════════════════╤═════════════════
│ Degenerations, │ Hypertrophy │ Dilatation
│ &c. │ │
─────────────────┼─────────────────┼─────────────────┼─────────────────
Primates │ 7.6│ .8│ .8
Carnivora │ 11.│ 2.1│ 2.2
Rodentia │ 8.│ 0.│ 4.2
Ungulata │ 5.4│ 1.2│ 3.
Marsupialia │ 19.│ .6│ 5.
│ │ │
Passeres │ 1.4│ 0.│ 0.
Picariæ │ _6.7_│ _1.1_│ 0.
Striges │ .8│ 0.│ 0.
Psittaci │ 3.4│ 0.│ .1
Accipitres │ 18.3│ 4.3│ .5
Columbæ │ 2.│ 0.│ 0.
Galli │ 9.3│ .7│ .7
Herodiones │ 4.1│ 0.│ 0.
Anseres │ 15.7│ .6│ 1.5
─────────────────┴─────────────────┴─────────────────┴─────────────────
TABLE 4.
_Table Showing Weight of Normal Heart in
Relation to Body Weight. Number of Specimens
used to Determine Weight Quoted in Parenthesis._
════════════════╤═══════════════════════════════
Average Heart of│Grams per Kilogram of Body.[12]
────────────────┼───────────────────────────────
Man ( 4)│ 5.67
Primates ( 4)│ 6.56
Carnivora ( 6)│ 6.78
Rodentia ( 5)│ 5.
Ungulata (10)│ 5.8
Marsupialia ( 3)│ 5.1
│ Average 5.82
Passeres (43)│ 19.8
Picariæ ( 9)│ 21.3
Striges ( 4)│ 7.33
Psittaci ( 6)│ 8.89
Accipitres ( 7)│ 12.32
Columbæ ( 4)│ 14.47
Galli (16)│ 11.08
Fulicariæ ( 3)│ 23.82
Limicolæ ( 2)│ 8.78
Anseres (14)│ 11.8
Struthiones ( 1)│ 12.7
│ Average 13.84
────────────────┴───────────────────────────────
For meaning of italics see foot note Table 1.
However, there are many reasons why great caution should be used in
evaluating the relative size of the heart. Welcher showed in his work
that the proportion is greater in small and young animals than in large
and adult ones. All the authors quoted agree that in birds and to less
degree but still clearly in mammals, there is a direct relationship
between the bodily activity of an animal and its cardiac bulk. This is
fairly well shown in the list of avian heart ratios, but not so clearly
in the mammals. What shall be considered the most active mammals—the
monkey, perhaps, with his tendency to be occupied constantly, yet we
find the greatest heart bulk among the Carnivora, animals prepared for
travel and struggle, and the smallest among the Rodentia, quiet and
timid animals. The avian order showing the greatest cardiac ratio, the
Fulicariæ, shore birds, is made up of some quiet hiding varieties, and
of some capable of very prolonged flight; the most constantly active
fliers (Passeres) also have a high cardiac weight proportion. The
inactive owls have the smallest heart bulk.
The contrast between the average heart-to-body weights of mammals and
birds is striking, the latter having two and one-half times as much as
the former, 5.8 _vs._ 13.8. Since this is the most prominent and best
supported statement in the table of weights, it may be used to compare
with the incidence of the pathology as seen in the two classes.
Degenerations and inflammations occur in mammals and birds as 9.5 is to
5.5.[13]
Hypertrophies occur in mammals and birds as 10.3 is to 4.3.[13]
Dilatations occur in mammals and birds as 2.4 is to .28.[13]
In other words, mammals are much more susceptible than birds to
degenerative and inflammatory processes, show an ability to increase the
muscle bulk two and a half times as great and are liable to chamber
distention nearly ten times as often. It might also be put that birds
cannot or do not need to increase their muscle, and that the chamber and
muscle balance is more perfectly arranged.
While in the preceding pages hypertrophy has been discussed rather from
the standpoint of its value as a compensating and reserve capacity, and
dilatation as a degenerative or decompensatory process on the part of
the cardiac mechanism, it may be that dilatation of the mammalian heart
is the usual method employed by the class in response to increased
demand. It seems certain, however, that the originally and normally
larger heart, both mammalian and avian, more often uses an increase of
its muscle to this purpose.
Hypertrophy was accompanied by myocardial disease in 44 per cent. of the
cases, while dilatation showed this change in only 24 per cent. This
supports the theory that dilatation is a normal response of the
myocardium under strain and the belief held in many quarters that the
muscle increases its bulk because some of it is damaged.
The differences between classes are not so conspicuous between orders.
However, the large heart of the carnivores increases both its muscle and
chambers, while the small heart of the rodents and marsupials more often
dilates. Analysis of the avian orders is inconclusive and somewhat
contradictory. Let it suffice to say that the birds which fly most, with
exception of the ducks, have a relatively low vulnerability, and the
soaring carnivorous Accipitres and the largest birds, Struthiones,
apparently have a high susceptibility to damaging influences and enlarge
their muscle bulk in response to increased work.
Aneurysms of the heart are quite rare; only two have been seen. They
were both located at the apex of the left ventricle in birds; they did
not rupture. Myocardial damage is evident in both cases but the cause is
not clear; parasites could not be demonstrated. Plimmer reports a case
of cardiac aneurysm at the apex from infestation of the heart muscle by
sarcosporidia.
SECTION III
DISEASES OF THE BLOOD VESSELS
The gross anatomy of the blood vascular system is constructed upon the
same general scheme throughout mammals and upon a comparable basis in
birds. Microscopically there is little variation throughout the orders
unless it be in the relative proportion of muscular and connective
tissues. The origin of the great vessels at their cardiac base and their
distribution to the pulmonary and to the greater circulations in no way
differ in these two classes in that it always consists of an efferent
pathway to the lung and a root vessel above the aortic orifice. The
former has usually quite a distinct origin on the right side, but in
some birds the posterior wall of the pulmonary artery may overlie the
entire aortic base; this, however, is not the rule for birds. The aorta
in most mammals remains a separate and distinct vessel for some
distance, after which it gives off the innominate and subclavians. In
the birds on the other hand, the stretch immediately above the aortic
valve is usually ballooned out somewhat, into a sort of sac or ampulla
from which the subclavians and descending aorta arise. This forms a
structure of rather trident shape, the lateral prongs being the
subclavians, the middle and posterior being the aorta proper. In some
birds the aorta may have the length of a centimetre or more then
dividing into the left subclavian and right aorta from which the right
subclavian comes off.
There is definitely more support to the heart and vascular roots in
mammals than in birds, in the latter class these structures lying quite
free between the lateral air sacs and well in front of the lungs. Nor is
there the richness of mediastinal areolar and fatty tissue in the winged
creatures.
The vessels of mammalia retain a considerable wall throughout nearly
their entire length. At first the wall is thin compared to the calibre
of the vessel while the arteries smaller in calibre, have a heavy wall.
In birds the arterial stalk at the heart is supplied with very heavy
walls, but after the second branching the relation of wall to calibre
seems to continue about the same. In this class the stalk vessels have
wall to calibre relation of 1 to 3 (measurements in 2 Passeres, 1
Psittaci, 1 Accipitres) whereas in mammals the relation varies from 1 to
5 to 1 to 7 (observations on 2 carnivores, 1 ungulate, 2 rodents). In
mammals the consistency of a normal artery wall remains much the same, a
firm, resilient, yellow-white tissue, quite opaque and standing open
upon cross section. In birds this description covers the main stalk, the
aorta in the abdomen and the first part of the carotid and iliacs. When
these characters are lost, the arteries become semitranslucent bluish
strands so that they are difficult to follow in the muscles of the neck
and extremities. This is particularly true in the Passeres, Picariæ,
Galli and Columbæ while in the Psittaci, Accipitres, and Anseres the
arteries are distinctly whiter than the veins but yet quite soft. In the
Herodiones and Struthiones, thick walled vessels may be followed as far
as the second joint in both extremities. These differences depend in
part upon the grosser construction of the central arteries in Aves and
in part upon the larger amount of elastic tissue in them than in the
secondaries and smaller vessels, and than in comparable mammalian
vessels.
It is impracticable to go into the minutiæ of histology in the different
orders, which indeed varies but little, although attention might be
directed to the facts that in all central vessels the relative amount of
elastica is greater than in smaller ones and that muscular tissue seems
to exceed in the latter. Considerable work has been done upon the amount
and arrangement of muscle bands in isolated genera, but no comprehensive
data are at hand upon orders. The strands of muscle do not seem arranged
so regularly as in mammals; the pulmonary artery of the cat, for
example, has a muscle arranged like an oblique band in waves or festoons
along the length. The mammals as a class seem more richly supplied with
arteries and veins than do the birds, and the square area of the
vascular system is likewise larger. This is distinctly different from
the amount of heart bulk as given in the discussion of kilogram-heart
ratios so that one might say that the birds are “overhearted and
undervesseled.”
In so far as the physiology of the two classes is concerned it is
obvious that a different regulatory system is necessary because, aside
from the variations of pressure incidental to pulmonary, muscular and
visceral work, there remains the altering pressure within the air sacs
of Aves, a force different under states of rest, of running, of deep
water swimming and of flying with or against the wind. Part of the
internal air pressure variation is cared for by the ability a bird has
to respire the air in its sacs and bones, but in prolonged exposure to
the pressure under water or during protracted flight some compensatory
mechanism doubtless exists. This seems to reside in part in the heavy
elastic quality of the arterial stalk and the very rich venous supply of
the abdomen, including the renal-portal system and the distensible
pelvic veins. Just where the governing power for this mechanism resides
is as much a matter of debate as in the case of the human being, but
certain researches would place it in the caudate lobe and pituitary
body.
Having discussed these general comparative data we can now pass to a
consideration of the pathology seen at this Garden. The subject will be
studied from the standpoint of the vessels as a system and the changes
peculiar to it. Naturally the most important lesions affect the great
stalks and the principal trunks, from which the processes may continue
into the smaller vessels. The essential alterations are inflammatory and
degenerative, of which the latter are by all odds the more important.
The former are either involvements of the vessel walls by frankly
infectious processes, or less easily proved to be bacterial in origin,
as is the case with periarteritis nodosa. Acute arteritis and phlebitis
are constantly encountered and present nothing unusual. General nodal
periarteritis has been seen in the lower animals, Lupke having
reported[14] before the German Pathological Society a big outbreak in
cows, but it is less common than among men; we have not discovered it
here.
THROMBOSES.
Thrombosis is practically always a parasitic or an infectious process
although at times considerable difficulty is encountered in explaining
the source of the worms or bacteria. Thus, for example, the iliac or
femoral thromboses which are at the bottom of intermittent claudication,
are frequently quite vague in origin. We have had one such case in a
deer in which a partly occluding thrombangeitis existed in both femoral
arteries and veins. Mesenteric thrombosis, a serious condition in cattle
and horses from infestation with sclerostomum or strongylus, has not
been proven at the Garden, but we have seen one case of numerous
thromboses of the venous radicals in the jejunal wall apparently due to
some nematode larvæ; the specimens were so soft by decomposition that
determination was not attempted. There occurred a thrombosis of the cava
and aorta originating from a necrotizing cloacitis, apparently
streptococcal in nature, in a Demoiselle crane. The clot, while not
totally occlusive, extended nearly as far as the heart in the vein and
the abdominal aorta. There is also on record a thrombosis of the vena
cava and right pulmonary vein in an American beaver, harboring
Hepaticola hepatica in the liver, with a fibrosing pneumonia due to this
parasite. Another case in which parasites seemed to take a hand
concerned a common raccoon with tapeworms (sp.?) in the small intestine
and microscopically discoverable parasitic parts in the lungs; these
organs were the seat of extensive congestion and venous thrombosis, the
latter containing really enormous numbers of diplococci. The parasites
probably paved the way for bacterial invasion. A frank case of septic
thrombotic aortitis was noted in a Rice Grackle, the infectious focus
apparently being a vegetative “tricuspid” valvulitis.
ARTERITIS.
In addition to these cases, productive inflammatory changes were
discovered five times affecting vessels in or near frank inflammatory
processes. The animals affected with this productive process were three
birds, a rodent and an elephant. In the case of two birds and the rodent
the process was associated with chronic intestinal lesions, while in the
elephant it was found as an endarteritis obliterans in large vessels of
the lung of chronic pulmonary tuberculosis occurring in this animal.
These instances serve as examples of the truly productive inflammatory
processes affecting vessels and illustrate the distribution through the
animal kingdom. Pathogenetically there are no essential differences, and
histologically they correspond to the forms seen in man. Had every piece
of tissue been subjected to microscopy wherein such lesions might have
existed, more examples might have been discovered, but these processes
excite no peculiar secondary effects so that attention is not drawn to
them directly. The only noteworthy difference between mammals and birds
is the fragile character of the clots in the latter class. This is
peculiar because the principal response of this class to an infectious
irritant is coagulation necrosis, liquefying enzymes apparently being
absent or small in quantity.
Fatty deposits in the aortic intima are by no means uncommon in the
human subject and are encountered at all ages, even in youth at a time
when progressive arteriosclerosis does not accompany them. There is a
belief in many quarters that this fat may be laid down and then removed.
Such deposits are exceedingly rare in wild animals; when they occur it
is in small indefinite patches and not the bands or rows as found in
man.
TABLE 5.
_Table Showing the Incidence of Degenerative Arterial Disease, the
Percentage in Animals Subjected to
Autopsy and the Principal Associated Pathology._
════════════════╤═════╤══════════╤═════════╤═════════╤══════════
│Total│Percentage│ Due to │Aneurysms│Myocardial
│ │ of order │parasites│ │ disease
│ │ │ │ │
────────────────┼─────┼──────────┼─────────┼─────────┼──────────
Primates[15] │ 3│ .6│ │ │ 3
Carnivora │ 16│ 3.3│ 5│ 7│ 1
Ungulata │ 13│ 3.5│ 2│ │ 1
Marsupialia │ 3│ 1.8│ │ │
Total │ 35│ 1.8│ 7│ 7│ 5
│ │ │ │ │
Passeres │ 3│ .22│ │ 2│
Picariæ │ _2_│ 2.2│ │ │
Psittaci │ 13│ 1.8│ │ 1│
Striges │ 3│ 2.2│ │ │ 1
Accipitres │ 13│ 6.6│ │ 1│ 4
Galli[16] │ 5│ 1.6│ 1│ │ 4
Steganopodes[16]│ _5_│ _25._│ │ │
Herodiones │ 1│ 1.│ │ │
Palamedes │ _1_│ _20._│ │ │ 1
Anseres │ 11│ 3.4│ │ 2│ 4
Struthiones │ _7_│ _22._│ │ │
Alectorides │ _2_│ _5.4_│ │ │ 1
Total │ 66│ 1.8│ 1│ 6│ 15
────────────────┼─────┼──────────┼─────────┼─────────┼──────────
Grand Total │ 101│ 1.8│ 8│ 13│ 20
────────────────┴─────┴──────────┴─────────┴─────────┴──────────
════════════════╤══════════╤═══════╤═════════╤══════════
│Valvulitis│ Renal │ Chronic │ Chronic
│ │disease│pulmonary│infectious
│ │ │ disease │ disease
────────────────┼──────────┼───────┼─────────┼──────────
Primates[15] │ │ │ │ 1
Carnivora │ │ │ 1│ 5
Ungulata │ 1│ 2│ 3│ 2
Marsupialia │ │ │ │
Total │ 1│ 2│ 4│ 8
│ │ │ │
Passeres │ │ │ │
Picariæ │ │ │ │
Psittaci │ │ 6│ 3│ 2
Striges │ 2│ │ │
Accipitres │ 2│ 5│ 2│ 4
Galli[16] │ │ 2│ 1│ 2
Steganopodes[16]│ 1│ 3│ │
Herodiones │ │ │ │
Palamedes │ │ 1│ │
Anseres │ 1│ 4│ 1│
Struthiones │ │ 1│ 2│ 3
Alectorides │ │ 1│ │
Total │ 4│ 25│ 9│ 11
────────────────┼──────────┼───────┼─────────┼──────────
Grand Total │ 5│ 27│ 13│ 19
────────────────┴──────────┴───────┴─────────┴──────────
For meaning of italics see foot note Table 1.
DEGENERATIVE ARTERITIS OR ARTERIOSCLEROSIS.
Whether or not it be exact to speak of the more protracted forms of
vascular disease usually called arteriosclerosis or atheroma as
degenerative, such changes form the most pronounced features of the
lesions, and we have made such a separation at this laboratory. Here is
not the place to engage in the academic discussion of the nature of the
process, but I wish to state that collectively the changes as seen in
such lesions in the lower animals are more degenerative than productive,
and that we have never seen true ulcerative atheroma as it not
uncommonly appears at the autopsy table in any large hospital. This
disease of the vascular walls has long been attributed to alcohol, gout,
syphilis and other such prolonged intoxications to which we might apply
the light term of “toxins of civilizations.” Too little credit, or
discredit has been given to chronic intestinal disorders, overeating,
and overdrinking of ordinary fluids, to entirely incorrect diets, and to
chronic bacterial diseases. Even though the exact counterpart of the
disease in man does not occur in lower animals, we shall see the
probable association with food and with habits, in a manner discordant
with former teaching of the causation of the disease.
The group to which the name degenerative arteritis has been applied is,
as has already been indicated, more productive than the analogues seen
in the human being, but indeed it is questionable whether the lesions
even in the lower animals are not more degenerative than productive.
Since, however, chronic arteritis is always associated with damage to
the elastic and muscular fibres of the media as well as with fatty
change and overgrowth of the intima, all the deforming and degenerative
cases will be classed together.
The general picture in mammals is one of diffuse rather than of plaque-
like thickening, but well outlined raised or depressed areas are
encountered. In the aorta and larger branches one may find irregular
streaking and loss of elasticity with fairly clear, pale yellow or gray,
flat sections of distinct opacity. Rarely these may contain calcareous
matter, a change most often seen in the carnivores. The lesions are very
largely limited to the aorta; 26 or 76 per cent. of the 35 cases had
this distribution alone. The arch seemed never to be affected alone, and
indeed it is rather commoner to find opaque patches stretching along the
thoracic or even abdominal portion; this is especially true of the
Ungulata.
[Illustration:
FIG. 2.—ARTERIOSCLEROSIS AND ATHEROMA. THORACIC AORTA. JACKAL (CANIS
AUREUS). THIS WAS CONTINUED TO THE MESENTERIC AND ILIAC VESSELS.
]
There have been also in mammals five cases of mesial change which have
given rise to the picture described by Mönckeberg and usually entitled
by his name. However, the noteworthy differences between the wild animal
and the human cases are the absence of advanced calcification in the
media under the concavities and the prominence of the changes in the
aorta near the heart to be found in the former. These few cases do not
permit an association of the arterial disease with any particular
pathology in other parts.
Considered minutely, the outstanding lesion in the class Mammalia is the
separation of the elastic fibres by fluid and debris, apparently derived
from the degenerated muscle fibres, associated with a decrease of round
and elliptical nuclei. Globules and hyaline pink staining material are
often collected between split-up elastic strands, which fibres in some
cases seem quite numerous, in others reduced. In the intima heaping-up
of cells and fibres is very moderate in degree while usually one finds
only subendothelial edema. When the process has advanced far, the
microscopy is like that of well developed human lesions. Arterial
degeneration due to parasites gives a different picture in that medial
degeneration is far advanced and some fibrinocellular activity is seen
upon the intima when this tissue remains. When, however, the infestation
has proceeded to weaken the wall sufficient for it to give way into an
aneurysm, little or no vestige of the true arterial wall is left.
In the Aves the distribution and anatomy of this process present some
differences. The aorta is as usual most conspicuously the seat of
change, but it is noteworthy that the dilatation or ampulla immediately
above the aortic valves and from which the main vessels spring, is
practically always free of lesions which are on the other hand most
marked in the thoracic and abdominal sections. One’s attention is
usually attracted to the aortic surface by its roughness although
visibly there may be no plaques, but upon close inspection a mottled
opacity may be detected. This all seems due in the few cases subjected
to tissue section, to hyperplasia of endothelia, with or without fibre
increase. The media may show muscular granularity or no change at all.
At the stage when plaques are formed, fairly well outlined, firm but
rather brittle, raised areas are detected, seated upon a distinctly
opaque gray wall. The remainder of the vessel may be smooth and elastic
but sometimes, in the Accipitres for instance, a general resistance to
pressure and tension is found. Microscopically such a vessel will show a
media the seat of ruptured muscle fibres, split-up or broken elastica
and some debris, while the intima is covered with active and distinct
fibrocellular exudate.
I have for comparison divided the cases into those in which the
superficial productive character was prominent and those seemingly
entirely a degeneration of the media, that is with inactive intima. In
mammals 77 per cent. of the cases were of the degenerative type while in
birds 50 per cent. were of this kind. The exact importance of this
difference is not easy to evaluate, but with the facts that the bird has
a greater elastic supply for its large vessels and a greater wall to
calibre ratio, it is interesting. The aorta alone was affected in half
of the birds, the remainder showing lesions in the carotids and
femorals.
The tendency for the media to degenerate would lay the basis for
concavities on the intimal surfaces after the type seen in Mönckeberg’s
sclerosis. A number of cases of this variety have been encountered, but
instead of being better developed in the vessels of extremities as in
man they have presented more definite pictures in the aorta and
pulmonary vessels. Examples will be quoted under the discussion of the
various orders.
[Illustration:
FIG. 3.—ARTERIOSCLEROSIS, ATHEROMA AND ANEURYSMAL DILATATIONS IN
THORACIC AORTA. WILD CAT (FELIS RUFFUS).
]
Primates are not often affected with degenerative arterial disease, two
of the instances observed showing this change confined to the coronary
vessels. As might be expected the myocardium in both was affected, and
in one animal had a definite concentric hypertrophy. A very interesting
case was encountered in a Lion-tailed Macaque (_Macacus silensis_). His
heart showed distinct fibrosis of the conducting pathways from auricle
to ventricle and of the papillary muscles. No atheroma was present in
the aorta, but in the pulmonary distinct sacculations of the Mönckeberg
type were found. Mesial degeneration was apparently responsible, but no
calcification had occurred. Death was due to acute gastritis.
Carnivora present about half the cases seen in mammals and 16 per cent.
of the total. Five of the sixteen cases owe their origin to parasitic
arteritis and were combined with aneurysms. As will be noted by
consultation of the list there is no outstanding accompanying pathology,
a fact which makes parasites more important. One case of mesial
degeneration, resembling the Mönckeberg type was observed in the
thoracic aorta of a bear.
Ungulata are generously represented, thirteen cases being recorded
distributed rather unevenly between the odd-toed (1 or 8.5 per cent.)
and even-toed groups (12 or 2.9 per cent.). The single case in the first
group occurred in a Zebra (_Equus burchelli_) wherein was found about
the middle of the thoracic aorta a diffuse thickening of media and
intima in a circular plaque approximately two centimetres in diameter;
it was by no means so well developed as similar lesions in the even-toed
ungulates. This recalls the expression of doubt by Zinserling as to the
occurrence in the horse of arteriosclerosis similar to that in human
beings.
The lesions in the Artiodactyla are both in plaques and diffuse, the
aorta and its branches sometimes being quite wrinkled but beset with
firm elevations with and without calcification. These changes are fairly
definite and, although they never attain the development seen in man,
resemble the stage of wrinkling and roughness in the preulcerative stage
of the human analogue. Two of the cases were associated with dilatations
of the mesenteric vessels and with periarteritis, a picture strongly
suggesting parasitic infestation; in one case ineffectual search was
made, in the other no record is made of the parasites. Renal disease
occurred only twice and myocardial damage only once. Chronic pulmonary
disease, present thrice, took the form of tuberculosis twice and pleural
adhesions with atelectasis once.
Marsupialia present three quite interesting cases, a Tasmanian Devil
(_Sarcophilus ursinus_) and two Kangaroos (_Macropus_). The first showed
distinct sacculations in the ascending aorta, suggestive of Mönckeberg’s
sclerosis but equally resembling several small or incomplete aneurysms.
The underlying vessel was opaque and stiff, continuing so to the middle
of the thoracic portion. The other marsupials showed distinct mesial
damage with early calcification and a roughened intima; once the
pulmonary artery was involved.
It will be noticed that the orders Rodentia and Lemures are missing from
those showing arterial disease although we have a reasonable number of
autopsies upon them.
Passeres are hardly good exponents of vascular disease, an interesting
thing in view of their large heart, heavy vessels, and flying habits. It
is, however, striking that two of the three birds of this group had
aneurysms of the aorta, one of which ruptured just above the origin,
partly into and partly outside the pericardium. Despite several
microscopical sections we were unable to find the tiny ends of the
breach and any evidence of parasites. In the other case a vegetative
growth occurred on the intima near the dilatation.
[Illustration:
FIG. 4.—ARTERIOSCLEROSIS IN AORTA. OTTER (LUTRA CANADENSIS). THERE IS
RELATIVELY LITTLE INTIMAL CHANGE, THE MEDIA BEING FIBROTIC AND
ALLOWING THE INTIMA TO BE DEPRESSED IN SMALL CONCAVITIES.
]
The Picariæ were represented by a Hornbill and a Toucan. The former
presented roughened yellowish elevations for two centimetres above the
aortic valve; this seemed the only involvement. The Toucan had a few
small scattered but deep yellow plaques in the same location.
Psittaci, although failing to be accredited with a high percentage of
arterial disease, nevertheless present some striking and interesting
changes. In the first place, the central vessels are not so
conspicuously the principal seat of atheroma as is the case in many
other orders, and the lesions are not so productive. It is usual to find
flat areas of opacity, perceptible as easily by section through the wall
as by holding up the opened vessel to the light, the seat of the density
being in the media. This can be followed into the wing arteries and,
upon microscopic section, these smaller vessels will show mesial
degeneration, thus being comparable to arteriocapillary fibrosis of man.
However frequent this picture may be, there are also instances of
overgrowth in the intima, prominences over opacities or raised plaques
at the points of branching, lesions which correspond to the activity of
the inner coat. It is interesting that renal disease, chronic pulmonary
and general infections occur in a goodly proportion of these birds.
Striges is an order of little importance. The lesions in the two cases
consisted of rather prominent plaques in aorta and large branches.
Accipitres stand out as giving the greatest percentage of any order of
which we have had a fair number upon which to make comparisons. Their
arterial lesions are frequently accompanied by renal, myocardial and
valvular disease. Mesial and intimal alterations are about equal in
degree, irregular patches going on to softening without ulceration, and
early calcification being quite prominent. The sickle at the branching
of the renals is a favorite site of deposit. Like the parrots their
arterial damage is not confined to the aorta, but may be found in the
carotids, femorals or small wing arteries. The most common situation is,
however, in the lower thoracic and renal regions.
Galli, represented by five specimens, seem to have their vascular
disease accompanied very often by myocardial and infectious disease.
Their arterial pathology consists of raised gray patches in the aorta
only.
Steganopodes give the highest percentage among avian orders, but this
must be held _sub judice_ because of the small number of specimens
subjected to autopsy. Renal disease occurred in three cases. Their
lesions are in the form of yellow opaque streakings in the aorta and its
branches, in one case following the carotid half way up the neck.
Plaques are not common, and when they occur are streaky and illy
outlined.
Herodiones, represented only by a heron, are negligible. This bird
showed a diffuse thickening with early thrombotic deposits attached to
the intima.
Palamedes are represented by a Screamer which showed around the orifices
of the renal arteries an early fatty deposit and mesial opacity.
Anseres present a considerable number of cases which are accompanied by
cardiac, renal and general pathology. The character of the lesions is
like that of the Accipitres and the distribution differs in only one
particular. In four of these eleven cases the elevations or opaque areas
were limited entirely to the stretch of aorta which might be compared to
the arch in mammalia, that is the part with which the right subclavian
is in closest contact and which bends almost directly backward to become
the thoracic aorta. This excludes the ampulla just above the aortic
valves. There seems no real reason for this and it may be accidental.
[Illustration:
FIG. 5.—AORTIC ARTERIOSCLEROSIS. SARUS CRANE (GRUS ANTIGONE). THE
LESIONS ARE ELEVATED AND IRREGULAR.
]
Struthiones, with seven specimens having arterial disease in the great
vessels alone, seem to have no especial characters unless these be in
the heavy furrowing and stiffness of the wall, with opaque, elevated,
indefinite patches, seen mostly in the descending aorta; once a long
tough and partly brittle stretch was found in the carotid.
Alectorides, with a relatively high percentage, present irregularly
outlined fatty and finely granular patches in the intima of the lower
aorta and abdominal vessels, and, in two cases, as far as the vessels of
the lower extremities could be followed.
The orders Columbæ and Fulicariæ are missing from the list of Aves
having arterial disease, yet a reasonable number of autopsy records are
at hand.
SUMMARY ON ARTERIOSCLEROSIS.
Having discussed the orders separately, a review of the whole situation
is desirable. Chronic arteritis, or as it is usually called
arteriosclerosis, is common to very many zoological orders, and its
principal lesions are comparable throughout the two classes under
consideration. A statement as to its incidence would best be made by
adopting an arbitrary number of observations as the desired minimum upon
which to draw conclusions, and I shall adopt one hundred as such a
figure. Accepting this as reasonable, a review of the table indicates
that the order of percentage incidence is: Accipitres 6.6, Ungulata 3.5,
Anseres 3.4, Carnivora 3.3, Striges 2.2, Psittaci 1.8, Marsupialia 1.8,
Galli 1.6, Primates 0.6, Passeres 0.22; the other orders have less than
one hundred specimens each. There is no doubt that carnivorous birds
have the highest incidence of chronic arterial disease. Next in order
come three varieties with nearly equal incidence, the ungulates,
anserine birds and carnivorous mammals. These orders have little in
common unless it be that in nature they are often engaged in prolonged
or strenuous effort, as in fight or flight. We possess no measurement of
their vascular supply but by consultation of the table giving heart
weights (page 63) it will be found that three of them have values below
that of the class in which they belong; the Carnivora alone have a
greater heart-to-body ratio than the average for its class Mammalia. Nor
do these orders have any direct dietetic relationship. The expected
longevity of these groups does not permit one to discover any reason for
arterial changes except perhaps that they have a reasonably good
viability under park conditions, and therefore many have a longer
opportunity to develop vascular disease. It so happens, however, that
the first four groups are the most likely to suffer from
gastrointestinal inflammation, of dietetic or bacterial origin.
It is interesting, but not easily explicable that the orders of great
activity, Primates and Passeres, are at the end of the list; their food
is very largely carbohydrate in character. Just why Lemures, Rodentia
and Columbæ should be missing is not quite clear, because orders of
comparative habits and food are included.
A review of the concomitant pathology reveals the fact that nephritis
more often accompanies these processes than any other single condition.
Among the chronic infectious disease in the table is included chronic
enteritis; this group falls well behind the renal diseases. The
relatively small number of cases of valvulitis speaks rather against an
active infectious origin of the vascular lesions.
ANEURYSMS.
Aneurysms have been observed all over the world and in nearly all the
larger orders. The London Garden has had an unusually large number to
report, the most striking being that described by Seligman in the 1906
Report of the Society, in a tiger thirteen years in captivity which had
fourteen sacculations from pea to plum size scattered along the aorta.
Even with the number of cases on record and those collected here it
would be unwise to draw deductions as to their incidence or as to the
possibilities of vascular dilatation in any given order. Horses have
aneurysms occasionally, cows and dogs rarely, according to Rievel. I
can, however, state that there has not occurred in our experience a
large growing pulsating aneurysm in the aortic arch region comparable to
the condition so well known in man. The literature to which we have had
access gives a definite impression that parasitism of vessel walls is
the most important factor in the causation of ectasia, and that simple
non-parasitic arteriosclerosis is relatively unimportant. Two of our
seven cases seem to have been free of parasites but the notes cannot
entirely assure one of this. The distribution of cases at this Garden is
found in Table 5.
[Illustration:
FIG. 6.—PARASITIC ANEURYSM IN THORACIC AORTA. PARADOXURE (PARADOXURUS
LEUCOMYSTAX). PARTLY SACCULAR, PARTLY DISSECTING ANEURYSM WITH OPEN
THROMBOSIS AS INDICATED BY THE GLASS ROD. PIECES OF WORM FOUND IN
WALL. COULD NOT OBTAIN WHOLE SPECIMEN, SPECIES UNDETERMINED.
]
A dilatation of the first part of the arch in a seal to a size which
might be described as an aneurysm caused us to make such a diagnosis,
correctly enough from the size and shape of the vessel but possibly
worthy of reconsideration in light of the fact that no damage to the
wall was found. At the heart and in the descending arch the diameter
measured 4–5 cm., while the first part of the aorta measured 7.5 cm.
This great irregularity in width could not be found in other seals
albeit this section of the arch is usually a trifle larger than its
origin and descending portion. The cava in seals is also large, but in
this particular animal it measured 6 cm. across at the liver where there
is a normal dilatation. These two spaces are looked upon as normal
reservoirs for blood during diving, but the case in question seemed to
have excessive “aneurysmoid” enlargements without mural disease. London
reports an aneurysm of the aorta in a seal.[17]
Aneurysms are not so common in birds, the incidence being in comparison
with mammals as 1 to 2.2. Two seats are prominent for their development:
the sinuses above the aortic valves and the first part of the subclavian
vessels; two of the six cases occupied the first position, two the
second, while one other lay in the arch of the aorta, the last in its
descending thoracic portion. Those developing over the valves seem to
arise from simple degenerative arteritis; those that occupy the other
locations are apt to be surrounded by plaques on the intima. Aneurysms
in birds reveal by microscopy some trace of all the vascular coats and
seem not to construct an adventitia from surrounding areolar tissue. The
veins have presented no peculiar pathology, except in tumors which will
be taken up later. A Derby’s Tyran showed a phlebitis and periphlebitis
of the left subclavian vein, of mycotic nature, which led to death by
rupture and hemorrhage.
SECTION IV
DISEASES OF THE BLOOD AND BONE MARROW
The production and physiology of the circulating blood seem closely
similar in the two classes under consideration, although the anatomy is
not the same in birds and mammals, variations also occurring within the
latter group. Pathological responses follow comparable lines in that
hemolyzing agencies, be they hemosporidia, absorptions from metazoan
parasites or bacterial toxins, produce a reaction in erythropoietic
centres, and positively chemotactic viruses call forth increases in the
colorless elements. We have also observed a decrease of leucocytes in an
Orang Utan suffering from influenza, a finding analogous to that in the
human attack. There is, however, a much less ready response on the part
of birds to any leucocyte-stimulating influence, in this class the
mononuclears seeming to bear much of the burden assumed by the myeloid
cells of Mammalia or at least appearing on the stage very quickly so
that any increase of the latter is overshadowed by them. Perhaps this
apparent difference may be further explained by the greater number of
colorless blood cells, structures which might be called the principal
secondary defences of the body and constantly at the disposal of the
organism, normally present in the birds’ blood; they amount to 25,000
per cubic millimetre in birds, while in the mammals very few varieties
have half this number. On the accompanying Table (6) will be found a few
differential leucocyte counts now known to us.
TABLE 6. _Differential Percentages of Leucocytes._
_The Figures are based upon Counts of Two Hundred Cells upon Two Slides unless
Otherwise Specified. Blood Films were taken from Apparently Healthy Animals in the
Exhibition Cages._
════════════════╤════════════╤═══════╤═══════╤═══════╤══════════╤══════════════════
Animal │ Polymor- │ Small │ Large │Eosino-│ Special │ Notes
│phonuclears.│Lympho-│Mononu-│philes.│ │
│ Per cent. │cytes. │clears.│ Per │ │
│ │ Per │ Per │ cent. │ │
│ │ cent. │ cent. │ │ │
────────────────┼────────────┼───────┼───────┼───────┼──────────┼──────────────────
Potto │ 20.│ 67.│ 7.1│ 5.9│ │
Perodicticus │ │ │ │ │ │
potto │ │ │ │ │ │
Rhesus Macaque │ 30.2│ 61.4│ 5.6│ 2.8│ │
Macacus │ │ │ │ │ │
rhesus. │ │ │ │ │ │
│ (Av. 5 counts) │ │ │ │
Raccoon-like Dog│ 62.2│ 32.│ 2.│ 3.8│ │
Canis │ │ │ │ │ │
procyonoides. │ │ │ │ │ │
Swift Fox Canis│ 65.│ 18.│ 13.│ 1.│ 3 per │
velox. │ │ │ │ │cent. Baso│
Dingo Canis │ 77.│ 15.4│ 3.8│ 3.8│ │
dingo. │ │ │ │ │ │
Timber Wolf │ 76.5│ 15.5│ 3.5│ 4.5│ │
Canis │ │ │ │ │ │
mexicanus. │ │ │ │ │ │
Wild Cat Felis │ 55.8│ 34.│ 7.│ 3.8│ │
ruffus. │ │ │ │ │ │
Gray Ichneumon │ 52.6│ 44.4│ 2.3│ .7│ │
Herpestes │ │ │ │ │ │
mungo. │ │ │ │ │ │
Indian │ 66.│ 20.│ 14.│ 0.│ │
Paradoxure │ │ │ │ │ │
Paradoxurus │ │ │ │ │ │
niger. │ │ │ │ │ │
Large spotted │ 60.│ 31.2│ 1.2│ 7.6│ │
Civet Viverra │ │ │ │ │ │
megaspila. │ │ │ │ │ │
Ocelot Felis │ 79.│ 15.6│ 3.5│ 1.9│ │
pardalis. │ │ │ │ │ │
Texas Skunk │ 44.1│ 46.3│ 4.3│ 5.3│ │_a._ There are
Mephitis │ │ │ │ │ │several grades of
mesomelas. │ │ │ │ │ │eosinophilic
│ │ │ │ │ │granulations,
│ │ │ │ │ │ranging from very
│ │ │ │ │ │fine to very
│ │ │ │ │ │coarse. They are
│ │ │ │ │ │entirely discrete,
│ │ │ │ │ │however, and the
│ │ │ │ │ │eosinophile cells
│ │ │ │ │ │are quite distinct
│ │ │ │ │ │from the
│ │ │ │ │ │homogeneous
│ │ │ │ │ │neutrophiles.
Tayra Felis │ 75.6│ 19.2│ 4.1│ 1.1│ │
tayra. │ │ │ │ │ │
White nosed │ 60.│ 20.│ 18.│ 2.│ │_b._ The
Coati Nasua │ │ │ │ │ │protoplasm of the
narica. │ │ │ │ │ │leucocytes shows
│ │ │ │ │ │practically no
│ │ │ │ │ │stain. Mitotic
│ │ │ │ │ │figures are
│ │ │ │ │ │frequent among the
│ │ │ │ │ │polymorphonuclear
│ │ │ │ │ │cells. The small
│ │ │ │ │ │lymphocytes show
│ │ │ │ │ │basophilic
│ │ │ │ │ │granules.
Crab eating │ 45.│ 42.│ 2.5│ 10.5│ │
Raccoon. │ │ │ │ │ │
Procyon │ │ │ │ │ │
cancrivorous. │ │ │ │ │ │
Ring tailed │ 39.2│ 54.7│ 4.3│ 1.8│ │
Bassaris │ │ │ │ │ │
Bassariscus │ │ │ │ │ │
astutus. │ │ │ │ │ │
Kinkajou Potos │ 47.4│ 42.5│ 6.│ 4.1│ │
caudivolvulus.│ │ │ │ │ │
Common Raccoon │ 46.│ 42.9│ 7.4│ 3.7│ │
Procyon lotor.│ │ │ │ │ │
Texas White │ 67.│ 19.│ 11.│ 3.│ │
footed Mouse │ │ │ │ │ │
Peromyscus │ │ │ │ │ │
leucopus. │ │ │ │ │ │
Kangaroo Rat │ 55.│ 33.│ 6.│ │ 5 per │_c._ Many
Perodipus │ │ │ │ │ cent. x │leucocytes were
richardsoni. │ │ │ │ │ cells. │noted, with deeply
│ │ │ │ │ │staining nuclei
│ │ │ │ │ │filling up most of
│ │ │ │ │ │the cells. The
│ │ │ │ │ │protoplasm was
│ │ │ │ │ │colored a deep
│ │ │ │ │ │brown. These were
│ │ │ │ │ │called x cells
│ │ │ │ │ │pending
│ │ │ │ │ │investigation.
Polecat Mustela │ 42.4│ 54.6│ 2.1│ .9│ │
putorius. │ │ │ │ │ │
Common Opossum │ 44.│ 39.│ 7.│ 9.│ 1 per │_d._ Polynuclears
Didelphys │ │ │ │ │cent. Mast│quite large, with
virginiana. │ │ │ │ │ cells. │deeply staining
│ │ │ │ │ │nuclei which are
│ │ │ │ │ │in many instances
│ │ │ │ │ │entirely separate
│ │ │ │ │ │and distinct.
Bridled Wallaby │ 58.3│ 38.8│ 2.│ 4.2│ │
Onychogalea │ │ │ │ │ │
frenata. │ │ │ │ │ │
Six banded │ 57.1│ 23.2│ 6.3│ 13.4│ │
Armadillo │ │ │ │ │ │
Dasypus │ │ │ │ │ │
sexcinctus │ │ │ │ │ │
Elephant Elephas│ 15.│ 47.4│ 7.6│ 5.8│ (Bilobed │_e._ The ordinary
indicus. │ │ │ │ │ 23.8) │polymorphonuclears
│ │ │ │ │(Basophile│are very few in
│ │ │ │ │ .4) │number, and those
│ │ │ │ │ │seen have nearly
│ │ │ │ │ │all a faint
│ │ │ │ │ │acidophilic or
│ │ │ │ │ │basophilic
│ │ │ │ │ │character. The
│ │ │ │ │ │eosinophiles are
│ │ │ │ │ │quite distinct and
│ │ │ │ │ │their granulations
│ │ │ │ │ │are large and
│ │ │ │ │ │globular. The
│ │ │ │ │ │cells called
│ │ │ │ │ │bilobed are
│ │ │ │ │ │unusual and can
│ │ │ │ │ │probably best be
│ │ │ │ │ │accounted for as
│ │ │ │ │ │directly dividing
│ │ │ │ │ │small lymphocytes.
│ │ │ │ │ │The staining
│ │ │ │ │ │properties and
│ │ │ │ │ │shape of the
│ │ │ │ │ │nuclei of the
│ │ │ │ │ │bilobed cells are
│ │ │ │ │ │most closely
│ │ │ │ │ │related to the
│ │ │ │ │ │lymphocytes. They
│ │ │ │ │ │are not always
│ │ │ │ │ │regular, however,
│ │ │ │ │ │but may be almost
│ │ │ │ │ │as irregular as
│ │ │ │ │ │the polynuclears.
│ │ │ │ │ │In practically
│ │ │ │ │ │every instance,
│ │ │ │ │ │however, a
│ │ │ │ │ │connecting isthmus
│ │ │ │ │ │may be found
│ │ │ │ │ │between the
│ │ │ │ │ │spherical nuclear
│ │ │ │ │ │portions. No
│ │ │ │ │ │mitotic figures
│ │ │ │ │ │seen. The
│ │ │ │ │ │protoplasm is
│ │ │ │ │ │homogeneous and
│ │ │ │ │ │pale blue or lilac
│ │ │ │ │ │in relatively
│ │ │ │ │ │large amount. No
│ │ │ │ │ │granules were ever
│ │ │ │ │ │seen.
────────────────┴────────────┴───────┴───────┴───────┴──────────┴──────────────────
It would seem, from a general observation of simple and infected wounds
and from a few blood counts, that the response of leucocytes in the
lower animals is greater than in monkeys and man. The ease with which
animals endure a wound and the rapid local pus formation about an
infection speak for an easy mobilization of their cellular defenders;
their connective tissue elements seem equally well brought into play. In
so far as birds are concerned perhaps the normally large number of
leucocytes and the participation of local tissue cells in response to
irritation is a preparatory protective mechanism because of their
relatively small amount of bone marrow which may not be able to mobilize
new cells rapidly; many of the birds, notably those prepared for long
flight, have much of their osseous system given over to air space. The
number of red blood cells is also greater in Mammalia, which show a
variation from 4,000,000 per cubic millimetre in some small genera to
12,000,000 per cubic millimetre in some ungulates, while birds vary from
2–5,000,000 per cubic millimetre. Despite these fundamental differences
in the classes, pathological changes of anemia, leucocytosis and
leucemia are comparable; polycythemia in lower animals is unknown to me
but may of course occur.
ANEMIA.
As in human pathology this condition may be divided into the group that
follows some disease which damages the red blood cells or their source,
called secondary, and those cases not preceded by such a condition,
called primary. Formerly this latter group, known as progressive
pernicious anemia, was copiously represented, but study has discovered
that worms, inorganic poisons and infections can produce a picture of
grave anemia so that the formerly large group has dwindled. We now
conceive a primary anemia to be one without discoverable responsible
antecedent pathology, therefore a disease of the bone marrow itself.
There is one variety, hemolytic anemia, which seems to be an
intoxication of the bone marrow with solution of red cells, but the
affected tissue puts up some struggle against the poison. In another
primary, the so-called aplastic anemia, no activity at all is shown by
the marrow, no young cells appearing in the circulation. Clorosis, or
green sickness of young persons, is a primary anemia and presents itself
as a moderate cell reduction with a disproportionately low hemoglobin
percentage. As a disease entity this does not occur in the lower
animals, so far as I am aware, but a very few hemoglobin estimations and
a reference to the literature would indicate that well marked hemoglobin
anemia does occur.
In so far as the pathology of anemia is concerned we are obliged usually
to judge by the appearance of the blood and tissues, the yellowish
pallor of the mucous membranes, the condition of the marrow and the
amount of pigment; severe rapid cases show hemorrhages and prolonged
cases have fatty degeneration of the parenchymatous organs. For a
decision of the primary or secondary nature we must judge the
accompanying pathology and the condition of the bone marrow.
SECONDARY ANEMIA.
Secondary anemia can be laid in general to insanitary housing or
inappropriate diet over a long period, to chronic bacterial infection of
low grade, to the action of blood parasites or those of the bowel which
either suck blood or elaborate an absorbable toxin, or to single great
or repeated small hemorrhages. We shall now consider the cases at the
Garden. Perhaps many other animals have had a substandard blood, but
these are the cases in which the gross appearance attracted close
scrutiny in this direction. London has had much anemia, probably from
their reported heavy infestation with parasites, but this factor has
with us apparently played a small rôle in the production of anemia.
IN MAMMALIA.
In so far as the Primates are concerned the one outstanding cause of
anemia is degenerative disease of the osseous system. In both rickets
and osteomalacia there is an irregular hyperplasia of the marrow, which
is usually more marked in the latter. In osteomalacia one finds
irregular areas of congestion or even hemorrhage besides masses of a
gelatinous fatty tissue while scattered about are pink spots where the
marrow is better preserved. In rickets, on the other hand, the tissue is
more uniformly congested and less sharply separated from the endosteal
osseoid material or the irregular epiphyseal spongiosa. The fibroid or
osteoid growth of osteomalacia seems to be fairly well differentiated
from the marrow tissue although it may send strands into the canal and
across the spongy area. Histologically there is not a distinct
difference in the appearances nor do they differ from the human
analogue. In those cases which develop late in life the red cell centres
are very few in number but usually active. In the blood, one finds a few
nucleated and stippled cells, but not much change in size and shape of
the erythrocytes.
It does not seem that the anemia can be the cause of death, for among
our thirty-nine cases of osteomalacia and rickets, the prosectors have
thought it of sufficient importance to record in the diagnoses but
eleven times. There are usually complications of pneumonitis or
enteritis to finish the animal before the poverty of the blood will do
so, and our records show only a Black Spider Monkey (_Ateles ater_), a
Silky Marmoset (_Leontocebus rosalia_) and a macaque (sp.?) with
osteomalacia and grave secondary anemia. It would seem, however, that
hemoglobin anemia must exist, for, despite one record of 40 per cent.,
Fleischl, no excess of pigment deposit is noted in the spleen, liver or
marrow.
Carnivora have shown a moderate number of diseases of the skeleton but
the occurrence of a marrow involvement seems less frank, although the
anatomical changes are similar. However, there are three grave secondary
anemias recorded in eleven carnivores suffering from osteomalacia and
rickets. Another prime cause of low blood value in this order is
gastrointestinal inflammation; in seventeen cases of anemia, of
secondary nature, five showed gastroenteritis of severe grade or
protracted character. Perhaps the most prolific single cause of this
blood change is parasitism, six of the seventeen cases showing
infestation, five of which are nematodes and two cestodes, one showing
both. The details of these are worth recording. Two young Jungle Kittens
(_Felis chaus_) from the same litter died of enteritis with a noticeable
anemia; they harbored in their upper small intestine ascarids, and one
of them had a few hookworms (sp.?). A Kinkajou (_Potos caudivolvulvus_)
died from a general mild infection, emanating from a pneumonia perhaps,
and showed a heavy infestation with tænia (sp.?). An American Wild Cat
(_Felis ruffus_) died from acute catarrhal enteritis and anemia; the
parasitological findings included Filaria fasciata, adults in abdominal
and gluteal muscles, larvæ in the blood; Dibothriocephalis felis,
Ascaris mystax and Uncinaria canina in the small intestines. While the
blood was thin and pale and some pigmentation existed, the condition
could not be called a picture of grave anemia. A noteworthy finding was
the deep pigmentation of almost the entire intestinal wall. Ascaris
mystax was found in an under-sized inbred gray wolf, killed because of
poor coat; there was a marked anemia and atrophy of the skin. An Ocelot
(_Felis chibigonazon_) gave a picture of anemia due to uncinariasis, but
is not so instructive as the following. A Swift Fox (_Canis velox_)
exhibited clearly a case of progressive secondary anemia from uncinaria,
and the history is worthy of a brief recital.
Muscles atrophic, greenish black over abdomen. Fat absent. Lung is
blotched by darker red markings where parenchyma contains distinct
excess of frothy pink watery fluid. No fluid or adhesions in
pericardium. Heart is contracted, and muscle is pale yellow and firm.
The only abnormality consists of slight yellowing of musculature. The
abdomen shows great omentum firmly adherent to fundus of bladder. No
fluid or other adhesions in abdomen. The liver is normal in size,
smooth in surface and has sharp edges, is friable and bright orange
yellow. The section surface is glistening, smooth and dry. Organ is
poor in blood content, greasy and breaks easily. Bladder is large,
contents fluid green bile; duct patulous. Spleen normal. Kidney is
small and smooth, diminished in bulk, normal location, smooth surface,
and pale yellowish gray, consistency, soft, flabby. Ureters normal.
Mouth and teeth normal. Stomach contains scanty brown fluid. Duodenum—
Mucosa bile-stained, contained a solitary nematode worm. In its lower
portion it becomes filled with a blackish red fluid, and its mucosa
becomes studded by heavily outlined punctate hemorrhages whose
positions are best seen through serosa. Jejunum similar in condition
to duodenum and contains four small nematode worms. At one point,
i.e., where the worm is located at beginning of ileum the blood
staining of mucosa is strictly in neighborhood of the worm.
Capillaries nowhere congested. Ileum contains slight amount of
brownish black material, mucosa normal. Large intestine and rectum
normal. Pancreas normal. Lymphatics normal. This is a case of death by
anemia as result of bites of hookworms. There were certainly more than
four worms present antemortem since no males were found, and this may
be explained by a possible diarrhœa which has flushed them out. This
idea is borne out by empty condition of gastrointestinal tract. Animal
Parasites—Uncinaria canina. The four small nematode worms above
mentioned conform in all respects to the given anatomical points of
uncinaria. All four specimens are perfectly formed females. The
location of the hooks was easily determined and established as being
in the most dorsal portion of buccal cavity, and as projecting forward
and ventrally in two groups of three each in same manner as described
heretofore in similar infestations in foxes. The large nematode worm
found in duodenum is, from its possession of three lips and its
general form, an ascaris. The mustache, however, which is so commonly
seen in ascaris worms from this region is absent. Postmortem blood of
heart shows red cells granulated and almost worthless for histological
study. Nucleated reds, however, are absent but other points valuable
in settling the question of anemia cannot be determined.
Lung.—There are no abnormalities in supporting tissue. Alveolar walls
are markedly congested. Bronchi normal and show no trace of larval
hookworm infestation. Air sacs contain many red blood cells together
with a few heart-failure-cells. Congestion of lung.
Liver.—No excess of fibrous tissue. Finer details of structure cannot
be made out owing to advanced autolytic changes. The only possible
pathological changes consist of localized areas where liver cells have
fused to form notable masses of pink granular material suggesting
local necroses. Autolysis.
Intestines.—Four sections are present and all show essentially the
same character of changes. Interstitial tissue between muscular tissue
and submucosa loosely arranged as though separated by edema.
On luminal side of muscular mucosa is a distinct zone of striking
tawny yellow color with hematoxylon-eosin combination. This zone is
smooth homogeneous and contains a few spindle and stellate cells with
no capillaries and with little or no fibrillation. It abuts upon the
fundi of the crypts. Interstitial tissue of mucosa is loose and
infiltrated with round and spindle cells in its deeper portions. Here
it is also congested but congestion is most marked toward lumen where
masses of free blood cells occur in interstitial tissue, within lumina
of crypts and within lumen of intestine itself; no parasites or ova
are found. Epithelium of crypts has granular cytoplasm; goblet cell
formation frequently seen; cilia well preserved. Edema; Subacute
catarrhal enteritis Hemorrhage.
Six instances of nephritis, four parenchymatous and two diffuse, are
recorded in the total of seventeen cases of secondary anemia in
carnivores. Except in the skeletal disease the marrow is very mildly
affected, some edema and reddening grossly and moderate hyperplasia
minutely, being the only noteworthy changes.
The next order is that of the Ungulata wherein we have found but two
cases of frank anemia, an Isabelline Gazelle (_Gazella isabella_) and an
Aoudad (_Ovis tragelaphus_). The former had several lesions of different
etiology and nature so that an impoverishment of the blood is not
astonishing: parasitic (?) cyst in lung, chronic infective arthritis,
calcareous tuberculosis, congestion and edema of lungs, osteomalacia,
and osteofibroma of maxilla. The condition of the aoudad was too
indefinite to permit conclusions.
The marsupials are represented by two common Opossums (_Didelphys
virginiana_) and a Rufous Rat Kangaroo (_Aepyprymnus rufescens_), two of
which suffered also from rickets. The condition of the bone marrow was
unfortunately not recorded, but in other rachitic marsupials this tissue
follows the changes seen in other orders. One opossum had a hypertrophic
gastritis with numerous Physaloptera turgida, a worm frequently
associated with chronic thickening of the mucosa; there was also an
early portal hepatic cirrhosis with enlargement of the spleen.
Among the Rodentia we have had anemias in a Beechy’s Gopher (_Citellus
grammurus beecheyi_) and a Southern (_Sciurus niger niger_) and Western
Fox Squirrel (_Sciurus rufiventer_). The first had a myeloma also, and
will be discussed later. One of the squirrels had osteomalacia, while
the other suffered with diarrhœa and showed hydropic degeneration of the
kidneys, conditions probably due to acute intoxication.
IN AVES.
The class Aves is represented by the orders Passeres, Psittaci, Columbæ,
Herodiones, Gaviæ, Picariæ, Striges, Galli and Accipitres; the first
four are well represented, but in the other orders only one or two cases
have occurred. The causes of anemia in birds are essentially those
discussed for mammals with the provision that greater attention must be
paid to parasites, particularly those of the blood. Several slightly
varying protozoa inhabit the blood corpuscles of birds, and numerous
embryos may circulate after they escape from a parent lying in some
organ or tissue. The rôle of blood parasites, intra- or
extracorpuscular, in the cause of death or of anemia is, however,
somewhat paradoxical. Plimmer seems to credit a heavy infestation with
great value in the cause of death. In the human being an infestation of
one cell in a hundred is a fair grade of malaria; such a relation is
apparently common in birds, and we have repeatedly seen a much heavier
seeding while Plimmer reports as many as 70 per cent. of the
erythrocytes to be carriers of hemogregarines (he has seen 92 per cent.
in reptiles). Can then the effect upon hemic function and vital
resistance be great? It has been our practice to interpret the finding
of circulating protozoa or of larval metazoa as merely reducing the
resistance of the birds so that they succumb more readily to incorrect
food, strange environment or infection.
It is perhaps well to show the state of our records in the Passeres by a
table.
Passeres—Secondary anemia associated with intestinal or visceral
parasites 11
blood parasites 9
intestinal inflammation 6
skeletal diseases and chronic infection (osseous) 3
nephritis 4
miscellaneous and unassociated anemias 8
(entries in this line not included under any
other heading)
Total cases 37
In the first group, two of the birds showed cestodes, one a tænia, the
other not examined for identification; three showed coiled filaria in
the air sacs, two, tropidocerca in the proventricular wall and five had
coiled filaria in the serosa of the stomach. The second group was
infested five times with Halteridium and five times with embryo filariæ.
Anemia was associated with gastrointestinal inflammation alone only
once, the remaining five cases having other finding of greater
significance. The three birds of the next group concerned one with
tuberculosis, one with mycosis and one with a long continued abscess. It
seemed worthwhile to separate four cases of anemia in which nephritis
was a prominent association, in three indeed being the only other
diagnosis. While it is impossible to state that either is dependent upon
the other, and they may of course be coincidental, it is nevertheless
noteworthy that such an obscure relation occurs here as well as in human
pathology. In one of these birds seen recently there was in all
probability a distinct hemoglobin anemia suggested by jaundice, pallor
of the tissues, absence of pigmentations and the finding of large pale
erythrocytes in the heart blood. The last group is a mixed one including
some birds in which only anemia was diagnosed, others with prolonged
hemorrhages, two tumors, intestinal sand, congestion of the lungs and
the like.
The parrots and their relatives are represented by nine specimens, among
which two had proventricular spiroptera, two had long standing
tuberculosis and two had osteomalacia. The notes of the other three are
not sufficient to warrant deductions.
Herodiones showed eight cases of anemia, five herons, one bittern and
two storks. Parasites are noted in only three examples, herons, and it
is noteworthy that these all had flukes in the proventricle or
intestine; one also had ascarids in the proventricle. Two of this order
suffered with long standing inflammation following bone injuries.
Perhaps the outstanding features of this order are the erythrocytic
picture and the condition of the spleen. The red blood cells seem very
fragile or soft, for one often encounters in their fresh or stained
preparation vacuoles or rifts in the protoplasm surrounding the nucleus.
At first we thought these were hemosporidia, but repeated attempts at
their coloration and the absence of pigment granules seem to warrant an
assumption that they are artefacts. In five of the seven instances there
is very definite evidence of present or past activity of the spleen. We
have not always considered it sufficiently prominent to call it a
splenitis, but follicular activity is commonly discoverable, and two
cases of definite fibrosis are recorded. The sun bittern (_Eurypyga
helias_) showed a chronic interstitial nephritis in the atrophic stage.
No other of the wading birds showed secondary anemia. There are seven
cases among the pigeons (Columbæ) where anemic tissues attracted our
attention. Three were associated with osteomalacia, in one of which the
marrow picture was that of an aplastic form being everywhere pale and
flabby without cells under the microscope; it is further interesting in
this case that there was a distinct but ineffectual attempt at bony
regeneration by the periosteum. In another case, this time brought to
death by an enteritis and cloudy swelling of the viscera, the marrow was
hyperplastic and red, there being activity in the basic staining areas
of the head and in the shafts. (Notes of the third case scanty.) None of
the seven cases seems to have been associated with animal parasitism;
one had tuberculosis. The other cases are obscure and not definitely
connected with other pathology.
Ten more cases of anemia were scattered among seven orders. There is
nothing striking or even individual about them worthy of special
mention.
SUMMARY OF SECONDARY ANEMIA.
A review of our records shows that among 5365 animal autopsies we have
recorded anemia of probable secondary character in 122 instances, 53
(2.8 per cent.) mammals and 69 (1.9 per cent.) birds. The orders
represented, with the percentage for the order, are Primates, 25 or 5
per cent.; Carnivora, 18 or 3.7 per cent.; Ungulata, 3 or .8 per cent.;
Marsupialia, 4 or 2.2 per cent.; Rodentia, 3 or 1.5 per cent.; Passeres,
37 or 2.7 per cent.; Psittaci, 9 or 1.3 per cent.; Herodiones, 8 or 8.
per cent.; Columbæ, 7 or 4.7 per cent.; Picariæ, 2 or 2.3 per cent.;
Striges, Galli, Gaviæ and Accipitres, each one case. A consideration of
their associated pathology reveals the fact that four changes are
prominently associated with secondary anemia, to wit: gastrointestinal
inflammation, 26 times (15 mammals and 11 birds); parasitism, 29 times
(7 mammals and 22 birds); osteomalacia, 24 times (18 mammals and 6
birds), and nephritis, 18 times (12 mammals and 6 birds); a few of these
cases overlap, but this is rather the exception than the rule, and this
does not militate against the importance of the connection with anemia.
It will be noted that practically all the important orders of animals
are represented, including species from all over the globe. There is,
however, no especial relation of anemia to the kind of diet or digestive
tract. Conclusions as to the meaning of these figures of incidence are
hardly justifiable. In so far as the blood picture is concerned we can
only record the qualitative appearance and the effect upon tissues. It
cannot be stated that to external observation a secondary anemia
presents any distinguishing features that a specimen in poor condition
may not exhibit. The monkeys formerly dying of tuberculosis had not
infrequently pale buccal mucosa and skin around the eyes, but upon
examination of their viscera, blood or marrow the quality of their blood
could not be called greatly substandard. Slide smears of secondary
anemia in many specimens would occasionally show stippling or a moderate
number of nucleated cells with anisocytosis and poikilocytosis. This is
much more frankly exhibited in the Aves, wherein displaced karyolytic or
pyknotic nuclei are very common. Mention has been made of the rifts in
the protoplasm, seen in Herodiones, and this has been observed in other
orders. Perhaps the most striking change is the increase of young
erythrocytes and of thrombocytes in the winged creatures. The nucleus of
the former reminds one of that of the human plasma cell.
The condition of the bone marrow corresponds with fair accuracy to that
which one is accustomed to see in the human being. Certainly this holds
good for the mammals, while among the birds, the few observations upon
which we feel like relying indicate a nodular erythropoiesis of rather
striking character. In the areas of reddening as seen grossly there will
be found under the microscope an orderly arrangement of large red cells
with loose chromatic nuclei about a very much larger cell of the same
type, apparently the primary erythroblast. Outside of this group, red
cells such as appear in the circulating fluid, are rather irregularly
distributed in a marginal zone. I have seen small areas like this in
apparently normal marrow, but the central grouping was not so large as
in the anemic cases; it thus appears that we probably have the anatomy
of erythropoiesis.
The deposition of pigment in the birds is in much coarser granules than
among the mammals, in the former case large masses sometimes obscuring
several liver cells or apparently blocking a lymphatic sinus; the
Kupffer cells do not seem to be heavily laden.
The extramedullary formation of blood cells has been a matter of
considerable interest and study in the human being, and as far as it
concerns the circulating mononuclears, the general opinion seems to be
that such a histogenesis exists. A decision in the negative is perhaps
reached by the majority in the case of erythropoiesis, and as far as my
observations go, this holds for all mammals. It seems worth while,
however, to record an occasional finding in some birds, especially
anemic ones, which may be of importance in their erythropoiesis. The
adult red cell is a clearly formed ellipse with a distinct, deeply
stained, sharply outlined nucleus of a shape corresponding to that of
the whole cell. Young red cells have a more nearly circular outline but
almost truly circular nucleus, the short diameter being at least
proportionately greater than is the corresponding short diameter of the
whole cell; this is also the nucleus whose internal structure resembles
that of the human plasma cell. Groups of such cells have been seen in
the interstices of the liver, sometimes as many as twelve, in a rather
orderly formation. An excess seems at times visible in the spleen but
not in orderly arrangement. Observations are under way toward
determining the relation of this finding to the amount of marrow, the
condition of the blood and the habits of the bird.
Primary Anemia.
As already specified primary anemia is apparently causeless, aside from
the assumption that it is a disease of the marrow itself. Since there
are only four cases, representing three orders and they cannot be
grouped as could the secondary variety, the individual instances will be
discussed separately.
Ring tailed Bassaris (_Bassariscus astutus_). Adult died after two
weeks’ stay in the Garden with a history of general failure of
condition. The diagnosis at autopsy was primary anemia, fatty
degeneration of the liver, hemorrhages in intestines and spleen,
hyperplastic bone marrow. The external appearance is of general good
condition, fair skin, mucous membranes pale. Lungs collapsed, and
gray-red. There are several small hemorrhages scattered irregularly
throughout respiratory tissue. Lymph Nodes—small, soft mottled gray-
red. Pericardium had slight excess clear fluid, and no adhesions.
Heart normal in size, and of pale brown color. The liver of normal
size, smooth surface and sharp edges, of a pale brown color, soft and
friable. Has indistinct markings like yellow brown mottlings on
section surface. gall-bladder contains some viscid brown bile. Spleen,
normal or slightly less in size, consistency firm, capsule pale pearl
gray, apparently not thickened. There are numerous small hemorrhagic
spots on section surface. Interlying pulp is homogeneous deep red.
Follicles not visible. Kidney, normal in size and shape. Trabeculæ
faint. Capsule smooth, strips easily, smooth surface, and brown.
Consistency soft. Medulla prominently striated, cortex homogeneous
salmon pink. Stomach contains a little glistening mucus. Mucosa pale,
flat yellowish, slightly opaque. There is a recent clot lying in some
mucus just above pyloric valve. There is, however, no open vessel
nearby. From pylorus to anus lumen contains some rather fresh smeared
out or slightly clotted blood and mixed in with mucus. Mucosa is flat
translucent, submucosa slightly injected in a mosaic fashion,
otherwise gut wall is negative. No recognizable food present.
Follicles not visible. Mesentery glands small, soft, pale yellow.
Bones seem entirely normal. Marrow of long bones is firm, bloody.
Marrow of ribs also deep red. Blood in intestinal tract is probably a
recent slow oozing from intestinal walls, and was probably the last
straw. Cause of this anemia could not be determined. Blood preparation
not made because it was too long after death. Liver shows moderate
fatty infiltration of marginal areas. Pigment is scarce, only a few
granules being present in the Kupffer cells, not more than is often
seen without marked anemia. There is a slight increase in interstitial
nuclei but not in fibres. No obstruction or increase of bile ducts.
Kidney.—Very mild swelling of tubular epithelium but no exudative
processes. Glomeruli show a few vacuoles but capsular space is
negative to pigment. Bone marrow (Femur) fairly cellular in
construction, but fat well mixed. Cellular areas well arranged,
active, most of cells are small members of the larger mononuclear
variety. Small lymphocytes abundantly represented. Most of the larger
cells are non-granular, with centrally placed nucleus. Megakaryocytes
fairly numerous, nuclei seem closely jammed into centre. No
recognizable certain nucleated red blood cells, moderately number
stippled cells, few adult red cells. Eosinophiles and basophiles quite
few. Pigment small quantity.
This is a case of primary anemia of moderate severity and short
duration, and probably of hemolytic character if one may judge by the
bone marrow, although excessive pigmentation of the liver and kidneys
was not found. Unfortunately the spleen was not minutely studied, nor
was the central nervous system investigated. Atrophy of the intestinal
tract did not exist.
Two cases occurred among the monkeys, but one example will answer, since
the two were essentially the same.
The case to be cited was that of a Japanese Macaque (Macacus
fuscatus). ♀ Young, weight three pounds two ounces, exhibited in the
Garden about four months, and apparently in good shape until two weeks
before death when it rapidly became emaciated.
DIAGNOSIS.—Aplastic anemia, chronic atrophic gastritis. Atrophy of
heart muscle, fibrosis of liver, slight local cloudy swelling of
liver. Perilobular diffuse nephritis (subcapsular type). Congestion of
spleen. Fibrillar fibrosis of spleen. Hemosiderin pigmentation of
spleen. Local amyloid infiltration of spleen. Calcareous infiltration
in medulla of adrenal.
Coat only fair, body emaciated. Pale muscles, fat scanty. Respiratory
tract normal throughout save for slight emphysema. The Pericardium
showed no fluid or adhesions. Epicardium glistening and slightly
thickened. Heart pale in color. Abdomen shows no fluid or adhesions.
Liver slightly decreased in bulk, smooth surface and sharp edges,
hard, and rusty brown. Gall-bladder distended, contained green fluid.
Spleen firm and normal in size. Capsule smooth, shape normal. Section
surface, dark reddish brown, trabeculæ distinctly visible. Kidney,
normal in shape, capsule smooth, strips easily, smooth surface,
glistening, pinkish gray, consistency hard. Section surface, poor
demarkation between cortex and medulla. R. Adrenal, thick orange
yellow cortex, solid small brown medulla. Mouth and teeth normal.
Stomach distended, contains gas and small quantity yellowish mucus.
Mucosa everywhere normal. Postmortem blood examined, stained by
Romanowsky, but red cells were disintegrated possibly by laking so
examination is not satisfactory. Histological Sections: Heart shows
normal epicardium quite free of fat. Myocardium peculiar in that
fibres immediately under epicardium show marked broadening in a very
narrow rather sharply indicated zone where nuclei are extremely large
although not especially chromatic. Transverse markings here easily,
although faintly recognized, have very indefinite borders, their
longitudinal fibrillæ being ranged in form of a coarse reticulum. This
comes about from frequent and extensive lateral anastomoses with
fellow fibres giving appearance of a syncytium. In deeper parts,
fibres are of more normal size but nuclei are still large and fibres,
now cut in transverse section do not appear to anastomose so freely;
there appears to be a slight excess of fibrous tissue in their deeper
parts. Arteries quite normal. Atrophy with regeneration.
Liver.—Capsule and interstitial parts on whole normal. Perilobular
fibrous tissues largely missing, but where remaining show an
overgrowth occurring in peculiar zonal arrangement and of old adult
almost hyaline type. Its fibres are often arranged strikingly in
whorls. Bile ducts, arteries and veins quite normal. Parenchymal cells
of normal size, finely granular, prominent normal nuclei and contain
small quantities of finely granular, golden brown pigment not really
as abundant as commonly seen in severe anemias. Blood capillaries
narrow, contain small quantities R.B.C., and Kupffer’s cells very
frequently contain fine granules like those of parenchymal cells but
of a greener tint. In a few isolated areas parenchymal cells
distinctly more swollen than others and many show disintegration of
nucleus. Hemosiderin pigmentation. Perilobular fibrosis. Slight local
cloudy swelling.
Kidney.—Capsule smooth, interstitial fibrous tissue of organ proper
highly fibrosed in peripheral parts, but slightly in deeper. No
lymphocytic infiltrations anywhere or sclerosis of vessels. Tubular
epithelium highly atrophic in subcapsular regions where tubules are
narrow. In deeper parts epithelium is at times so swollen as to
occlude lumina, where they are coarsely granular and occasionally show
some karyolysis, a pink hyaline or finely granular material. Tufts
never show fibrosis, normal size. Bowman’s capsule heavily thickened.
Chronic diffuse nephritis (subcapsular type).
Spleen.—Slightly hyalinized capsule, normal thickness. General
reticulum of pulp slightly fibrosed and poor in lymphocytes. Sinuses
broad, crowded with red blood cells, but only small numbers of
lymphocytes. Coarse granular blood pigment abundant, showing greenish
cast on focusing. Malpighian follicles normal size, slightly fibrosed,
and in several instances show a deposit of smooth pink material
between cells. Congestion. Fibrillar fibrosis. Hemosiderin
pigmentation. Local amyloid infiltration.
Adrenal.—Organ appears normal in all respects save for presence of a
few small irregular areas of calcification in medulla. These occur
apart from any recognizable necrotic or fibrous areas. In one place
one appears to lie within lumen of blood vessel. No fibroses or
special congestions anywhere in organ, and cells show normal details
and normal numbers of vacuoles. Calcareous infiltration of medulla.
Stomach.—Muscular tunic normal. Submucosa thin, has densely arranged
bundles of smooth, pink character. Mucosa distinctly thinned, shows
comparatively few regions holding acid cells, consisting for most part
of peptic type of gland. These are short and of broader calibre
towards lumen than deeper, suggesting a hyperplasia of luminal
portions; stroma richly infiltrated with lymphocytes, not fibrosed or
congested. Epithelium of crypts has rarefied appearance, shows no
special degenerative changes. Chronic atrophic gastritis.
Bone marrow appears as widely separated large, fat globules with
intervening granular edematous material and no hematopoietic elements.
Blood capillaries numerous and highly congested.
Although the notes fail to discuss the gross appearance of the bone
marrow, the amount of alteration in its microscopy and the relatively
small output of pigment in the liver, seem to substantiate the
determination of aplastic anemia; it is unfortunate that the blood
smears could not be used in the decision. At all events the condition of
the intestinal tract, of the heart, liver, spleen, and adrenal, justify
us in classing the case as one of primary anemia. The next and last
instance is of the same type, although I am inclined now to differ from
the diagnoses made at the autopsy table, that of aplastic anemia, and to
place it in the hemolytic variety. The rapidity of the fatal attack, the
redness of the marrow, the excessive pigmentation, and the prominence of
recent degenerative lesions in the organs are much more like the changes
of a primary hemolytic intoxication than of an aplastic anemia.
Gray Fox (_Canis cinereo_). ♂ Weight four pounds, adult, was in the
exhibition two years, but in good condition until two weeks before
death, when it stopped eating and rapidly fell away.
DIAGNOSIS.—(Aplastic) Primary anemia. Zenker’s Hyaline of heart and
skeletal muscles. Mucoid degeneration of bone marrow. Congestion of
bone marrow. Atrophy of hemopoietic elements in bone marrow.
Hemosiderin pigmentation of liver. Atrophy of liver. Congestion of
liver. Congestion and fatty infiltration of kidney. Patulous lumina in
adrenal and absence of pars glomerulosa.
External appearance of coat good. Decomposition advanced in
intestines. Skin and subcutaneous tissue faintly yellow. Poorly
developed, dark muscles and fat. Respiratory tract normal throughout.
Pericardium glistening, transparent, and pale, with no adhesions.
Heart a little too pale, consistency slightly soft. Normal or slightly
increased size of liver, with smooth surface and sharp edges,
consistency friable, and of a brownish red with rusty coloring. Spleen
normal. Kidney normal in size, shape, location, and consistency.
Capsule strips easily, and of a faintly yellow, under general red,
coloring. Adrenal normal. Mouth and teeth normal. Stomach, serosa and
wall normal. Mucosa shiny, autolytic, muddy red. Ileum, agminated
follicles swollen. Feces from colon examined microscopically. Pancreas
normal. Bone marrow tibia and femur gelatinous and red, not slightest
trace of yellow. Blood films from heart’s blood show poikilocytosis
and anisocytosis; only one nucleated red.
Microscopic Notes.—Heart has torn but normal pericardium. No
abnormalities of interstitial tissue or vessels. Fibres of normal
width but show transverse markings irregularly since cytoplasm becomes
hyaline and swollen in many places along its course. Nuclei prominent,
slightly pyknotic. Zenker’s Hyaline.
Bone marrow consists of a matrix of granular or fibrillar mucoid
tissue within the delicate reticulum of which highly developed
capillaries are placed, together with stellate spindle and sealring
cells. In a few places only are myelocytes recognizable and then in
decreased numbers. Plasma cells sometimes found containing much blood
pigment.
Liver.—Capsule normal; perilobular fibrous tissue only slightly
overgrown, moderately infiltrated with lymphocytes and heavily with
blood pigment. Arteries, ducts, veins, normal. Parenchymal cell a
little smaller than normal with nuclei of normal type, and crowded
with fine granules of blood pigment. Latter lie in usual
pericanalicular position. Blood capillaries narrow, moderately
congested and Kupffer’s cells also contain abundant pigment granules.
Thyroid.—Interstitial framework shows no fibrosis or cellular
infiltrates. Blood vessels normal. Acini fairly uniform in size, none
ever attaining large proportions, but some being distinctly below
normal. They are uniformly filled with a very pale pink hyaline
material which in some way gradually increases in color intensity
toward one side, attaining in a few examples usual intensity of
colloid. Lining epithelium is low cuboidal, shows no special
hyperplastic features or atrophy.
Kidney.—Capsule normal. Interstitial tissue normal. Blood vessels
slightly congested. Tubular epithelium granular, disintegrated and
frequently contains numerous fat globules and obscured nuclei. Lumina
of about normal size containing variable quantities of pink granular
detritus. Glomerular tufts normal in size and appearance. Subcapsular
space and Bowman’s capsule normal.
Adrenal.—Capsule and pericapsular tissue normal. Parenchymal cells
throughout poor or practically free of vacuoles, such appearing in
only limited portion of pars vesicularis. Interstitial framework and
vessels normal. Structure of columns in pars vesicularis is peculiar
in that they extend quite to capsule with no intervening pars
glomerulosa, and again in that most peripheral parts are expanded at
times showing a lumen, while deeper parts show broad cells extending
fully across the column. Pars reticularis contains no pigment and
medullary cells quite normal. Skeletal muscles show comparatively few
fibres with transverse markings. Most are swollen, hyaline, lumpy, and
have pyknotic nuclei. Interstitial parts show no inflammatory change.
Tissues treated by Prussian blue test for iron. Kidney, adrenal, heart
found to contain none. Spleen, liver contain abundance. That in spleen
responds to test showing that it is all iron containing. Two kinds of
pigment found in liver. In periphery of lobule as much contains iron
as that which does not, while in deeper parts iron predominates. Many
times both kinds are recognized in one cell. On the whole it is the
finest granules which contain more iron (are bluer) while iron free
pigment occurs in bile canaliculæ. That in Kupffer’s cells stains
strongly blue.
SUMMARY OF PRIMARY ANEMIAS.
A review of these instances of grave anemia brings one to the conclusion
that there is a strong similarity to the disease in man. Perhaps we have
constructed a picture that is too narrow for the animal kingdom in
general, but surely these few instances deserve to be distinguished from
the secondary cases already presented if for no other reason than that
no associated etiological condition was exposed. It was hoped in
studying the anemias of lower animals, and this hope extends over all
the subject of this book, to be able to throw some light upon causation.
The thought of incorrect diet came at once, but we are confronted with
the paucity of cases among our records. Moreover, secondary anemia from
digestive and dietetic troubles is clear, but how we can use this
argument for an essential change in hematopoiesis and natural
hematolysis, is far from evident. It will be noticed that I have
studiously avoided grouping any case with parasites among the primary
cases, nor will there be found any evidence of generalized infectious
disease. Most of the reported instances of pernicious anemia in the
lower animals have been associated with one or other of these factors,
although certain authors (Kitt, Hutyra and Marek) maintain that a
causeless variety probably exists.
LEUCEMIA.
This condition is fairly well recognized by veterinarians as occurring
among domesticated animals, but in the records of this Garden it has
occurred rarely, indeed only once in a mammal and but five times in
birds. It is interesting that, in the wealth of material at the disposal
of Plimmer and his associates, only one case, a polecat with lymphatic
leucemia, is noted, and but very few avian instances. Herewith is
submitted the protocol of our single mammalian case; perhaps we have
missed others of a mild grade dying during the early stages because
their resistance to infection was reduced. Unfortunately, perhaps
because of the postmortem changes, but more likely because it appeared
at first as if we had to do with a case of generalized tuberculosis, the
bone marrow in this case was not examined. Nevertheless the infiltrative
character of the lesions, the absence of distinct tumors and the
numerous mononuclears in the blood as seen in sections seem to justify a
diagnosis of leucemia, in all probability of the lymphatic type. There
follows this case one with similar gross and microscopic picture which
has no visible increase of leucocytes, but a very distinct myeloid
picture in many places.
Common Opossum (_Didelphys virginianus_). ♂ Adult. No evidence of
illness. Found dead. Lymphatic leucemia (involving all viscera and
lymph nodes). Diffuse nephritis. Both lungs have become entirely
involved in a firm, gray-yellow mass not adherent to any serous
surface. Practically no normal lung tissue is left. This seems like
tuberculosis but no tubercle bacilli could be found in a good smear.
Estimation of the normal cubic capacity of an opossum lung was made to
be about five cubic inches. In this case not over one-half cubic inch
remained respirable. Bronchial lymphatic glands were enlarged, firm,
yellow gray, with no recognizable lymphatic tissue. Heart muscle was
firm and flaccid, pale and striated. Liver very large, firm and tough,
with smooth surface and sharp edges. Color pale brown. Section surface
glistening, dry, smooth, opaque. Common bile duct patulous. Spleen,
slightly increased, firm, tough consistency, capsule smooth. Section
surface, smooth, firm, brown-red, pale pulp, prominent follicles, and
trabeculæ faintly visible. Right kidney, slightly decreased, normal in
shape. Capsule smooth, strips with difficulty, tears surface. Surface,
granular, color brown, consistency firm. Thickness of cortex, narrow
irregular, markings irregular and obscure. Small mass of fibrous
material in cortex about 3 × 3 mm. like those in lungs. There are also
numerous pale yellow gray areas in cortex and outer medulla, round and
streaky, distorting the striated architecture. Right adrenal converted
to a yellow gray mass like lungs. The mesenteric and retroperitoneal
lymph nodes are firm, gray-yellow. This includes those under diaphragm
and around cœliac axis.
The histology of the organs may be described together. The infiltrate
described is a densely packed mass of large cells with large, well
staining nuclei and a very narrow rim of protoplasm. It is not limited
by any definite wall or septa. It has no interstitial tissue. There is
no blood supply in the densest masses but the walls of the blood
vessels remain intact wherever the mass surrounds them. In the lungs
it has involved all structures indiscriminately, and has destroyed
practically all of the respiratory surface. It seems to follow by
preference the peribronchial space. A few glands may be seen in the
centre of this mass, but they are rapidly undergoing degeneration. In
the liver the infiltrate is chiefly beneath the capsule extending
inward but a very short distance. There are no large masses as in
other organs but small infiltrates are seen at the portal areas. The
spleen shows a diffuse excess of pulp cells and many of the cells
above described, the difference being only in the size of the nucleus
which is smaller in the pulp cells. There are very small round cells
relatively. Follicles are absent, connective tissue not altered. Note
states follicles prominent; this is due to nodal hyperplasia of the
large mononuclears above described. The parenchyma in the kidney is
anemic, the epithelium is slightly pigmented but this is probably not
abnormal. Between the tubules especially of the outer layer of the
medulla and medullary ray but also in the cortex and around the
glomeruli are diffuse, irregular, infiltrating masses of the cells as
described above. In some places in the kidney hyaline casts are being
formed probably due to the degeneration of the epithelium by pressure.
There are a few distentions of the tubules. The capsular space is
free. In the neighborhood of the collections the capsules are a trifle
thicker than normal. Lymph nodes, similar to spleen in that most of
the bodies are thoroughly overrun with the large mononuclears. The
sinuses, both marginal and internal, are practically obliterated by
these cells. In the blood vessels of the lungs and liver there are
many large mononuclears, perhaps not as large a number as might be
seen in leucemia, but decidedly in excess of normal.
Common Marmoset (_Callithrix jacchus_). ♂ Adult. Had cage paralysis
for two months before death and declined gradually from that time.
DIAGNOSIS.—Bronchopneumonia. Myeloid hyperplasia of bone marrow.
Myeloma in pancreas. Fatty degeneration of liver. Constipation.
Nematodes in cecum. Animal is thin, skin bare in spots. Both lungs are
pale pink with large areas of deep red consolidation. Heart is
dilated, increased in size with firm, red-brown muscle. Liver is firm,
red-brown, with smooth surface and sharp edges. Section surface is
glistening, smooth and moist. Lobular outlines are clear by reason of
pale lines. The gall-bladder is normal in size and contains fluid pale
green bile; duct patulous. Spleen is normal in size, smooth capsule,
soft, purple pulp, follicles small and faint, trabeculæ fairly
prominent. Kidneys normal in size and shape. Capsule smooth. Section
surface smooth and brown and firm. The glistening section surface has
a narrow cortex, swells slightly, with prominent striæ. Intestines
throughout are pale on serosa. Wall thin. Mucosa flat, pale pink.
Contents creamy mucus in the upper intestine. Large intestine contains
large masses of very firm feces. Cecum is distended with feces and a
great quantity of nematode worms. They are not attached to mucosa nor
does mucosa seem altered because of their presence. Skeleton and
muscles.—Long bones of extremities break easily, but with snap. Skull
can be dented with fingers. Bone marrow of femur bright red.
MICROSCOPICAL NOTES.—Liver shows moderate degree of fatty degeneration
with capillary congestion. Kidneys negative. Some postmortem change in
last two organs. Spleen, marked congestion. Hyperplasia of large lymph
cell type, particularly in follicular centres. Blood destruction
moderate. Bone marrow seen in condition of marked activity of myeloid
type. Aside from enormous crowding of strands there does not seem to
be any atypical cell. Intestines show practically no change. Same
condition holds in pancreas. In several places in pancreatic ducts
cross sections of nematodes may be found. In among lobules of pancreas
is a well encapsulated cellular mass without particular architecture.
It consists of cells of large lymphocyte or endothelioid series. There
are numerous cells of size and staining characters of small
lymphocytes. There are no megalocytes but there are some
indistinguishable from myelocytes. This may be an intrapancreatic
lymph node. One small lymph node found in section; it shows a picture
quite like the marrow except for megalocytes. Blood vessels do not
show an excess of leucocytes in free or coagulated blood.
Perhaps this latter case belongs to the aleucemic leucemias or
pseudoleucemias. These two conditions are recognized by the difference
in circulating leucocytes, a piece of information not at our disposal.
The whole subject of hemato-lymphatic affection must remain unsettled in
so far as a diagnostic name is concerned, for in very few cases has the
blood of our animals at autopsy been in a state permitting reliable
observations upon stained smears, because of coagulation, lysis or
decomposition. After considering a few more of the diseases of the blood
and marrow, the lymphatic apparatus will be considered. But there is a
borderland to which a word might be devoted at this time, that group to
which various names—Hodgkin’s disease, pseudoleucemia, general
adenopathy, adenie, aleucemic leucemia—have been applied and which has
been accepted as occurring in the domesticated animals. Since I have
been occupied for several years in a study of this clinicopathological
complex in the human being, such cases have been searched for most
diligently, but without success. The New York Zoological Park records a
case of Hodgkin’s disease, without specifications, in 1901, and at the
London Garden a pseudoleucemia was found. The paucity of leucemia and of
the aleucemic adenopathies in lower animals and their relative frequency
in man excite speculation as to their interdependence; but more of this
under the lymphatics.
AVIAN LEUCEMIA.
The class Aves is rather better represented in the group of leucemias,
but here the well known infectious disease may confuse the picture. The
birds affected were Psittaci 3 (1 parrot, 1 parrakeet, and 1 amazon),
Herodiones (stork) 1, and Galli (Gambel’s quail), 1. There was no close
association of these cases either in time or housing. One of the parrots
and the stork had a picture suggesting that given by Warthin for avian
leucemia while the remainder presented greater evidence of a generalized
infection, such as Moore described, associated with the finding of the
B. sanguinarium; this organism was isolated once, but no secondary cases
succeeded upon the death of this bird. It seems hardly profitable to
quote protocols of this relatively unimportant condition, especially
since it is fairly well known.
The separation of the two groups just specified might be discussed,
however, for it is by no means certain that they are or are not
different. When a pathological picture of leucemia gives a decided
impression of an acute infection there are very prominent involvements
of the viscera but no lymph nodal masses. On the other hand, in the
cases with nodular masses corresponding to the scanty lymph tissue of
birds, there is much less infiltrative involvement of viscera and less
parenchymatous degeneration. This suggests that they are different
processes, but an analogous contrast may be found in the pathologic
anatomy of acute and chronic leucemia in man, and I am inclined to view
them as stages of the same disease. In one of our infectious cases noted
above the lesion was certainly myelogenic for the infiltrate in the
organs and the cells in blood smears showed an enormous number of
eosinophilic and basophilic polynuclears greatly in excess of normal.
The study of two of our cases confirms the picture as given for
lymphatic and myeloic leucosis by Ellermann[18], but material
corresponding to his lymphoidocytes or erythroleucotic group has not
come to our attention. Cells with deeply staining basophilic protoplasm
and a lymphoid nucleus are certainly to be found with reasonable ease in
the avian marrow normally and, more than this, can be detected by
careful search in nearly all cellular infiltrates of organs not leucemic
in nature. Perhaps, as Ellermann states, they are collateral stages in
normal erythrogenesis.
THE BONE MARROW.
Since the foregoing conditions so vitally concern the bone marrow, it is
but natural to give to this structure a separate consideration. From
what is known of the origin, physiology, anatomy and regeneration of the
marrow from the work of Ponfick, of Neusser, Bunting, Selling, Werigo
and many others, it seems highly probable that the principal conclusions
reached in the study of human medicine and experimental pathology, apply
to the whole group of animals here under discussion. The peculiar
arrangement already mentioned as encountered in the marrow of birds
differs little if any from the erythropoietic centres seen in man after
experimental anemia, although it may be somewhat more orderly.
Myeloblasts or megakaryocytes are not numerously present in any order,
but seem more prominent in the mammals than in birds. In so far as the
mononuclear groups are concerned, one can state with reasonable
certainty that they differ little throughout the animal kingdom. They
occur in islands, strands, or infiltrate—like groups, are mixed granular
and non-granular in character and, with exception of the frankly
oxyphilic cells, are distinctly basic in tinctorial affinity. In a case
probably myeloma, soon to be discussed, there is not a single
acidophilic or multinucleated cell to be found in two sections. As might
be expected from the greater eosinophilic content of the circulating
blood in the Aves, greater numbers of such cells are to be found in the
marrow and they are, understandingly enough, sometimes found in distinct
nodes and groups containing mono- and polynuclear varieties. Concerning
the platelets, no sufficient data are at our disposal to warrant a
general statement. In the avian marrow they can be made out quite
clearly, as in the blood, and have a greater diameter and a sharper,
more chromatic nucleus than in the higher mammalian blood. Mast cells
are quite common in lower mammals and birds, in whose blood they
maintain an appreciable percentage, while in the marrow they stand out
clearly. It is noteworthy, in the light of Graham’s statement that the
hemic basophile is but a degeneration form of the eosinophile, that in
the bird’s marrow, large mono- and polynuclear cells with both kinds of
granules easily may be found by Romanowsky stain. An increase of
eosinophiles, seen in avian as well as in human parasitism, is not
necessarily accompanied by basophilia.
Hyperplasia and atrophy of marrow in the lower mammals follow much the
same conditions as in higher groups. During acute general infections, as
by the paracolon bacillus in carnivores, it is common to find a distinct
increase in the mononuclear centres, while in suppurative lesions a
polynucleosis results. The bird, however, responds less readily with
leucocytes, judged by cross sections of blood vessels and the activity
of the marrow. The latter may show a myeloid picture, but mononuclears
without granules, with deeply staining nucleus and protoplasm, are
usually more numerous; two cases recently studied, one of tuberculosis
and one of pneumonia with general congestion, had similar bone marrow—
pale homogeneous red with distinct mononucleosis, more outspoken,
however, in the former case. Pigment is not common in the avian marrow.
The relation of the marrow to general conditions has been mentioned in
the foregoing pages, but perhaps the following diagnoses will illustrate
other connections seen among our records:
Bactrian Camel (_Camelus bactrianus_).—Hydatid disease of lung and
liver. Hemorrhagic enteritis. Atrophic bone marrow. Calcified areas in
thyroid.
American Gray Wolf (_Canis mexicanus_).—Cretinoid. Hemorrhagic external
pachymeningitis with craniotabes. Secondary hyperplasia of thyroid with
colloid. Chronic lymphatic hyperplasia. Chronic interstitial nephritis.
Chronic enteritis. Osteogenesis imperfecta. Hemorrhagic bone marrow.
Concentric hypertrophy and dilatation of heart.
MYELOMA.
Perhaps no pathological condition has given rise to more varied opinions
than the tumor-like hyperplasias of the bone marrow, growths resembling
bone sarcoma with and without giant cells—myeloma, chloroma,
pseudoleucemia ossium and many others. In brief only two cases occur in
our series which could be admitted to this category. There have been
osteomata, but they were so clearly local tumors that they cannot be
included in myeloid neoplasms that are assumed to be systemic in nature.
Here is not the place to engage in a discussion of the correct
classification and nomenclature since there are included only the
aleucemic newgrowths usually assumed to originate from blood-making
cells. The first case seems to be a myeloma because of the involvement
of many bones and the infiltrates in the liver. Judging by the cross
section of blood vessels there is no leucemia, but of course this is not
final, although somewhat supported by the normal size of the spleen and
lymph nodes; lymphatic structures need not be enlarged in myeloid
leucemia although they usually are.
Beechy’s Gopher (_Citellus grammurus beecheyi_). Adult ♂ . Gradual
loss of power in limbs beginning about two weeks ago. No other
symptoms.
DIAGNOSIS.—Multiple myeloma. Anemia. Acute parenchymatous nephritis.
Chronic ulcerative gastritis.
External Appearance.—General condition fair, hair in good condition.
Fully developed animal. Muscles contained no fat.
Respiratory Tract.—Thymus, large soft gray homogeneous. Both lungs are
distended, pale, homogeneous, yellow pink, boggy, do not crepitate,
but contain no edema. Lymph nodes, small soft anthracotic. Pericardium
contained no fluid.
Abdomen.—No adhesions. Size of liver normal or slightly small, firm
and pale brown-red. Architecture irregular showing areas of perfect
homogeneity and others where lobules are clear outlined by paler
interstices. Gall-bladder distended, contains brown fluid. Common bile
duct, patulous. Spleen, normal or slightly small, consistency soft,
capsule smooth, location normal; section surface, homogeneous pale
pulp, faint trabeculæ. Kidney normal in size and shape, capsule
smooth, strips easily, smooth brown surface; section surface
glistening, opaque; consistency firm; thickness of cortex normal and
of medulla normal; homogeneous cortex, glomeruli not visible.
Adrenal.—Narrow, brown, opaque cortex; pale brown, opaque medulla.
Bladder, small quantity of cloudy urine showing albumin, bile and many
granular casts, few hyaline casts. Teeth carious broken; mouth pale.
Stomach distended; serosa and wall pale, contained gas; mucosa pale,
flat, translucent except in pyloric segment where it is slightly
thickened, irregular, opaque and there are several saucer shaped
depressions covered with black, shiny material; these seem like
sluggish ulcers. Intestinal tract throughout seems normal save for its
pallor. Few natural fecal masses in lower gut.
Skeleton and Muscles.—All bones are irregular in thickness, very
brittle and show in their length irregular swellings made up of
periosteal growth and probably increase in marrow. The latter is pale
yellow with punctate hemorrhages. Skeleton seems too soft to give
support, but there is little deformity.
Microscopy.—Bone section shows a myelomatous growth of costal marrow,
new myelocytes predominating. The cells are packed in disorderly
fashion through the marrow. They are chiefly lightly granular but a
few distinct promyelocytes are found. The hyperplasia is invading
cartilaginous bone with absorption. In some places cartilage is of
fetal type. Perichondrium is active but there is no round cell
infiltration. Ossification is imperfect at costochondral junctions.
Kidney shows granular and vacuolar degeneration of epithelium with
flattening of tubular lining. Nuclei are for most part normal.
Epithelium of tufts and Bowman’s capsule is likewise granular and
vacuolated. Distal and discharging tubules seem to be most affected.
No well defined casts are found.
Liver.—The fine markings mentioned in the notes correspond to areas of
infiltration of large pale mononuclears without granules. There is no
fibroblastic or polynuclear increase around them. Very small necroses
seen in hepatic lobules. Very slight increase of connective tissue is
noted.
This seems to be a tumor of true myelocytic origin; none of the cells
was of the plasma type as usually depicted. The second case stands in
the files as a myeloma, yet the full description and slides have been
mislaid. It is cited briefly for record.
Samoli Ostrich (_Struthio molybdophanes_). Adult ♂ . Would not eat for
three weeks.
Diagnosis.—Tuberculosis of lung, liver, spleen, kidney, mesenteric and
cervical lymph glands. Myeloma of periosteum of pelvis.
Skeleton and Muscles.—Large tumor mass lying on inside of pelvis
measuring about ten inches by twelve inches with a thickness of about
four inches. It is sharply defined and separated from adjacent muscle
by a capsule. Inner border is directly below the peritoneum, and outer
border lies directly on bony pelvis. Traced to its origin it seems to
come from pelvis yet tumor peels off bone easily, leaving a rough
surface. The tumor is soft and succulent, of a red gray color and
contains some fat and much irregularly placed masses of bony tissue.
SECTION V
DISEASES OF THE LYMPHATIC TISSUES INCLUDING SPLEEN
Since we have followed diseases of the blood from the simple anemias to
a place where mononucleosis in the circulatory system and in the fixed
tissues is the prominent feature, another step reaches the area whence
most of these cells emanate—the lymphatic system. The anatomical and
physiological position of the lymphatic circulatory apparatus is closely
analogous in the classes under discussion, and it stands in an
anatomico-clinical sense, closer to the hematopoietic system than to any
other structures, throughout the whole animal creation. This anatomical
division of the circulation is closely comparable, for pathological
purposes, in the mammals whereas in the birds one finds noteworthy
variations. In the class Aves lymphatic radicals are extremely numerous,
the plexuses in the extremities and thorax perhaps being complemental
for the rather scantily supplied blood vessels. About the fibulo-tibial
and femoral muscles the tiny lymph vessels form an extraordinarily dense
and intricate lacework, a replica of which may be found in muscles of
the upper limb, while in the pelvis and thorax a rich plexus is
distributed around both kinds of blood vessels and also lies within the
walls of air sacs. The air sac walls in the chest display lymphatic
lines very well in birds that have been for many years exposed to
railway dust, the natural pearl gray glistening membrane looking as if
black pepper had been evenly dusted over it. The lymph glands or
compound nodes so easily discovered in mammals are practically absent in
birds. Along the large thoracic vessels and in the pelvis of some
anserine and struthious varieties, small illy defined masses of
lymphatic tissue may be discovered by careful search but they do not
possess nodal arrangement and capsule. Lymph follicles on the other
hand, are quite numerous in the respiratory, and especially, the
intestinal tract. Groups of follicles may also be found in the lining of
the upper ends of these tracts in such situations that the names
faucial, pharyngeal, or even tubal tonsils are justly applied. I do not
find any reference to a lingual tonsil in birds, but this structure is
found, with of course many modifications, down as far as the monotremes.
The lymphoid tissue of the nasopharyngeal region is so placed in animals
as to be exposed to aerial and food infections, just as it is in man. It
is, however, noteworthy that chronic inflammations leading to
hypertrophy or to obstruction have not come to our attention. There is
only one diagnosis of chronic tonsilitis in our records, a determination
based upon the nodular red-brown prominence of the tonsillar region, but
there were no true hypertrophy and areas of fibrosis combined with
necroses as seen in human medicine; this case concerned a Chacma baboon.
HYPERPLASIA.
In so far as the reaction to infectious or toxic agents is concerned
there seems to be a fairly uniform character through the mammalian
groups, but in the Aves there are a few differences worthy of mention.
It is at once admitted that these observations upon birds are based upon
a very few sections of isolated lymphatic tissue, but they are supported
by records of the changes in nodes in mucous membranes and viscera, and
by those in the spleen. The first and perhaps most noteworthy difference
is in the paucity in birds of large mononuclears of the endothelial
type. Their position in chords, sinuses and germinal centres is taken by
deeply staining mononuclears, of the size and general character of large
lymphocytes as seen in the blood. The hyperplasia in the follicles is
much more dense but it is outdone by that in the chords. Since the nodal
tissue of birds is not so sharply delimited by some sort of capsule, it
is but natural that the hyperplasia should be diffuse; in the intestinal
wall it may extend laterally twice or thrice the width of the normal
follicle. Necrosis, unless the disease be mycotic, tuberculous or
parasitic, is uncommon.
It may be well to discuss for a space the reaction to infection of the
thoracic and intestinal lymphatics in mammals. The amount of
lymphadenoid tissue in the mediastinum is very great in some mammals,
notably the Ungulates, while in others, the Rodents and Primates, for
example, it is not so plentiful. Nevertheless the gross and minute
changes are usually of the edemato-exudative type—large, pink, soft,
moist glands. In the abdomen, on the other hand, one usually finds well
outlined, firm, yellow nodes in the mesentery and behind the peritoneum.
This is not only to be discovered in various chronic diseases of the
intestine but even in acute, so-called toxic enteritis seen in
carnivores from food poisonings. One must therefore ask if the local
nodes abundant in the intestinal mucosa do not take up the poisons which
cause the acute hyperplasia and are in turn backed up by the stalk
glands. Even in so acute and overwhelming a disease of the intestine as
hog cholera (which we have not had here) the glands retain their general
structure, although hemorrhagic, while in late stages they become firm,
sharply outlined and pigmented. In birds there may be swelling of the
omental bursæ, but as there are no lymph glands no masses are found.
The response on the part of the lymphatic tissues as a system, or some
large section of this system, is shown in the following figures. It is
our practice to include in the diagnosis general acute or chronic
lymphadenitis or inflammation of a large drainage area. Acute changes
have been mentioned 103 times, in which the important orders are
represented as follows: Primates 21, Carnivora 46, Ungulata 15, Rodentia
3, Marsupialia 13, Pinnepedia 4. Chronic changes are mentioned 43 times
as follows: Primates 7, Carnivora 19, Ungulata 14, Marsupialia 1, and
Pinnepedia 2. This great proportion among the Carnivora does not
indicate that they have more lymphatic structures for such an advantage
is probably possessed by the Ungulata, but perhaps should be interpreted
as an evidence for this order of the ready response to irritation on the
part of the tissues in question. They probably suffer more, as we shall
see later, with inflammation affecting drainage tracts. The hyperplasias
or inflammations included in the figures above most often accompany
gastroenteritis, pulmonary diseases or long standing infectious
processes such as arthritis, while there are also lymphatic enlargements
both local and general, associated with skeletal degenerations
(rachitis-osteomalacia) and with thyroid disease. The former may be
described as lymphadenitis, the latter as lymphatic hyperplasia.
Unlike lymphadenitis, a condition associated with some definite
infectious or toxic cause, systemic hyperplasia of the lymphatic tissue
may be apparently primary and causeless. In a pathological and clinical
sense alike these hyperplasias are protean in their manifestation,
making a satisfactory classification extremely difficult. For our
purposes they are divisible into acute and chronic, associated with an
increased number of circulating lymphocytes and without such a
lymphocytosis.
The first, acute systemic lymphatic hyperplasia, is known in man as
status thymicolymphaticus, a well recognized condition chiefly
encountered in youthful males having some of the stigmata of the
opposite sex. There is no record, nor have I any recollection of a
pathological state in a wild animal comparable to this condition.
If acute generalized lymph node increase be associated with
lymphocytosis, acute lymphatic leucemia exists; there is no case in our
records. Chronic enlargement of lymph nodes with increase of circulating
mononuclears is chronic lymphatic leucemia; a case of this has been
cited under leucemia.
LYMPHOMATOSIS.
Chronic enlargements of the lymphatic tissues without leucemic blood
present a bewildering number of varieties, the best known names of which
are Hodgkin’s disease, aleucemic leucemia, pseudoleucemia and
lymphomatosis. On occasion they are at first localized tumors, being
generalized only late in the course; under these circumstances they are
usually classed with neoplasms in the form of leucosarcoma and
lymphosarcoma. Examples of lymphatic disease answering the above
description are limited to two, but even these must be explained in
certain particulars. There has already been quoted under leucemia a case
of a common Marmoset (_Callithrix jacchus_) which was probably aleucemic
leucemia of the myeloid variety; the enlargement of lymphatic nodes was
trifling. The case to be cited answers in most respects to the
descriptions of systemic lymphomatosis, but there were found two
conditions, enteritis and parasitism, which might be responsible for
sufficient general toxemia to stimulate lymph nodes and follicles to a
state of active growth. Even accepting these two cases as examples of
this group, it is very plain that chronic systemic primary lymphatic
hyperplasia is an exceedingly rare entity in wild animals. There has
been no case resembling Hodgkin’s disease of man.
California Hair Seal (_Zalophus californianus_). Young ♂ four months
old. Appeared to be in good health, no loss of flesh or activity.
DIAGNOSIS.—Lymphomatosis. Fatty degeneration of kidneys. Emphysema.
Chronic follicular and catarrhal enteritis. Nematodes in intestines.
External appearance good. Both lungs distended and are tense; it seems
almost like a spastic dilatation—a simple emphysema—beneath pleural
surface are many minute petechiæ. Lung mottled red and gray. This
color is present on section. Lobules clearly outlined and separable
with fingers. Bronchi and vessels widely open, the latter containing
small amount of fluid blood. Lymph nodes—Mediastinal, tracheal and
those visible in neck are variously but definitely enlarged, firm,
irregular and roughly nodular, both in appearance and to touch. On
section they are red and gray, follicular border not preserved and
merging with medulla; connective tissue visible; gray juice expressed.
Pericardium normal. Epicardium, glistening, transparent and pale.
Heart position, size and interior normal. Abdomen contained no
adhesions or fluid. Pale brown-red, firm liver with smooth surface and
sharp edges; markings not clear; section surface smooth; watery blood
expressed from section. Gall-bladder normal, contents limpid, brown.
Common bile duct patulous. Somewhat enlarged spleen, soft, yet
resilient; capsule smooth; section surface pulp homogeneous brown-
purple; follicles gray, slightly enlarged, clear, sharply outlined;
trabeculæ faintly visible, more prominent where they are near
follicles. Kidney normal in size, shape and location, with smooth,
pale brown surface; capsule smooth, strips easily, section surface
glistening, consistency soft yet resilient; thickness of cortex
slightly wide, of medulla normal; individual lobules clear yet no
increase of connective tissue between; pyramids quite pale; top of
medulla a little darker; cortices, pale, striæ quite faint and seem
irregular; glomeruli not visible. R. Adrenal—In upper pole are two
cysts about 1.5 and .8 cm. across; no scar at this point. L. Adrenal—
Wide pale purple, regular homogeneous cortex under very dense capsule;
medulla reddish brown, homogeneous, quite bloody. In left adrenal is a
pale gray, fairly well outlined area between medulla and cortex at
upper pole about 3 mm. across.
Stomach.—Contains glass and stones; mucosa, soft, smooth, flat, yellow
and pink, translucent rugæ; cardia about normal; pylorus, valve
prominent but probably not hypertrophied. Duodenum—Beginning at
pylorus and extending through to ileum where follicles commence,
intestine contains small amount white, creamy material, serosa
negative, mucosa smooth flat, pale pink, translucent. There are small
nematodes, probably uncinaria, some of which are attached quite
firmly. Here and there throughout the gut are bits of thickened mucosa
or submucosa, 2–5 mm. across. Some of these have a tiny opening from
which clear fluid can be expressed. Ileum shows smooth flat
translucent mucous membrane; empty; individual follicles faint but
discernible. Colon reddened mucous membrane, nematodes and little
mucus. Pancreas, soft, normal in size and position, color pink gray.
The lymphatics of peritoneal cavity are all enlarged; most of
retroperitoneal are also. Regional lymph glands are also enlarged. The
description given for mediastinal answers here. The glands of
mesenteric stalk present chain of sausage-like masses. Glands in
mesentery are but slightly affected. Glands within and without
peritoneum at kidney are especially enlarged. Large gland behind
stomach and pancreas and in front of upper end of spleen is much
enlarged, thick and roughly circular; it shows much fibrosis. The
regional glands are distinctly enlarged but proportionately not so
much as the internal ones. Smear of juice expressed from peritoneal
glands shows large and small lymph cells in about proper proportions.
There are a few plasma cells. No granular cells.
Smear from bone marrow shows enormous number of premyelocytes and mast
cells. Polynuclears in their early stages are not numerous. Small
groups of lymphocytes, lightly packed together, noted here and there.
Blood smears unsatisfactory.
Microscopical.—Lung shows distended vesicles with considerable
congestion of septa and in some places red blood cells in alveoli.
Kidney.—Glomeruli contracted, relatively anemic; capsule negative;
epithelium throughout in state of granular degeneration probably
fatty; connective tissue not increased.
Intestines.—Show slight hyaline change in muscle fibres and nodular
degeneration and disappearance of protoplasm, leaving bare nuclei and
outline of the cells; submucosa loose; mucosa shows infiltration of
round and plasma cells, diapedesis, degeneration and desquamation of
epithelium. Section of ileum shows a hyperplasia of lymph follicles
with active centre in which large endothelial cells predominate. Small
swellings in submucosa consist of chronic granulation tissue, but
there is no foreign body and no evidence of preëxistence of a lymph
follicle.
Lymph nodes loosely arranged but in places solidly small lymphoid;
chords and sinuses contain chiefly small lymph cells in which are some
mast and plasma cells; follicles small and loose, and centres contain
chiefly large lymph and plasma cells; connective tissue not increased
yet there are some fibroblasts in follicles.
Spleen.—Shows almost entirely hemorrhagic pulp; blood destruction not
active; follicles large and made up of about equal mixture of small
lymph, plasma and large lymph cells; connective tissue prominent
probably because of excess of blood around it.
LOCAL HYPERPLASIAS.
In this group and touching the purely hyperplastic, come the
hypertrophies of the lymphadenoid tissue of the nasopharynx; this can be
disposed of by stating that no true chronic hypertrophies have been
seen. With most cases of gastroenteritis in ungulates, and many in
carnivores, there is a swelling and redness of the tonsillar region but
an exudative or necrotizing process does not occur.
THYMUS.
The thymus is rarely visible in our specimens but when found has usually
been normal. An increase in size and a decrease of consistency of this
organ is noted in marasmus (inanition) from failure of care of the young
by the parent, but so far as can be determined this has not been
adequate to cause tracheal compression. In a few cases of rachitis in
the canines, the organ is large and pale along with the rest of the
lymphatic system. In one of the tumors of the mediastinum to be
discussed, the suspicion arose that the growth originated in the thymus;
adenomata and sarcomata have been described in the lower animals.
TUBERCULOSIS.
Tuberculosis of the superficial lymph glands is rare as an independent
lesion in the lower animals. Dr. C. Y. White was fortunate in seeing a
monkey with a chain of fibrocaseous nodes in the cervical region, upon
which before death he offered the suggestion that it was of tuberculous
nature. In Primates almost all drainage glands exhibit some miliary or
caseous process. One monkey rejected upon the tuberculin test had what
was apparently a primary lesion in the glands at the tracheal
bifurcation. In the Ungulata, lymphatic tuberculosis assumes two forms,
the caseous and the cellular. The former is generally understood while
the latter is more uncommon. It is occasionally seen in the “fungous
tubercle” of cows, but we have seen it in deer and in another order,
Carnivora. In the latter, tuberculosis being uncommon, examples in the
lymph nodes were noted but twice, once caseous and once solid; this
latter was made up of firm, homogeneous yellow pink masses of glands in
the mediastinum, showing under the microscope solidly packed epithelioid
and giant cells.
Lymphatic tuberculosis in the birds is rare; only one case is recalled
(unfortunately record cannot be found) as small yellow, discrete firm
nodules in the mediastinum and neck. The minute picture was of a solid
arrangement of large vacuolated mono- and polynucleated cells which were
so packed with bacilli that the preparation could not be decolorized.
TUMORS.
The neoplastic enlargements are represented by a lymphosarcoma of the
mediastinum in a Dorcas Goat; there were secondary growths in the liver,
the kidney and several isolated lymph glands. Secondary growths from
original tumors not in the lymphatic system are curiously rare,
certainly much less frequent than is found in the human being. In
ninety-two tumors which are known to give metastases, only three
involved the lymphatic glands and only one of these could be considered
as involving nodes not in the ordinary drainage pathway.
THE SPLEEN.
The spleen is an organ whose exact position in the scheme of things
remains mystifying through the whole series of animals. Its functions
have been arrived at largely by exclusion, somewhat by conjecture and
speculation, while the acceptably proven duties are indeed few. Although
this is not the place to enter into a discussion of all the points at
issue concerning the anatomy and function of the organ, a few facts
might be mentioned of comparative and perhaps pathological value. While
the spleen has been looked upon always as the origin of blood cells in
the embryo, cases in man are on record where no spleen was discovered, a
condition suggesting that its absence is not incompatible with life;
that such is the case is obvious for experimental or therapeutic removal
of the organ is well known.
It was suggested by Virchow that at times the spleen assumes the duty of
the bone marrow and the swelling of the viscus in certain anemias seems
to support this statement. However, there is no physical relationship
between the size of the animal and that of the spleen, nor between the
available quantity of bone marrow, the obvious richness of circulating
blood and amount of lymphatic tissue. This is well shown in the water
mammals which have a great deal of blood in vessels and viscera yet
their spleen is relatively smaller than birds of somewhat comparable
size (the ostrich, for example). The Carnivora and Rodentia among the
mammals, have quite large spleens proportionately, while comparable
birds, Accipitres and Striges, have relatively small ones, and an
absolutely small amount of marrow.
Another anomalous example of the function of this tissue is found in the
hematopoiesis of birds. While there seems to be some evidence that in
the spleen and liver red blood cells may be formed, there is perhaps at
most times sufficient bone marrow to keep the blood cells at a proper
number. There is no inverse relation between the amount of bone marrow
and that of splenic bulk; that is in diving birds with their hollow
bones the latter is no greater than in gallinaceous birds which have
abundant marrow in all the skeleton.
It has been suggested that the spleen supplies an activator for
pancreatic ferments. This receives a sort of support from the greater
size of the organ in carnivores and smaller relative size in ungulates,
since in the former concentrations of digestive enzymes are more often
needed. Because of the greater excretion of iron in splenectomized
animals or those being starved, Fischer has thought that the spleen has
some power to metabolize this element; this receives some support from
the statements concerning the size of this organ in the carnivorous
orders. From experimental studies it appears that some relation exists
between the lymphocytes and resistance to implanted tumors. If one apply
this idea to the amount of lymphatic tissue and the incidence of
spontaneous new growths, it is found that no definite relationship is
discoverable either in terms of size of spleen or richness in lymphatic
nodes. Carnivores, rodents and marsupials show a high tumor incidence
and have a good lymphatic supply. Aves, on the other hand, with a poor
nodal apparatus and a variable splenic bulk, show many fewer tumors than
do the mammals. The mononuclears of avian blood rise normally as high as
60 per cent., of which 40–45 per cent. are of the small size.
The size of the spleen is subject to great variation not only within
orders but actually within genera; it even seems that one sometimes sees
two or three members of a species kept in the same enclosure, maybe with
the same disease, maybe without any obvious disease, yet with definite
variation in the size of the organ. This irregularity is recognized by
veterinarians (Hutyra and Marek) who ascribe it to some unknown disease,
past or present, and to normal variation. The lack of uniformity is seen
more clearly in birds than mammals. In the former it might be due at
times to low grade or inactive parasitism or, conjecturally, to toxins
from incorrect diet; we shall see later that infection and intoxication
seem to have a different effect. Some writers have mentioned the
possibility of an idiopathic splenomegaly (?), a condition associated in
youthful human beings, with anemia and lymphadenopathy, and occasionally
going over into a sort of leucemia. The existence of such a condition is
difficult to admit or deny; we have met nothing which could not be
aligned in some fairly well defined group. Birds have a relatively
larger spleen than mammals and in addition the organ seems to respond
more actively in infections or intoxications, since it may reach, under
active stimulation, a size ten times that of the normal organ.
ENLARGEMENTS OF SPLEEN.
Acute enlargements of the spleen, be they of congestive or
“inflammatory” nature are quite common among the lower animals, a fact
that is recognized in veterinary medicine. Congestions of the spleen are
most often seen during acute infections and diseases of the heart and
liver. The diagnosis has been made among mammals proportionately more
than in birds, 27 or 1.5 per cent. to 35 to 1 per cent.
REASON FOR CONGESTIVE ENLARGEMENTS.
Perhaps this is partly due to the circulatory anatomy since in the
former the arterial and venous supply is usually by one large vessel of
each kind, whereas in birds the splenic branch of the cœliac axis breaks
up into several small arteries and the venous return is accomplished by
numerous venules some of which reënter the posterior cava almost
directly, others joining with the mesenteric to form the portal; by this
arrangement a more elastic system is assured. The same condition is
found when analyzing the records of chronic passive congestion; in
eighteen recorded cases, fourteen were mammals and four birds. In these
cases the principal associated pathological lesions were pleural and
pulmonary in seven, cardiac in three, renal in three and hepatic in
four. While the anatomy of the splenic blood supply may help to explain
the small number of congestions in Aves, it will not answer for the
inflammations which occur in large numbers in this class; this will be
discussed in the following pages.
Hemorrhage and infarction of the spleen are not very common, there being
eleven of the former and ten of the latter and all occurring with the
same indication or history of infectious disease; in one case, an
opossum (_Didelphys virginiana_) an injury probably caused a massive
hemorrhage shaped like an infarct. It is, however, curious that of the
twenty-one cases only five occurred in birds, of which only one
hemorrhage was in the shape to which the term infarction is best
applied. There have been, as one might expect, a few cases of infected
infarction, with abscess. It is perhaps worth noting that no case of
hemorrhagic cyst or inspissated coagulum has been seen. Only one case of
rupture is recorded secondary to acute splenitis during an acute
septicemia.
INFLAMMATIONS.
It has been the practice at this laboratory to classify splenitis in
three ways, (1) acute diffuse splenitis—general congestion with perhaps
small hemorrhages, swelling but retention of general architecture and
with no undue prominence of the follicles; (2) follicular hyperplasia—
where this is the prominent gross and minute finding, the pulp being
less pronouncedly involved; (3) acute splenic tumor—where the organ is
greatly enlarged but with loss of the usual markings. Perhaps this
separation is not warranted upon a strict etiological basis, and yet as
we shall see it holds true fairly well in the toxic and infectious
lesions. Moreover, from the following list it is evident how the various
orders call upon the splenic tissue in disease.
TABLE 7.
_This Shows the Percentage of Various Forms of Splenitis in the Animals
Coming to Autopsy._
═════════════════╤═════════════════╤═════════════════╤═════════════════
│ Acute Diffuse │ Follicular │ Acute Splenic
│ Splenitis. Per │ Splenitis. Per │Tumor. Per cent.
│ cent. │ cent. │
─────────────────┼─────────────────┼─────────────────┼─────────────────
Carnivora │ 7.│ 3.│ 1.3
Primates │ 2.5│ 4.9│ 2.
Ungulata │ 2.4│ .3│ 1.2
Rodentia │ 2.6│ 4.7│ 1.
Marsupialia │ 9.2│ 3.│ 3.7
Pinnipedia │ _33._│ │
Proboscidea. │ _33._│ │
Edentata │ _12.5_│ │ _6.2_
│ │ │
Passeres │ 3.│ 3.│ 3.8
Psittaci │ 6.5│ 2.3│ 4.1
Anseres │ 5.2│ 7.2│ 5.2
Herodiones │ _1._│ _6._│ _2._
Galli │ 2.6│ 1.5│ 4.7
Struthiones │ _10._│ _10._│ _1._
Accipitres │ 7.5│ 3.7│ 1.6
Gaviæ │ │ │ _5._
Picariæ │ _4._│ │ _1.3_
Striges │ 6.8│ 3.4│
Fulicariæ │ _3._│ 6.│
Steganopodes │ │ _10._│
Columbæ │ .7│ .7│
─────────────────┴─────────────────┴─────────────────┴─────────────────
For the meaning of italics see foot note Table 1.
The points to draw from this chart are first the greater variety of
lesions seen in the birds, which apparently make greater use of the
organ in defence, and the preponderance of acute diffuse hyperplasias in
mammals. It is noteworthy that the Primates and Marsupialia show more of
the acute hypertrophy of the spleen going under the name of tumor. It
would be interesting and valuable to be able to discover exactly what
determines and constitutes the conditions usually termed hyperplasia and
inflammation of the spleen and an attempt was made in this direction by
tabulating the data from Table 7 in terms of each diagnosis, classifying
these latter also as infectious and toxic. The results of this effort
are not conclusive, and while they permit of some discussion of the
lesions, do not allow finished conclusions. The figures obtained by
study are not illuminating. One can state, however, that in infections,
either specific or not specific, more elements of the spleen were
engaged in the process than when the condition did not resemble a
communicable disease, but might be called toxic. Under the former
condition the diagnosis of splenitis or acute tumor predominated, while
under the latter follicular hyperplasia is more often recorded.
Anatomical alterations in these two groups are described in the
definition given in a previous paragraph and deserve no special
discussion except in so far as they concern the changes in the avian
splenic tumor when under magnification.
Microscopically there is a total loss of the relations in the acute
splenic tumor of birds, the chords and follicles being replaced by a
rather regularly arranged mass of small and large mononuclears, granular
cells of the circulating types and red blood cells; pigment always seems
increased. Endothelial cells do not take part in the general mass of the
organ but along lymph and blood vessels their bulk and number are
increased so that if the packing be not too dense one may find double
lines of these cells passing through the hyperplastic tissue. There is,
however, a group of seven cases (six birds) to which the term
endothelial hyperplasia in the spleen has been applied. All of them show
an unusual prominence of the vascular linings and of the follicular
centres and perivascular areas; besides this there is a moderate general
hyperplasia. An examination of the history and autopsy results in the
birds indicated that they had all suffered with some rather protracted
intoxication and showed a moderate anemia (four of the spleens were well
pigmented).
The more chronic changes of this organ, be they moderate or of a grade
to which one must apply the term fibrosis, are rather uncommon when one
considers the number of animals with prolonged infection, anemia,
skeletal diseases and hepatic cirrhoses; these are the conditions that
take a prominent place in the associated pathology and history. There is
no essential difference in the organ throughout the animal kingdom, and
one may find as far down as the struthious birds analogies to the
processes of domestic and human animals.
SPECIAL SUBJECTS—AMYLOID.
Amyloid changes in the spleen have occurred in the following orders:
Primates, Carnivora, Rodentia, Marsupialia, Passeres, Galli, Gaviæ, and
Anseres, fourteen cases in all. This infiltration is usually ascribed to
long continued suppuration or chronic infection, every one admitting,
however, that once in a great while a case is seen wherein no cause can
be discovered. In this laboratory we have a high percentage of cases
without adequate accompanying pathology so that we have called six of
the above cases primary or idiopathic. The gross appearance of the
spleen is in all these cases that of an enlarged, firm, homogeneous body
without the sago spots usually described for this change.
Microscopically the infiltration occurs first in the vessel walls,
thence spreading to the sinus walls and reticulum. Joest in discussing
this infiltration[19], states that it is comparatively rare among the
domestic animals, where it may appear under the usual conditions or as a
primary affection; it seems at times to follow unsuitable feeding.
According to this author, the “sago” type is more common than the
“bacony;” this has not been our experience. The most conspicuous example
is given here.
European Badger (_Meles meles_) Adult ♀ . Gradual failure for two
weeks.
DIAGNOSIS.—Amyloidosis. Chronic parenchymatous nephritis. Emphysema of
lungs.
Muscles atrophic; fat scanty. Heart is dilated and muscle is red-
brown. Aorta is jaundiced and there is a small patch of atheroma near
the anterior leaflet of aortic valve and about 5 mm. above it. Abdomen
contains a slight amount of clear fluid, no adhesions. Liver is normal
in size, smooth surface, sharp edges, firm consistency, yellow color.
The section surface is glistening, smooth and moist. The spleen is
very hard, greatly enlarged (25 × 6 × 2 cm.) and lies across the
abdomen over the intestines. It is pale red and very bacony. In iodin
the tissue stains a mahogany brown. The kidney is normal in size. (5½
x 3 cm.). The capsule is smooth and strips easily leaving a smooth,
yellow surface. Organ is firm. The section surface is glistening, has
a relatively narrowed cortex and relatively wide medulla. The
glomeruli are barely visible but stain a mahogany brown in iodin. The
adrenals are 12 × 10 × 4 mm. The cortex is wide, dull yellow and
regular. The zone beneath fades into the cortex although rather
abruptly. The centre of both glands is occupied by an irregular pale
yellow, sharply outlined nodule suggestive of solid medulla, tubercle
or tumor. The zone between cortex and this is gray, irregular and
firm. This is practically a normal figuration. The stomach is empty,
mucosa apparently normal. Intestines were not opened but serosa seems
normal; when opened after Kaiserling fixation they seem normal. The
pancreas is normal in size, firm and pale. Lymphatics of the mesentery
are slightly enlarged, soft, homogeneous pale yellow.
HISTOLOGICAL NOTES.—Lung seems somewhat atrophic and there are some
vesicular ruptures. One small patch of amyloid found in blood vessel
wall. Liver shows slight capillary congestion and granularity of
parenchyma. There is a marked blood vessel amyloid deposit not only in
interlobular spaces but in intralobular capillaries. Spleen, no trace
of splenic tissue recognizable in section. It is composed of more or
less eosin-staining material surrounding single, or small collections
of round or plasma cells. Kidney shows marked amyloidosis of glomeruli
and slight deposit in blood vessel walls and in the increased
connective tissue. There is a general moderate fibrosis; irregular
tubules; low epithelium and hyaline casts. Heart muscle fibres are
small and stain deeply. No amyloid in section. No pigmentation
although section is suggestive of brown atrophy. Adrenal is
practically negative. There seems to be slightly more connective
tissue than normal but parenchyma may be considered normal. At one
place in the cortex there are some structures of deep layer included
in vesicular layer. This seems like a structural malformation.
NECROSES.
Focal necroses of the spleen affecting chiefly follicular centres but
also chords, are not at all uncommon in avian spleens, especially where
parasitism occurs, not only with hemic protozoa and embryos, but also
with intestinal or visceral nematodes and trematodes.
SPLEEN IN ANEMIA.
The spleen in the anemias shows much less definite change than one would
expect. In the secondary form of anemia among mammals one finds a slight
excess of pigmentation and an occasional fibrosis but often the size of
the organ is recorded as normal. When the impoverished blood seems
secondary to skeletal degenerations there is a diffuse or follicular
enlargement. In the birds, on the other hand, there is nearly always
some grade of enlargement which is due in the well studied examples to a
richness of blood cells. There may be a slight increase in follicles,
but these bodies are usually small and solid. In two instances a
prominence of large endothelial cells was discovered. Pigment is seldom
increased, but it may be very excessive.
In the primary anemias little more than the above is to be found.
Fibrosis is more evident and perhaps pigmentation less so, but the
variations are more of degree than kind. The spleen in leucemia can only
be discussed upon the case already reported (_q. v._).
[Illustration:
FIG. 7.—EUROPEAN BADGER (MELES MELES). PRIMARY AMYLOIDOSIS. THE
ENORMOUSLY ENLARGED SPLEEN IS SEEN LYING ACROSS THE STOMACH BELOW
THE LIVER, WHICH ORGAN IS EXCEEDED IN SIZE BY IT.
]
SPLEEN IN HEPATIC FIBROSES.
The fibroses of the liver are not infrequently associated with some
enlargement of the organ under discussion. At this laboratory hepatic
cirrhoses are divided into Portal, Biliary, Fatty, Perilobular and
Vascular. By a study of the spleens in these cases a few facts have been
obtained. In mammalian portal cirrhoses there is usually a very moderate
but definite increase in the size of the spleen due to connective tissue
increase in the trabeculæ and reticulum, with very small compact
follicles. Among the birds the organ seldom shows more that a moderate
congestion and diffuse hyperplasia. In the mammalian biliary cirrhoses
there is almost without exception a definite enlargement due to fibrosis
and follicular hyperplasia. Among the birds the process is very far from
uniform, there being just as often no change, as a congestion and
hyperplasia, or as a mild fibrosis; it is notable, however, that
pigmentation is commonly met in this class. No noteworthy change is met
with in the spleen of fatty hepatic cirrhoses. We have no record of
cyanotic induration of the spleen accompanying a similar condition in
the liver. When the condition of perilobular hepatic fibrosis has been
met a distinct increase of the splenic pigment is usually found. In
reviewing the facts in this paragraph one is forced to the conclusion
that, with the exception of the frank infective cases, there is no
definite relation of the splenic changes to those in hepatic cirrhosis,
a fact made perhaps the more significant in view of the idea held in
some quarters that the primary change in this pathological process
occurs in the spleen.
PERISPLENITIS.
Perisplenitis of an acute or fibrosing variety as a part of peritonitis
or as the result of an injury to the splenic region, has been
encountered on numerous occasions and offers nothing worthy of comment,
but the so-called “sugar-icing” spleen, associated with perihepatitis
and general peritoneal thickening, and with an obscure relation to
tuberculosis has not been seen. As we shall learn later peritoneal or
massive intestinal tuberculosis is not common in the lower animals. A
diffuse fibrous thickening of a pearl gray glistening appearance, has
occurred in five monkeys harboring the Filaria gracilis in the
peritoneum.
TUBERCULOSIS.
In tuberculosis of this organ the capsule is almost invariably thickened
over the nodules, but not over the whole organ and rarely in the diffuse
variety. There is almost always, however, in this prolonged infectious
disease some reaction on the part of the spleen, particularly when
several other viscera are involved. In such cases a low grade of general
hyperplasia and fibrous tissue increase is found. This is especially
true in the Primates and Carnivora in long continued pulmonary
tuberculosis, and it is in this form that one does not often see
tuberculous lesions proper in the spleen itself. Tuberculosis of the
spleen is not very common in adult human beings and domesticated
animals, while in the young it is seen in a fairly high percentage of
cases. In the wild animals this organ seems much more susceptible to the
settling of tubercle bacilli as will be attested by the facts to be
cited, and yet there are some conspicuous exceptions to this statement.
Just why certain groups, or orders should show splenic tuberculosis very
frequently while others fail to do so is far from clear.
The appearance of the lesion is fairly comparable throughout the animal
kingdom, variations among the Aves being chiefly in the more frequent
occurrence of the diffuse tuberculous splenitis. Miliary, caseous and
conglomerate masses occur separately or together and without very
distinct relation to other pathological involvements.
The relative incidence of tuberculosis in the spleen is set forth in the
section devoted to this infection, but may be mentioned here in a
general way. The organ is about equally susceptible to the disease in
mammals and birds according to the figures, but the high percentage for
the former is due to the frequency with which tuberculosis is met in the
Primates. With this order deducted there is no doubt that the avian
spleen has a greater vulnerability for the tubercle bacillus than has
the mammalian organ. Rodentia as a mammalian order stand next to the
Primates, whereas the Carnivora and Ungulata relatively seldom show
splenic tuberculosis. Among the Aves one finds that Columbæ, Galli and
Accipitres have the highest splenic susceptibility, but beyond this one
hardly dare venture because of the irregularity in the number of
specimens seen at autopsy. Suffice it to say that a greater number of
cases of tuberculosis are seen in the spleen of the class for which the
intestinal origin of tuberculosis appears most important.
In the cases of actinomycosis and its congeners, such as the Kangaroo
maxillary mycosis, which we have seen at the Garden, no specific changes
have been seen in the spleen, unless a single or double nodule of the
same variety as the original focus may be considered specific. Such was
found in two cases, one a tapir with low grade inactive actinomycosis,
the other a kangaroo with maxillary streptothricosis. Two deer came to
autopsy with a gross picture suggestive of anthrax; no bacilli could be
found in the semifluid spleen, but a member of the hemorrhagic
septicemia group was found. The latter group of infections has been
fairly well represented, although not in epizoötic form, and the almost
invariable splenic change has been that already discussed as diffuse
splenitis. Three secondary tumors are recorded, two cancers and one
renal adenoma.
SECTION VI
THE RESPIRATORY SYSTEM AND ITS RELATED STRUCTURES
It is customary to divide the descriptions of normal and diseased
conditions of the upper entrance to the body into respiratory and
alimentary parts, the nose, nasopharynx and larynx belonging to the
former, the mouth, buccal cavity and pharynx to the latter. As a matter
of fact they can for most purposes be considered as the structures
contained in the anterior head and furthermore their pathological states
are more often followed by extensions into or implications of the
respiratory organs proper than of the alimentary tract. From a
comparative standpoint the incidence of specific infectious diseases and
of the involvement of accessory nasal sinuses present the most
interesting subjects. There are several infections, believed to be
specific, observed among domestic mammals and birds but their actual
individuality has hardly been unexceptionally proved. This refers to the
communicable rhinitis of cows, pigs, rabbits, and birds, especially
parrots, the follicular catarrh of horses, and croupous nasopharyngitis,
all of which have been ascribed to a particular virus, without finished
evidence in many instances. Some of these diagnoses doubtless cover or
are confused with the early symptoms and signs of the disease of protean
manifestations, distemper, and indeed the Bact. septicus and relatives
of the bird cholera organisms are reported as being responsible for
them. No intention of excluding well recognized entities like bird
diphtheria, foot-and-mouth disease or influenza, exists. I shall refer
below to small groups of epizoötics which do not conform strictly with
word pictures drawn by Hutyra and Marek, Moore, or Ward and Gallagher.
RHINITIS, SINUSITIS.
The nature of inflammations of the nasopharynx suggests at once that
there may be some anatomical reason for their distribution and
character. A general review of the anatomy of the mammalian and avian
nasopharynx reveals the relatively greater space in the former,
especially in the passage from the nose to the pharynx, and emphasizes
the exposure of the opening of the upper larynx in the bird, lying as it
does in the posterior part of the tongue and surrounded by the
constrictores glottidis. A dissection of the accessory nasal sinuses
exposes the relatively large size of these spaces in the lower mammals,
and the capacious openings into the nasal cavities.[20] In the Primates
and Lemures the anatomy more closely resembles that of man, the sinuses
being relatively smaller and the communicating passages narrower. In the
bird on the other hand, while the sinuses may be extensive in some they
are usually small, yet in all the communication with the turbinate area
is by a narrower slit or tortuous canal, frequently, as in Galli,
running from below upward into the maxillary sinuses. The extent of the
turbinate and the richness in mucosa is probably greater in all mammals
than in birds; certainly this seems true of Carnivora and Ungulata
_versus_ Accipitres and Galli.
If the seriousness of a rhinitis be dependent upon the extent of
involvement of the sinuses and the blocking up of their outlets it would
be expected that the variety of animal having the smallest drainage
channels would show the greatest evidence of these diseases. Our records
would indicate that 32 birds (.96 per cent. of the autopsies upon Aves)
had rhinitis whereas only 7 mammals (.39 per cent. of autopsies on this
class) presented the condition. Extension to the sinuses occurred in
only one-third of each of these figures, a complication which in turn
produced generalized infection more often in mammals than in birds as 4
is to 3. These figures are perhaps too small for conclusions but it
would seem that rhinitis occurs more often in birds with their small
sinuses and channels while sinusitis and general infection occur more
often in mammals with their large sinuses and extensive turbinate
apparatus. The most conspicuous orders represented are, in line of
numbers Anseres 12, Psittaci 7, Accipitres 5, Carnivora 3. Nine of the
twelve waterfowl were part of an epizoötic which will be discussed under
specific diseases.
Bacteriologically the mammalian cases that have been worked out were due
to _Streptococcus pyogenes_ in several instances, including the
generalized cases, and to a mixture of streptococci, golden
staphylococci and members of the colon-aerogenes group. In one case in a
tapir a member of the B. septicus group was found. Moulds were
discovered in three avian cases and filaria in one. No pentastomum or
œstrus has been discovered. In thirteen instances the lungs have been
involved, apparently secondary to the nasopharyngeal disease.
There have been two small outbreaks of an acute nonspecific infection—
that is not suggestive of cholera, psittacosis or infectious enteritis—
among the parrots in which during a short time 4 and 6 parrots died with
nasopharyngosinusitis as the prominent lesion. One outbreak was studied
bacteriologically without definite result. There was no uniform internal
pathology unless, in one outbreak, congestion of the cerebellum may be
mentioned. Fowl diphtheria and its associated condition from which a
satisfactory separation has not been accomplished, epithelioma
contagiosum, has happily given us little concern, so that it is not
possible to record any instructive facts upon its cause or differential
diagnosis. There was recorded in the 1911 Report of the Society the
occurrence of two fatal cases in cassowaries from which it was possible
to isolate the B. columbarum and one bird with the same clinical
appearances whose recovery seemed to be due to the use of human
diphtheria antitoxin. In light of more information and consideration of
the accepted variability of this disease, it is possible that this bird
may have recovered without the injections or with the use of normal
serum. Nowadays it is possible to obtain antiroup serum which is stated
by Blair of New York to be efficacious. The disease has been observed in
a wild turkey and an Abyssinian Ground Hornbill, beside the two
struthious birds mentioned above.
MYCOSIS.
Mycotic disease of the nasopharynx seldom restricts itself to this
cavity, usually extending by continuity to the esophagus, or by
inspiration to the lungs whence it spreads to the air sacs. This
condition of the upper passages has occurred here only in Psittaci and
Accipitres although it is reported by veterinarians as occurring in
Anseres and Struthiones. In the first order four birds were affected,
two showing extension to the esophagus and a like number having
pulmonary and serous membrane involvement. These cases were all due to
aspergillus whereas those next to be mentioned were caused by an oidium
close to the “albicans” variety. In four Mississippi kites the prominent
changes were found in the pharynx and esophagus down as far as the
proventricle with only a few rather trifling lesions in the nasal area.
Infiltrative and necrotizing processes characterized the action of the
oidium while that exerted by the aspergillus was more superficial and
extensive. In one case of a parrot the whole nasal cavity was completely
filled with a yellow gray exudate whereas the esophageal wall of the
kites was thoroughly infiltrated by a gray-brown, friable, necrotic
mass. Attempts at treatment were made in the case of the latter, using
potassium chlorate and saline solution on cotton swabs. The result was
entirely negative and the applications seemed to have no effect upon the
course of the infection.
There are on our records in addition to the above, several cases of
necrotizing processes about the head seeming to emanate from wounds to
the mucosa by foreign bodies, by decomposition of pieces of food in
crevices or by damage by masses too large to be swallowed. In the few
instances where we have tried bacteriology, no definite result has been
obtained unless the frequent occurrence of organisms bearing a
resemblance to Bact. necrophorus be important. This organism however may
be found in many necrotic processes in animals; I do not look upon it as
specific in the locations just cited.
Mammals as a class do not present many inflammatory conditions around
the anterior head, aside from the specific diseases like distemper (?),
actinomycosis, Kangaroo disease and the like. Monkeys occasionally have
acute coryza, which may indeed seem transmissible to others but it
seldom leads to any serious consequences and is untreated, except by
segregation. Tuberculous lesions are not recorded. There has been no
glossitis aside from lesions involving the pharynx. The tonsils have
been discussed under the lymphatic apparatus and it only need be
repeated here that inflammation and hypertrophy of these organs are
exceedingly rare. Specific or individual diseases of the salivary glands
are also rare although these organs may be involved by extension. This
general region is not often affected with tumor, unless the jaw be
included which bone is the seat of several tumors in antelopes and
opossums. Aside from these we have seen an epithelioma of the tongue in
a black bear (_Ursus americanus_).
LARYNX.
The larynx is an organ of fairly uniform construction through the
mammalian orders but is conspicuously different in the Aves where it is
double. The upper end of the trachea in the latter class is surmounted
by a cartilaginous box lying beneath the root of the tongue through
which an anteroposterior slit-like opening forms the glottis; there is
no epiglottis. This is only an air passage, the voice being made in the
syrinx or lower box which lies at the bifurcation of the trachea. The
structure of the upper box is quite simple with its lateral plates
controlled by the glossal muscles and two external retractors but the
syrinx is very complicated and variable in the different orders and even
in the same family. It possesses an internal and external set of muscles
and in some birds can be opened at one point to permit air to pass to
the cervical or thoracic air sacs. Detailed discussion of its anatomy is
hardly profitable since there is nothing peculiar about its diseases. On
one occasion only have we seen distinct pathological change—what was
probably an extension of mould disease from it to the cervical air sac.
It is involved in true tracheitis and bronchitis but even these are rare
in birds.
The larynx on the other hand is constantly reddened in cases of
pharyngitis and may be the seat of mould colonies. Edema of this
structure is, however, not very common, it being recorded but twice in
birds in association with nearby inflammation and five times in mammals;
in the latter cases three were of acute infectious nature, one was a
tumor and the other osteomalacia. It is common to find the laryngeal and
tracheal mucosa swollen and wet in chronic bone degenerations without
the condition being severe enough to call it edema.
LARYNGITIS.
Acute laryngitis of active catarrhal or purulent nature has been met
five times in mammals and twice in birds while more chronic lesions have
occurred only in the former, four times. Tuberculous laryngitis has been
observed in a cockatoo and a lemur; they are interesting enough to cite.
There are no cases recorded among monkeys despite the large number dying
from the disease; this implies of course that no suspicion of its
existence was had at postmortem but perhaps some would have been
detected had every larynx been subjected to microscopic section. A
citron-crested cockatoo was found when posted to have general miliary
tuberculosis. The bright red rim of the glottis attracted attention and
upon slitting open the organ, pinhead size, sharply outlined yellow
tubercles were found on both sides. A black and white lemur was killed
because of a positive tuberculin test. He was in good condition and
exhibited as his only lesions retropharyngeal lymph nodes with
precaseous miliary nodules and small miliary tubercles on the
epiglottis, true and false vocal chords and in the mucosa of the main
ventricle, each lesion being surrounded by a narrow sharply injected
zone. This seems like a recent double implantation since the
retropharyngeal glands probably do not drain toward or from the larynx.
The larynx has been the seat of only one tumor, a squamous cell cancer
in an Azara’s agouti. The tumor caused ulceration and edema of the whole
mucosa sufficient to produce fatal asphyxia.
The trachea is of relatively little comparative or pathological interest
aside from its inflammations which however are so closely associated
with bronchitis that they will be included under that heading. Perhaps
the most important condition of this tube is its infestation with
_Syngamus trachealis_ since this leads to inflammations not only of the
related mucosa but predisposes to pulmonary infection. The occurrence in
the Galli is well known but perhaps it is not so well recognized that
this worm occurs also in crows (Passeres) and swans and geese (Anseres).
For the diagnosis of this condition it is customarily stated that a
frothy mucus in the mouth is very suggestive; this is true in the cases
seen here but in addition a mucopurulent stomatitis is exceedingly
common and when the two are combined the picture is almost confirmatory.
Although worms are credited with considerable weight in the production
of pneumonia in Ungulata, they have only been seen once within the
tracheal tube.
THE BRONCHI.
The bronchi will be discussed as a separate part of the respiratory
system in so far as possible since they present a very decided
difference in anatomy between mammals and birds and because the
incidence of their disease is other than will be found for the lungs.
However, distinction has been made between changes in the grosser tubes
and those in the finer bronchioles, especially because capillary
bronchitis so-called is really a pneumonitis in which the mucosa of the
larger passages need not participate. The mammalian tubes are not really
greatly different in their construction, passing through ever smaller
branchings which give an increasing square area of tube capacity and
more extensive mucous surface. The avian main bronchus breaks up very
shortly after entering the lung into a varying number of spaces lined
with low epithelium lying upon a fibrous support and without cartilage.
These spaces then open into secondary air spaces of a size visible to
the naked eye which are in turn surrounded by microscopic alveoli. The
largest spaces, first mentioned, continue to grow smaller toward the
lower part of the lung where they usually communicate with one or other
of the various ostia of air sacs. Bronchial diseases in birds must
therefore be limited at the place where the bronchi lose the
cartilaginous rings since below this the surface functionates as
pulmonary tissue.
BRONCHITIS.
The accompanying list, Table 8, will show the distribution of bronchitis
not accompanying pneumonia or due to mycosis. It is striking that
carnivorous animals are more prone to bronchitis than any other order
(the struthious birds are too few to be important). There is a very
decided preponderance of mammalian cases over avian, there being not
only more cases but proportionately more orders affected. The character
of lesions in the mammals is nearly always catarrhopurulent or freely
purulent while ulcerative changes are not uncommon. Peribronchial
infiltrates are seldom found without some evidence of pneumonia; nor is
it common to meet the pale lines extending from bronchi between the
lobules, such as are seen in human streptococcal disease. Avian
bronchitis is usually hemorrhagic or catarrhal and with exceeding rarity
becoming purulent; when this occurs the cause is frequently found to be
tuberculosis or mycosis. Inflammation of the larger passages is nearly
always accompanied by pulmonary congestion, a serious condition in birds
as will be seen later. A few of these cases have been studied
bacteriologically with no definite result, nor have these cases occurred
in such groups that an epizoötic was suggested. Bact. avisepticum, Bact.
canisepticum, Bact. coli, Bact. aerogenes mucosum, and Ps. pyocyaneus,
Streptococcus hemolyticus and non-hemolyticus and staphylococci have
been found.
TABLE 8.
_Showing the Percentage Incidence of Bronchitis and of Parasites in the
Autopsies upon the Various Orders._
════════════╤═══════════════════╤═══════════════════╤═══════════════════
Orders │ Simple Bronchitis │ Verminous │Inactive Parasites
│ │ Bronchitis and │of Lung (Encysted)
│ │ Pneumonitis │ &c.
────────────┼─────────┬─────────┼─────────┬─────────┼─────────┬─────────
„ │ Cases │Per cent.│ Cases │Per cent.│ Cases │Per cent.
────────────┼─────────┼─────────┼─────────┼─────────┼─────────┼─────────
Primates │ 7│ 1.4│ 3│ .6│ 5│ 1.
Lemures │ │ │ │ │ 1│ 1.2
Carnivora │ 14│ 2.9│ 8│ 1.6│ 8│ 1.6
Insectivora │ │ │ │ │ │
Chiroptera │ │ │ │ │ │
Rodentia │ │ │ 2│ 1.│ │
Ungulata │ 5│ 1.3│ 2│ .5│ 10│ 2.7
Proboscidea │ │ │ │ │ │
Hyracoidea │ │ │ │ │ │
Edentata │ │ │ │ │ 2│ _12.5_
Marsupialia │ 3│ 1.7│ 2│ 1.1│ 3│ 1.7
Monotremata │ │ │ │ │ │
│ │ │ │ │ │
Passeres │ 4│ .29│ 7│ .5│ 2│ .16
Picariæ │ │ │ │ │ │
Striges │ │ │ │ │ │
Psittaci │ 4│ .58│ │ │ │
Accipitres │ 1│ .5│ │ │ │
Columbæ │ │ │ │ │ │
Galli │ │ │ 1│ .3│ │
Hemipodii │ │ │ │ │ │
Fulicariæ │ │ │ │ │ │
Alectorides │ │ │ │ │ │
Limicolæ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │
Impennes │ │ │ │ │ │
Steganopodes│ │ │ │ │ │
Herodiones │ 1│ 1.│ │ │ 1│ 1.
Odontoglossæ│ │ │ │ │ │
Palamedes │ │ │ │ │ │
Anseres │ 2│ .67│ 3│ 1.│ │
Struthiones │ 1│ _3.3_│ │ │ │
────────────┴─────────┴─────────┴─────────┴─────────┴─────────┴─────────
For meaning of italics see footnote Table 1.
A review of the active verminous lesions of the bronchi and the
pneumonitis to which parasites lead, shows again the highest number
among the Carnivora, with negligible percentages among the Aves. The
forms concerned are, when determined, ascarides, strongylus, hepaticola,
fasciolopsis, cytoleichus, pneumonyssus and paragonimus; these will be
discussed later. The lesions in the bronchi are mucocatarrhal or
hypertrophic; occasionally actual ulcerations are seen. What is more
important however is the peribronchitis leading to interstitial
pneumonitis and to bronchiectasis of the smaller bronchi, or to areas of
atelectasis by total occlusion of some small air passage. This pathology
is fairly well recognized among veterinary pathologists but there are
two points which seem worthy of special emphasis, namely, the relative
mildness of the changes in the larger bronchi and the importance of the
worms as causes of pneumonia. In regard to the first it can be pointed
out that the trachea and its branches need not be altered at all while
the middle sized bronchi present a mottling of small recent congestion
with pigmentations from old hemorrhages, together with slight
unevennesses of the surface. Small bronchi on the other hand are the
seat of ulcerative internal processes and quite marked peribronchitis,
as indicated by round and connected tissue nuclei or perhaps polynuclear
increase under active acute inflammation; it is in the latter case that
acute pneumonitis is present.
To what extent do the parasites predispose to pneumonia? Compare for
this purpose the two columns of Table 8 showing active and inactive
pulmonary parasitism. In Rodentia and Galli alone do we note that active
parasitism is effective, there being no passive cases. In all the other
orders, animal invaders of the lung are more often encountered as
quiescent or encapsulated bodies, therefore as findings incidental to
the autopsy and perhaps not concerned in the cause of death. In Ungulata
the inactive parasitisms are five times as frequent as the active
inflammatory lesions. It might be added that the list is made up of
cases wherein we saw parasites whether determined or not, an explanation
of the apparently small number of cases; there were many more in which
such invaders were suspected but not found and therefore excluded.
BRONCHIECTASIS.
Bronchiectasis affecting the smallest tubes, or bronchiolectasis, is not
at all uncommon in verminous pneumonitis and is explained as due to the
degeneration of the wall, the surrounding progressive ulceration, to
accumulation of inspired air and its retention by the obstruction. There
is described a generalized bronchiolectasis, chiefly in young human
beings, due to a destructive bronchiolitis; this has not been seen.
Non-verminous bronchiectasis of the middle sized bronchi such as is seen
in human chronic bronchitis, simple or tuberculous, is quite uncommon.
Widening of the bronchial lumen may be divided, as I see its
pathogenesis, into (a) that due to congenital weakness of the walls, (b)
that due to obstruction permitting air to pass into but not out of a
bronchus because of a ball-valve obstruction or weakness of expiratory
power, (c) that due to external pressure by tumors or distortion by
fibrous tissue either within the lung or pleura and (d) that due to
inflammatory weakening of walls, augmented by loss of supporting
pulmonary tension, accummulation of secretion and the dilating effect of
inspiration preparatory to and incidental to coughing. How important the
last three auxiliary factors may be in the cases explicable under a, b,
c, can easily be speculated upon and may vary in different cases.
Bronchiectasis is reasonably common with pulmonary diseases of man,
particularly of chronic character, but is certainly not frequent among
animals. Under the first group (a) we can record one case, a Siberian
tiger which died of enteritis and its complications to which were added
a mild inactive bronchitis and a bronchiectasis of diffuse distribution.
The lungs were irregular in shape, dull, gray-red in color and gave a
variable boggy and vesicular sensation to the fingers. On opening the
lung, dilatations of the bronchi were found, affecting chiefly the
larger secondaries but apparently not the bronchioles. Parasites were
not found nor were inflammatory reactions apparently adequate to explain
the distentions, so that we looked upon this case as congenital. Cases
coming under the headings b and c are not recorded. Inflammation almost
certainly represents the most important single factor in the
pathogenesis of this lesion and could be demonstrated in two cases, a
Clouded Leopard (_Felis nebulosa_) and a Red River Hog (_Potamochærus
porcus_). While I feel that parasites probably laid the foundation for
the dilatations in these cases, none were found after, in one case at
least, a very thorough search, although in the second animal a single
cyst of _Cysticercus tenuicollis_ was found in the peritoneum. In both
animals there was a low grade interstitial pneumonitis and
peribronchitis with dilatations of the middle sized and end bronchi,
these being supplied with thick walls but containing very scanty
secretion.
We have on record chronic ulcerative pulmonary tuberculosis in six
primates, two carnivores and nine ungulates. It is highly probable that
among this number some cases of ulcerative bronchiectasis occurred but
if so they were not conspicuous enough to mention in the diagnosis and
in only two protocols do I find a discussion thereof, once in a monkey
and once in a carnivore. All the cases of our records were diffuse
ectasias, fusiform, or irregular and none of the distinct saccular
variety.
From the foregoing facts it would seem that in human cases more weight
should be laid to the effect of the dilating power of coughing and its
preparatory exertions. While I am aware that the comparative incidence
of human and lower animal bronchiectasis cannot be based upon the meager
figures at our command, these dilatations certainly can be expected in a
general autopsy service more in man than in lower animals. Chronic
bronchitis is relatively rare, aside from the verminous varieties. I
have seen little retained exudate in the bronchi, probably because
quadrupeds seem with ease to raise and swallow the secretions. Nor do
animals give vent to paroxysms of coughing such as the human being feels
forced to do. Suggestive deductions from these points are that
inflammation is the principal factor in acquired bronchiectasis and that
the retention of secretion with violent inspiratory efforts are potent
in man for the dilatation of the tubes.
THE LUNGS.
The essential respiratory organ of the animal body, the lung, is all
through this kingdom a structure intended to expose the blood to free or
combined atmosphere in order to permit gaseous interchange, therefore
being arranged so that there is a close apposition of the two factors,
separated only by such cells and membranes as may be necessary to
protect the circulation; perhaps these anatomical elements possess at
the same time some vital force to further the exchange of useful and
useless matter. In the two classes under discussion there is no
difference whatsoever in the primary factors of respiration albeit some
variations exist in reference to oxygen and carbon dioxide interchange,
moisture of the air, and the physics of inspiration and expiration. The
chemical variables have in our limited knowledge of comparative
physiology apparently little effect upon morbid anatomy but it is
probable that some pathology may be in part explained on physical
grounds.
The mammalian respiratory box is a relatively elastic affair, but
collapsed at the end of expiration which is largely a passive or recoil
process. The avian thorax is believed to be normally a tensely distended
space from which air is expelled by pressure of the pectoral contraction
upon the broad sternum driving the latter back upon the air sacs which
in turn drives it from the lungs. Also by this means, air is distributed
through the bones and air spaces, a measure necessary in flight,
especially in a head wind when tracheal inspiration is said to be
suspended at times. The communications of the lungs, air sacs and bones
make it possible for birds to breathe internally when the trachea is
closed and externally as well if a bone be opened. The balance of air
pressure in the lungs and related spaces is dependent upon the patency
of the ostia communicating between the bronchial ends and the air sacs,
from which the bony cavities obtain their supply. Should all these be
closed there is first a standstill of current and a limitation of the
respiration of the lungs. Fortunately it is extremely rare that this
occurs for it is obvious that it is incompatible with flight, and with
life indeed. The principal effect upon the lungs of obstruction to the
passages seems to be expressed in congestion but in how far this is due
actually to the closure of foramina and how far to the cause of
obstruction is sometimes difficult to evaluate. It should be remembered
that the air sacs are usually looked upon as mucous surfaces continuous
with the bronchial wall, there being a deep layer to each membrane
possibly continuous with the serous membranes. In mould disease of the
lungs there is very commonly a colony lying in the ostium supplying the
anterior, lateral and posterolateral cavities.
The lungs in birds are not free as in mammals, being fitted into the
troughs made by the anterior ridges of the ribs, to the serous covering
of which they are lightly attached by delicate fibres running between
the two. This more or less definite fixation, together with the pressure
of the air in the sacs give the free play of the lungs a limited
excursion. They are naturally very elastic by reason of a good supply of
elastic fibers and large air spaces, a condition aided by their
attachments to the supports of the diaphragm and to the insertions of
the air sac walls. Notwithstanding this elasticity and the great
capacity of the organ for blood, it seems as if congestion of the lungs
is a very serious matter, since from the foregoing review of anatomy,
accommodation of excess blood and any consolidation must be difficult.
As a matter of fact the mere excess of blood known as active congestion
seems able to kill small varieties.
CONGESTION OF LUNGS.
Birds of flight seem to have little resistance to this condition and
often it is the only diagnosis one can make at autopsy. The causes of
this condition include exposure, dust, gorging (?), indigestion,
enteritis and infection in birds while in mammals acute gastrointestinal
disease stands out as the most prominent accompaniment. To what extent
dust and exposure operate I do not see, although they are frequently
mentioned as causes. The overfilling of the crop, esophagus and
proventricle, the turgescence incident to gastric indigestion or the
pressure of foreign bodies in large amount are supposed to operate by
exerting pressure on the anterolateral air sacs with closure of their
ostia and also by right lateral torsion of the heart with twisting of
the very delicate pulmonary veins.
I have sought to show that protozoa or embryo nematodes in the blood
might embarrass the lungs to a state of congestion, a thought suggested
by some findings in the London Gardens, but only about ten per cent. of
our cases of hemic parasitism are accompanied by it.
The incidence of congestion of the lungs not due to stasis as from
cardiac diseases, is 2.4 per cent. in mammalian autopsies, in only 7 per
cent. of which figure did it represent the principal morbid anatomy,
whereas in birds it occurred to the extent of 7.6 per cent. of
postmortems, in 17 per cent. of which it was the sole or principal cause
of death. This seems to bear out the feature of delicacy of the
pulmonary vascular mechanism in these latter animals. This condition
seems to be indicated by simple dyspnœa in birds, relief for which has
occasionally been afforded by removal from the exhibition cages and
protection separately in a warm dry room; this is partly hypothetical of
course and congestion is to be looked upon as serious, particularly in
passerine birds.
PNEUMONIA.
Pneumonia as a clinical disease is a relatively uncommon, although quite
serious sporadic condition in animals. However accompanying the
specific, more or less epizoötic diseases such as influenza, distemper
and the choleras it may be a frequent and quite pronounced complicating
feature of the case. Pneumonia _per se_ has exacted a reasonable toll in
this Garden but unfortunately recognition being impracticable, diagnosis
and treatment have not progressed. Nor has it been practicable to group
our cases pathologically because of the lack of history and the
difficulty of making bacteriological observations at many autopsies.
Fortunately we have had practically no epizoötic pneumonias, an
experience shared with other gardens judging by their published reports.
Etiologically, and of course this applies to non-verminous, non-mycotic
and non-tuberculous cases, the pneumococcus has stood out prominently as
a cause with a few additional cases due to the streptococcus and the
Bact. aerogenes mucosum group; London reports four cases in monkeys due
to the Friedlander bacillus. Some time ago Doctor Weidman subjected our
pneumonias to an analysis and was able to show that there is no
parallelism between the seasonal incidence of pneumonia in man and
animals, rather indeed that the Garden is more apt to have a greater
number of cases in the summer, a sort of “closed season” for man. This I
am inclined to interpret as connected with the larger number of visitors
during that season. Doctor Weidman was further able to show that the
only real examples of lobar fibrinous pneumonia strictly comparable to
the human infection occurred in the Primates. I have uncovered one in a
lemur and one in a carnivore. The pneumococcus has been far and away the
greatest producer of our pneumonias, in two typed cases being of the IV
variety. There will be given below a summary of the pathological types
of pneumonia encountered, to be followed by some notes upon the
principal gross and minute anatomy in special orders. Table 9 will show
the numerical distribution of types among the orders. All the principal
mammalian orders are represented while the birds seem relatively less
susceptible to the disease and, except the Passeres, show a trifling
incidence.
TABLE 9.
_Showing the Number of Cases of the Various Forms of Pneumonia Found in Each
of the Orders._
════════════╤═════════╤═════════╤═══════╤══════╤══════════╤═══════╤═══════════
│Fibrinous│Catarrhal│ Acute │Septic│Hypostatic│Chronic│Pleurogenic
│ Lobar │ │Inter- │ │ │Inter- │
│ │ │stitial│ │ │stitial│
────────────┼─────────┼─────────┼───────┼──────┼──────────┼───────┼───────────
Primates │ 4│ 22│ 2│ 1│ 1│ 2│ 2
Lemures │ 1│ 3│ │ │ │ │
Carnivora │ 1│ 34│ │ 4│ │ 1│
Insectivora │ │ │ │ │ │ │
Chiroptera │ │ │ │ │ │ │
Rodentia │ │ 6│ │ 3│ │ │
Ungulata │ │ 14│ │ 5│ 1│ 1│
Proboscidea │ │ 1│ │ │ │ │
Hyracoidea │ │ │ │ │ │ │
Edentata │ │ 1│ │ │ │ │
Marsupialia │ │ 13│ 1│ │ 1│ │
Monotremata │ │ │ │ │ │ │
│ │ │ │ │ │ │
Passeres │ 1│ 59│ 2│ 2│ │ │
Picariæ │ │ │ │ │ │ │ 1
Striges │ │ 3│ │ │ │ │ 1
Psittaci │ 1│ 15│ │ │ │ 1│
Accipitres │ │ 1│ │ │ │ │
Columbæ │ │ 2│ │ │ │ │
Galli │ │ 2│ │ │ │ │
Hemopodii │ │ │ │ │ │ │
Fulicariæ │ │ 1│ │ │ │ │
Alectorides │ │ │ │ │ │ │
Limicolæ │ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │ │
Impennes │ │ │ │ │ │ │
Steganopodes│ │ │ │ │ │ │
Herodiones │ 1│ │ │ │ │ │
Odontoglossæ│ │ │ │ │ │ │
Palamedes │ │ │ │ │ │ │
Anseres │ 1│ │ │ │ │ │
Struthiones │ │ │ │ │ │ │
────────────┴─────────┴─────────┴───────┴──────┴──────────┴───────┴───────────
Primates present a definite group of variations from the other orders,
notably in having four clear cases of lobar fibrinous pneumonia, and in
certain histological findings. In reference to the lobar cases, a review
of their history does not indicate that any might have been surely
diagnosed by their symptoms, and only possibly by signs in one case
during the stage of red hepatization; unfortunately no temperature
records are at hand. In one case it was possible to see a group of
alveoli with the fibrin collected in a strand which, according to
classical description, passes through the septum to the adjoining
alveolus.
There were two cases, a Chimpanzee (_Pan niger_) and a Galago (_Galago
maholi_) with a microscopical picture suggestive of those we met in the
influenza epidemic, and indeed the lung of the former resembles grossly
the lung of influenza pneumonia. The spotty areas of watery purple color
correspond under magnification to celluloedematous semisolid sections
showing a sanguineous exudate, few polynuclear cells and many swollen
epithelia. The microscopic picture of the bronchocatarrhal pneumonias
shows conspicuously thickened septa decidedly wider than one is
accustomed to see in human cases and apparently due more to round cell
infiltration than to congestion or polynuclear increase.
Bronchopneumonia or capillary bronchitis with zones of cellular edema in
the vicinity is a rather usual picture in the deaths from degenerative
bone disease. It cannot be said that there is anything very peculiar
about it, although a frequent note met in the autopsies describes spotty
areas of hemorrhage and nearby atelectasis.
The case of lobar pneumonia found in a ring tailed lemur (_Lemur catta_)
showed very delicate fibrinous reticulum and relatively few cells in the
exudate, a picture apparently due in part to beginning resolution since
the whole upper left lobe was in a stage of gray hepatization.
The peculiarity of the Carnivora seems to lie in the reaction of the
epithelia, these cells being quite large, swollen and occasionally much
vacuolated. Such a picture was most pronounced in the terminal
bronchitic pneumonias in cases which might be called distemper. Many
instances of pseudolobar catarrhal or bronchopneumonia are recorded but
we also observed the fibrinous lobar form at the stage of red
hepatization in a Texas skunk (_Mephitis mesomelas_). Concerning the
orders Rodentia and Edentata no especial notes seem necessary for their
inflammatory reactions are essentially like the others in that
epithelial cells are much swollen and prominent.
Pneumonias of Ungulata are well known to pathology and offer in
causation and microscopy little that is peculiar. It might be emphasized
however that the gross appearance of the bronchocatarrhal variety
closely simulates that of lobar pneumonia, therefore to be called a
pseudolobar form, in that extension to various parts of a lobe seems to
occur. Moreover in the bronchitic varieties associated with enteritis,
with or without infectious foci in the pharynx or larynx, there may be
two or even three stages of the pneumonitic process in one lung or lobe.
It seems that this pseudolobar appearance occurs definitely more often
in ungulates than in the other orders.
[Illustration:
FIG. 8.—NORMAL AVIAN PRIMARY AND SECONDARY ALVEOLI. NOTE THE DELICACY
OF THE SEPTAL PROLONGATIONS THAT BOUND THE PRIMARY ALVEOLI, ALL OF
WHICH ARE WIDELY OPEN.
]
[Illustration:
FIG. 9.—EARLY BRONCHOPNEUMONIA OF SUPERFICIAL ORIGIN. NOTE SOME LITTLE
EXUDATE IN SECONDARY ALVEOLUS. WIDE SWOLLEN SEPTA AND BOTH ALVEOLI
REDUCED IN SIZE.
]
Marsupialia offer two rather easily grouped classes of bronchopneumonia—
one associated with enteritis and one secondary to “Kangaroo disease” of
the jaw; they differ in microscopy correspondingly. The simple
bronchitic and peribronchitic infiltrate and superficial exudate
occurring with enteritis or with a general infection is relatively
diffuse, giving in some instances the impression of an interstitial
process and showing notably swollen septa; there may be fibrin but this
is exceptional and scanty. When mycosis of the jaw has been the origin
or occasion of the infection the picture is that of frank aspiration
pneumonia, therefore more like a septic infarct. However the amount of
fibrin is sometimes very great and whole alveoli will be filled with it,
perhaps accompanied by red cells, polynuclears and epithelia. Epithelial
cells however play a small part in the minute anatomy. Hemorrhage and
edema are prominent but true abscess formation and gangrene are not.
Possibly the animals die too soon for the latter to develop.
Pneumonia in Aves aside from that due to moulds is apparently much less
common than among the Mammalia, one order only, the Passeres, showing an
incidence comparable to the important orders of the latter class. The
other orders, and this applies particularly to those of which we have an
adequate number, are quite insusceptible to simple pneumonia, none of
them showing over two per cent. There are listed for Aves three
instances of lobar fibrinous pneumonia. These cases can be described
together since in all the findings were about the same. A whole lung or
goodly portion thereof was uniformly involved in a red or gray
consolidation of rather fine granular character which on section study
seemed to be made up of the same lesion all over, with fibrin a
prominent part of the exudate. The coagula were largely within the
secondary alveoli but the primaries also contained it. The microscopic
section may not have represented the process at all places, and since
the arrangement of fibrin is similar in definitely catarrhal lesions,
these may of course have been instances of pseudolobar pneumonia.
Our data are too few to draw any conclusions as to the behavior of the
various orders but one note may be permitted. The passerine birds have a
great tendency to dense cellular infiltrates while parrots show more
coagulative or fluid exudates.
PRODUCTION OF INSULAR PNEUMONIA IN BIRDS.
Insular consolidations in which catarrhal and infiltrative processes are
prominent, the bronchopneumonias, seem to arise in two ways. One course
of events apparently follows infection _via_ the bronchial mucosa, the
other _via_ the blood stream and a study of the resulting lesions may
help toward an understanding of the development of pneumonia in man.
When infection unquestionably has been superficial, that is _via_ the
bronchus, the first thing to happen is a swelling of the septal
prolongations dividing the primary alveoli and an extension of their
ends farther into the secondary alveoli with the result that the inlet
to the primary air sacs is narrowed and the space in the secondaries is
reduced. Upon the surfaces there then develops the usual catarrhal
exudate while in the deeper parts marked congestion makes its
appearance. Fibrin may develop and be mixed with the cells both in the
larger and smaller alveoli but it is more evident in the former. (Figs.
8, 9, 10.)
[Illustration:
FIG. 10.—LATER BRONCHOPNEUMONIA OF SUPERFICIAL ORIGIN. NOTE GREATER
EXUDATE, GREATER SWELLING OF SEPTA. PRIMARY ALVEOLI PRACTICALLY ALL
CLOSED. MUCH OF LUNG HAS BECOME CONSOLIDATED.
]
[Illustration:
FIG. 11.—INSULAR PNEUMONIA, BEGINNING AS CELLULAR INFILTRATION OF
DEEPER PARTS OF SEPTA AND OF INTERSTITIAL TISSUE. FOUR AREAS OF
DENSE AIRLESS CONSOLIDATION. ALL SECONDARY AND MANY PRIMARY ALVEOLI
WIDELY OPEN.
]
The other process by which insular pneumonia develops seems to begin in
the septa of the smaller alveoli and in the perivascular areas. This has
been looked upon as hematogenic or pleurogenic. The first change occurs
in the surroundings of the primary alveoli where there appears a
richness of nuclei, of round, moderately well stained character, among
which one may see a few granular and red blood cells. Soon the epithelia
of adjacent alveoli increase in number and a fibrinocellular exudate
appears, at first probably in the smaller sacs. However when the lesion
is intensive the course of events must be rapid for the identity of a
group of primary alveoli is soon lost and the exudate may extend to the
larger air space. (Fig. 11) In severe or late cases a decision as to the
course of origin is often impossible. The most instructive point of this
part of the study is the closing of primary alveoli by the swelling of
their septal ends and the early occlusion of the secondary alveolus by a
catarrhofibrinous or even pus-like material. It is quite possible that a
similar course of events transpires in the pathogenesis of human
pneumonia, the superficial avian form being comparable to the aspiration
form, the interstitial form comparable to the septicemic variety.
ABSCESS AND GANGRENE OF LUNG.
Abscess and gangrene of the lung are degenerative processes dependent
upon embolism, or inspiration of infective matter and it is usually
assumed that gangrene succeeds upon abscess when the blood or air supply
of a part of the pulmonary tissue has been obstructed mechanically or by
inflammation. A review of our material adds little to the etiology or
pathogenesis of these two lesions, well recognized as they are by
veterinarians. As opposed to human beings, lower animals probably suffer
more from them, for an explanation of which one can probably look to the
B. necrosis or necrophorus, an organism quite common in feed, and
acknowledged to be of great importance as a secondary invader during
specific infectious diseases. It has been found in embolic abscesses and
in the organs in calf diphtheria and similar other conditions. It has
been cultivated here twice, once from a lung abscess, once from Kangaroo
disease. It doubtless occurs in human necrotizing processes but is
seldom emphasized or even heard about; possibly none is due to it or its
congeners.
TABLE 10.
_Table giving Analysis of 20 Mammalian and 3 Avian Cases of Abscess and
Gangrene of the Lung_
════════════╤═══════════════╤════════════════╤════════
Animal │ Causative │ Pneumonia, │Abscess
│condition upper│septic or other │ or
│ respiratory │ │Gangrene
│ tract │ │
────────────┼───────────────┼────────────────┼────────
Sooty │Negative │Catarrhal │Gangrene
Mangabey │ │pneumonia │
Cercocebus │ │ │
fuliginosus │ │ │
│ │ │
Rhesus │Negative │Septic from │Abscess
Macaque │ │suppurating │
Macacus │ │gland │
rhesus │ │ │
Am. Wild Cat│Aspiration │ │Gangrene
Felis ruffus│vomitus from │ │
│violent │ │
│gastroenteritis│ │
│ │ │
│ │ │
│ │ │
Puma Felis │Acute purulent │No │Abscess
concolor │nasopharyngitis│ │and
│ │ │gangrene
│ │ │
│ │ │
Ichneumon │Negative │Sepsis, scalp │Abscess
Herpestes │ │wound │
mungo │ │ │
│ │ │
│ │ │
Raccoon │Negative │Pneumonia │Abscess
Procyon │ │followed by │
lotor │ │sepsis │
│ │ │
│ │ │
Skunk │Cellulitis face│Sepsis, very │Abscess
Mephitis │and neck │mild │
mephitica │ │ │
Puma Felis │Perforating │Secondary │Abscess
concolor │abscess around │terminal │
│jaw │pneumonia, │
│ │sepsis │
│ │ │
│ │ │
Porcupine │Negative │Enteritis, no │Abscess
Erethizon │ │special sepsis │
dorsatus │ │ │
│ │ │
│ │ │
│ │ │
Kangaroo Rat│Negative │Right sided │Abscess
Perodipus │ │bronchopneumonia│
richardsoni │ │ │
│ │ │
Squirrel │Abscess under │No │Abscess
Sciurus p. │eye and in │ │
carolinensis│masseter muscle│ │
│ │ │
│ │ │
│ │ │
Mule Deer. │Actinomycosis? │Arthritis. │Abscess
Mazama │nasopharynx │Myositis │and
hemionus │ │Tenosynovitis │gangrene
│ │ │
│ │ │
Axis Deer. │Negative │Negative │Abscess
Cervus axis │ │ │
│ │ │
│ │ │
│ │ │
│ │ │
│ │ │
│ │ │
Tapir. │Abscess of │Died from │Abscess
Tapirus │parotid │enteritis │
indicus │ │ │
│ │ │
│ │ │
│ │ │
Gazelle. │Negative │Sepsis from │Abscess
Gazella │ │infected wound │
isabella │ │ │
│ │ │
│ │ │
Kangaroo. │Negative │Catarrhal │Abscess
Macropus │ │pneumonia │and
rufus │ │ │gangrene
│ │ │
│ │ │
│ │ │
│ │ │
│ │ │
│ │ │
Kangaroo. │Kangaroo │Sepsis │Abscess
Macropus │mycosis of jaw │ │
rufus │ │ │
│ │ │
Kangaroo. │Kangaroo │ │Abscess
Macropus │mycosis of jaw │ │
giganteus │ │ │
│ │ │
Kangaroo. │Negative │Sepsis from │Abscess
Macropus │ │infected wound │
robustus │ │ │
Devil. │Negative │Negative sepsis │Abscess
Sarcophilus │ │ │
ursinus │ │ │
│ │ │
│ │ │
Crow. │Negative │Filaria in │Abscess
Gymnorhina │ │blood? │
leuconota │ │ │
Heron. Ardea│Negative │Negative │Abscess
tricolor │ │ │
ruficollis │ │ │
│ │ │
│ │ │
Goose. Anser│Syngamus in │Negative │Abscess
fabalis │trachea │ │
│ │ │
│ │ │
│ │ │
│ │ │
────────────┴───────────────┴────────────────┴────────
════════════╤═════════╤══════════════╤══════════════
Animal │Single or│ Position │ Bacteria
│Multiple │ │
│ │ │
│ │ │
────────────┼─────────┼──────────────┼──────────────
Sooty │Massive │Upper part │Streptothrix,
Mangabey │single │lower lobe and│necrosis
Cercocebus │ │adherent part │bacillus.
fuliginosus │ │upper lobes │
│ │left side │
Rhesus │Single │Occupied │
Macaque │ │nearly all │
Macacus │ │right middle │
rhesus │ │lobe │
Am. Wild Cat│Bilateral│Right middle │
Felis ruffus│ │lobe, left │
│ │lower lobe, │
│ │left bronchus │
│ │ruptured, │
│ │right middle │
│ │lobe ruptured │
Puma Felis │Bilateral│Right upper │Streptococcus
concolor │ │and left lower│pyogenes.
│ │lobe abscesses│
│ │biggest, right│
│ │middle also │
Ichneumon │Bilateral│Scattered │
Herpestes │ │small │
mungo │ │abscesses, │
│ │under pleura │
│ │especially │
Raccoon │Bilateral│Probably all │
Procyon │ │lobes, right │
lotor │ │middle │
│ │contains │
│ │largest │
Skunk │Single │Left lower │
Mephitis │ │lobe, single │
mephitica │ │small │
Puma Felis │Bilateral│Numerous small│
concolor │ │abscesses, │
│ │irregularly │
│ │scattered │
│ │through both │
│ │lungs │
Porcupine │Bilateral│Multiple small│
Erethizon │ │scattered. │
dorsatus │ │Parasitic? No │
│ │notes │
│ │parasites or │
│ │bacteria │
Kangaroo Rat│Single │Left lower │
Perodipus │ │lobe, small │
richardsoni │ │abscess, │
│ │record scanty │
Squirrel │Multiple │Left lung │
Sciurus p. │ │scattered, │
carolinensis│ │small │
│ │abscesses, │
│ │parasites not │
│ │seen │
Mule Deer. │Bilateral│Scattered both│
Mazama │ │lobes under │
hemionus │ │pleura, upper │
│ │right inferior│
│ │tip gangrenous│
Axis Deer. │Single │Apparently │Streptothrix.
Cervus axis │ │primary │
│ │streptothrix, │
│ │abscess in │
│ │cardiac tip of│
│ │upper lobe │
│ │with extension│
│ │toward hilum │
Tapir. │Bilateral│Multiple │Staphylococci.
Tapirus │ │subpleural pus│
indicus │ │pockets, │
│ │surrounded by │
│ │catarrhal │
│ │pneumonia │
Gazelle. │Bilateral│Multiple │
Gazella │ │subpleural and│
isabella │ │internal, both│
│ │lungs about │
│ │the same │
Kangaroo. │Double │Lower middle │Pneumococci
Macropus │left │left lobes, │streptothrix.
rufus │ │seat of a │
│ │ruptured │
│ │gangrene │
│ │surrounded by │
│ │pneumonia, │
│ │right lung │
│ │pneumonic │
Kangaroo. │Bilateral│More on right │Streptothrix,
Macropus │ │side, sharply │cocci.
rufus │ │outlined │
│ │abscesses │
Kangaroo. │Single │Abscess and │Streptothrix
Macropus │ │atelectasis, │
giganteus │ │right middle │
│ │lobe │
Kangaroo. │Single │Lower right │
Macropus │ │lobe │
robustus │ │ │
Devil. │Multiple │Largest middle│Probably
Sarcophilus │ │of right lung,│streptothrix.
ursinus │ │many small │
│ │scattered │
│ │abscesses. │
Crow. │Multiple │Scattered tiny│
Gymnorhina │ │abscesses, no │
leuconota │ │worms seen │
Heron. Ardea│Single │Upper pole, │
tricolor │ │right lung, no│
ruficollis │ │apparent │
│ │antecedent │
│ │cause │
Goose. Anser│Single │Lower half │
fabalis │ │right lung │
│ │occupied by │
│ │abscess, which│
│ │has penetrated│
│ │air sac │
────────────┴─────────┴──────────────┴──────────────
The distribution of abscess and gangrene in the lungs in terms of the
antecedent disease, therefore its causation, may however be of interest.
The lower animals move more in the horizontal position, they seldom
cough, they are subject to several different diseases with principal
lesions in the anterior head (diphtheria, actinomycosis, etc.) but not
to chronic lymphatic infection, they push their snouts into all kinds of
filth thereby probably taking into the nose and throat many objects
which can find their way to the bronchi, and finally they are not
subjected to various instrumental operative procedures when they chance
to have a focus of pathology in the nasopharynx. For these reasons the
position of abscess and its sequels may be instructive. It has recently
been stated that abscesses of the lung in human beings following
anesthesia for infections of the upper respiratory tract, occur most
often in the upper parts of the lung whereas those following pneumonia
develop more in the lower lobes. For the animals of this series, these
facts are not borne out. In the accompanying list will be found our
acceptable cases of abscess and gangrene. Little can be said about
incidence save the fact that the highest percentage and number occur in
the Carnivora. It will be found that the right lung is affected nine
times predominatingly while the left lung is affected seven times. The
lobe most often singled out for an isolated lesion is the lower left,
the right middle being the next most often affected. These figures
concern the mammals alone, the three birds being considered too few to
discuss. It cannot be said from these figures that there is in animals
any definite distribution of pulmonary abscess and gangrene.
Nor do these figures correspond to those appearing in literature of
human pathology. In man inspiration of foreign bodies, including
bacteria-laden mucus, usually carries them into the right lung because
of the larger and more directly vertical bronchus to that side. Emboli
go as a rule also to the right lung more than to the left because of the
greater size of the pulmonary artery and more direct blood current to
that side. In these animals right side lesions are more numerous but the
left lower lobe is the principal segment of the lung to be affected. The
cases are too few and the anatomy too variable to permit any deductions.
There is in the affected animals no uniform anatomical peculiarity which
would explain the predominance of the right lung as a whole or the left
lower lobe as a unit.
PNEUMONOKONIOSIS.
Pneumonokoniosis, because of its importance in industrial diseases, has
been subjected during recent years to considerable intensive study in
human medicine, from which activity some interesting and useful
information has been obtained as to its genesis and effect upon the
function of the lung. This condition is of course a purely environmental
one, the degree and particular kind of “dusting” being dependent upon
the duration and nature of exposure of the particular individual. This
Garden is situated beside an active railroad trunk line so that the
opportunity for coal dust inhalation is continuous. The degree of
anthracotic pigmentation of the lungs and related serous membranes is
really negligible and with one questionable exception, we have not seen
fibrosis due to this cause in any animal. The one exception, an amazon
presented and living in the Garden but three months, at necropsy showed
an interstitial chronic bronchitis and pneumonitis stretching out from
the hilum, all of the affected area being deeply pigmented. The picture
was comparable to what might be expected from a second degree
anthracotic fibrosis of Landis and Pancoast. Many specimens come to
autopsy with some grade of pigmentation, but none, except the one above,
with resultant fibrosis. The degree of anthracosis is usually so slight
that it has been considered important enough to include in the diagnosis
but eighteen times and curiously enough seventeen of these were observed
in birds. Were there more cases it might be profitable to plot their
exhibition period but the use of this small number might lead to error;
the average length of exhibition of the birds was about a year. It is
common to observe some black specklings of the air sacs, as if pepper
were dusted on them as has been said before, but even this is rarely
marked. It is most often seen in the Anseres, Psittaci and Struthiones
but a goodly number of cases occur in the long-lived Passeres.
The distribution of the pigment is essentially the same throughout
Mammalia—peribronchial, submucous and in the lymph nodes at the root of
the lung. In the birds it is first seen in the subepithelial spaces of
the septa of the small alveoli where they project into the secondaries,
later accumulating in the connective tissue of the main septa.
Collections under the pleura and at the root of the lung are rare, the
dust usually spreading out along the air passages into the air sacs.
Other forms of pneumonokoniosis are unknown. Although animals must
inspire much dust from dry feed and from floors it must be caught early
and removed by snorting or by the lymphatic drainage. It seems fairly
well accepted that dusts are dangerous to the degree that they contain
inorganic substance and as these animals are not exposed to concentrated
mineral or metallic dusts, no effects are seen.
INFARCTION OF LUNG.
Infarctions of the lung, while not at all common, are interesting
because of their incidence in the Carnivora and in the distribution. The
figures concern the mammals only since the decision for or against
infarct in the birds is very difficult because of the frequency in this
class of hemorrhage with pulmonary congestion. There were eleven single
or double non-septic infarcts, of which seven occurred in Carnivora, one
in an ungulate, two in Primates and one in a rodent. The existence of
parasites was excluded in most of the cases but could not be entirely in
all. Eight of these infarcts were on the left side, five of these being
in the lower lobe.
EMPHYSEMA.
Emphysema of the atrophic and chronic vesicular types with the soft,
fluffy, pigmented or pale pink organ has not occurred in the animals
under observation. Acute vesicular emphysema, such as is seen in chronic
bronchial and cardiac diseases, has been encountered several times.
Cardiac lesions were found four times, nephritis eleven times, acute
enteric conditions seven times, hepatic diseases seven times. Two cases
of wide spread amyloid disease showed a deposit of this substance in the
alveolar walls. It is quite common to find some grade of emphysema in
monkeys dying from osteomalacia and rickets. The process is then most
prominent in the upper lobes and along the free anterior margins. The
incidence in the orders is Primates 5, Lemures 2, Carnivora 2,
Pinnipedia (drowning) 1, Rodentia 1, Ungulata 4, Marsupialia 4. The best
example was found in a Skunk (_Mephitis mesomelas_) having a general
infection, emanating from the cranial sinuses, and cardiac dilatation.
Emphysema does not seem to occur in birds for only one was seen which
seemed to present this condition. This was a Bald Eagle (_Haliæetus
leucocephalus_) with chronic renal and enteric disease and cardiac
hypertrophy. The lungs were tensely distended under their serous
covering and showed a few small bullæ anteriorly. Unfortunately a
histological preparation is not at hand.
TUMORS.
Tumors of the lung are moderately common, both of primary and secondary
origin. Thus we have seen three primary and six metastatic growths in
mammals and one of each kind in birds. The primaries were: carcinomata
in a civet (_Viverra tangalunga_), a bandicoot (_Thylacomys lagotis_), a
kangaroo (_Macropus rufus_), and a lorikeet (_Glossopsittacus
concinnus_). The secondaries were: carcinomata in a black bear (_Ursus
americanus_), a polar bear (_Ursus maritimus_), a lion (_Felis leo_),
and a dasyure (_Dasyurus maculatus_); sarcomata in a prairie wolf
(_Canis latrans_), and a raccoon-like dog (_Canis procyonoides_);
adenocarcinoma in a chestnut-eared finch (_Amadina castanotis_).
The histological character of the primary cancers would place them in
group of the nodular and infiltrative types of Kauffman. They all seem
to have taken their origin from the smaller bronchi, the usual starting
point. The growths were small in the civet and bandicoot and strongly
suggest that the tumors arose in bronchi occupied by parasites; such
bodies could not be demonstrated. It is the usual thing to find in cases
of parasitism of the bronchi that if there be no ulcerative destruction
of tissue the epithelium undergoes some form of hyperplasia, and even
structural metaplasia in the air tubes supplied with cuboidal or
cylindrical cells. Epithelia many layers deep have been encountered,
usually arranged in orderly fashion but frequently “papillomatoid,”
suggesting the epidermal layers yet not so far as to show protoplasmic
bridges. Distention of various degrees, affected by the contents of the
tube and the surrounding inflammation, are common. Such a picture
naturally resembles epithelioma and indeed growths of this nature are
reported as due to verminous pneumonitis.
There are, especially in cats and dogs, small scattered adenomatoid
growths[21] under the pleura and in the pulmonary substance, thought to
originate in the alveolar epithelium and occasionally growing to large
size; the case in the kangaroo may have had this origin. _It was the
only primary tumor to give metastasis_ (to the spleen and gastric wall),
the secondaries being decidedly adenomatous in character.
Metastatic growths come from the following originals: two from the
thyroid, well known to give pulmonary embolism in dogs; one each from
the breast, uterus, adrenal, intestine and kidney. The form assumed is a
gray and red mass lying under the pleura or an isolated nodule in the
substance. Sarcomatosis, the form apparently spreading out from the
hilum and growing in isolated grayish tubercular masses, has not been
seen.
THE PLEURA.
The pleura is a tissue apparently quite susceptible to infection in
mammals and so closely associated with the air sacs in birds as to be a
part of the same membrane, therefore the two being affected together.
Throughout the higher class all orders give copious examples of the
involvement of the pleura, principally of course as an accompaniment or
a sequel to pneumonitic or bronchitic processes but also as a part of
acute infectious diseases, such as hemorrhagic septicemia,
pleuropneumonia and the like. However two orders present such a number
of instances of pleuritis that they deserve notice. The seals,
Pinnipedia, of which we have twenty autopsy records, showed inflammation
of this membrane four times, three of which were dependent upon
pulmonary infection and one apparently due to general septicemia with
trifling damage to the lung proper. One of the first cases had gone on
to empyema of the classical type, a shrivelled dry almost carnified lung
with a thick fibrinopurulent covering. The lung of the seal is well
divided into lobules, the external surface being generously supplied
with lymphatic channels under the pleura, an arrangement which should
carry away infection one would think. Perhaps this high percentage of
pleurisy in our Pinnipedia is but accidental. The marsupials, while
having a notable percentage of pleurisy both among all the cases and in
relation to the number of postmortems, are not so striking from the
etiological standpoint since practically all of these have suffered with
Kangaroo mycosis or pneumonia. In over half the cases of this infectious
disease some grade of pleuritic exudate has been observed, only one,
however, going to the stage of empyema.
One cannot speak so definitely of pleuritis in birds since this tissue
merely represents in them the covering of the lung and is firmly
attached posteriorly to the ribs and anteriorly to the air sacs.
Exudates show as collections upon the air sac side of the combined
membrane, pleuritis proper in birds being an infiltrative affair coming
through the pulmonary tissue and therefore being a part of pneumonitis.
I notice a tendency in a few articles to write of pleuritis when the
process is confined to the thorax but this gives the impression that the
disease is peculiar. There seems no difference in the gross and minute
appearance between thoracic serositis and panserositis. The course of
procedure seems to be from the anterior or mesial pulmonary ostia into
respectively the cervical and thoracic air sacs and this seems to hold
good whether the infection be mycosis or fowl cholera or fowl pest.
There are records of 104 cases of serositis in birds of which 45 were
among parrots, the remainder being well distributed among the various
orders; only two each occurred in Galli and Anseres, orders prominently
affected under domestication. This high percentage of pleuroperitonitis
among parrots and their congeners can only be explained upon the ground
of a continued infection of our stock by the virus of fowl cholera and
by mould. One case of undoubted fowl cholera occurred recently and as
the records are reviewed a few are discovered where the organism was
found. The virus must be of low grade for we have had no severe and
devasting epizoötic. Mycosis is constantly with us no matter what we do
in hygienic measures. There was a small group of cases of pulmonary and
serous membrane mycosis combined with staphylococcus infection which
carried off six birds. The pathology of this group was interesting
because one could follow the infection of the bacterium. The anterior
pulmonary ostium was surrounded or covered by a mycotic mass and
spreading downward from this was a grayish yellow turbidity of the air
sac walls with a delicate sticky or almost mucilaginous exudate
extending into the lateral abdominal and posterior sacs.
[Illustration:
FIG. 12.—ENDOTHELIOMA OF PLEURA. LEOPARD (FELIS NEBULOSA).
]
[Illustration:
FIG. 13.—ENDOTHELIOMA OF PLEURA IN FIG. 12. DETAIL OF ONE OF THE WARTY
EXCRESCENCES.
]
There is on record one tumor of the pleura, an endothelioma, in a
Clouded Leopard (_Felis nebulosa_). It was the usual plate-like
thickening with warty excrescences. No metastases occurred. (Figs. 12
and 13).
SECTION VII
THE ALIMENTARY TRACT. PART 1.—PHARYNX, ESOPHAGUS, STOMACH AND INTESTINES
The portion of the anatomy that we now approach varies in construction
almost as much through the animal kingdom as do the external shape and
covering of the various orders and much more than do the other systems.
The reason for this is obvious, an arrangement accommodative to the
differing food chiefly, but not a little to the ease with which animals
obtain and assimilate their nutriment. It would be impracticable to
describe all the variations of the orders discussed in this study, but
since certain gross and minute differences are of importance in
comparative pathology they will be discussed at the appropriate places.
It is my purpose to present in a subsequent section a discussion of food
in captivity from the standpoint of its quality and quantity in relation
to pathology.
Doubtless the quality of food is the largest factor in the production of
disease both of the alimentary tract and elsewhere, but I am not at all
sure that the quantity may not be equally important, in certain groups
at least. Thus, for example, the ungulate has nearly always available in
bedding a substance that he can and will eat, and the prevalent idea
that an animal will eat only as much as is good for him seems not to
hold at all times, since overfilled rumens are only too common. It might
be thought, however, that captivity creates a sort of pica, or that
enforced idleness is conducive to gorging. The use a few lines above of
the word “doubtless” may have arrested the attention of some, yet when
the whole subject is reviewed it seems entirely justified. Plimmer puts
incorrect food at the head of the list of the causes of enteritis,
Brooks emphasizes the importance of certain grasses and musty fodder,
systematic writers detail among the principal causes of gastritis
spoiled food, and in zoological gardens specific disease like hog
cholera and enterohepatitis are relatively uncommon while nonspecific
gastroenteritis is the most frequent diagnosis in causes of death.
The other factors to which enteritis is ascribed are animal and
vegetable parasites and mechanically operative foreign bodies, the last
being unimportant. Just how important the first mentioned are is a
matter of some question which must be subjected to considerable study
before any solution can be expected.
If for no other reason than that the gross and minute pathological
anatomy of gastroenterocolitis is the same through the mammals and birds
(aside from a few specific lesions like enterohepatitis, typhoid fever,
etc.), while the food and bacteria vary, it would seem probable that the
ultimate cause is the same, a poison which can be formed alike in the
carnivorous and herbivorous gut, and not dependent upon bacteria, but
upon the chemistry of the food or of the intestinal mucosa. To put the
matter more simply, the lesions being the same under nearly all
conditions is not the cause the same, and is it not a poisonous product
from food or the intestinal lining. It is profitable here only to
mention the marked similarity of enteric lesions under the differing
conditions and in different orders. We shall study chartwise, the
various forms of inflammation from the cardia to the anus in terms of
their anatomical diagnosis and most probable etiology in an attempt to
throw light upon the matter, and later present the physiology. System
requires, however, some attention first to anatomical order so that a
brief review of the esophageal and pharyngeal conditions is indicated.
PHARYNX.
The buccal-pharyngeal cavity in mammals is used chiefly as a passage way
for food and as the place where some of them triturate and insalivate
the bolus. Certain orders, Primates, rodents and marsupials, use this
cavity thoroughly at the first mastication, others use it little at
first but may ruminate, the ungulates, while strict carnivores use it
very little. The Aves use their pharynx almost exclusively as a passage,
and, despite the presence of a certain amount of salivary gland tissue,
probably do not digest any substance in this cavity. The crop or
ingluvies is a sac to permit of salivary digestion but is really a
storehouse to allow rapid feeding without overfilling of the
proventricle. The esophagus extends from the pharynx to the cardiac
opening of the stomach in mammals and widens into the glandular stomach
or proventricle in birds, the upper end of which lies in front of the
lower third of the left lung behind the heart.
Inflammations of the buccal, pharyngeal and esophageal walls are
relatively common in certain orders especially ground birds and grazing
ungulates. This would seem to be explained on the basis of injury to the
mucosa by sharp or pointed objects picked up while feeding. The
character is usually necrotizing, but need not be, and the bacteriology
is not specific. Definite infectious diseases like diphtheria and
actinomycosis are not included here, but it might be mentioned that the
second disease cited is believed to be started by the penetration of the
organisms into wounds made by sharp grasses. Certain orders, notably
Ungulata, Passeres, Psittaci and Struthiones, are quite susceptible to
mycotic infestation and we have seen an outbreak of thrush in Kites
(Accipitres). It is, however, interesting and possibly significant of
peculiar protective powers in the upper alimentary tract, that strict
carnivores have failed to show ulcerative, purulent or necrotizing
inflammations of the mucosa from the mouth to the cardia. There has been
no important data upon ingluveal indigestion or esophageal obstruction.
Birds especially, and occasionally mammals, gorge themselves or take too
large a bolus, but it seems as if this is only fatal where some distinct
important pathology is present which has reduced their resistance. In
the lower esophagus one has to deal with worms in connection with the
proventricle in birds, but no mammals seem to have suffered with
temporary or permanent strictures. “Crop-binding” has occurred in the
following orders: Psittaci, Galli; and overfilling of the esophageal
dilatation was seen in Accipitres and Herodiones; Columbidæ with their
double crop were not affected by this abnormal collection of food in the
esophagus.
DILATATIONS OF ESOPHAGUS.
The mammals have shown three dilatations of the esophagus interesting
enough to detail briefly:
Mongoose Lemur (_Lemur mongoz_) ♂ . Sacculo-fusiform dilatation of
esophagus, probably congenital, with adjacent fibrosis of lung. In
poor condition for several years but recovered satisfactorily from a
bad cut inflicted by cage-mates. At autopsy the general condition is
poor, hair missing in spots, all skin dry and atrophic with patches of
keratotic dermatitis. All tissues anemic, muscles lusterless. Right
lung collapsed, brown and pink, spotted with anthracosis. Left lung
pushed forward and to left by a mass in the posterior mediastinum.
Lower lobe in its posterior portion is adherent to esophageal mass.
Lower half of this lobe beginning where bronchus ends and extending
over anterior-posterior surfaces shows marked fibrotic processes and
at one point in tissue between end of bronchus and adherent esophagus
there is no lung tissue remaining. No recent consolidations. Bronchial
lymph nodes, small, firm homogeneous pale brown with specks of
anthracosis. Heart contracted, normal in size, firm red-brown. Aorta
is firmly adherent to esophageal mass where bronchus crosses it. The
lower half of the esophageal from the hilum of the lung to the cardia
is the seat of a dilatation, fusiform for the most part, but with a
saccular portion anteriorly. This latter presses the left bronchus
upward and heart forward. The wall of the tube is slightly irregularly
thickened but there is no cicatrix and mucosa shows slight
hypertrophic condition. A large mass of food occupies the dilatation.
Stomach is empty save for gas. Mucosa is soft, smooth, pale pink.
Duodenum shows slight swelling of the rather pale yellow submucosa and
mucosa, but the tips of the villi are injected. Intestine contains
only a little slimy mucus. Large intestine contains a mass of
constipated feces. The esophageal dilatation seems to have been
congenital although it is barely possible that the fibrosing
pneumonitis and pleuritis may have aided and caused it by traction. It
has been doubtless the cause of the animal’s inanition.
Black Bear ♂ (_Ursus americanus_). Sacculate dilatation of esophagus
with chronic esophagitis. Chronic hypertrophic gastritis. Chronic
lymphadenitis. Fatty degeneration of liver. Acute catarrhal enteritis.
Had been vomiting more or less, nearly every day for two months and
did not eat for six days before death. Mouth, pharynx and esophagus
are full of macerated, unrecognizable food. Pharynx seems normal.
Larynx is yellow, mucosa rough and slightly thickened in places
especially just above the vocal chords. No excess of mucus. Esophagus
in neck is dilated. Mucosa is rough, irregular yellow brown. This
dilatation proceeds downward so that at thoracic opening tube is twice
normal size. Upon entering thorax this dilatation turns to right and
in irregular saccular form extends to diaphragm compressing heart and
lungs to left. The main course of it then recrosses the midline, aorta
being slightly twisted as it regains position in front of vertebræ.
The wall is irregularly thickened from pseudomembranous patches and
some hypertrophy of mucous and submucous layers. Muscle and serous
coats are considerably thinned. The sac is full of macerated food and
gas. The right lung is compressed small resilient red gray. No
adhesions in either pleura. On section the lung tissue is found to be
slightly edematous, red gray, compact and while not atelectatic yet
crepitates much less than normal. Left lung is the seat of passive
congestion in lower lobe and lower half of upper lobe. The upper half
of lobe is compressed and subcrepitant like the right lung. Lymph
glands of neck and thorax are much enlarged firm with large irregular,
clear outlined follicles and brown firm homogeneous pulp. The aorta
shows slight roughening, the intima being smooth and homogeneous.
Lion ♂ (_Felis leo_). Ten and one-half months old. Cystic
parenchymatous goitre, dilatation of esophagus, ulcerative enteritis.
Acute glomerular nephritis. Chronic hyperplasia of spleen. Fatty
infiltration of liver. Bronchopneumonia (from pressure of goitre).
Ascaris in intestines. Had lump on neck for several weeks, ate very
little and seemed to have hard work to get anything down. Stopped
eating toward the last and vomited water and foam. There is a small
ulcer with everted lips just below left incisor on lower lip which the
keeper says is of several months’ duration. The thyroid is much
enlarged and forms a large mass in the upper chest and extends far up
in the neck. Because of this mass the lungs are pushed far down in the
chest. Heart also lies very low. The thyroids are enormously enlarged
and cystic, the right measuring 13 × 8.5 × 5 cm. and the left
19 × 9 × 5 cm. The lungs are pale pinkish white. Air content increased
in places, decreased in others. No hypostatic congestion. The lungs
seem normal except at the apex where they are collapsed probably from
pressure on lung by enlarged thyroid which dips down into the chest
for at least three inches filling entirely the apex of the chest. One
bronchial lymph gland was about the size of a walnut, the rest were
normal. The heart seems normal except for its slightly low position.
The abdomen contains about 300 c.c. of deep yellow highly albuminous
fluid. No adhesions. The liver is softer than normal, glistening,
smooth, moist and very yellow particularly at the edges. The gall-
bladder contains a green mucoid bile and the duct is patulous. Spleen
and kidneys are normal. Mouth and pharynx are normal. The esophagus is
much dilated above the thyroid. The enlarged thyroid pressing upon it,
has acted as a distinct obstruction. In this pouch was a large amount
of food probably (from the history) eaten two days before. The
esophagus below this point was normal except for the presence of thin
mucus. Stomach empty save for two small bits of meat. The duodenal
walls are much thickened, mucosa covered with small ulcers many with a
hemorrhagic base; there were present also a few small, round worms.
[Illustration:
FIG. 14.—DILATATION OF ESOPHAGUS. LION (FELIS LEO). DILATATION
PROBABLY DUE TO OBSTRUCTION BY ENLARGED THYROID BODY. IN
ILLUSTRATION DISTENTION OF ESOPHAGUS CAN BE SEEN IN THE FORK OF THE
THYROID LOBES.
]
Here are presented three different dilatations, the first probably
congenitally started and aided by pulmonary fibrosis, therefore
secondarily a traction diverticulum, the second probably entirely
congenital, and the unusual third case due to obstruction by an enlarged
thyroid. In this connection might be mentioned small saccular
diverticula in the proventricle of a Fire Finch (_Lagonosticta
senegala_), and at the pylorus in a Puma (_Felis concolor_). Neither of
these seemed of any significance and played no part in the death of the
animals; they did not seem to be artificially produced, by worms, for
example.
THE PROVENTRICLE.
The proventricle or forestomach of birds, is the seat of active
secretion of the gastric juice in nearly all orders, although Jobert
believes that the mucosa of the gizzard may contribute some digestive
fluid, and there are active glands in this tissue in a few orders. The
proventricle does not act as a reservoir during digestion, but as soon
as the juices are well mixed with the bolus the food is passed on to the
gizzard. The organ has a rather free position, at least as far as its
left lateral and downward movements are concerned for the left lateral
abdominal air sac is free on that side of the gastric complex and the
left lateral thoracic also extends down the side of the proventricle.
Upward and anteriorly is the heart. Some of the cases of proventricular
spiropteriasis have shown very marked congestion of the left lung,
possibly due to the closure of the anteroinferior air sac aperture on
that side. Aside from parasitism, affections of this organ are not very
numerous.
Infestation with spiroptera and with less dangerous worms was quite
serious at one time, but since routine examinations of all suspicious
birds has been practiced this parasitism has been under control. This is
a subject of especial importance to collections, and will be described
in a special section. The susceptibility of the proventricle to damage
seems from our figures to be very distinctly a matter of zoological
order. In so far as parasites are concerned, the parrot group stands
away ahead of all others having an incidence among autopsies upon
Psittaci of 16 per cent.; after them come the Picariæ with 9 per cent.,
and Columbæ and Passeres each with 4 per cent. When, however, non-
verminous conditions are reviewed the anserine birds are found the most
susceptible, 3 per cent. of the autopsies upon this order revealing
proventricular lesions; after them come the Columbæ, 2 per cent., and
Psittaci, 1.5 per cent. In this group are included inflammations of all
kinds, dilatations and distentions and some lesser matters.
This part of the stomach has been involved in our cases of fowl
diphtheria, showing a distinct mucopurulent inflammation with
penetration into the depths of the glands; no separation of the mucosa
occurred, but ulceration was seen. Perforation was observed thrice,
twice by ulceration around a worm while it was boring into the muscular
layer and once, in an ostrich, by the penetration of a nail. Obstruction
of this division of the stomach by impaction of food and stones is not
common, but does occur. The reason for such obstruction is usually very
obscure. Sometimes it seems due to the feeding of seeds and the like in
too finely divided form, whereby food and pebbles are taken up together.
Some of the smaller birds have had in times past too many small pebbles
in the cages, while others have had too large seeds, thus apparently
trying to use the pebbles to crush them. It would seem also that the
birds had really eaten too much and could not accommodate it in the
gullet and gizzard; this seems surely true in three or four Accipitres.
Most often, however, we have had to fall back upon the inadequate
explanation of pica or perverted appetite.
Impacted proventricles and gizzards have been observed thirty-four
times, in eight of which it seemed the sole cause of death, and
therefore probably entirely due to foreign bodies in food. The theory is
accepted that dilatation and obstruction will not occur if the motor
power of the gastric wall be normal and no inflammation exist. In this
regard we can only discover five birds (the mammals will be discussed
later) with any distinct inflammatory or degenerative disease of this
part of the anatomy and two with lesions elsewhere which might affect
the musculature; this leaves the vast majority of gastric obstruction in
birds unexplained on basis of defective motor power, therefore probably
dependent upon the character of material consumed. The anserine birds
and parrots are most often affected by this form of obstruction.
Acute or chronic dilatation of the forestomach and gizzard is very rare
in birds, it having occurred only thrice in our records, a finch, a
parrot and an owl; the causes were entirely unknown since the cavities
were not overfilled with food.
THE STOMACH.
Impaction of the mammalian stomach is a diagnosis made but once in our
records, an Indian Antelope (_Antilope cervicapra_), and this is viewed
with suspicion. The rumen was undoubtedly tightly packed, being
distended to its fullest capacity with rather dry and not properly
softened grain. However, postmortem changes had advanced and therefore
observations in the whole body were not dependable. The bulk of food
which can be accommodated by the rumen is very large, and had this not
been dry and firm the condition might not have been interpreted so
seriously. Many animals come to autopsy with a well filled, indeed even
with a well packed stomach, but there is usually sufficient reason for
this or there is distinct pathology to account for death.
All this of course implies a stomach of normal or approximately normal
dimensions since distention beyond this, or dilatation of the stomach,
is more definite. In veterinary medicine, gastric tympanites (rumen
alone or all stomachs, or the simple stomach) is ascribed to food that
ferments easily when taken in excess or in the presence of defective
motor power, to constrictions by scars and to obstructive tumors;
excessive feeding is sometimes mentioned but given a subordinate rôle.
Our records throw very little light upon the subject since only five
cases were observed. Four of these five seem to be due to acute
fermentation independent of gross physical obstruction, while one, a
Cape Hunting Dog (_Lycaon pictus_) showed an old chronic ulcerative
gastritis with both healed and active ulcers distorting the pyloric end
of the organ. Three of the first mentioned four were monkeys and one was
an ocelot. The stomach of the voracious monkey is at time of dissection
usually well filled, but in these cases there seems no doubt that gas
and excess fluid had distended the cavity enormously, in one instance
apparently assisting in acute cardiac dilatation. There were no obvious
reasons for assuming any damage to the gastric motor mechanism.
[Illustration:
FIG. 15.—ROUND ULCERS IN STOMACH WALL. COMMON OPOSSUM (DIDELPHYS
VIRGINIANUS). THERE IS GENERAL MODERATE CHRONIC GASTRITIS WITH ROUND
ULCERS NEAR THE CARDIA.
]
GASTRIC ULCERS.
Gastric ulcer, so-called peptic or round ulcer of the stomach, having a
chronic course and leading to radiating scars of the mucosa is not
common in the lower animals, but frequent enough in the human being. The
form of ulcer in question has at present no adequate explanation, or at
least there is no one cause which will answer for all cases. Local
injuries from within or without the stomach, bacterial embolism,
entrance of bile through the open pylorus and many other factors have
been named in the causation but can seldom be used in any given case. In
the lower animals with their relatively frequent parasitic infestation,
another factor is added. In analysis of our statistics I have separated
ulcerative gastritis from parasitic and mycotic ulcerations and from
peptic ulcers; the first is discussed in later paragraphs. Parasitic
ulcers of the stomach occur chiefly in our native marsupial, the
opossum, and in some Carnivora; physaloptera, strongylus, ascaris, and
gastrophilus have been found. The kangaroos are frequently affected (8
cases) with an acute or subacute ulceration of the gastric wall, without
much general gastritis. The lesion is peculiar in appearance. The
youngest ulcers are black or dark gray, flat necroses of the mucosa
alone and indeed the process very frequently penetrates no deeper. Older
lesions spread laterally and may be preceded by a very narrow congested
line but there is no raised edge nor does there seem to be submucous
infiltration. If the process be rapid a loose dirty slough may form.
Certain of the advanced cases of Kangaroo mycosis will present more
infiltrative lesions of the gastric wall leading to large and well
defined necrotic areas; they may at times penetrate the whole wall
outward. (See page 580.)
True peptic ulcers have been found in Primates, 4; Carnivora, 5;
Pinnipedia, 2; Insectivora, Ungulata and Hyraces each one. The London
Garden reports that gastric ulcerations occur most often in Carnivora
and Marsupialia. Those in the last three orders of our list were small,
usually multiple and relatively superficial. The ulcers found in
Primates and Carnivora present the usual pictures seen in man. In one
example in each of these orders radiating scars of healed defects are
mentioned in the notes. None of them seems to have led to cancer, and in
only one, a wolf (_Canis lupus_), was the scar tissue sufficient to
cause definite impediment to the motility of the stomach. Six of the
fourteen examples appeared on the greater curvature, the remainder on
the lesser. Ten ulcers were in the pyloric division, the other four
being scattered. No other pathology is found common to these cases which
might be drawn into etiological association.
TUMORS.
Tumors of the gastric complex are not at all common, there being only
the following to report: Primates, Hamadryas Baboon (_Papio hamadryas_),
diffuse adenoma; (none in Carnivora with the most ulcers); Marsupialia,
Red Kangaroo (_Macropus rufus_), malignant papilloma with metastases.
The former tumor, shown in Fig. 17, was a diffuse soft excrescence
beginning near the pylorus and stretching along the lesser curvature
toward the cardia. Histologically it was made up of glandular acini
growing in all directions but always maintaining normal relations of
cells and basement membrane. There were no metastases and other reasons
for death existed. The tumor of the kangaroo stomach was a true
epitheliomatous cancer with metastases to liver, spleen, and kidney.
Only one secondary tumor was observed, from a carcinoma of the lung in a
Red Kangaroo (_Macropus rufus_).
[Illustration:
FIG. 16.—MULTIPLE GASTRIC ULCERS. COMMON WOLF (CANIS LUPUS). CHRONIC
GASTRITIS WITH NUMEROUS IRREGULAR ULCERS OF THE PEPTIC TYPE.
]
[Illustration:
FIG. 17.—PAPILLOMA OF STOMACH. HAMADRYAS BABOON (PAPIO HAMADRYAS).
]
THE INTESTINE.
Inflammation of the gastrointestinocolic tube is the most important
single condition with which handlers of animals have to deal, and
unfortunately it can seldom be diagnosed clinically, early and
accurately enough, to make treatment useful. At this Garden some
evidence of acute or chronic disease of the tube has been present in 31
per cent. of our autopsies. The reports of other gardens would indicate
that their figures might be quite close to this. What is the cause of
this high mortality? Incorrect feeding, qualitatively or quantitatively
has been put at the top of the list by Plimmer, but he adds other less
important factors: Bacteria of infectious power, protozoa, foreign
bodies and parasites or their mural cysts. In order to evaluate
approximately how each of these acts let us review the causes as they
are generally known and later discuss the pathology as seen in the
various orders.
(1) Overloading of the stomach by too much food or by rapid eating of a
hungry animal is of importance under certain domestic circumstances
where times of feeding are irregular or intervals are too long, but this
cannot occur in any well regulated menagerie. It is possible, however,
that overfilling might occur in certain Ungulata, which have hay and
straw nearly always available, if the food in their reach happens to be
particularly agreeable or tasty to them.
(2) Insufficient mastication would seem to be important only in those
orders which depend upon this action to triturate, insalivate and
macerate their food, of which Homo, Primates, Ungulata and Marsupialia
are the principal ones.
(3) Disturbance during and after feeding has always been believed to
affect digestion unfavorably, and it may be that visitors to a
collection exert such an effect; this factor is probably negligible.
(4) The appropriateness of the food is a very important factor in the
health of an animal under captive conditions. Diet lists are made up by
officials largely according to the known habits and general physiology
of an animal, but the food offered can at best only approximate what the
wild beast obtains for himself. It does not follow because a selected
diet may seem to provide all the elements contained in the food
available under natural conditions that it actually does so, especially
since we are aware that some essential food factors, known under the
term vitamins, are necessary to best development. These substances vary
in closely similar foods, and seem to be higher in simple natural foods
than in prepared diets. We have seen in this Garden that the inorganic
constituents must be correctly represented in the food, else
degenerative osseous condition may develop. Inappropriate diet may
express itself at once after the receipt of an animal, by its sickness
or death, or after some time in the development of chronic tympanites,
chronic intestinal catarrh or bony deformities.
(5) The physical condition of food is a matter of no small moment. The
taking of soft food in large quantities especially by herbivorous
animals, permits too short a sojourn in the gastric fundus and is often
followed by pyloric and duodenal disease. Too firm food may pack the
rumen, fundus or proventricle as the case may be, and be succeeded by
distention of these parts and catarrh of the pyloric and intestinal
area. The effect of foreign bodies mixed with food is difficult to
evaluate unless of course they be of such a nature (pointed metal and
the like) as directly to traumatize the mucosa. Many birds and mammals
come to autopsy with a relatively large number of stones and small
sticks in the stomach without any distinct evidence that they have been
hurt thereby. In the bird the stones may be so large and numerous as to
leave little room for food, or small enough to pass out into the
intestine where they undoubtedly may pave the way for bacterial action.
Smoothly polished pebbles in small quantity seem to have little effect
in mammals. Hair balls are not common and unless of large size are
apparently unimportant. Considerable sand mixed with food has a
distinctly irritating effect. It is perhaps best known as a chronic
gastric disorder of horses; we have seen it in zebra.
(6) Spoiled food is obviously a very prime factor in inflammations of
the gastrointestinal tract. Its operations are illy understood except
perhaps when products of fermentation or putrefaction prevent digestive
action or are absorbed. If in small quantities not sufficient to cause
acute fermentative inflammation or intoxication, such substances
frequently taken may doubtless produce chronic catarrhs. Many animals
are fed upon vegetable mashes, or stews which can decompose, while bad
meat may occasionally be fed. We had a rather serious outbreak of
enteritis in small Carnivora from the use of fowl heads obtained at
hotels; some of these cases were shown to be due to B. paracoli, thus to
be looked upon as infections. Dirty food while not spoiled may carry
with it organisms of decomposition, or of infective qualities, or the
dirt may act as an irritative foreign body. We have found that for
delicate ungulates (antelopes) it is highly desirable to screen grain,
and that the grade of hay should be of the best.
(7) Infectious conditions are of great importance under certain
circumstances but with the exception of hog and fowl cholera, the
dysenteries and a few other diseases, do not as a rule play a great part
in mortality as specific diseases unless of course an epizoötic appear.
The greater problem is to understand bacterial action in the face of
other factors. Are infectious germs introduced with food and drink in
every case of gastroenteritis or do some other factors activate those
already present in the gut tract? Unfortunately these questions cannot
be answered directly. We can, however, point out which groups of
bacteria are most common in some of the orders, which orders are most
susceptible to bacterial invasion and which to local lesions with
intoxication. The greatest problem in the field is the interrelation of
germs of various sorts in the intestinal tract. Certain varieties are
known to develop intoxicating aromatic substances, others to elaborate
or excrete fatty acids, still others to form antiferments but the
conditions existing in the various kinds of intestinal tracts are too
little understood to help very much in this study.
(8) Animal parasites have long been considered as one of the causes of
gastrointestinal inflammation, a condition largely due to copying from
book to book of a few facts and more impressions. The sum of reliable
information to-day would seem to indicate that a few parasites—uncinaria
being the most conspicuous example of this type—draw considerable blood
from the mucosa, that a few, like uncinaria and dibothriocephalus,
elaborate an absorbable toxin, that some, notably ascarids, produce an
irritating substance, and that many possess the power in themselves or
by some excretion to act as antiferments. These factors, were they all
combined in one worm, might probably irritate the mucosa sufficiently to
produce inflammation, but it is not easy to imagine that they would
cause an acute specific condition. It is much more easily conceived that
with tiny hemorrhages or ulcerations of mucosæ, bacteria might get in
their work or if considerable ferment were neutralized, maldigestion,
flatulence or indigestive irritation would ensue. With certain worms
like esophagostomum there is considerable evidence to show that a
chronic fibrous disease of the intestinal wall arises, but in this case
the parasite resides in the mucosa and acts as a foreign body. It would
seem, however, that the most important influence that animal parasites
exert is to be found in the preparation of the mucosa for the action of
bacteria. Masses of parasites may of course physically obstruct the
lumen and lead to intestinal stasis and dilatation.
INFLAMMATION.
In analyzing the cause of a gastroenteritis and its consequent effect
upon the wall of the tube and upon the viscera, certain physical,
chemical and physiological factors must be considered. Whether this may
be directly the effect of bacteria or poisons from worms or some other
factor seems of little moment since in any fully developed case,
symptoms and effects are comparable. Moreover it seems that pathological
anatomy, both gross and minute, is essentially the same from Primates to
struthious birds, the highest and lowest of the two classes here
considered. By this is meant that the acute congestive condition of the
gut tract with solution of the surface, to which we have applied the
name of toxic enteritis, seems to be met with in this form throughout
all the orders. So too catarrhal inflammations are the same to the naked
eye and under the microscope, due allowance being made for the fact that
mammals use polynuclear cells for exudative purposes while birds employ
mononuclears. Concomitantly with these conditions, a degenerative
process may be going on in the liver and kidney, and hyperplasias,
especially in the true infective processes, will be found in the related
lymphatic structures.
The majority of students to-day place responsibility for gastroenteritis
upon the bacteria known to be present in the various intestinal tracts,
mentioning especially colon and proteus groups, streptococci, the
necrosis bacillus and anaerobes of the Welch class. In a few of our
studies of intestinal bacteria in cases of enteritis one thing has been
very definite and that is that in the intestinal content of animals
whose food is largely meat, Gram-negative bacilli have predominated,
whereas in herbivorous animals Gram-positive organisms have been most
numerous. From the observations of Kitt, Strassberger and some others,
the normal flora of domesticated animals is subject to wide variations
so that our observations must receive confirmation before they are
finally acceptable. We have on several occasions isolated from
carnivorous intestines Bact. paracoli, Bact. suipestifer and other
members of this group. We have no reliable cultural data upon the
herbivorous intestine and can only quote the Gram pictures as mentioned
above. On two occasions, an eland and an elk, a very large number of
forms corresponding to necrosis bacillus were seen; to this organism
Kitt gives considerable power in the production of necrotizing
processes.
TABLE 11.
_This table shows an analysis of all cases of gastroenterocolitis. The
left half of the table is an analysis of orders upon which one hundred
or more autopsies have been done, the right half of orders with fewer
than that number. The left half is expressed in percentages, the right
half in number of cases only since percentages might be misleading. Left
hand table: First column is percentage of gastroenterocolitis per order;
next five columns the percentages in which each of the factors in the
headings was believed responsible; the last three columns show the
participation of each of the divisions of the intestinal tract; thus
Primates had all told 24.8 per cent. of inflammations of which 7.2 per
cent. were in stomach, 18.3 per cent. in the intestines and 8 per cent.
in the colon; obviously many had all three sections affected. Right hand
table is constructed on a similar basis except that number of cases is
quoted, not percentages, and the total is put in the last column._
════════════╤═══════════════════════════════════════════════════════
│ Percentages in orders with sufficient autopsies.
────────────┼─────────┬────┬────────┬─────────┬────────┬────────────
│Per cent.│Food│Bacteria│ Animal │Physical│Undetermined
│ of │ │ │Parasites│Objects │
│Autopsies│ │ │ │ │
────────────┼─────────┼────┼────────┼─────────┼────────┼────────────
Primates │ 24.8│ 1.8│ 4.4│ 3.6│ │ 15.
Lemures │ │ │ │ │ │
Carnivora │ 46.1│ 2.9│ 7.2│ 5.8│ .2│ 30.
Pinnipedia │ │ │ │ │ │
Insectivora │ │ │ │ │ │
Chiroptera │ │ │ │ │ │
Rodentia │ 25.│ 5.│ 2.│ 2.│ │ 16.
Ungulata │ 24.8│ 6.6│ 2.2│ 2.│ .8│ 13.2
Proboscidea │ │ │ │ │ │
Hyraces │ │ │ │ │ │
Edentata │ │ │ │ │ │
Marsupialia │ 33.1│ │ 10.│ 10.1│ │ 13.
Passeres │ 23.6│ .1│ 4.5│ 1.8│ .15│ 17.
Picariæ │ │ │ │ │ │
Striges │ 41.5│ 1.5│ 5.3│ .7│ │ 34.
Psittaci │ 36.6│ .3│ 10.7│ 3.7│ .15│ 21.8
Accipitres │ 40.7│ │ 4.5│ │ .5│ 35.7
Columbæ │ 17.8│ │ .6│ 3.│ .6│ 13.5
Galli │ 38.6│ │ 5.3│ 19.6│ │ 13.7
Hemipodii │ │ │ │ │ │
Fulicariæ │ │ │ │ │ │
Alectorides │ │ │ │ │ │
Limicolæ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │
Impennes │ │ │ │ │ │
Steganopodes│ │ │ │ │ │
Herodiones │ │ │ │ │ │
Odontoglossæ│ │ │ │ │ │
Palamedes │ │ │ │ │ │
Anseres │ 29.6│ .3│ 4.4│ 2.3│ .6│ 22.
Struthiones │ │ │ │ │ │
Crypturi │ │ │ │ │ │
────────────┴─────────┴────┴────────┴─────────┴────────┴────────────
════════════╤════════════════════════╤════════════════════════════════
│sufficient autopsies. │Number of cases in orders with under 100 autopsies each.
────────────┼───────┬──────────┬─────┼────┬────────┬─────────┬────────
│Stomach│Intestines│Colon│ │Bacteria│ Animal │Physical
│ │ │ │Food│ │Parasites│Objects
│ │ │ │ │ │ │
────────────┼───────┼──────────┼─────┼────┼────────┼─────────┼────────
Primates │ 7.2│ 18.3│ 8.│ │ │ │
Lemures │ │ │ │ │ 8│ 2│
Carnivora │ 21.│ 41.│ 6.6│ │ │ │
Pinnipedia │ │ │ │ │ 1│ 1│ 1
Insectivora │ │ │ │ │ │ │
Chiroptera │ │ │ │ │ │ │
Rodentia │ 7.│ 20.5│ 3.5│ │ │ │
Ungulata │ 9.1│ 20.│ 2.5│ │ │ │
Proboscidea │ │ │ │ │ │ │
Hyraces │ │ │ │ │ │ │
Edentata │ │ │ │ │ │ │
Marsupialia │ 22.│ 21.│ 3.5│ │ │ │
Passeres │ 1.2│ 22.│ 3.│ │ │ │
Picariæ │ │ │ │ 1│ 10│ 4│
Striges │ 6.│ 40.│ .7│ │ │ │
Psittaci │ 1.7│ 35.4│ 1.3│ │ │ │
Accipitres │ 5.2│ 39.│ 1.│ │ │ │
Columbæ │ 4.5│ 13.5│ .7│ │ │ │
Galli │ 2.6│ 21.6│ 19.6│ │ │ │
Hemipodii │ │ │ │ │ │ │
Fulicariæ │ │ │ │ │ 6│ 1│
Alectorides │ │ │ │ 1│ 1│ 2│
Limicolæ │ │ │ │ │ │ │
Gaviæ │ │ │ │ │ 1│ 1│
Impennes │ │ │ │ │ │ │
Steganopodes│ │ │ │ 1│ 1│ │
Herodiones │ │ │ │ │ 1│ 3│
Odontoglossæ│ │ │ │ │ │ │
Palamedes │ │ │ │ │ │ │
Anseres │ 2.5│ 27.7│ 6.6│ │ │ │
Struthiones │ │ │ │ │ 7│ │
Crypturi │ │ │ │ │ │ │
────────────┴───────┴──────────┴─────┴────┴────────┴─────────┴────────
════════════╤═════════════════════════════════════════════════════
│Number of cases in orders with under 100 autopsies each.
────────────┼────────────┬───────┬──────────┬─────┬───────────────
│Undetermined│Stomach│Intestines│Colon│ Total Animals
│ │ │ │ │ Showing
│ │ │ │ │Gastroenteritis
────────────┼────────────┼───────┼──────────┼─────┼───────────────
Primates │ │ │ │ │
Lemures │ 13│ 4│ 19│ 3│ 23
Carnivora │ │ │ │ │
Pinnipedia │ 8│ 7│ 8│ 1│ 11
Insectivora │ │ │ │ │
Chiroptera │ 2│ 1│ 1│ │ 2
Rodentia │ │ │ │ │
Ungulata │ │ │ │ │
Proboscidea │ 1│ │ 1│ │ 1
Hyraces │ 2│ │ 1│ 1│ 2
Edentata │ 2│ │ 1│ 1│ 2
Marsupialia │ │ │ │ │
Passeres │ │ │ │ │
Picariæ │ 24│ 5│ 36│ │ 39
Striges │ │ │ │ │
Psittaci │ │ │ │ │
Accipitres │ │ │ │ │
Columbæ │ │ │ │ │
Galli │ │ │ │ │
Hemipodii │ │ │ │ │
Fulicariæ │ 8│ 1│ 15│ │ 15
Alectorides │ 10│ 2│ 13│ 3│ 14
Limicolæ │ 1│ │ 1│ │ 1
Gaviæ │ │ │ 2│ │ 2
Impennes │ 3│ 1│ 3│ │ 3
Steganopodes│ 8│ 1│ 10│ │ 10
Herodiones │ 25│ 1│ 24│ 6│ 29
Odontoglossæ│ │ │ │ │
Palamedes │ 1│ │ 1│ │ 1
Anseres │ │ │ │ │
Struthiones │ 14│ 8│ 20│ 3│ 21
Crypturi │ 1│ │ 1│ │ 1
────────────┴────────────┴───────┴──────────┴─────┴───────────────
THE TABLE.
Our records have been analyzed from the standpoint of diagnosis and the
most probable cause. The first will be taken up in discussing each of
the orders. The probable causes are divided into food, bacteria, animal
parasites, physical objects and undecided, in other words a
classification based upon the most prominent or definite evidences as
seen at postmortem combined when possible with antemortem observations.
When findings were inconclusive or contradictory, cases were called
undecided, naturally a very large group. Fermentative processes in the
presence of obviously undigestible material, are classified with food as
a cause. When evidences of septicemia existed in absence of the other
factors, it is held that bacteria were responsible. Cases were grouped
under animal parasites when these were the most definite findings.
Physical objects are relatively unimportant and self-explanatory. To the
etiological chart there are appended columns intended to show the
percentage or case incidence of the disease of the grosser subdivisions
of the gastrointestinal tract which indicate in a general manner what
part of the tube in the various orders is most susceptible to disease.
While of course conclusions must be drawn with great caution, there can
be little doubt, for example, that carnivores and marsupials have more
gastric disease than any other order, and that the high place for the
colon is held by the gallinaceous birds. This charting was suggested by
the work of Dr. Raymond Pearl upon statistics, wherein he takes as a
basis of classification the part of the body which succumbs to disease-
producing organisms or from which a disease starts. It cannot be stated
that there is a clear cut relationship between enteritis and the
expectancy of life.
MAMMALIA.
The PRIMATES as an order have their share of inflammations of the
gastrointestinal tract and present points of interest. Acute digestive
disorders succeeded by acute dilatation of the stomach, or in less
fermentative cases by acute catarrh of the intestine, are not at all
uncommon. The reason for this is not discovered by reviewing the diet
and manner of feeding. The buccal pouches, distensible esophagus, the
freely movable stomach, and relatively elastic gastric wall would seem
to permit of very considerable dilatation to accommodate the large
quantities which the monkey sometimes crams into himself. Nine fairly
acceptable records of gastric overfilling exist and two of them seem to
have been followed by tympanites sufficient to embarrass respiration, in
one case there occurring an acute cardiac dilatation with myocardial
degeneration. The animals give no symptoms of this condition and in the
last case cited the beast, while old, ate well and was not distended the
evening before death.
When acute gastritis exists (twenty cases) the animal seems uneasy but
does not vomit. On one occasion I was called to see a monkey which was
retching and seemed in pain. Lime juice was offered and taken, followed
by gentian and cardamon, which seemed to give some benefit. Somewhat
later this was repeated in another case, but observations where this
might be useful are rare.
The pathology of gastric conditions offers little to contrast with that
of man. The enormous distensibility of the fundal pouch often suggests
to the observer the rumen of ungulates. Acute gastritis of one kind or
another and acute catarrhal enteritis are the most common lesions noted
in the Primates. Involvement of the intestine or colon need not carry
with it an increase of signs of illness, although at times one will see
an evidently sick animal with diarrhœa. Anatomically the lesions are
commonly restricted to the stretches of gut _above_ the ileum, it being
rather rare that this division or the colon is affected. Pathologically
the lesions are catarrhal with definite involvement of the follicles in
about one-third of the cases. In this order toxic and pseudomembranous
forms are quite rare and ulcerative lesions uncommon. Colonic disease as
a sequel to inflammation higher up is sometimes seen in the follicular
varieties, but takes a minor place compared to amœbic dysentery of which
we have had several cases; this will be discussed under a separate
heading. Degenerative disease of the skeleton is almost always
accompanied by a low grade of enteritis but not necessarily gastritis or
colitis. The pallor of the mucosa, while at times striking, may be
relieved by follicular spots and petechia or pigmentation. Often,
however, animals suffering from osteomalacia and rickets come to their
end by an acute inflammation of the gut tract.
The bacteriology at our disposal allows no conclusions. Aside from a
case probably due to Ps. fluorescens and one with colon bacillus
abscesses in the liver, no reliable data are at hand.
Reference to Table 11 reveals the fact that among orders with sufficient
autopsies to permit percentages, the alimentary tract in monkeys is in
the group of low figures, that the intestinal section is relatively more
often affected, and that the colon is more often diseased than in other
mammalian orders, and is exceeded only by the gallinaceous birds.
The LEMURES, of which we have eighty-six autopsies, do not differ much
in anatomy from the Primates, however greatly they disagree in habits
and outward appearance; their diet is the same. Clinically the slothful
behavior of a normal lemur probably obscures symptoms and signs of
illness, for our antemortem notes with the exception of a few
observations of loose stools, fail to offer a lead as to diagnosis. This
order has a large incidence (twenty-three cases) of gastroenteric
conditions as shown in Table 11, but some explanation of the figures is
deserved. In the first place, only one case of acute gastritis occurred,
and this was apparently a part of a general infection, and if induced at
all by food this was only secondary. Indeed as one reviews the records
it does not seem that the lemurs are easily disturbed in their gastric
digestion. Acute and subacute inflammations from bacterial action seem
definitely more prominent since they take the catarrhal, follicular and
deep submucous form and are frequently associated with generalized
infectious processes. One amœbic case was observed and there was another
in which a heavy cestode and nematode infestation seemed to have paved
the way for bacteria.
CARNIVORA.
The food of this order is received into the fundal part of the stomach,
the distensible but normally capacious left and superior two-thirds of
the organ. The general shape of the viscus, that of a gourd, permits a
fairly sharp separation of the fundal and pyloric sections, so definite
indeed that the pathology of the two parts was studied. The intestines
vary in length, but in the land carnivores are relatively short, narrow
in lumen and rich in wall. A cecum, or at least a blind end of the large
gut made by the insertion of the small intestine above the tip of the
colon, is suggested in all families, although, as in the bears, it may
be quite insignificant or rudimentary. Theoretically no stasis should
occur at this point. The colon is short in all carnivores and, like the
small gut, with a heavy wall. The comparative simplicity of the
carnivorous gut tract, the ability of many of these animals to disgorge,
the suggestion of high resistance of the upper end of the tract to
infection and the ease with which diarrhœa can clear out the tube, would
seem to warrant the expectation that inflammation would not be serious.
Such, however, is not the fact for, on the contrary, they have shown a
higher incidence than any other order for which we have adequate
comparison. Anatomically considered their stomach occupies the second
place in vulnerability, next to the marsupials, and their intestines the
highest place; this indicates of course that combined gastric and
intestinal disease has often occurred. Involvement of the colon occupies
the second place, in ordinate susceptibility, being exceeded only by the
monkeys, due to heavy parasitic infestation, but would occupy the first
place were the eleven amœbic dysenteries in monkeys subtracted from
their total, a subtraction which might be allowed since it represented
an epizoötic outbreak.
Etiologically considered, it would seem as if the influence of incorrect
feeding were of little importance, and from one standpoint this is
probably the case. Acute fermentative or irritative processes are not
common at all, while more inflammatory pictures, catarrhal, erosive or
ulcerative, are the rule. There is another phase to the term incorrect
food, that is incorrect in its cleanness. During 1912–15 there was an
increasing mortality among the cats and dogs fed upon horse meat, mutton
and fowl heads. Early in 1916 the butcher shop was reconstructed and
thoroughly cleaned and covered galvanized pans supplied in which to
transport the food; these pans were scrubbed and scalded after use.
Since that time, infections inflammations of the stomach and intestines
have shown an ever increasing downward incidence, which result, there
having been no material changes in other directions, I do not hesitate
to ascribe to the improvement of butchering and dispensing engineered by
Dr. W. B. Cadwalader.
Helminths seem to be of importance in this order both by reason of the
percentage of autopsies in which they presented the most probable or at
least most suggestive cause and because uncinaria and strongylus have
been seen attached to the wall and a large bulk of known irritative
cestodes have occupied the lumen. Physical objects, stones, bones, wire,
may cause irritation enough to activate bacterial action or may actually
penetrate the wall; the latter action is well known. In so far as
practical application of this is concerned, it teaches to feed whole,
unsplintered or ground bone.
The distribution and character of pathological lesions according to the
region of the stomach is what might be expected from the shape and
physiology of its parts. True inflammatory processes are best, and in
some cases only seen in the pyloric half of the viscus, while the
changes in those few cases believed to be fermentative or irritative in
nature were largely confined to the fundus. Dilatation of the latter
part may be understood because there the muscular coats are about equal
to the mucous in thickness and one-half the width of those at the
pylorus, but why inflammatory processes should not be so developed in
the fundus is not clear unless the greater availability of mucus
protects the secreting wall. Not only does acute inflammation reach its
most definite form in the second part of the stomach, but the irregular
pigmentation, mammillated overgrowth and atrophy or ulceration of
chronic disease are likewise best seen in this part.
Acute enteritis, of all varieties, is seen more beautifully in
carnivores than in any other order of mammals, and nowhere can it be
studied better. Its gross appearance is that of the text-book and its
minute character even more instructive. I have used a slide of acute
catarrhal enteritis in a lion for the illustration of this lesion for
the _Text-book of Pathology_ by Doctor Stengel and myself. However, as
is known to all who have paid any attention to enteritis, the postmortem
findings are usually much less definite than clinical observations would
warrant one to expect. The Carnivora not uncommonly show intestinal
congestion, mucous membrane swelling without edema or opacity,
congestion of the spleen, cloudy swelling of the liver and kidneys and
perhaps mesenteric lymph node edema. This picture we have viewed as a
toxic affair of some sort or a bacterial infection not yet far enough
advanced to produce catarrhal or ulcerative enteritis and septicemia. In
such cases the carnivorous intestinal mucosa offers instruction. The
epithelium is vacuolated or fringed on the free edge or may be missing
altogether. In the depths mucus formation is very active, and where it
is going on, round cells seem attracted, collecting in groups in the
villus or in the subjacent submucosa. Perivascular round cell increase
may be noted. Plasma cells and granular eosinophiles are common, but I
cannot state how important the latter are in the general picture because
of the frequency of parasites in carnivores. The central vessel of the
villus and the arterioles of the submucosa are injected. Lymph follicles
may or may not be enlarged, but if so usually fail to show a germ
centre.
Colitis alone is not common in this order, but as an extension process
or involvement at the same time as the upper levels it occurs
occasionally. The only fact I wish to record and one which I would
emphasize because of having seen it recently in a human case of chronic
colitis, and since it does not appear important to systematic writers,
is superficial blood supply. The capillary network of the colonic villi,
while rich, is in the form of a fine plexus just under the epithelium.
In the cases studied these vessels become quite distinct and possess
much more definite walls, often bordered by mononuclears, while
connective tissue is more evident at the bases of the villi and deeper.
This may help in deciding the existence of a colitis.
Bacteriologically the most instructive experience to report is the
discovery that a small outbreak of enteritis among small Carnivora,
chiefly cats, fed upon fowl heads was due to Bact. paracoli, or at least
this organism was found in the intestinal mucosa, spleen, and heart’s
blood of three cases. The type of enteritis was hemorrhagic and
follicular. There was also a case of septicemia apparently emanating
from enteritis due to Bact. suipestifer in a lion (_Felis leo_). These
facts bring strongly to attention the modern teaching that meat
poisonings of the Gärtner type are to be considered as infectious and
not of the so-called ptomaine group.
PINNIPEDIA, while related closely to the Carnivora, are grouped in a
suborder in our classification and because of their restricted diet are
treated here in a separate paragraph. The tract is peculiar in the
strong tubular stomach sharply bent upon itself, the great length of the
small gut (upwards of a hundred feet in some genera), and the practical
absence of a cecum. Pathologically speaking, the most striking lesion of
these animals is ulcerative gastritis, a process usually most marked
along the posterior-superior surface, but not confined thereto. Upon
inspection the gastric mucosa, normally supplied with low regular rugæ,
is much distorted by swellings upon the top of which are irregular
ragged ulcers with rounded elevated but not frayed margins. The density
of the edges indicates much infiltration of the deep mucosa and
submucosa; this can be confirmed by microscopical examination. One
attempt to study this gastritis bacteriologically was fruitless.
Sections of one case showed streptothrix-like masses while in another
case bacterial colonies and yeast-like bodies were found in adjacent
lymph nodes. The genesis of this condition might lie in injury by fish
fins or by foreign bodies, of which large numbers are found at times (a
pint and a half of stones, marbles, and sticks were found in one
stomach). Gastritis has been the starting point of septicemia on two
occasions, and three times an acute exacerbation or new implantation of
infection occurred, with extension into the intestine. It is interesting
that all the deaths of Pinnipedia with gastroenteric conditions occurred
in the winter months.
INSECTIVORA are represented by two common European Hedgehogs. In one
there were three shallow but shelving ulcers in the stomach which had
bled sufficiently to weaken the animal; free blood was found in the
intestine. The other specimen was diagnosed at postmortem as having
catarrhal enteritis involving nearly the whole small gut, but
histological section did not confirm this.
As one descends the zoological scale the first gastrointestinal tract
prepared for the nutritional care of bulky food is to be found in the
RODENTIA. This order presents a great variety of shapes and arrangements
of the stomach, but the outstanding feature, with very few exceptions
(cf. spermophiles), is the development of the cardiac and fundal
divisions ostensibly for the reception of a large bulk of coarse food to
be digested at leisure. Some genera like the hamster (_Cricetus_) have a
stomach closely resembling the ruminants, while that of the spermophile
suggests the equine stomach. The pyloric end, variable in many ways,
greatly resembles the abomasum. So too the duodenum is large, loose and
distensible while the copious small gut ends in a very large cecum,
shaped at times in a manner which has led to the term “colonic stomach.”
The colon is variable and not always supplied with longitudinal bands
and sacculations.
In regard to incidence of gastrointestinal disease, rodents occupy a
middle position in the table. The stomach seems a vulnerable section of
the tract. Dilatation of the left hand section is common, due, to all
appearances, to fermentative processes which have as a result the
softening of the mucosa so that even immediately after death it will
separate almost entirely. In these cases the pyloric part need not
participate but may remain flat, smooth, soft and pink. This condition
is slightly more common in the compound than in the simple stomachs. In
some of this order, especially rats and cavies, there is a fermentative
gastroenteritis expressed by injection and edema of the pylorus and
duodenum, and much frothy mucus. It was at first thought that some
relation might exist between this condition and the absence of the gall-
bladder, but it occurs in varieties possessing this structure. The
reaction of the intestine to irritation in this order is peculiar in two
ways, the occurrence of mucus and the activity of the lymphatics. In all
the inflammations from and including the stomach to the cecum, mucus is
conspicuous. At times it is thin or loose and mixed with contents, while
at others it forms a relatively close covering for the mucosa almost
like a false membrane. Rodentia are peculiar in the promptness and
clearness with which the follicles of the intestinal wall and mesentery
enlarge in inflammation. They appear as pale, well outlined or diffuse
opacities in the wall or as distinct plaques prominent on the surface.
The PROBOSCIDEA are represented by one Elephant (_Elephas indicus_), in
which a mild catarrhal change was seen in the middle stretches of the
small intestine. This was of little importance as a cause of death,
there being several other diagnoses, and was probably a terminal affair.
HYRACES, of which we have a total of seven examples, present two mild
involvements of the intestine but none of the stomach. It would appear
from the records that the intestinal condition had little to do with the
death of the animals, and unfortunately no microscopic slides were made.
Because of the curious formation of the large gut, notes of both ceca
were made in one case, and can be condensed as follows: “The upper or
anterior cecum presented a shaggy pearl gray mucous covering, closely
attached to the mucosa. This cavity and the posterior ceca were packed
with dry crumbling feces. Small thin-walled cysts were seen in the tips
of the lower ceca. Duodenum was congested and mucosa swollen. Stomach
contained dry, poorly digested food. No parasites were found.”
The EDENTATA are represented by an Armadillo (_Tatu novemcinctus_) and
an Anteater (_Myrmecophaga tridactyla_.) The former had a prolapse of
the rectum accompanied by colitis but it is impossible to decide the
priority of the two conditions since the former is known to have existed
long enough to have permitted the latter to develop. The Anteater had a
distinct mucocatarrhal enteritis in which bacteria played a part since
involvement of the liver, spleen, kidney and lymph nodes also existed.
The beast was in good condition upon arrival, but did not become
accustomed to the proffered diet, and was distinctly anemic at death.
The UNGULATA, so-called for their hoofed and horned character, are also
associated anatomically by the construction of their gastrointestinal
tract. However, the order of the list as given on page 44 does not
represent their historical development nor does it accord with
anatomical arrangement of the tube under discussion. The last three
families of Artiodactyla are perhaps the simplest in the construction of
this tube, or at least take an equal place with the Perissodactyla,
while the remaining families of the former suborder have a complex tract
of generally similar architecture. This whole order has, however, an
alimentary tract anatomically suited for the consumption of bulky
vegetable stuffs and shows an attempt at adjustment between the food,
the methods of mastication, the area of digestive surface, and the bulk
necessary for nutrition. The number of factors opened up by the many
variations between this complex tract and that of the carnivorous simple
tract is so great that I shall attempt only to contrast the anatomy and
pathology of the simpler ungulate tracts and the complex ruminant
apparatus.
The simpler gastrointestinal tract is possessed by the Perissodactyla,
and by the following families of Artiodactyla, the Phachocœridæ, Suidæ
and Tayassuidæ. This consists of a stomach with a single cavity (some
Peccaries have partitions but no true septa with strict histological
differences) divided into esophageal, cardiac, fundal and pyloric areas,
dependent upon the nature of the lining epithelia and the absence or
presence of glands, as well as the nature of the tubules. The duodenal
section is ample and may be sacculated while the intestines are small in
calibre and rather sturdy in wall. The cecum is relatively very large,
well supplied by longitudinal bands and sacculations; the colon is
relatively short but quite capacious and sacculated.
The ruminants and other remaining members of the Artiodactyla have a
compound stomach suited to the separation of coarse and fluid foods and
the retention of water, and so arranged that boluses of different
densities are distributed as needed. These divisions are histologically
as well as grossly different. The first three, comparable to the
esophageal section of the simpler stomach, are reservoirs or channels,
while the fourth or true digestive section, is divided into areas
corresponding to fundus and pylorus, possessing the appropriate type of
gland. The duodenum in this group is narrow, as is the rest of the small
gut, and has delicate walls. The cecum proper is short and of variable
width, but never as great as in the group first discussed, while the
colon, an intricately wound tube, is narrow and very long. Certain of
the first group (Peccaries) have a colon of this type, but it is not so
complicated as in true ruminants.
These complications seem designed to permit of a long retention of
coarse food of low nutritive value per bulk for a time sufficient for
full digestion; reverse adaptation of large size of stomach and colon
may be explained on the same basis. Let us now examine these two groups
to discover their pathological reactions and the nature of the lesions.
TABLE 12.
_Showing the Percentage Incidence of Various Forms of Inflammation in
the Alimentary Tract of Ungulata._
══════════════════════════════════╤═════════════════╤═════════════════
Lesion │ Group A │ Group B
│ Perissodactyla │ Ruminants and
│ and Swine, Wart │ Relatives Per
│ Hogs, Peccaries │ cent.
│ Per cent. │
──────────────────────────────────┼─────────────────┼─────────────────
Acute fermentative gastritis │ 18.│ 2.1
All other forms of gastritis │ 16.3│ 5.
Acute toxic or fermentative │ 1.6│ 2.3
enteritis │ │
All other forms of acute enteritis│ 1.6│ 8.4
Chronic enteritis │ 0.│ 1.9
Colitis and typhlitis │ 0.│ 3.1
──────────────────────────────────┴─────────────────┴─────────────────
Ungulates as a class stand in a position equivalent to the Primates in
the incidence of gastrointestinal diseases. They show a conspicuous
percentage of cases apparently due to incorrect food and, coupled with
this, a high percentage of gastric involvement, being exceeded in this
respect by the marsupials only (there is an adequate reason for this—see
below). Cases ascribed to bacterial or parasitic agents are not
numerous. Analysis of the records of the two groups discussed above
brings out some interesting facts. Consultation of Table 12 shows
percentage comparisons, based on the number of autopsies, of lesions in
the various sections of the tract. Group A, that with the simple stomach
and the short capacious colon, is represented by forty-four specimens,
while Group B embraces 321 animals. Perhaps the use of these two widely
differing figures for comparison is open to some objection which might
be final and decisive were not the figures so definite. At a glance one
can see that Group A has involvement more marked high in the tract while
Group B has more disease in the intestine and colon. Certainly gastritis
is more common (five times) in the A than in the B group, while
enteritis is more common in B (over three times). No case of chronic
enteritis or of involvement of the colon is recorded in animals with a
simple stomach and a wide hind-gut. This may be read either in terms of
vulnerability of the stomach or in the degree of resistance of the
respective groups.
Consideration of the local factors of the stomach brings to light at
once the fact that incorrect food entering the simple stomach could
attack the softer, less resistant glandular section of the fundal and
pyloric areas whereas the rumen and psalter of the compound organ, with
their stratified epithelium devoid of glands, act as barriers or as
places where detoxication of irritants might take place. In both groups
bulky food is packed to the left, the esophageal and cardiac section in
the simple form, the rumen in the compound. Soft or liquid food may pass
into the psalter and abomasum of the ruminant stomach almost directly
since it has not the force or bulk to push aside the valve-like fold of
wall at the junction of esophagus, rumen and reticulum. For this reason,
if for no other, the character of soft food supplied to this order must
be unexceptionable.
It has not been possible to follow out the layering of diets as
Scheunert did when showing the course of various foods before they are
mixed at the beginning of the pyloric compartments. We have seen two
cases in ruminants which seem to indicate that soft food had passed into
the right side cavities of the stomach, there to cause irritation, while
the rumen remained quite normal. It seems, however, accepted by
veterinarians that excessive soft food may be followed by trouble in the
digestive stomachs, while excessive dry food may cause distention of the
left hand sections. So far as I know, the relative incidence of gastric
disorders in the above outlined groups has not been pointed out before.
The pathological types of gastroenteritis do not present many unusual
features. Simple injection of vessels during digestion seems more
evident in this than any other order, while mucus production seems less
marked. The mucosa of the reservoir portions may, in simple overfilling
and fermentative distention (gastric tympanites), be quite normal or
dull red; when active fermentation has occurred it may be digested and
peel off. More or less true inflammation as seen in the digestive
stomachs is definitely better expressed in the compound ruminant organ
than in the simple equine variety where congestion and edematous
swelling with hemorrhage form the usual picture. True catarrhal changes
both gross and minute, are often well seen and ulcerative lesions are
not uncommon; ulcers are unusual in the simple stomach. These statements
hold good also for the small intestine. Enteritis affects the duodenum
and jejunum more in the Perissodactyla and swine than in the ruminants.
Ungulata do not react with hyperplasia of the mural lymphatics as do
many other orders, but the swelling of the mesenteric nodes is often
noteworthy. As might be expected this is more definite with catarrhal
changes and therefore best seen in the ruminants. In the colon, however,
the solitary follicles are often quite prominent in simple inflammation.
Histologically the greatest changes seen in this order are superficial
degenerations with mononuclear increase in the deep submucosa, mostly
arranged in perivascular fashion. The villi do not contain the large
number of cells seen in the Carnivora.
MARSUPIALIA.
Consultation of the figures for this order in Table 11 arrests attention
at once because of the peculiar percentages found under the detailed
factors. Thus food is of no moment as a disturber of the alimentary
tract, while bacteria and parasites are high in importance. The gastric
segment is more often attacked than any other portion and slightly more
often than in the nearest order, Carnivora. These unusual figures
deserve explanation, to which purpose it will be necessary to consider
the anatomy of the organ and to discuss why bacteria and parasites stand
so high in etiology.
Marsupials are divided into six families in our classification (see page
44) which in regard to their diet, range from largely carnivorous (the
first two) through those choosing mixed insects, fruits and vegetables
(the second two) to those eating vegetables and grain (the last two).
The stomach of these animals does not vary exactly according to their
diet, the first four, opossums, dasyures, bandicoots and wombats,
possessing an organ closely similar in outline and construction and
resembling the carnivorous variety, while the phalangers and kangaroos
have a stomach entirely different from the first four although somewhat
similar to one another. The first group has a round or irregularly
elliptical organ with the esophagus and pylorus close together along the
lesser curvature. The wombats have a bank of glands surrounded by a
capsule, near the cardia. The stomach of the first four animals is
divided into cardiac, fundal and pyloric parts by the construction of
their mucosa, the first mentioned division being a high, rounded pouch,
rumen-like, well to the left. The phalanger’s stomach is more elongated,
the two openings well separated and a fissure is found in the right end
of the lesser curvature which serves to separate the pyloric part from
the rest. The Macropodidæ all have a stomach resembling the human colon
in being elongated, with longitudinal bands gathering it into
sacculations. There is a distinct esophageal section to the left with a
blind sac suggesting an ungulate rumen, a long tubular fundal, and a
sacculate pyloric division.
The small intestine of the order starts with the opossums as a stout
muscular and mucous tube fitted for meat eating, but as one proceeds to
study the families downward in the list this tube becomes more delicate
and longer. In the first two families the cecum is rudimentary and the
colon very short as in cats, but the length and capacity of these parts
increase through the bandicoots and wombats until in the strict fruit,
vegetable and grain eaters, phalangers and kangaroos, the cecum is long
and capacious and the colon relatively long and roomy.
TABLE 13.
_Showing the Incidence of Gastroenteric Disease in the Two Forms of
Marsupial Intestinal Tracts._
═══════════════════════╤═══════════════════════╤═══════════════════════
│ Group A │ Group B
│Carnivorous Stomach and│Herbivorous Stomach and
│ Intestines 103 │Intestines 73 Specimens
│ Specimens Per cent. │ Per cent.
───────────────────────┼───────────────────────┼───────────────────────
Acute gastritis │ 9.6 │ 15.
│ Bacteria Verminous │ Bacteria Verminous
Chronic gastritis │ 0. 13.6 │ 5.4 0.
Acute enteritis │ 2.9 │ 1.5
Colitis incl. typhlitis│ 1.9 │ 4.3
───────────────────────┴───────────────────────┴───────────────────────
Table 13 contains an analysis of the forms of gastroenteritis as they
were described in the two groups of tracts, that resembling the
carnivorous, that similar to the herbivorous intestinal construction,
and according to the factor believed to be responsible. In the first
group gastritis of an acute nature occurred in 9.6 per cent. of the 103
specimens. They were chiefly catarrhal in character and seem for the
most part secondary to verminous infestation; at least six of the ten
cases were associated with parasites. The process microscopically is
catarrhal and deeply infiltrative. Group B has a high incidence of
gastritis and here the evidence of bacteria or toxins is quite plain.
Several of the cases were in animals showing also Kangaroo disease of
the jaw with pneumonia or septicemia; the gastric lesion of
streptothricosis will be described under that heading. The character of
gastritis without jaw disease is somewhat different from that with it.
Pathologically the process is a congestive and superficially necrotizing
affair, forming upon the tips of the folds, small gray erosions or flat
shallow irregular ulcers, which upon histological study consist of loss
of tissue of the mucosa and some deep congestion with round cell groups
but no reaction deep in mucosa or submucosa. True catarrhal inflammation
has occurred, but not like in the opossums.
Chronic gastritis in the simple stomachs is almost exclusively in
opossums harboring _Physaloptera turgida_, a worm which fastens itself
more or less firmly in the mucosa and probably, with the assistance of
bacteria, causes sufficient irritation to produce a hypertrophic change
in the deeper layers and a destruction of the glands where it holds and
a distortion of those nearby. One is reminded that Fibiger found
spiroptera to be responsible for adenocarcinoma in rats; no tumor
formation has been found in these animals, although one opossum with
such a stomach had an adenocarcinoma mammæ. Small hemorrhagic spots may
occur in the deeper layers, possibly where the worms have bitten. The
rugæ are irregular or interrupted by knobs and papillæ.
Group B, stomachs showing chronic change, were all kangaroos. The three
cases resembled the infiltrating necrotizing lesions as discussed under
ulcers (page 175). The process showed an infiltration of the subsurface
tissues with a gray slough over the densest part. The mucosa as a whole
was irregularly rugous and spotted with red gray areas.
Altogether one gets the impression that in the simpler stomach, reactive
inflammation is most prominent, while in the colonoid stomach
degeneration is greater than reaction.
Intestinal lesions in marsupials are not common and not peculiar except
in that they carry out the pathological reaction as seen in the stomach.
The carnivorous intestine shows frank catarrhal changes, the herbivorous
presents congestions and superficial necroses. These two groups then
follow the descriptions as already given for carnivores and ruminants.
The colon presented in the first group, simple catarrhal or follicular
change. In the second division the lesions resembled those in the
stomach; they were only once of the three instances associated with
streptothricosis.
AVES.
The class Aves has been treated in the chart precisely as have the
mammals, but it is not possible to make the accurate diagnoses or to
separate groups of lesions according to anatomy as was done for the
latter class. Upon the average there is more gastroenteritis among birds
than mammals, but when looking for an explanation of this, it was
unfortunately necessary to enter in the “undecided” column of Table 11 a
very great number of cases. This column would be greater relatively were
it not for the parasites in parrots and gallinaceous birds, the entries
for which are high. Besides this fact and that the owl stands at the
top, the pigeons at the bottom of the list numerically, no further
general statements are allowable. There are several orders with high
values among those of which insufficient autopsies are at hand to cast
percentages.
The avian alimentary tract seems to have developed according to the
character of food the different varieties of birds consume if one may
judge by the construction of the bill, the gastric musculature and the
intestinal wall. Zoological classification has only secondarily
considered this point, it being made incidental to the habits and
habitats of birds. For this reason the orders as outlined on pages
44–46, placed as they are in historical evolutionary position, represent
with few exceptions groups which have differing diets and, by the same
token, differing gastrointestinal tracts. Classifications based upon
habits of life (Raptores, Cantores, Natores), prove likewise too broad
or too heterogeneous, while systems making character of food the chief
criterion though apparently correct in reasoning and helpful in certain
orders, (Accipitres, Galli) are found to present copious exceptions;
moreover we are imperfectly informed of the exact diet that many
families require or resort to in absence of their preferred food. I
shall therefore discuss the chief diseases and distributions according
to our classification, preceding the discussion by a brief résumé of the
anatomical peculiarities of the avian alimentary tube.
The first digestive burden falls upon the proventricle where the
principal juices are secreted while the muscular stomach or gizzard
assumes the duty of gastric mastication. The lateral muscular bellies of
its heavy wall grind the food and mix well the gastric juices. Its
mucosa probably supplies only lubricant. In birds whose food is hard,
corn and the like, this grinder is supplied with a dry horny internal
layer, while a thick, moist, soft, epithelial surface is sufficient for
carnivorous birds. All kinds of gradations exist between these extremes.
The mucosa of the proventricle is always soft, but quite deep to permit
the placement of compound tubular glands.
The relation of size of these two parts is subject to many
variations.[22] The proventricle is larger proportionately in meat
eating, fish-eating and fruit eating birds, the gizzard having the
greater size in granivora and insectivora. In certain birds the mucosa
of the two is separated by a very soft thin zone, an important fact in
Psittaci since at this place spiroptera seem to penetrate to the
glandular layer of both organs.
The duodenum begins in practically all birds, from a spherical cavity at
the pyloric end of the gizzard, to be accredited anatomically to both
sections. It passes downward, forms a long loop enclosing the pancreas,
its distal end lying under the liver and near the gall-bladder. Near its
end it receives the major bile and pancreatic ducts; smaller ducts from
the liver and pancreas may enter near the pylorus or elsewhere along the
loop. The small intestine is usually simple in its coils, but in the
birds that eat grain, grass and greens, may be long and complicated. So
too the colon, usually a very short segment, may be increased in the
just mentioned group while the ceca are only of any considerable length
in herbivorous birds. The length of the ceca is, according to Owen,
related to the availability of food and the need the bird may have for
exhausting the nutritive value of it. In carnivorous birds as in similar
mammals, the whole gut, but especially the hind-gut, is very short and
the ceca small or absent. But so they are in picarian birds which are
chiefly herbivorous, but may eat meat.
GASTRITIS.
The double-muscle stomach, that with the two lateral plates and tough
epidermal internal coating, is seldom the seat of disease. An excess of
greens in the diet sometimes seems to soften or macerate the lining,
while an excess of pebbles may cause erosions. Upon severe irritation
this internal layer assumes the appearance of tanned leather and may
crack. The proventricle of such a gizzard seems rather resistant to
disease, particularly one would say, to infective processes, for
catarrhal or ulcerative inflammation is uncommon. The saccular stomach
with uniform muscular walls continuous with those of the proventricle,
such as is seen in raptatory birds and parrots, offers a somewhat
different picture. The internal membranes of these organs are definitely
softer, seeming to swell with great ease, and the glands themselves are
smaller both at the fundus and outlet, a construction which may favor
their closure by swelling from simple congestion and edema. Catarrhal
and ulcerative processes are definitely more common in such organs than
in the first type or true gizzard.
ENTERITIS.
Enteritis of all orders is most outspoken in the duodenal loop, but a
determination of the lesion must be made with some care. All the signs
of intestinal inflammation—congestion, swelling and opacity, excess
mucus or mucopurulent covering—must be present to justify a gross
diagnosis of enteritis and even when these exist one fails at times to
confirm the finding by microscopical section. These changes may be
simulated by digestive activity so that it is but reasonable to demand
them all in a clear cut fashion before applying the term enteritis.
However, it is well known that cases in both human and veterinary
medicine giving a satisfactory clinical picture of this disease may fail
to show to the naked eye and under magnification the changes expected.
In the human being, the carnivore and the ruminant, the ileum presents
the most definite picture of enteritis. In the bird, the duodenum shows
the prominent lesions, and with the exception of specific diseases like
blackhead, is always involved when the smaller coil of small intestine
is affected. This is true whether the enteritis be nonspecific or be
associated with cholera of chickens, ducks or parrots.
The colon presents peculiar lesions in but few birds. Ulcerative and
necrotizing processes have been encountered in three orders, Psittaci,
Anseres and Herodiones, suggestively like the specific forms seen in the
ceca. Microscopy and one unsuccessful culture failed to reveal a mould
or protozoön. The condition appears as a gray white plaque in the
cloacal wall or it may spread up to the colon and around the urethral
orifices. At times it is superficial upon the mucosa and may be covered
by a pseudomembrane.
The chief interest in the ceca centres about enterohepatitis either of
heterakis and amœbic origin or that supposed to be due to coccidia or
Bac. scoticus. This specific form has been encountered only in Galli
(three of the four families). It has been so well described by Hadley,
Smith, Morse and Cushman that it is unnecessary to discuss it since we
have nothing to add to its pathogenesis or pathology. At a later time
some attention will be given to our experience with Quail disease. What
is more interesting from a comparative standpoint, besides having a
bearing upon blackhead, is the discovery of heterakis in the ceca, and
hemorrhage and fatty change in the liver without amœbæ or coccidia in
either place (unfortunately no bacteriology was done), in a Sebastopol
Goose (_Anser domesticus_), a bird which has ceca not unlike the
gallinaceous varieties. This is a single observation and must be treated
expectantly.
Microscopically the avian digestive tract in its various inflammatory
states presents a few noteworthy features. The primary reaction,
sometimes the only one, to irritation is injection of the vessels in the
villi or deeper mucosa. To this, however, is nearly always added a
granularity of the epithelium, without much evident mucus (goblet cell)
formation. When the epithelial degeneration is marked there appears a
round cell increase in the deep mucosa shortly followed by a similar
infiltration into the villi. True catarrhal enteritis as described for
the cats is not as common as some combination of the changes just
detailed, but when it occurs is best developed in the carnivorous avian
tract. The most striking cellular finding is the round cell of the
infiltrate. It is of the middle lymphoid size with clear protoplasm, or,
when late in the disease, may be small and so-called adult.
Polynuclears, unless eosinophilic, and endothelioid cells are rare.
The foregoing are general remarks concerning the pathology of the avian
tract, and we are now ready to discuss briefly the reactions of the
orders. I shall, however, omit mention of those in the right half of
Table 11.
Passerine birds are represented better than any other order because they
are more numerous in nature and therefore exhibited more generously in
collections. This order is not especially vulnerable as to its
alimentary tract, but this tube is often affected by tiny stones, bits
of rust from cages and by acute general nonspecific infections to which
these birds are quite susceptible. Upon many occasions intense
congestion with and without tiny hemorrhages in the duodenum are all
that can be found in the little birds and the diagnosis of enteritis is
put down. Only about one-tenth of these birds have shown more or less
definite catarrhal changes. Many birds have heavy infestation with worms
which may activate bacteria.
The Striges and the Accipitres will be discussed together because of the
similarity of their tracts and their diets. The reaction of their
gastric complex has already been mentioned and what was written there
can be extended to the intestine. The type of lesion is catarrhal and
seems to be “meat bred” although this cannot be proven. They never have
given positive heart’s blood cultures so that the disease seemed not to
be septicemic. Liver and spleen have harbored colon and paracolon
bacilli. It will be noticed that they have the highest incidence of
gastric disease.
Psittaci, birds with a tract similar to the last two but with a captive
diet of seeds, fruit and vegetables although they may eat small animals
and insects in the wild, present figures under bacteria and parasites
which explain the involvement of the alimentary organs. We have had two
acute outbreaks of what seemed to be fowl cholera, judging by the
pathology and the isolation of _Bact. gallinarum_ and we have frequent
deaths with the same gross anatomy from which bacterial isolation has
not been tried or was unsuccessful. At all events the enteritis of
parrots is often a definitely infectious affair. We have also isolated
_Bact. psittacosis_ on two occasions. Separation of the birds and
cleansing of the exhibition spaces seemed to stop the disease. The
lesions are hemorrhagic and superficially necrotizing in this group
whether or not they are septicemic. Some have also shown a follicular
appearance both grossly and minutely, one of which cases was associated
with _Bact. psittacosis_.
The effect of animal parasites is chiefly exerted, for this group, in
the proventricle where the S_piroptera incerta_ occupies the lumen and
penetrates the mucosa or burrows under the inner lining of the gizzard.
Enteritis is not especially associated with this infestation, death
resulting more from inanition than infection; some few cases have had
enteritis, others pulmonary disease.
Columbæ are not susceptible to disease in the parts under consideration.
This order seems to have some tissue resistance, for their lesions are
quite frankly catarrhal, more so than in most grain-eating birds.
The figures set against the Galli are swollen by the number of cases of
enterohepatitis of one sort or another. Extracting these from the total
leaves the order among the lowest. Their lesions are congestive and
hemorrhagic, although they may show catarrhal cases. They seem to be
able to summon mucus more readily than many other birds.
Anserine birds, though not very high in figures, present three
conditions worthy of note. In the first place, acute simple gastritis
occurs often, sometimes associated with foul green food, sometimes
without any apparent cause. From the number of times that foreign bodies
are present it seems probable that they contribute in some way.
Excessive stones and sand, bits of glass, collar buttons and the like
are sometimes found. Then the form of acute enteritis has always a
hemorrhagic tendency, at least in the submucosa, while the mucosa may be
swollen, opaque and covered with mucus. Upon histological study these
intestines show intense swelling by cellular infiltrate and
disappearance of the tips of the villi. The third observation concerns
what is apparently a subacute or chronic process although this is not
supported by microscopy. Certain birds will have a cast of mucus and
epithelial detritus rather closely adherent to the wall. Under the
microscope there may be slight evidence of chronic inflammation or there
may be little amiss. These birds have usually been large ones, and
several have come from the separate goose pens, not from the open lake
where many birds are kept.
The struthious birds deserve a word. They have had a great deal of
enteritis and mostly of infectious nature. Two instances have arisen
from bird diphtheria, one from cholera and six from what later seemed to
have been anthrax but was not diagnosed at the time. The character of
the lesions in the struthious intestine tends to be hypertrophic and
superficially erosive if not ulcerative. The changes are found with
greatest clearness in the lower duodenum and small coil.
CONSTIPATION.
Having discussed the inflammatory conditions of the gastrointestinal
tract we now come to the more or less definitely mechanical
abnormalities, whether or not they depend upon preëxisting inflammation,
and the subject of constipation will claim first attention. In the human
being this condition is the result of bad habits more than any other one
thing or all things together, I think it will be admitted. In the lower
animals perhaps no such thing as habit of defecation exists so that one
can with more certainty hold incorrect food, chronic catarrhs or
physical obstruction as responsible. Veterinarians look upon excess of
dry food and irregularity of work and food periods as the principal
causes of constipation. These factors do not hold in zoological
collections. As a matter of fact constipation is of minor importance in
this menagerie, but a certain few cases are worthy of note. It has been
mentioned in the diagnoses in only a little over 1 per cent. of the
total, and of these the records indicate its importance only ten times
(.2 per cent.); a few notes of these cases are appended. The first place
of incidence is taken by marsupials (six kangaroos and one opossum), the
second by ungulates (largely ruminants) and the third by Primates. It
will be noted that with exception of the opossum, herbivorous mammals
occupy the first places of incidence, carnivores falling well behind the
orders named. This condition is quite infrequent in birds and is usually
associated with the presence of seeds or parasites or with impaction in
the ceca.
Primates, almost exclusively feeders upon carbohydrate and soft protein
food, have shown as causes of constipation two outstanding conditions. A
low grade of colonic catarrh with excessive pouchings of this tube has
had constipation associated with it three times. One of these cases had
small coproliths in the diverticula, one other a fecal concrement in the
cecum. Another group of these cases with evidence of delayed passage of
feces shows chronic peritonitis with adhesions, one of which seems
certainly due to filaria in the peritoneal sac.
The seat of constipation in monkeys is practically always the colon. The
carnivores while occasionally showing hard fecal masses packed into the
colon, more often exhibit a constipation in the ileum. One case
presented a nearly empty colon with a long scybalum just above the cecal
valve. There is no peculiar associated pathology in the notes at my
command.
Ungulata, showing next to the highest incidence, has its stoppage
chiefly in the colon, but the lowest stretch of the ileum may contain
balls of feces. In nearly every case one finds some grade of colonic
catarrh. In two instances, there being a proctitis, it seemed as if the
animal voluntarily restrained from defecating because of pain. The caput
coli is the seat of stoppage in the Rodentia.
Marsupials give such a high relative incidence that especial search of
their records was made, without, however, very definite result. In three
of the seven cases an acute general infection existed, in one an acute
peritonitis which seemed to emanate from a small ulcer in the ileum, in
one an injury to the anal region was found while in the remaining two
the notes would suggest that the lower intestine was atonic, judging by
its distention, translucency and pallor. In five the stoppage took place
in the large bowel alone, in the others both divisions being affected.
It is often difficult to establish a diagnosis of constipation in birds
because many varieties form a long rather dry mass in the lower small
intestine, to be moistened in the cloaca for discharge. Still again the
groups with capacious ceca are apt to have them filled normally with
firm casts. Diagnoses of fecal inspissation and stoppage in the smaller
tube have been made seldom, but one must consider also the obstruction
offered by excessive urate collections either in the cloaca or lower
ileum which will amount to a constipation if the cloaca be over-dilated
and dried urates mixed with dirt or feathers cover the anal opening.
The causes of this condition in birds are usually mechanical,
inflammation being found in a small minority of cases. In the small
passerine birds, seeds, sand, or parasites form the commonest findings.
This is also true of parrots, while excessive urate collections are
noted for both these groups. The gallinaceous birds present two reasons
for fecal stoppage—disease of the ceca (see pages 205–6) and cloacitis
probably secondary to anal closure by excessive urate collection. Uratic
stones, varying from one to five millimetres in diameter, have been
found in the cloaca in several orders. In only one case, a pheasant, did
they cause ulceration and cloacitis. Sand, rust, grains and the like are
found frequently, and sometimes in groups of birds, indicating that the
specimens had not been put upon the correct flooring or caging. Unbroken
seeds may obstruct the lumen.
MECHANICAL OBSTRUCTION.
Although the following is not constipation it is well to cite at this
place an experience which amounted to mechanical intestinal obstruction.
A number of finches were subjected to postmortem and found to have whole
white millet seeds in their intestines, this being the only discoverable
cause of death. Investigation revealed that during the night mice ate
the canary seed in the pans, leaving only the millet, which the hungry
birds consumed whole. Small birds can take a few millet and crack them
when eating leisurely, but apparently not when hungry. When the food was
removed at night the trouble ceased.
Obstruction by sand is well illustrated by a peculiar form of pica, in a
goose, which is worth citing, and calls to mind the sand disease of
horses:
Canada Goose ♂ (_Branta canadensis canadensis_).
DIAGNOSIS.—Masses of sand in entire intestinal tract. The general
condition externally and internally is good. The crop is distended
like a sausage, quite firm and the overfilling is obviously due to
sand in which very few stones, which could be called pebbles, are
found. This mass continues into the esophagus making the whole tract
impassable for food. The mucosa is a little pink and dirt-stained in
places but is not visibly inflamed. The gizzard is contracted over a
mass of sand but no food. Sand in more or less definitely packed
condition is found all along the gut tract, in one place in the small
coil it being quite as tight as in the crop and no lumen remaining.
Sand and bits of shale are found in ceca. The organs are apparently
healthy, slightly pale perhaps, but certainly not distinctly anemic.
No infection exists. The aorta, just above renals, has a 15 mm. × 2
mm. pale opacity of same consistency as the rest of the vessel, just
perceptibly higher than surrounding surface.
“Sand disease” has occurred in a Persian Wild Ass (_Equus onager_)
causing in this case ulceration, perforation and peritonitis, a Common
deer (_Mazama virginiana_) and a Chapman’s zebra (_Equus burchelli
chapmani_). The collection of sand is always greatest in the caput coli,
but may coat the large bowel to the anus.
Larger and more definitely obstructive physical objects are found in
both mammals and birds. We have on record a lion (_Felis leo_) and a
tiger (_Felis tigris_), which swallowed pieces of bone large enough to
be stuck in the small intestine and completely occlude it. Smaller
objects like buttons have been found even in the passerine tract. Worm
masses may occupy such a large part of the lumen of the tube as to
constitute a physical obstruction. This is definitely less important in
mammals than in birds, especially in the passerine order of the latter
class.
Dilatation of the intestine aside from that occurring in connection with
fermentation, constipation or ileus, in other words chronic atonic
dilatation, has not been encountered. Acute dilatation has been found in
several orders under the picture known for domesticated animals. Its
pathology and incidence have already been discussed.
ILEUS.
Ileus or acute intestinal obstruction may be divided for our purposes
into intussusception, volvulus, strangulation and paralysis from
interruption of mesenteric circulation. Examples of all these varieties
have been encountered and illustrative cases will be cited. In so far as
incidence is concerned, the Ungulata and Carnivora greatly outnumber all
other orders, showing seven cases each; the sum total in all other
orders is but eight. Upon re-reading some of the protocols I have,
however, excluded three invaginations in the carnivores, one each in the
ungulates and rodents, as probably being postmortem or shortly
antemortem occurrences; two had very early peritonitis but other things,
sufficient to account for death, were present. These deductions bring
the total cases of ileus in mammals to seventeen. Five cases in birds
will be discussed briefly.
Primates present one case of volvulus, one of intussusception and one of
internal strangulation. The first displayed the entrance of four inches
of ileum into the colon with such swelling of the wall as to prevent
reduction. The exciting cause seemed to be an enteritis, the cause of
death a peritonitis. A white-collared mangabey (_Cercocebus collaris_)
was the victim of volvulus probably favored by an anomalous position of
the transverse and descending colon which lay to the right, the latter
traversing the abdomen obliquely from right to left to reach the pelvis.
The volvulus occurred in the ileum just above the cecum, the twisted
part being found adherent by the peritonitis. The third case is a
strangulation due to peritonitis from filaria and adhesions between
stomach and colon from a colitis and pericolitis due to cestodes, one of
which was found deeply implanted in the colonic wall.
Two cases of intussusception are noted (after deductions above) for the
Carnivora. They both occurred in the ileum, one restricted thereto, the
other extending into the colon. In both a vague history of being “off
their feed” or giving evidence of intestinal trouble could be obtained
from the keeper. The three excluded cases had invaginations in the
middle and lower small intestines but not at the cecal valve. Volvulus
did not occur in the Carnivora.
A paradoxure (_Paradoxurus hermophroditus_) died as the result of a
strangulation of a six-inch knuckle of gut which had passed through a
hole in the omentum. The animal had not been eating well for a month but
gave no signs by which this ileus could have been diagnosed. Perhaps it
had existed for sometime but only shortly before death had swollen
sufficiently to cause obstruction.
Having excluded a doubtful invagination in a small rodent there remains
an interesting though somewhat obscure case in a porcupine (_Erethizon
dorsatus dorsatus_). This animal suffered with an acute hemorrhagic and
catarrhal enteritis while the colon seemed free of change until the
rectum was reached. Here was a stretch of a foot with the purple,
lusterless but translucent appearance of a strangulated intestine
although no involution or twisting remained. This was looked upon as a
volvulus which had untwisted a few hours before death.
Intussusception was seen only once in the Ungulata, a tapir (_Tapirus
terrestris_) with chronic enteritis. Here the ileum had passed into the
colon for a distance of nine inches, it being much swollen and congested
but not gangrenous. Its condition warranted the idea that the process
was antemortem but a peritonitis had not arisen, death having occurred
from the slight extra shock in an animal suffering with chronic
malnutrition. Volvulus was encountered three times, two deer and a
zebra. The last was the animal already described that carried such a
heavy load of sand in the gut tract, a factor in the production of the
twist probably although this might have been aided by a fibromyoma of
the colonic wall. The location of the volvulus in this order was twice
in the dilated descending colon, the third in the jejunal area. This
last was a twist which resembled an internal strangulation because of
the intricate knot-like windings of the small bowel.
The marsupials present two interesting cases. A rock kangaroo
(_Petrogale pencillata_) had chronic gastric ulcerations with local
peritoneal adhesions which apparently obstructed nearby coils of
intestine so that they became inflated and twisted over. An opossum had
a volvulus of the stomach which performed one and a half turns from left
to right; its protocol follows.
Common Opossum ♂ (_Didelphys virginiana_). Ileus. One and one-half
complete volvulus turns of stomach on duodenum. General condition
fairly good. Abdomen quite prominent, a condition found to be due to
great dilatation of the stomach which occupied the whole anterior part
of the abdominal cavity. The organ is blue and the vessels stand out.
Postmortem changes are occurring everywhere favored by the obstruction
to the circulation. The dilated stomach has undergone a volvulus upon
the third part of the duodenum making one and a half turns. The spleen
lies upon the right side well below the liver; it is swollen, soft and
deep purple. The duodenum in its upper half takes part in the
dilatation and beginning gangrene. The pedicle of the twist is made of
the duodenum, esophagus, edge of the mesentery and the middle part of
the pancreas; the end of the tail of the last is gangrenous. There is
no apparent obstruction lower down to explain the twist of the
stomach.
Among the Aves the following cases only are worthy of report. A parrot
(_Melopsittacus undulatus_) was found to have a tightly packed mass of
worms in the end of the duodenum above which the bowel was distended,
elongated, doubled on itself and of a deep red color; below this the
small intestine was empty. A closely similar condition was found in a
Screech Owl (_Otus asio asio_) the obstruction occurring just above the
end of the small gut. A Sparrow Hawk (_Falco sparverius_) had an
invagination two cm. in length, a short distance above the end of the
small intestine. No peritonitis existed but the presence of an acute
enteritis helps to explain the intussusception.
HERNIA.
Hernia is not a common occurrence among the lower animals but our
experience is instructive in two particulars, to wit, its absence in the
orders preceding the Rodentia and the frequency of the traumatic
variety. There being no general remarks to be made upon the subject, it
seems well to give a summary of the findings in each of the seven cases.
A Western Fox Squirrel (_Sciurus rufiventer_) showed a diaphragmatic
defect on the right side, a rounded opening with smooth edges, through
which a loop of intestine had passed, entering behind the liver and
reaching into the pleura as high as the pulmonary apex where it was
adherent; this was probably of long standing. Two more loops were found
wedged in the diaphragmatic hole, one of which was gangrenous.
An Indian Antelope (_Black Buck_) (_Antilope cervicapra_) presented an
irreducible incarcerated but not strangulated umbilical hernia. The
peritoneum was fused with the aponeurosis at the ring but the gut was
not adherent at this point while it was attached within the sac outside
the muscle, thus forming the incarceration. Apparently the sac had
dissected between the muscular layers for it could be followed for
several centimetres in some directions. A Hog Deer (_Cervus porcinus_)
had apparently suffered an injury in the flank for at one point the
muscles were irregularly cicatrized and a rent was present through which
several loops of intestine and a band of omentum had escaped, being
adherent to fascia. No injury to the skin was apparent.
Another Indian Antelope showed a clean traumatic rupture of the muscle
_and peritoneum_ in the right inguinal region _without_ penetration of
skin. An acute hernia had occurred which was lightly adherent to fascia
and an acute peritonitis was beginning. The bowel was however not
strangulated.
An aoudad (_Ovis tragelaphus_) seems to have suffered an injury by a
pointed object (horn?) just to the right of the ensiform cartilage for
at this position there is a circular hole, with smooth healed edges, in
the aponeurosis, permitting the emersion of a peritoneal sac containing
omentum. All parts were adherent but no acute inflammation existed.
What may have been a hernia or a relaxation of the transversus perinei
was observed in an Undulated Grass Parrakeet (_Melopsittacus
undulatus_). A bulge about the size of the finger end was seen
externally, beside and behind the anus. This proved to contain several
loops of bowel and a mass of fat.
A lateral abdominal hernia was seen in a Barbary Turtle Dove (_Turtur
risorius_). It consisted of a peritoneal sac and two loops of intestine.
This protrusion, while firmly fixed in its unnatural position, was in no
way constricted.
RECTAL PROLAPSE.
Prolapse of the rectum may in a sense be looked upon as a hernia or at
least as a relaxation of the anal and perineal muscles with protrusion
of parts normally situated intracorporeally. Although not frequent it
has been incurable in the animal, as it frequently is in man without
operation, a measure we have not adopted. Just what determines weakness
in the pelvic outlet is entirely obscure for indeed we have seen here
wounds and inflammations of the perineal area without prolapse of the
rectum and in none of the cases of prolapse did the pelvic floor seem
injured or diseased. It is but speculation to blame the annular muscles
of the anus. Tenesmus, or at least reasons for this straining action,
have been sought, with the result that in our cases lesions of the egg-
laying apparatus in birds and enteritis in mammals have stood out most
prominently. In no case have hemorrhoids been encountered nor has a
tumor pendant from the colonic mucosa, drawn the bowel toward the anal
opening. It might be added parenthetically here that hemorrhoids are
practically unknown for quadrupeds, Hutyra and Marek failing to mention
them independently and only one reference being found in the
_Jahresbericht fur Veterinär Medizin_ (Schmidt 1914–169); this case is
more like angioma than hemorrhoids. If tenesmus be active in the
production of rectal prolapse then it would have to be assumed that this
straining effort can be induced by enteritis since eversion of the
rectum has occurred with this disease in the absence of colitis, the
condition usually expected in the presence of tenesmus. The thirteen
cases have been seen in Mammalia, 8, (Carnivora, 2, Rodentia, 1,
Ungulata, 3, Edentata, 1, Marsupialia, 1) and Aves, 5, (Passeres,
Picariæ, Striges, Psittaci and Galli each one). Three mammals had
enteritis, one had foreign bodies in the bowel and one had many
ascarids; three had no demonstrable or suggestive causes. Two of the
five birds had enteritis high in the tract, one had uratic calculi in
the cloaca, and three had trouble in the egg-laying apparatus: one too
large an egg, one a broken egg and one a salpingitis.
DIVERTICULA.
It is almost certain that in a human pathological service of fifty-five
hundred autopsies, one or more diverticula of the Meckel variety would
be encountered and perhaps several of other kinds. In our material only
pouchings or false diverticula of the colonic wall are recorded, and our
personnel has often spoken of the absence of these gross abnormalities
of the alimentary tract. The two cases, notes of which are given, are
instances of hernial pouchings of the colonic mucosa and serosa, a
condition which is well known in human medicine. It may be said to occur
in two varieties, one in which the pouchings have heavy walls formed by
a thickened mucosa, muscularis and peritoneum and one in which the
bulgings have delicate walls, then being small herniæ of the inner coats
through rifts in the outer. Such a division is probably unnecessary or
misleading since the latter may be only a forerunner of the former.
However the clinical evidence of the simple variety is scanty and may be
little more than constipation while the peritonitic variety gives a
clinical picture of pain, constipation and a mass in the left abdominal
area, then known as diverticulitis or pericolitis sinistra. In these
cases the colon is much distorted by the irregularity of its mucosa and
by inflammatory thickening of the muscularis and serosa. Diverticula
arise from defects of the muscular coat, or secondarily after
inflammation or prolonged constipation, by weakness of muscle, or as
hernial protrusions around the entrance of blood vessels where the
muscle is thin. Such sacculations permit feces to collect and continue
the inflammation, thus further weakening the gut and producing
constipation, the whole vicious cycle being favorable to the formation
of more sacculations; coproliths may form in the diverticula. The two
monkeys now reported seem to have varying grades of the same condition,
a long standing colitis with diverticula, constipation and the
collection of inspissated feces in the sacculations. These animals did
not have hemorrhoids.
Black Ape ♀ (_Cynopithecus niger_). Coprostasis. Coproliths in
diverticulum. Chronic colitis. Cor bifida. The large intestine is of
the same calibre as the small intestine should be when not distended.
The sacculations as seen before opening the organ are salient, forming
distinct pouches. In one or two cases they are so pronounced as to
constitute diverticula 7 cm. long. In two instances the serosa at the
fundi of these diverticula is markedly hyperemic and very thin. In
many cases the sacculations contain coproliths. The wall of the organ
is distinctly thickened, puckered, inelastic and opaque. Mucosa is
thrown up into coarse rugæ.
Japanese Macaque ♂ (_Macacus fuscatus_). Chronic hypertrophic colitis.
False diverticula of colon. The large intestine contains a moderate
quantity of quite constipated feces. The serosa is smooth. The wall
shows at several stretches enlargements of the normal sacculations,
forming false diverticula. The wall of the gut in these herniæ is
thinner than in the surrounding parts; no ulcers exist; no local
peritonitis is present. The mucosa everywhere is irregular in
thickness, less translucent than normal and thrown into irregular
rugæ; tenacious mucus covers it. No ulcers.
TUMORS.
Only one tumor was observed in the mammalian intestinal tract proper.
Dasyure (_Dasyurus maculatus_) Adenocarcinoma of the intestines. On
postmortem there was a pale diffuse thickening of the coats of the small
gut over a large area; numerous soft, light yellow, sharply
circumscribed, elevated (like secondary tumors) nodules in the liver and
spleen, and a pea-size whitish nodule around a bronchus in the right
lung. Histological section of primary growth not made but a cross
section of the intestine in the vicinity shows an adenomatous change
with considerable increase in the connective tissue. The nodules in the
liver, spleen and lung and the appearances of the abdominal lymph nodes,
found microscopically, are precisely similar. They consist of
irregularly arranged epithelial nests and distorted acini, around which
are sharply outlined spaces, filled with the remains of degenerated
blood or a granular material. The metastases are always sharply
outlined.
Aves supply three papillomata which are interesting in that one occurred
in the proventricle, and two grew in the duodenum in the vicinity of the
upper biliary opening and presented within the lumen soft masses which,
while not occluding the passage, offered some little obstruction as
indicated by a slight distention above their location. In two, carefully
studied, no indications of parasites or of cancer could be found. The
birds concerned were an amazon, an owl, and a rhea.
SECTION VII
THE ALIMENTARY TRACT, PART 2. THE LIVER
A consideration of the liver is anatomically and physiologically the
next step in the discussion of diseases of the alimentary tract. While
this organ may participate in most of the pathological states of the
tubal part of the system, it is comparatively seldom the primary seat of
change and when damaged seems to be possessed of great accommodative and
reconstructive power. This must be true, and fortunately so, since we
ascribe to it the major detoxicating function of the body. Nevertheless
it is noteworthy that the largest solid organ of the animal body shows a
relatively low percentage of changes threatening to life. In the sense
of Pearl’s method of statistics, it does not “break down” easily. In
pathology it is the custom to list with great care all the changes,
gross and minute, in the liver, but with a few exceptions they are
secondary or incidental. They do however reflect many things, especially
referable to diet and to chronic infection from the intestinal drainage
area. It is in these directions that the organ will be studied in the
following pages.
Anatomically the liver is situated in the right upper part of the
abdomen subjacent to the diaphragm in both mammals and birds, being held
in position by attachment to this transverse partition, by ligaments or
folds of peritoneum, and by the other abdominal viscera. Its general
relationships do not offer great variations since in all animals means
are afforded for a dual blood supply and an outlet for the hepatic
secretion, the bile, into the higher intestines. Naturally variations in
the size of the lobes are observed and there has been considerable
speculation as to their independence and association. From the
standpoint of comparative pathology, little can be ascertained to assist
in this matter unless the position of abscesses and hepatitis relative
to cholecystitis have a bearing; some discussion of this will appear
later. We have not observed any peculiar pathology of the lobes of
Spigelius and Riedel. In so far as the size and arrangement of the organ
is concerned a few general facts of significance may be mentioned.
It was formerly thought that the liver varied inversely as the size of
the animal but Magnan[23] and others have shown that the matter is not
so simple. In the first place if there be an actual mathematical formula
it is that the liver varies in size inversely as the surface area of the
body, but this is not the whole story. It seems that the relation of
size of the organ to its weight is not constant and that it is better to
judge of the organic capacity by the latter. In herbivorous animals,
both birds and mammals, the liver is lightest per kilo of body weight;
next in weight are in order, fisheaters, meateaters, insectivora,
seedeaters, fruiteaters and omnivora. There is besides this a roughly
inverse ratio between the size of the liver and the length of the
intestine and in the class Aves inversely as the size of the lungs also.
From the immediately foregoing statements it is apparent that a
bewildering variation occurs and that only rough measurements of the
relative volume of the liver are available. An attempt was made in the
Marsupialia, which present all the variations given, to discover if any
peculiar pathology corresponded with the above groups; as it was
fruitless, no change from our zoological treatment will be made.
Lobar arrangement varies from the relatively simple double avian type to
the manifold lobulations of the seal or the marsupial but I can find no
literature to indicate that lobes or lobulations have a direct effect
upon functions. There must be a difference of blood supply for in
certain infectious diseases like enterohepatitis and amœbiasis, the
cystic and extreme right lobes are more affected than the left parts of
the organ. In the bird this is not so difficult to follow since the
three divisions of the portal vein, while they combine at times in an
ampulla within the hilum of the liver, seem directed to certain lobes,
that from the left portal seeming to point toward the right side. The
avian portal system differs from the mammalian in having a large branch
from the renal area, the so-called renal-portal system, pass to the
liver, and by having a free anastomosis between the portal area and the
caudal vena cava whereby blood from the pelvic district may pass into
the general circulation without going through the liver. There is no
unanimity of opinion as to the function or importance of this
connection[24] and from the data collected here there is no peculiar
renohepatic pathology.
The gall-bladder is not a constant organ in either mammals or birds and
indeed it may be absent or present in very closely related species (Two-
toed Sloth present, Three-toed Sloth absent). When present in mammals it
is usually a dependent bag while in birds it commonly lies upon the
cystohepatic duct, between the liver and the last curve of the duodenum,
in some varieties filling from the bottom, the inlet being guarded by a
valve. This cystic duct in nearly all birds, comes exclusively from the
right lobe while the hepatic duct, with which the cystic has no
connection, is formed by combination within the liver of radicles from
both sides. It passes to the duodenum well in advance of the cystic
duct, in some birds, _e.g._, the Struthiones, very near the pylorus,
that is on the descending limb of the duodenal loop. By this means
obstruction to the biliary stream is rendered difficult. The common duct
combines with one of the pancreatic outlets in most mammals but the
abdominal salivary gland in lower animals has more often patent separate
ducts or multiple ducts than it does in man. Birds have one to four
pancreatic ducts separate from the biliary openings.
The gall-bladder is missing in most varieties of the following groups:
pigeons, parrots, wrens, ostriches, rheas, cuckoos, toucans among the
birds; most odd-toed ungulates, hyraces, Indian elephants, all deer,
peccaries, three-toed sloth, and many rodents. The varieties lacking
this reservoir are herbivorous in the main, true carnivores seeming
always to be possessed of such a structure. Among the important
herbivorous ungulates, Bovidæ, Tragulidæ, Camelidæ and Suidæ have this
bile reservoir almost without exception. Because of the interest now
being shown in the pathology of the gall-bladder and its passages and of
the pancreas, it was hoped that evidence of definite practical value for
human pathology would be at hand in our study if we divided the animals
into groups with and without a bile reservoir. The result is not
unequivocal but worthy of note; it is discussed on pages 238 and 255.
Microscopically the well known lobular arrangement of the liver is
rather faithfully carried out among the mammals albeit the most
systematic and complete architecture is to be found in the pig while the
marsupial seems the most disorderly, thus resembling the avian organ. In
the latter class all the parts are indistinct, the cells having an
unclear outline, the tubules being intricately wound and the
interlobular connective tissue being scanty and not anastomosing in a
definite framework. The intralobular reticulum is especially difficult
to detect. Groups of cells are often found at portal spaces; these are
large and small mononuclears and granular cells, probably of the
hematopoietic system. It is possible that blood formation is performed
in the liver and spleen in some adult birds but such a function is
denied for the mammal except under very unusual conditions of bone
marrow atrophy.
Glycogenic and fatty conservation is a function possessed by both
zoological classes as are the detoxicating and bile-producing powers.
However it is highly probable that urea and creatin in metabolism is not
cared for by the avian liver as it is by the mammalian, judging by the
researches of Paton and of Richet.
FAT DEPOSITS.
The care of fat by the liver is very well shown by examining the
incidence of fatty metamorphoses through the various orders. In the
first place Mammalia show a slightly higher percentage of fatty change
than do Aves and should show a greater difference were it not for the
large number of cases in two orders of the latter. Among mammals,
lemurs, rodents and marsupials store fat in the liver more than other
orders but in the second and third, it is chiefly the carnivorous
varieties that have this property. Just why the slothful herbivorous
lemurs should be first on the list is not evident especially since the
grain-eating Ungulata are least apt to present fatty livers. With this
exception, mammals with plentifully available hydrocarbons in their diet
are most apt to show its deposit in the organ under discussion. Among
the birds the gallinaceous varieties stand far ahead of all others, the
passerines following next. Galli show the condition in association with
acute infections, chronic diseases and in health. Unless there be
distinct reason for it at autopsy, it may almost always be said to be
normal. Passeres, especially the smaller forms, frequently come to
autopsy with such excessively large livers, and indeed with a very large
pad of abdominal fat, and nothing else, that one is compelled to look
upon this overburdened organ as incapacitated by the deposit. These two
orders increase the percentage value for the birds. Striges, Anseres,
and Accipitres also show a good number of cases but there is among the
Aves no such clear relationship between food fat and fat infiltration as
may be found in the Mammalia.
AMYLOID DEPOSITS.
Amyloid deposit is reported with reasonable frequency in domesticated
animals, causing in them a fairly definite entity, being as usual
related to the effects of long continued or repeated infectious disease.
Wild animals suffer from this condition but rarely and therefore to our
few cases will be given a short discussion separately. An Indian
Paradoxure (_Paradoxurus niger_) had patches of amyloid irregularly
distributed through the organ. The animal had a carcinoma of the head of
the pancreas, an obstructive biliary cirrhosis in a state of atrophy and
a chronic nephritis with arteriosclerosis. There was nothing peculiar
about the distribution of the deposit as there was in the next case, a
Badger (_Meles meles_) where amyloid was found around the interlobular
vessels and extending in the lobules along their canaliculi. This latter
case seemed without cause and we have considered it a primary
amyloidosis, the spleen, heart muscle, kidneys, intestines and other
structures being affected. (See Fig. 7.) A third mammalian case
concerned a Dasyure (_Dasyurus viverrinus_) which showed distinct
intralobular collections. Its cause was a chronic suppurative process in
the jaw bone.
Avian livers are somewhat more prone to show amyloid deposits, eight
cases being on record. Four occurred in the Passeres, one each in
Columbæ and Impennes and two in Anseres. Three were associated with
chronic infectious disease and two with well established nematode
parasitism. The remaining three, classed as primary, were not related to
any other lesions, in two the amyloid liver being the only finding.
The next abnormal deposition related to the physiology of the organ is
blood pigmentation. Normally hemic pigment is dispensed with very
rapidly but under unnatural conditions it accumulates. In only one order
is there any noteworthy percentage of hemosiderosis, the carnivores, the
remainder showing a very trifling incidence.
DEGENERATIONS.
Going further into the physicochemical alterations of the liver brings
us to consideration of those changes known as degenerations—
parenchymatous, fatty, hydropic, hyaline, all of which we shall group
under one heading. They occur in a great variety of conditions and do
not appear to be specific, nor as the records are analyzed do they
appear to occur preëminently in any one disease of the lower animals.
The percentages are however higher for orders and families whose diet
contains relatively more protein, carnivores, the higher marsupials,
accipitrine, and wading birds.
ACUTE ATROPHY.
A very important degenerative disease of the liver is acute yellow
atrophy or, better expressed, acute degenerative atrophy for it is a
total destruction of the whole or large parts of the parenchyma. It is
apparently toxic in origin being related to the toxemias of pregnancy,
to certain organic and inorganic soluble poisons; some cases arise
without discoverable cause. We have seen no cases in the mammal but two
in birds. Both were females, one in active ovulation, while the other
had no related pathology and the condition of the ovaries could not be
determined since they had been destroyed after death by rats. The
macroscopic and minute anatomy offers nothing new. Jaundice was present
but not intense.
HEPATITIS.
True inflammatory lesions are to be defined as some form of
parenchymatous change to which are added congestion, infiltration of
round or polynuclear cells, stagnation in the bile ducts or perhaps
actual degeneration of their lining cells. It seems necessary to
stipulate these things because in the chronic forms, usually called
cirrhosis, it is necessary to have all of them, plus efforts at
regeneration, in order to determine it as a chronic progressive process.
Acute hepatitis is a rare condition in mammals except when it is
combined with septicemia or severe enteritis. In birds on the other hand
the liver is, aside from the intestinal wall, perhaps the most frequent
seat of pathology in the abdomen. This is because of its almost constant
involvement in infective enteritis, and in such conditions as fowl
cholera, fowl typhoid, coccidiosis and cecal amœbiasis, all of which we
have sporadically. When one searches for special distribution among the
orders, only one of them stands out as having a high percentage, the
Galli, an order which seems to have a very vulnerable liver.
The macroscopic anatomy of hepatitis in birds is peculiar in showing a
definite swelling with spots of gray or yellow color, sometimes
coalescing to form irregular areas. These are much more definite than in
the mammalian organ where swelling and hemorrhage are the commoner
findings. These pale spots are of two origins. They may be focal
necroses of the hepatic cells, with or without circumferential
congestion or hemorrhage to make them stand out. In amœbic, coccidial
and typhoid livers such is the type of change. In septicemia and
cholera, the mottlings are made up of increased interstitial mononuclear
areas, with blood cells and shadow cells numerously present. I have seen
what was in all probability a stage of repair after both these kinds of
change. In the former, regeneration seemed to take place from adjoining
liver cells, there being in the section no evidence of increased bile
ducts to make new hepatic cells. It seemed also that phagocytes were
derived from blood cells and not from Kupffer’s cells. In the
infiltrative lesion disappearance of the liver cells from the groups
leaving compressed and deeply granular remnants was all that could be
determined. Regeneration seemed to be progressing in the manner just
outlined.
NECROSES.
The degenerative and infiltrative areas of acute hepatitis are simulated
by focal necroses in livers not the seat of a general hepatitis from
which they can be differentiated only by the microscope. These small
areas of local tissue death are quite common in all pathological
processes but are most common in the liver, possibly because of its
exposure to toxins from the intestine. Their exact origin is not
determined, various explanations being given. The somewhat distinct
distribution in mammals _versus_ that in birds may help in the final
decision. In the former, focal necroses are more often encountered
midway in the anatomic lobule and around the central vein whereas a
perivascular location seems the usual position in the bird.
Massive necroses of the liver may be of considerable importance in
veterinary medicine. They take their origin in several different ways.
The commonest in our records are those due to cecal coccidiosis and
amœbiasis (quail disease and blackhead) while from the primary seat of
these two infectious diseases, the cecum, may originate the virus of
nonspecific hepatic necroses. We have observed several birds, passerine,
psittacine and gallinaceous, which at autopsy showed a distention of the
cloaca, ceca, and lower small intestine with urates and slime but no
mural inflammation and a large area of necrosis in the liver. This
suggests perhaps a “white diarrhœa” but it did not occur in epizoötics
and other morbid anatomy of this specific disease was absent. These
frequent instances of association between the colonic area and the liver
seem to suggest the transfer of necrotizing organisms, just as amœbæ
travel, and to indicate measures to clean out the tract when birds
become “plastered.” Massive necroses also arise from mould disease, and
from infection with the necrosis bacillus, emanating from nearby
infectious foci, or _via_ the normal passageways from the intestine.
Massive areas of degeneration may form by the coalescing of numerous
foci, in any septicemic disease.
ABSCESS.
In man, amœbæ, flukes, cestodes and biliary tract infection are the
commonest causes of purulent collections within the liver. In the lower
mammals parasites play practically a solitary rôle at least as the major
influence in localizing the collection, bacteria from the intestine
doing the rest. We have one case of massive abscess in a porcupine
suffering with septic pneumonia, the suppuration in the liver being due
to the colon bacillus, the general septicemia probably being from
distemper. Monkeys have shown more abscesses than any other order, three
being observed. One was due to infestation with trichocephalus which had
apparently penetrated from the colonic wall into the liver through
adhesions formed between these two structures. Another seems certainly
amœbic but these protozoa could not be found, while the third followed
an ulcerative enterocolitis of unknown cause. Two cats were seen with
parasitic abscesses; one harbored _Distoma_ or _Clonorchis sinensis_,
the other a nematode of ascaris type.
The topographic distribution of these six hepatic abscesses was
interesting. The position of the abscess is not mentioned in one case
but of the remaining five three were entirely in the right lobe, one had
the major lesion on the right side and smaller separate abscesses spread
over the organ, and one with about equal distribution in all lobes. All
three confined to the right side were solitary.
Abscesses of considerable size are not met with in the bird as in the
mammal perhaps because the former does not form real pus, necroses
developing instead.
Congestion of the liver is a matter of small importance from the
standpoint of pathology unless it be of sufficient duration to cause
cyanotic atrophy and induration. However the facts that congestion of
this organ occurs three times as often in the mammal as in the bird and
that vascular cirrhosis has not been seen in the latter class, are
interesting and noteworthy. In addition ascites of hepatic origin has
not been seen in the birds. The explanation for this lies in the rich
anastomosis between the intestinal area and the caudal vena cava so that
the blood does not have to pass through the liver to reach the heart.
This arrangement would reduce the back pressure in passive congestion
and relieve the liver in the congestion due to toxic or inflammatory
distention of small vessels.
CIRRHOSIS.
The chronic inflammations or so-called cirrhoses of the liver have been
subjected to a great deal of study and many theories have been expounded
as to their cause and classification. Here is not the place to discuss
the academic question of nomenclature but rather to adopt an acceptable
working classification and to analyze our material thereon. A cirrhosis
is a chronic inflammation of the liver indicated by increased connective
tissue with evidences of degeneration and attempts at regeneration on
the part of the hepatic cells. Certain cases of increased connective
framework fail to show the last two features and, since they must be
grouped near the cirrhoses because of the prominence of connective
tissue, they are called _fibroses_, _perilobular in type_. Among the
instances carrying out the full stipulations are livers with evidence of
a perivascular fibrosis and obstruction, to which are added degeneration
and regeneration of the lobular margins; such are PORTAL CIRRHOSES in
human medicine associated with passive congestion in the intestinal
area, and ascites. In a second variety, fibrosis seems to succeed upon
obstruction to the biliary lumina or upon peribiliary inflammation,
BILIARY CIRRHOSES. The effects of this are to dam back bile with the
production of varying degrees of jaundice and for the inflammation to
spread into the lobules, thus distorting their internal architecture;
this form is therefore unlike portal cirrhosis which alters the size and
shape of lobules as a whole. Fatty change is very prominent in certain
cases and it has been a custom, perhaps without warrant, to put such
livers into a separate group. It may be that they represent a different
chemical process. When there exists for a long time a venous stasis in
the liver, necrosis is apt to occur in the cells subjected to pressure
and the absence of fresh blood. This gives rise to a “nutmeg” liver upon
which may succeed a definite perivenous fibrosis.
This then is a working classification of the hepatic cirrhoses. Perhaps
many slightly differing varieties might be constructed but this grouping
will permit comparison and contrast with human cases, and with instances
in the various orders. Because of the relatively small total, thirty-
two, it is perhaps unwise to attempt any conclusions as to distribution
but it is certainly noteworthy that twenty-six occurred in mammals. This
means 1.6 per cent. in mammalian autopsies against .2 per cent. in
avian. Among the former class the carnivores stand at the head of the
list, followed in order by the marsupials, ungulates, primates, and
rodents.
Carnivora have shown a few typical portal cirrhoses from a pathological
standpoint but only one, in a badger (_Taxidea taxus_), was combined
with the classical picture of intestinal hyperemia and ascites. Two of
the cases were combined with chronic enteritis which may, of course,
have been secondary but there was also a hyperplasia of the spleen which
bespoke some grade of infection. None of the four showed involvement of
the biliary tract. One animal, a skunk (_Mephitis mesomelas_), was
jaundiced; it had anemia, nephritis and enlarged spleen but no
intestinal inflammation; perhaps the associated anemia may have been
responsible for the pigmentation. Biliary cirrhosis occurred in two
Carnivora, in both associated with enlarged spleen and nephritis. One
showed jaundice and the other, with a huge liver from congestion and
interstitial infiltration, had a small ascites. Fatty cirrhosis was
diagnosed in a raccoon but this is viewed with some reservation because
this animal easily stores fat and in this case it may not have been a
part of the process. In none of the foregoing cases did parasitism enter
into the causation of the change and I shall always specify when such a
factor was probable. The only vascular cirrhosis in our records occurred
in a Gray Wolf incident to a longstanding myocarditis (Gray Wolf, _Canis
lupus mexicanus_, Myocarditis, Adenomatoid goitre, Chronic
gastroenteritis, Vascular cirrhosis of liver, Subacute diffuse
nephritis, Edema of lungs, pericardium, and peritoneum). Two examples of
perilobular fibrosis appeared in this order, a raccoon (_Procyon lotor_)
and a paradoxure (_Trichosurus vulpecular vulpecular_). The only
noteworthy feature was, in the former, a very marked biliary stasis on
the lobular margins and in the connective tissue; this animal was not
jaundiced.
Ungulata are normally well supplied with definite interlobular strands
which, in a few varieties, completely encircle the lobule but always
show as clear fibrous septa going out from the portal areas. This
richness of connective tissue renders more difficult a decision of
increase so that unequivocal degenerations and regenerations with
inflammatory changes have been demanded as criteria for cirrhosis. It
has been recognized that cattle get a definite increase in their
interstitial tissue without serious reaction in the parenchyma. With the
knowledge of these facts in mind it has been possible to detect two
distinct portal cirrhoses, two biliary cirrhoses and three perilobular
fibroses. It is however evident by examining the rest of the autopsy
notes that the chronic inflammations have had with one exception, little
influence on the animal’s life and death and the associated pathology is
not instructive in etiology. One old deer with the definite portal type
had ascites and intestinal hyperemia which hastened his end.
The type of cirrhosis in the marsupial is progressively inflammatory and
of the biliary variety. In two of the three cases there was active
infection somewhere in the body, one a long continued streptothricosis,
the other and more important a choledochitis with involvement of the
pancreatic head. The third case showed a nephritis and a
pericholedochitis and pericholecystitis. In all three there was definite
evidence of biliary obstruction within the liver and in the occurrence
of general jaundice.
Monkeys have presented one portal, two biliary, and one perilobular
cirrhoses. The London Garden reports a cirrhosis with gall stones in a
Chimpanzee. The case of the Barbary Ape is so good that it is quoted in
brief.
Barbary Ape ♀ (_Macacus innuus_). Found dead. Never known to be sick.
On exhibition nine years. Acute dilatation of stomach. Acute
gastritis. Portal cirrhosis of liver. Acute parenchymatous nephritis.
Chronic passive congestion of lungs. Chronic splenitis and
perisplenitis. Ascites. Mild passive congestion of abdominal
circulation. On opening the abdomen a dilated stomach occupies most of
the anterior part, displacing the intestines downward and backward.
The upper lobes of both lungs are uniformly deep red, soft, collapsed,
subcrepitant. Subclavian vessels—veins distended with red clot,
arteries with small amount of chicken fat clot. The heart is dilated
on the right side, filled with currant jelly clot. The liver is small,
surface hobnailed, edges rough, consistency tough, color brown.
Section surface glistening, moist, granular and opaque, mottled by
irregular brown areas separated by paler brown intercommunicating
bands. Gall-bladder is small, contains viscid yellow bile and duct is
patulous. Areolar tissue about the bile ducts is thick and opaque, the
duct wall itself is thick and yellow. Gall-bladder tightly attached to
capsule of liver. Spleen is slightly enlarged, soft and tough. Capsule
is smooth, opaque and thickened on gastric surface. The trabeculæ are
prominent, pulp mottled gray-red, few recent hemorrhages. Capsule of
the kidneys is smooth, strips easily leaving a smooth brown surface
with dilated vessels. Organ is soft. Section surface is glistening,
striæ wide and indistinct, glomeruli faintly visible. Microscopic
section of liver shows high grade of fibrosis almost entirely confined
to portal areas with a marked increase in bile ducts although no place
is found where these bile ducts are running into lobules suggesting
attempt at regeneration. Liver cells show high grade of fatty
degeneration in some places, whole lobules being necrotic. There is no
pigmentation and connective tissue is fairly rich in cells. Fibrosis
quite well advanced. Cells about equally fibroblasts, round cells and
polynuclears. Bile ducts very well preserved and cellular infiltrate
rather less directly around them than at other parts of connective
tissue. The section of kidney shows moderate congestion, granular and
vacuolar degeneration of epithelium generally distributed except in
proximal tubules where there is swelling and desquamation. Detritus
present in tubules and capsular spaces. Tufts swollen.
The biliary forms of Primates were associated in one case with an
undetermined parasite in the bile channels, in the other with
tuberculosis and chronic enteritis. In all the cases the relative
inconspicuousness of bile in ducts or in cells is worthy of mention. The
perilobular fibrosis in a small cebus was trifling in extent but was
associated with considerable round cell infiltration in isolated areas;
there was also nephritis, splenitis, and enteritis.
The only representative of the rodents is a capybara (_Hydrochœrus
hydrochœrus_), their largest variety. This case was originally described
as a typical Lænnec or Pictou cirrhosis but I now class it as a portal
form. The distinct insular arrangement of the lobules, the failure of
involvement of the bile channels and the ascites are reasons for the
present decision. The animal suffered also from tuberculosis (not in
liver) and myocarditis.
The Indian Elephant, “Bolivar” (_Elephas indicus_), an old specimen, is
the only member of his order to show cirrhosis. It may be considered as
a senile process in part but the extreme distortion and compression of
the lobules press the conclusion that it was a progressive inflammation.
[Illustration:
FIG. 18.—PORTAL CIRRHOSIS OF LIVER IN ATROPHIC STAGE. BARBARY APE
(MACACUS INNUUS). THE DILATATION OF THE STOMACH ALSO SHOWS IN
PHOTOGRAPH.
]
[Illustration:
FIG. 19.—ATROPHIC PORTAL CIRRHOSIS OF LIVER. INDIAN ELEPHANT (ELEPHAS
INDICUS).
]
Aves fail to show lesions which could be called portal cirrhosis, five
of their six cases being biliary and one fatty with signs of continued
infection. The macroscopic anatomy of the avian liver with chronic
fibrosing hepatitis is fairly uniform and suggestive. In the first place
it is grossly nodular, lumpy, not finely granular or “hobnailed.” The
sensation to the finger is resilient rather than tough. The color is
variable but green and dull purple are the usual shades. On section no
peculiarities present themselves unless it be that one can find pale
spots on a dark background, which may correspond to the mammalian
connective tissue strands. Microscopically the increase of cellular
groups at portal spaces and the extensive growth of connective tissue
between the liver columns are the noteworthy features. There is nothing
in mammalian cirrhoses to compare with the intralobular growth of fibres
in birds. There is of course no regularity so that the degree of
replacement or necrosis of parenchyma is hard to estimate. Bile ducts do
not proliferate but seem, once obstructed and surrounded, to succumb to
the inflammation. The six cases in birds are: Psittaci, 3, Galli,
Anseres, Struthiones each one. The cases in the last two orders were
associated with parasites, to which bacteria or toxin may have been
added. It is interesting to note that the two frankly progressive
obstructive biliary cases in the parrots showed general jaundice.
It was formerly customary in many quarters to speak of atrophic and
hypertrophic cirrhosis. Now it is generally thought that any form will
be large or small as growth and regeneration on the one hand, or
contraction, atrophy and degeneration on the other, may be predominant
at the time the organ is seen. It is perhaps misleading to judge by our
notes of what happens, but it is curious that in the thirty-two cases,
the pathologist could state only in seventeen instances that the liver
was larger or smaller than normal. This means therefore that the liver
of cirrhosis need not deviate greatly from its customary size. Nine of
the seventeen times the organ was considered smaller than normal, eight
times it was greater. These variations did not strictly correspond to
type, but the portal form, frequently called atrophic, was more often
small than was the biliary form.
Gastrointestinal disease accompanied cirrhosis in fourteen instances.
Nephritis was present nineteen times. The spleen was enlarged six times,
in all of which definite evidence of infection existed in the body.
Choledochitis existed four times, twice with biliary cirrhosis, twice
with perilobular fibrosis; cholecystitis existed twice, once in a
monkey, and once in a bird with parasites. Pancreatitis was seen in
three biliary cirrhoses and once in a perilobular fibrosis.
The relation of the existence of cirrhosis to the presence of a gall-
bladder is interesting. Among the thirty-two animals twenty-one have
gall-bladders, eleven have not. The exact number of animals in our whole
list with and without this structure, unfortunately cannot be given with
exactness. As nearly as I can figure it out, sixteen per cent. of our
animal posts have been on varieties without a gall-bladder, eighty-four
per cent. with it. This would make the absence of this reservoir a
factor favoring the development of cirrhosis since one-third of the
cirrhoses are in groups devoid of this bag, yet these same groups
supplied only one-sixth of the total postmortems.
GALL STONES.
Our experience with concrements in the biliary system is limited to six
cases which can be detailed in brief.
American Beaver ♀ (_Castor canadensis_) showed a soft purplish liver
with groups of tortuous yellow lines; these prove to be groups of
hepaticola with fatty degeneration around them, but successful
regeneration is going on; bile ducts are not seriously involved over
any great part of the organ; the bladder is distended greatly with
thin, yellow-green fluid; duct is not patulous; common duct narrowed
at middle and above this constriction lies a small concrement; bladder
contains two large and several small pale yellow-green friable stones;
mucosa injected and covered with mucopus; the pancreas is not
affected.
American Beaver ♂ (_Castor canadensis_) shows a slight bile
obstruction and pigmentation through the liver but no pus or
cirrhosis; bladder is collapsed containing only a little limpid brown
fluid; wall is slightly roughened but not opaque; there is a blue-
black stone 1.5 × 1 cm. free in the cavity; duct patulous; pancreas
and intestine not affected.
Brant Goose ♂ (_Branta bernicla glaucogastra_) liver shows slight
fatty change; bladder much distended, contains twenty-six small, quite
hard, greenish stones; one is impacted in the cystic duct which is not
patulous.
Pigtailed Macaque ♂ (_Macacus nemestrinus_) shows a normal liver;
bladder contains a small black concrement, very hard, no cystitis.
Polar Bear ♀ (_Ursus maritimus_) showed a chronic cholecystitis and
cholangitis, the stone (?) in this case consisting of a solitary,
black, friable mass, six mm. in diameter.
Mongoose Lemur ♂ (_Lemur mongoz_) showed a normal liver; bladder of
about normal size but the duct can be forced only by considerable
pressure; there is a small stone and a granule in the tortuous cystic
duct; no cholecystitis.
The specimens that are preserved show these to be chiefly inspissated
bile, those from the first beaver and the goose being the only ones to
rise to the dignity of gall stones; it would seem that there was plenty
of opportunity for calculi to form in the bladder of this beaver. In no
case is there a cholangitis or cirrhosis dependent upon cholelithiasis.
While stones have been shown as infrequent there is a condition of the
bile which may be quite important. In Passeres, Accipitres, and Striges
one frequently sees a very dense inspissation of the bile both in the
cystic area and in the lesser independent bile duct. This need not be,
indeed usually is not, associated with hepatitis or cholecystitis. There
is no one thing more common than another in relation with it but the
diagnoses most often made are enteritis, distention of the proventricle
and gizzard, and constipation.
INFLAMMATION OF THE BILIARY SYSTEM.
The biliary tract from its origin in fine intrahepatic radicles to the
bladder and to the end of the common or intestinal ducts is the seat of
many inflammations both acute and chronic, but since they are supposed
to lead to damage to the liver and pancreas and to the production of
gall stones, it is well to consider the system as a whole. As a matter
of fact separate analyses of cholangitis, choledochitis and
cholecystitis do not reveal different figures for each or for different
orders. The vulnerability of this tract is found to be directly as the
percentage of cirrhosis, to wit, the carnivores stand first, then the
marsupials, ungulates, Primates and rodents; among the birds the order
is Accipitres, Anseres, Struthiones, Psittaci, and Galli. It is
difficult in most instances to evaluate the various possible etiological
factors, but, due caution being exercised, gastrointestinal inflammation
could be held responsible in seventeen of the total of fifty cases. In
twelve of the seventeen this process was wholly or largely in the
duodenum. The next factor was general infection, at the head of which
pneumonia and “distemper” occupied about equal places. In marsupials,
the streptococcal and streptothrical infections to which these animals
are susceptible, was the prime factor. This group almost always has
definite signs of stasis both in the liver and, as indicated by
jaundice, in the general tissues. Pancreatitis was present in seven of
the fifty cases and in five of the seven, enteritis was also found.
Common duct stones were not observed. I shall have something to say
about pericholangitis and pericystitis under the head of pancreatitis.
TUMORS.
The liver presents a good share of the tumors appearing in solid viscera
but, with the exception of a few points, they offer little of interest.
In the first place three angiomata have been seen and while they may not
be tumors in the accepted sense of the word, may be considered briefly.
A single cavernous angioma was seen in a goose. It occupied a large part
of the right lobe but did not seem to affect mechanically the function
of the organ since conditions wholly foreign to the liver were the cause
of death. A leopard presented several small groups of telangiectatic
angiomata lying mostly at portal spaces, a few also under the capsule.
The liver of a thrush was likewise scatteringly beset with small
angiomata. The original notes and recent examination do not reveal
parasites or perivascular sarcomatous change.
Simple adenomata were observed in a woodchuck (_Arctomys monax_). This
diagnosis is made with the appreciation that nodular regeneration of the
liver after damage and in cirrhosis sometimes suggests tumor, but with
adenomata an increase of supporting framework may occur. The liver of
this animal presented numerous .3 to 10. cm. irregularly spherical,
encapsulated, firm or slightly resilient, brown masses which under the
microscope consisted of large pale vacuolated cells in columns or
strands not connected with bile ducts. The last feature speaks in favor
of the diagnosis of adenoma. The damage to the organ was probably
considerable and the portal circulation must have been impeded since
passive congestion and ascites were present. Enteritis and nephritis
seemed the causes of death.
Adenomata or fibroadenomata of bile duct origin were seen in four
animals, a Red Fox (_Canis vulpes pennsylvanicus_), a Gray Fox (_Canis
cinereo argenteus_), a Jaguar (_Felis onca_) and a Common Deer (_Mazama
virginiana_). The first two present similar pictures, pinpoint to 8.
mm., gray, well outlined areas some of which are clearly cystic, others
opaque and more solid. In the first fox a larger mass was found near the
hilum. Careful study and consultation has failed to discover parasites
in these cases, although their presence was strongly suspected, so that
we were forced to conclude, in view of the rather typical microscopic
picture, that they are adenomata of bile duct origin. Their scattered
distribution, but with a tendency to be more numerous beneath the
capsule, corresponds with a human case just brought to my notice. The
mass in the liver of the deer was single and resembled an infarct, with
cysts exposed by cross section. This tumor was found on the
diaphragmatic surface of the right lobe.
Tumors of an atypical, therefore malignant, epithelial variety were
found four times, in an Alpaca (_Lama pacos_) and three parrakeets;
these birds are very prone to have all kinds of tumors. The records of
the first animal could not be as satisfactory as might be desired
because of an advanced state of decomposition but there was a carcinoma-
like growth of the gall-bladder area and a large hard alveolated tumor
occupying one-half of the liver. The colon had been involved by the
former, with perforation. Two of the parrakeets showed a simple
carcinoma with well developed fibrous tissue bands running in all
directions through the large mass. The whole growth was comparable to
the usual picture of these massive tumors when they are primary in the
liver. All these three cancers seem to take their origin in the liver
cells but the third had such an interesting involvement of the
connective tissue that its minute anatomy will be given; it was
denominated adenocarcinoma sarcomatodes.
Undulated Grass Parrakeet ♂ (_Melopsittacus undulatus_). Section of
liver shows organic capsule normal. Nothing remains of the original
structure by which it might be recognized, suggestion in places of
granular cells resembling liver cells being only occasional
occurrences and in small numbers. Where liver cells do occur they are
highly granular in various degrees of atrophy and show various grades
of nuclear retrogression. Greatest part of section consists of dense,
white fibrous tissue in which lymphocytes are rather diffusely placed
together with large numbers of epithelium-lined spaces. These spaces
are often elongated after manner of imperfect ducts but are of
irregular form, have single layer of low cuboidal epithelium and
richly staining nuclei. Upon search certain acini are found to have
especially hyperchromatic nuclei and penetration of basement membrane.
In such localities collections of epithelial cells are to be seen in
plug form in lymphatics and acini of imperfect development of lumen
are found. In addition to these epithelial lesions connective tissue
ones are seen, occurring generally in restricted localities. The
interstitial framework is seen to consist of closely placed spindle
cells, some of which are especially elongated after manner of
imperfect ducts but are of irregular form, directed in a definite,
purposeful manner, but interlace in the whorling manner noted in
fibromas. Nuclei are, however, entirely too chromatic for a connective
tissue tumor. Whenever a vessel occurs in these regions its lining
endothelium is always swollen and nuclei in its wall will be
proliferated and of embryonic type. This latter condition is apt to
occur in patchy manner, part of wall appearing normal and other parts
containing these peripherated elongated nuclei.
Secondary tumors were observed in the liver seven times as follows: Red
Kangaroo (_Macropus rufus_) from malignant papilloma of the stomach;
Spotted tailed Dasyure (_Dasyurus maculatus_) from cancer in the small
intestine; Dorcas Goat (_Capra hircus_) from sarcoma in lymph nodes in
mediastinum; Raccoon-like Dog (_Canis procyonoides_) from mixed tumor of
thyroid; Undulated Grass Parrakeet (_Melopsittacus undulatus_) from a
brain tumor probably glioma; another of same species from a sarcoma of
pectoral muscle; European Robin (_Erithacus rubeculus_) adenoma of
adrenal (_hypernephroma_).
SECTION VII
THE ALIMENTARY TRACT, PART 3.
THE PANCREAS
The pancreas, an organ functionating as a gland with an internal
secretion and by pouring a digestive juice into the duodenum, remains a
structure of constant anatomy throughout the zoological classes under
discussion in that it is composed of compound racemose lobules whose
outlets join to form large discharging ducts, and of interstitial
bodies, the islands of Langerhans, without connection with the secreting
acini but having some relation with the blood and lymph vessels. The
organ originates embryologically by sprouts from the side of the
primitive gut just below the part destined to be stomach, and from an
outbudding of the common biliary duct. These two sprouts or pouches
combine to form one organ, but this does not necessarily effect a union
between their lumina. In some birds and mammals (Accipitres and some
Ungulata) the lobes of the pancreas remain distinct during life, and the
discharging tubules seem to empty only their respective lobes. However,
there is no uniformity in the matter, and indeed the anatomy of the
ducts is subject to very great variation despite the rather similar
beginnings of the organ. Those who are interested in this point may
consult Beddard,[25] Letulle and Nathan-Larrier,[26] and Opie[27]; there
will be given in the following pages the average findings of anatomy of
the gland body and of its ducts.
The region of the pancreas in lower animals, especially those which
travel constantly on four feet, is one of great activity, and the organs
are more freely movable than in the human being. The only exception to
the latter part of this statement may possibly be found in the cats and
dogs, in which there are firmer attachments of the duodenum and pancreas
to the vertebral column and the liver; this is brought about by the
short gastrohepatic omentum and the abrupt curvature of the duodenum
toward the back, under the mesenteric stalk. In the Ungulata and
Marsupialia and in some Rodentia, the pyloric, duodenal, and pancreatic
attachments are relatively loose, and torsion of the pylorus seems to be
allowed for, since in these animals great distention of the stomach is
the rule. Among the Aves the anatomy is wholly different. The birds have
no attachment of the duodenum and pancreas to the posterior abdominal
wall, except indirectly through a narrow strip comparable to the
gastrohepatic omentum, one division of which passes to the beginning of
the duodenum, the other to its end, and by a thin tail of pancreas which
goes toward the spleen. The bulk of the pancreas lies in the U made by
the long free duodenal loop, the two organs being covered by the serous
membranes forming the middle abdominal sac. It will be seen from the
foregoing that the movability of the pancreas is considerable—a highly
necessary provision, because the stomach and duodenum are also movable
and subject to distention by food and alteration of position during
flight.
In the class Mammalia there are usually two ducts, one entering the
duodenum in combination with the bile duct, the other variously above or
below this common opening. As will be seen in Table 14, however, there
are several exceptions to this statement, there being but one duct
opening independently of the bile duct. The general anatomy is closely
similar throughout this class, so I shall confine my notes to the
exceptions from the general rule, especially where they seem to be of
importance in the etiology of pancreatic lesions.
In the class Aves the pancreas consists usually of two or three distinct
lobes lying one in front and two behind the cleft between the limbs of
the duodenal loop, and it discharges its secretion into the duodenum by
two or three ducts separately, and almost invariably above the bile duct
openings. One duct always opens near the top of the distal end of the
duodenal loop, near the bile duct. In the gallinaceous birds that have a
bile duct opening into the duodenum near the pylorus, there is usually a
pancreatic duct opening there also. In some birds a third duct passes
from the body of the pancreas to the duodenum at different places along
the loop. It does not seem probable that dislocation of the duodenal
loop would seriously interfere with the passage of the pancreatic
secretions, since the gland is so intimately related with the duodenal
serosa, but obstruction to the biliary flow due to changes in position
of the intestine is easier because the bile duct is separate and loose
and arises from the end of the gall-bladder. The ducts of both these
structures pass very obliquely through the duodenal wall a matter of
importance, as will be seen when discussing the infiltrative forms of
enteritis. The gall-bladder is not present in all birds, but this is
probably of no importance, as the hepatic ducts are wide and run
directly from the liver to the duodenum. The pancreatic ducts are short
and are closely bound around by glandular tissue up to a place quite
close to their entrance into the intestine.
The musculature of the gall-bladder and the ducts seems comparable in
mammals and birds, and a constrictor or sphincter usually called the
muscle of Oddi, is present in all but pigeons (Oddi). There may be found
also muscular fibres in the major ducts of the pancreas, but they are
not so heavy nor distributed so definitely as similar tissue in the bile
duct walls. The mucosa of the pancreatic duct is much more folded in
birds than in mammals, seemingly, therefore, more adapted to obstruction
by swelling from any cause.
Passerine birds have two pancreatic ducts usually on the ascending loop
of the duodenum, or there may be one ahead of the pyloric biliary duct.
The picarian varieties possess three ducts as a rule, one near the
beginning of the pylorus, one near its end and a third of inconstant
location. Owls have a system like Passeres, but the relation between the
organ and the intestinal loop is looser and the ducts are wider. Columbæ
have two pancreatic ducts in the ascending limb of the duodenum.
Gallinaceous varieties have a double biliopancreatic system, a duct of
each kind entering the descending and the ascending duodenal reaches,
with the biliary placed after the pancreatic in each instance.
Accipitres have always two and oftentimes three ducts as do Anseres,
both orders frequently having the third duct opening at the bottom of
the duodenal loop where stagnation can and does occur. Fulicariæ have
usually three ducts.
The foregoing are the orders presenting pancreatitis and therefore those
whose anatomy concerns this study directly. The irregularity in number
and arrangement of ducts continues through all the avian orders which
show a greater aberration from standards than do the mammals.
Theoretically the birds should cast some light upon the unsettled
question of the causes of pancreatitis, and as a matter of fact such a
result seems to have been realized. In 1915 I published an article upon
a study of this subject which indicated that acute inflammations of this
organ may arise _via_ the lumen of the duodenum and pancreatic ducts,
while chronic processes were the result of periductal passage of
pathogenic agents. Further study would seem to indicate that disease of
the biliary tract is of importance in lesions of the pancreas since a
decidedly large number of cases is found in mammals, where the relation
of ducts is definitely more intimate than in birds. The work of
Archibald,[28] Deaver and Sweet,[29] and Judd[30] seem to agree with the
findings upon our material. This need not be, however, in discord with
the idea that acute inflammation is superficial in origin, chronic
lesions deep or lymphogenic. The discussion will be resumed in a
subsequent paragraph.
The amount of pancreas to be found in birds is greater than that in
mammals. According to our figures the organ represents ¹⁄₄₀₀th of the
body weight in the former and ¹⁄₆₀₀th in the latter. These figures are
averages of a small number of instances and are not final. It is,
however, obvious to casual daily observation that birds as a class have
a large pancreas.
The minute structure of the organ is governed by the same general rules
throughout the two classes under consideration. Birds do not have as
many interstitial islands as do mammals, but they are more compact and
seem more definitely constructed of coiled tubules. In so far as the
internal structure of the organ is concerned there has not developed in
our study pathology peculiar to any animal. The importance of the ducts
and position of the organ will be discussed later.
Recognition of pancreatic disease during life is practically impossible.
In human medicine the signs and symptoms are vague and inconstant,[31]
diagnosis often being a matter of exclusion. Veterinarians, except under
the best hospital conditions make no attempt to diagnose pancreatic
lesions but, since the improvement of surgical practice, at times
operate upon cases of evident pain and distention which prove to be
pancreatitis. These things were evident in a deer that I saw and that
died on the following day from acute hemorrhagic pancreatitis; I made no
attempt at this diagnosis, believing it to be acute tympanites. The
feces were normal, according to the judgment of persons qualified to
give an opinion.
The condition of the pancreas at autopsy on animals not dying with
lesions of this organ deserves some attention since it may confuse the
uninitiated. If the organ be seen in its normal resting stage shortly
after death, it is not difficult to recognize the condition as normal
for the species. Activity is indicated by a darker or redder color and
an increase of consistency. In carnivorous or omnivorous animals and
birds the pancreas in this state is a body with a distinct bulky
character, whereas in strictly herbivorous varieties, especially
ungulates, the structure is diffusely pink and doughy. This is important
since the early stages of self-digestion and decomposition assume this
same character in all varieties, while later stages present a deep red,
swollen, wet organ. These appearances must be differentiated from acute
hemorrhages or inflammations, a distinction based upon actual local
blood collections or extravasations and areas of degeneration in true
disease. Oftentimes differentiation must be made under the microscope
and in advanced decomposition, determination is impossible. When there
is torsion of the stomach, notably in ungulates, the pancreas is often
found decidedly congested. This, it seems, is due to a twist of the
duodenum and passive congestion of it and the pancreas—the only simple
explanation despite the apparent provision for a high degree of
mobility, as already explained. The organ is nearly always mildly
congested in severe grades of acute duodenitis, although it need not be
pathologically involved. It is, however, noteworthy that the pancreas is
an organ with a low morbidity index, especially when one considers its
proximity to a structure showing the highest disease index in the body,
the intestine. The succeeding paragraphs will reveal in comparison to
other organs only a small number of cases of degeneration, inflammation
and tumors. This has been ascribed to the freedom of blood supply and
the power of tryptic digestion.
An expression of this relative immunity to pathologic change is met in
analyzing the data upon the simplest lesions, degenerations, to be
expected in many states of disease. Only a small number of cases present
themselves, and they are under expected conditions, namely in
association with acute general infection, sometimes definitely
septicemic in nature. About half of them were discovered
microscopically, affecting the islands of Langerhans in vacuolization or
granular disintegration. Focal necroses of the organ were met four
times, three turkeys and a cockatoo. It is noteworthy that all these
birds had some involvement of the liver, twice a complete acute
hepatitis and twice a cholangitis. This is the more interesting since we
shall learn that the liver is less often involved in avian than in
mammalian pancreatitis. Hemorrhages occur occasionally in the pancreas
in acute general infections and are seen in acute inflammations of the
intestines; the percentage incidence with the latter is, however, very
small. Pancreatic apoplexy proper has not occurred, for all the
instances of large hemorrhage into the organ have been combined with
changes forcing a classification of acute pancreatitis.
PANCREATITIS.
Pancreatitis in the acute form is divided by many writers into
exudative, hemorrhagic and necrotizing, while for the chronic variety an
inter- and intra-acinus form has been described. It is questionable
whether it is fair in acute cases to focus attention by special
nomenclature on different macroscopic pictures, unless it be for
descriptive purposes solely, since there is nothing at hand to indicate
that differing agents cause one kind every time. The physical findings
seem to depend rather upon the speed of operation of the causation than
upon its essence. Sudden obstruction of the pancreatic duct is believed
to produce necrotizing processes to which hemorrhage may be added by
digesting of blood vessels. Exudative cases seem due to extension of
ulcerative inflammation, from a perforated gastric ulcer for example, to
which digestive pancreatitis may be added. The interacinus chronic
inflammations are usually considered as due to obstruction or infection
through the biliary or pancreatic ducts whereas vascular disease
produces intra-acinus connective tissue overgrowth. Analysis of the
records of this laboratory would seem to indicate that necrotizing and
hemorrhagic processes belong together, exudative in a class by
themselves, and that chronic disease may be either interlobular or
intra-acinar without regard to associated pathology. I have therefore
studied our cases from this standpoint.
Pancreatitis has occurred in thirty-eight mammals and birds among the
5365 autopsies, an incidence of 0.7 per cent.; class incidence in
mammals twenty-seven or 1.5 per cent.; birds eleven or .3 per cent.
(Table 14.) Among the higher class all the important orders are
represented, but by no means in equal degree, whereas in the birds, less
than half of the orders are listed, with the important Psittaci missing,
despite a high death rate.
It is perhaps well to be guarded in stating the relative vulnerability
of the pancreas in various orders, but one cannot avoid the observation
that Carnivora stand well in advance of the others (3. per cent. of
autopsies), to be followed by Ungulata (1.9 per cent.) and Rodentia (1.7
per cent.). Nor can one fail to see that mammals have inflammations of
this organ five times as often as do birds.
TABLE 14.
_Showing Cases of Pancreatitis, their Pathological Nature, the Character
of Ducts of the Particular Animal, the Associated
Pathology, All of Which Data are Collected at the Bottom into Totals for
Zoological Classes and Orders._
════════════╤════════════╤════════════╤══════╤═════╤═════════════
Order │ Acute │ Chronic │Number│Open │Cholecystitis
│Hemorrhagic │Pancreatitis│ of │with │
│ or │ │Ducts │Bile │
│Necrotizing │ │ │Ducts│
│Pancreatitis│ │ │ │
────────────┼────────────┼────────────┼──────┼─────┼─────────────
Primates: │ │ │ │ │
Marmoset │ │Chr. Dif. │ 2 │ 1 │ 0
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
Carnivora: │ │ │ │ │
Wolf │Ac. Hem. │ │ 1 │ 1 │ ?
Fox │Ac. Hem. │ │ 1? │ 1 │ 0
Bear │ │Chr. │ 1 │ 1 │ 0
│ │ │ │ │
│ │ │ │ │
Raccoon │ │Chr. sl. │ 1? │ 1 │ 0
Bear │Ac. Nec. │ │ 1 │ 1 │ 0
Coati │Ac. Hem. │ │ 2 │ 1 │ 0
Badger │Hem. and │Chr. │ 2? │ 1 │ ?
Ocelot │Ac. Hem. │ │ 2 │ 1 │ +?
Bear │Ac. Hem. │ │ 1 │ 1 │ 0
Wild Cat │ │Chr. │ 2? │ 1 │ 0
Lion │Ac. Hem. │ │ 2? │ 1 │ 0
Skunk │Ac. Nec. │ │ 2? │ 1 │ ?
Raccoon │Ac. Nec. │ │ 1? │ 1 │ 0
│ │ │ │ │
Rodentia: │ │ │ │ │
Beaver │Ac. Hem. │ │ │ 1 │ 0
Porcupine │Ac. Hem. │ │ │ 1 │ 0
Ungulata: │ │ │ │ │
Antelope │Ac. Hem. │ │ 1 │ 0 │ 0
Deer │Ac. Hem. │ │ 1 │ 0 │
Deer │Hem. │ │ 1 │ 0 │
Deer │Hem. │ │ 1 │ 0 │
Elk │Ac. Nec. │ │ 1 │ 0 │
Nylghaie │Ac. Hem. │ │ 1 │ 0 │ 0
Peccary │Ac. Hem. │ │ 2 │ 1 │ 0
Marsupialia:│ │ │ │ │
Phalanger │Ac. Nec. │ │ 1 │ 1 │ 0
Opossum │Ac. Nec. │ │ 1 │ 0 │ 0
Opossum │Ac. Nec. │ │ 1 │ 1 │ 0
Devil │ │Chr. │ 2? │ 1 │ +
Passeres: │ │ │ │ │
Finch │ │Chr. │ 3 │ 0 │ 0
Thrush │Nec. and │ │ 3 │ 0 │ 0
│Hem. │ │ │ │
Chaffinch │ │Chr. │ 3 │ 0 │ 0
Picariæ: │ │ │ │ │
Hornbill │Acute │ │ 3 │ 0 │ 0
Striges: │ │ │ │ │
Owl │ │Chr. │ 3? │ 0 │ 0
Accipitres: │ │ │ │ │
Kestrel │ │Chr. │ 3? │ 0? │ 0
Columbæ: │ │ │ │ │
Dove │ │Chr. │ 2 │ 0 │ 0
Galli: │ │ │ │ │
Pheasant │ │Chr. │ 2 │ 0 │ 0
Fulicariæ: │ │ │ │ │
Gallinule │Ac. Hem. │ │ 3? │ 0 │ 0
Anseres: │ │ │ │ │
Gadwall │Ac. Hem. │ │ 3? │ 0? │ 0
Struthines: │ │ │ │ │
Ostrich │Ac. Hem. │ │ 3? │ 0? │ 0
════════════╪════════════╪════════════╪══════╪═════╪═════════════
_Totals_ │ │ │ │ │
Primates │ 0 │ 1 │ │ │
Carnivora │ 10 │ 4 │ │ │ 4?
Rodentia │ 2 │ │ │ │ 1
Ungulata │ 7 │ │ │ │
Marsupialia │ 3 │ 1 │ │ │ 1
────────────┼────────────┼────────────┼──────┼─────┼─────────────
_Mammalia_ │ 22 or 1.1% │ 6 or .32% │ │ │ 6
Passeres │ 1 │ 2 │ │ │
Picariæ │ 1 │ │ │ │
Striges │ │ 1 │ │ │
Accipitres │ │ 1 │ │ │
Columbæ │ │ 1 │ │ │
Galli │ │ 1 │ │ │
Fulicariæ │ 1 │ │ │ │
Anseres │ 1 │ │ │ │
Struthiones │ 1 │ │ │ │
────────────┼────────────┼────────────┼──────┼─────┼─────────────
_Aves_ │ 5 or .14% │ 6 or .17% │ │ │
Grand Total │ 27 or .5% │ 12 or .22% │ │ │ 6
────────────┴────────────┴────────────┴──────┴─────┴─────────────
════════════╤═════════════╤═════════╤═════════════╤═════════╤═════════
Order │ Cholangitis │ Hepatic │Inflammation │ Acute │ Chronic
│ or │Cirrhosis│ outside │Enteritis│Enteritis
│Choledochitis│ │ Pancreas │ │
│ │ │ │ │
│ │ │ │ │
────────────┼─────────────┼─────────┼─────────────┼─────────┼─────────
Primates: │ │ │ │ │
Marmoset │ 0 │ 0 │Lymphadenitis│ 0 │ 0
│ │ │ adjacent │ │
│ │ │ glands │ │
│ │ │ │ │
Carnivora: │ │ │ │ │
Wolf │ + │ 0 │ 0 │ + │ 0
Fox │ 0 │ 0 │ 0 │ ? │ 0
Bear │ 0 │ 0 │ Areolar │ + │
│ │ │ tissue and │ │
│ │ │ glands │ │
Raccoon │ 0 │ 0 │ 0 │ 0 │ 0
Bear │ 0 │ 0 │ Slight │ + │ 0
Coati │ + │ 0 │ 0 │ 0 │ 0
Badger │ + │ Atr. │ 0 │ 0 │
Ocelot │ +? │ 0 │ 0 │ + │ 0
Bear │ +? │ 0 │ 0 │ + │ 0
Wild Cat │ 0 │ 0 │ 0 │ + │ +?
Lion │ 0 │ 0 │ 0 │ + │ +
Skunk │ + │Infective│+ Lymphnodes │ 0 │ 0
Raccoon │ 0 │ 0 │ 0 │ 0 │ 0
│ │ │ │ │
Rodentia: │ │ │ │ │
Beaver │ + │ 0 │ 0 │ 0 │ +
Porcupine │ 0 │ 0 │ Lymphnodes │ + │ 0
Ungulata: │ │ │ │ │
Antelope │ 0 │ 0 │ 0 │ 0 │ 0
Deer │ ? │ 0 │ + │ + │ 0
Deer │ 0 │ 0 │ + │ 0 │ 0
Deer │ 0 │ + │ 0? │ 0 │ 0
Elk │ 0 │ 0 │ Lymphnodes │ + │ 0
Nylghaie │ 0 │ 0 │ 0 │ + │ 0
Peccary │ 0 │ 0 │ 0 │ + │ 0
Marsupialia:│ │ │ │ │
Phalanger │ 0 │ 0 │ 0 │ + │ 0
Opossum │ 0 │ 0 │ 0 │ + │ +
Opossum │ 0 │ 0 │ 0 │ + │ 0
Devil │ + │ 0 │ + │ 0 │ +
Passeres: │ │ │ │ │
Finch │ 0 │ 0 │ 0 │ ? │ ?
Thrush │ 0 │ + │ 0 │ 0 │ 0
│ │ │ │ │
Chaffinch │ + │ 0 │ 0 │ 0 │ 0
Picariæ: │ │ │ │ │
Hornbill │ + │ 0 │ + │ + │
Striges: │ │ │ │ │
Owl │ +? │ 0 │ 0 │ 0 │ +
Accipitres: │ │ │ │ │
Kestrel │ 0 │ 0 │ + │ 0 │ +
Columbæ: │ │ │ │ │
Dove │ 0 │ 0 │ 0 │ 0 │ +
Galli: │ │ │ │ │
Pheasant │ + │ 0 │ 0 │ 0 │ +
Fulicariæ: │ │ │ │ │
Gallinule │ + │ 0 │ 0 │ + │ 0
Anseres: │ │ │ │ │
Gadwall │ 0 │ 0 │ 0 │ + │ 0
Struthines: │ │ │ │ │
Ostrich │ 0 │ 0 │ 0 │ + │ 0
════════════╪═════════════╪═════════╪═════════════╪═════════╪═════════
_Totals_ │ │ │ │ │
Primates │ │ │ 1 │ │
Carnivora │ 4 │ 2 │ 3 │ 7 │ 2
Rodentia │ │ │ │ 1 │ 2
Ungulata │ 1 │ 1 │ 3 │ 5 │
Marsupialia │ 1 │ │ 1 │ 3 │ 2
────────────┼─────────────┼─────────┼─────────────┼─────────┼─────────
_Mammalia_ │ 6 │ 3 │ 8 │ 16 │ 6
Passeres │ 1 │ 1 │ │ │
Picariæ │ 1 │ │ 1 │ 1 │
Striges │ 1? │ │ │ │ 1
Accipitres │ │ │ 1 │ │ 1
Columbæ │ │ │ │ │ 1
Galli │ 1 │ │ │ │ 1
Fulicariæ │ 1 │ │ │ 1 │
Anseres │ │ │ │ 1 │
Struthiones │ │ │ │ 1 │
────────────┼─────────────┼─────────┼─────────────┼─────────┼─────────
_Aves_ │ 4 │ 1 │ 2 │ 4 │ 4
Grand Total │ 10 │ 4 │ 10 │ 20 │ 10
────────────┴─────────────┴─────────┴─────────────┴─────────┴─────────
════════════╤════════
Order │ Fat
│Necrosis
│
│
│
────────────┼────────
Primates: │
Marmoset │ 0
│
│
│
Carnivora: │
Wolf │ 0
Fox │ 0
Bear │ +
│
│
Raccoon │ 0
Bear │ 0
Coati │ +
Badger │ 0
Ocelot │ +
Bear │ 0
Wild Cat │ 0
Lion │ +
Skunk │ 0
Raccoon │ small
│
Rodentia: │
Beaver │ 0 0
Porcupine │ 0
Ungulata: │
Antelope │ ?
Deer │ 0?
Deer │ 0
Deer │ 0
Elk │ 0
Nylghaie │ 0
Peccary │ +
Marsupialia:│
Phalanger │ +
Opossum │ +
Opossum │ +
Devil │ +
Passeres: │
Finch │ 0
Thrush │ 0
│
Chaffinch │ 0
Picariæ: │
Hornbill │
Striges: │
Owl │ +
Accipitres: │
Kestrel │ 0
Columbæ: │
Dove │ 0
Galli: │
Pheasant │ 0
Fulicariæ: │
Gallinule │ 0
Anseres: │
Gadwall │ 0
Struthines: │
Ostrich │ 0
════════════╪════════
_Totals_ │
Primates │
Carnivora │ 5
Rodentia │
Ungulata │ 2
Marsupialia │ 4
────────────┼────────
_Mammalia_ │ 11
Passeres │
Picariæ │
Striges │ 1
Accipitres │
Columbæ │
Galli │
Fulicariæ │
Anseres │
Struthiones │
────────────┼────────
_Aves_ │ 1
Grand Total │ 12
────────────┴────────
Further analysis of the data leads into a consideration of the anatomy
of the viscus in terms of the acceptable theories of the origin of the
lesion. It is commonly believed that infection of the gland occurs by
passage of organisms through the duct opening in the intestines,
especially when there is swelling of the mucosa of both. For the human
being the idea is current that infection or obstruction of the common
bile duct may spread to the pancreatic duct, and that mechanical or
inflammatory obstruction of the papilla of Vater may permit the bile to
pass up the pancreatic duct. This theory is based upon certain
observations, notably those of Opie, in cases, where a gall stone
obstructed the ampulla, bile entered the pancreas and acute pancreatitis
arose, partly by the activating action of the bile upon the pancreatic
juice and partly by bacteria introduced at the same time. This method of
origin is perhaps accepted in most quarters, but there are some who
believe that infection of the gland may occur by the infiltration of
lymphatics around the pancreas by disease of adjacent parts—gall-
bladder, stomach or lymph nodes. Quotation has already been given to
reference literature, and I shall not go further into theory except in
pointing out how our material may help to answer the question.
In the first place it seems perfectly obvious that infection might in
any animal travel from the intestine to the pancreas _via_ its ducts,
the main question to be settled being the relative importance of the
infection _via_ the bile duct. Let us now see if the variations in
anatomy will cast any light upon the matter.
Among the 1860 mammals, there are as far as I can determine 1275 which
have one pancreatic duct opening in conjunction with the bile duct, 585
in which the former has an intestinal opening independent of the latter.
Among this 1275 there are nineteen cases of pancreatitis, while among
the 585 there are eight cases, or as 14.9 to 13.6. All Aves have
separate biliary and pancreatic ducts and relatively little
pancreatitis, although frequently suffering with its most common
accompaniment, namely duodenitis. There is therefore some evidence that
more pancreatitis occurs when there is a physical proximity or
combination of bile and pancreatic ducts.
Active infections of the biliary system in relation to pancreatitis are,
however, not as conspicuous as might be expected. In the mammals twelve
of the twenty-seven cases showed cholecystitis or cholangitis; in every
instance the form of pancreatitis was acute. Among the eleven avian
cases four showed inflammation of the biliary channels, but not of the
bladder. Hepatic cirrhosis was observed four times. In a thrush and a
skunk obvious infectious cirrhosis existed, and in both a necrotizing
pancreatitis was found. A badger suffered with atrophic cirrhosis of the
liver and a chronic pancreatitis with acute exacerbation. A deer showed
marked perilobular fibrosis with a recent hemorrhagic pancreatitis
probably due to duodenal torsion. Nothing very distinctive is to be
found in these cases, but they merely make the total of involvements of
the liver and its adnexa up to twenty. It is to be emphasized that
pancreatitis was not associated with lithiasis in ducts or bladder as
described on page 240. Peripheral cholecystitis and plastic
inflammations about the pylorus and lesser omentum are exceedingly rare
in wild animals, while they are not common in human surgical practice.
They did not occur at all in mammals in this series, the only external
inflammations being in lymph nodes in cases of frank infectious
character. There were distinct adhesions between liver, duodenum and
pancreas in two birds, one with acute, the other with chronic
pancreatitis.
In so far as the kind of pancreatitis is concerned mammals had twenty-
two acute and six chronic forms, one animal having the former implanted
on the latter, while birds had five acute and six chronic. The
preponderance of acute over chronic lesions in mammals again recalls the
association of the biliary and pancreatic ducts, but if one expect that
such a relation establishes acute inflammation, the relatively high
figures for Rodentia and Ungulata, with a single duct removed from the
bile duct conflict with the data for orders having two ducts such as the
Carnivora. Every case in the former orders was of acute nature; only two
had any hepatic disease, four had lymph gland hyperplasia in the
pancreatic region, and seven had acute enteritis. The preponderance of
acute over the chronic cases in mammals and the nearly equal number in
birds is, however, apparent.
The collateral pathology with the most definite relationship to
pancreatitis is enteritis and one may say that the former occurs in
proportion to the incidence of the latter. Acute forms, twenty-seven,
were associated with acute enteritis nineteen times. Chronic enteritis
was found with chronic pancreatitis in six of eleven cases.
There is a rough relationship between the type of pancreas and the
nature of the lesions. The organ may be divided for this purpose into
the compact organ firmly held in place by attachments to the lesser
omentum, spleen and duodenum, and the velamentous organ which spreads a
considerable distance along the duodenum and sends out digitations into
the mesentery and thin processes toward the spleen. The first type is
seen in primates and carnivores and birds, while the second is
characteristic of rodents, ungulates and marsupials. The compact variety
showed all but one of the chronic cases while the loose organ was
affected by the acute pancreatitis in twelve of thirteen cases.
The microanatomy of the cases may throw a little light upon our subject.
I was able to see the duct in one case of acute pancreatitis (bear). It
showed a simple catarrhal inflammation with a very moderate
circumferential round cell increase. The destruction of glandular areas
by edema, hemorrhage and necrosis offers nothing of importance except in
a few birds. In these the necrosis is more definite about cross sections
of ducts, and the islands of Langerhans are frequently spared until
necrosis is locally complete. In a case of chronic pancreatitis in a
bird, a cross section of pancreatic duct was found in the intestinal
wall; a chronic catarrhal and infiltrative enteritis existed in this
specimen. A very definite mantle of round cells was found about the duct
while the mucosa showed no change, although the lumen seemed large.
Interlobular fibrosis was the rule, only one case of intra-acinar
pancreatitis being encountered; this specimen, a bird, showed great
distortion of the acini and of the islets.
The study of comparative pathology of pancreatitis does not settle its
etiology, but some very suggestive facts may be learned. The association
of hepatic and biliary disease and of enteritis in the causation of
pancreatitis seems amply confirmed, and the latter factor is in our
series numerically the greater. It is suggestively shown that
inflammations of the pancreas occur more frequently in the zoological
class in which the ducts of the organ and of the liver empty into the
duodenum together or in close association. Moreover, infections of the
liver and adnexa are very important in the mammals, more so than birds
in which enteritis, notably chronic in type, usually accompanied the
involvement of the pancreas. This is consistent with the incidence of
bile tract disease as already discussed under that subject, and it is
interesting to note that the mammals showing the greatest number of
cases of choledochitis and cholangitis also show the high case incidence
of pancreatitis. The birds that have bile tract disease have little
pancreatic disease. These facts when considered in connection with the
free biliary supply of the avian duodenum, the disassociation of the
ducts of the two glands and the close apposition of the pancreas to the
duodenal wall, suggest strongly that direct infection of the pancreas
can occur from the intestinal wall along the walls of the ducts perhaps
via the lymphatics. This is supported by the observation of at least one
case in which there was a definite inflammation under the adventitia of
the pancreatic duct, its mucosa being normal. The study also suggests
that acute pancreatitis is more often associated with acute lesions in
the intestines and with hepatic or gall-bladder disease, and that
chronic pancreatitis seems more often the result of chronic or repeated
intestinal inflammation. Peripheral inflammation such as occurs in
gastric or duodenal ulcers, has not been encountered in a distinct
character so that its value cannot be estimated.
[Illustration:
FIG. 20.—ADENOMA OF PANCREATIC DUCTS. CORSAC FOX (CANIS CORSAC).
]
Cystic change in the pancreas has been observed a few times, but never a
large visceral collection or the so-called extra-pancreatic cysts of the
omentum. One acinus cyst was seen in a drake, one congenital cyst in a
lark, and multiple ductal cysts were seen in a baboon and a duck. The
parenchyma in all cases seemed entirely capable of functionating.
TUMORS.
Tumors of the pancreas have been three in number, two being of academic
interest only. One of these concerned an apparent adenoma of the ducts
within the organ, discovered microscopically in the sections from a
Corsac Fox (_Canis corsac_). This is the only specimen we have had, and
I can find no description of the normal microanatomy of this species, so
that with a knowledge that certain carnivores have convoluted ducts, the
determination is made tentatively; it corresponds microscopically to a
ductal adenoma. The pancreas of a raccoon (_Procyon lotor_) showed a
true adenoma of glandular acini as two separate but closely applied firm
nodules surrounded by a capsule, and with distorted acini as seen under
magnification. The most important tumor was found in an Indian
Paradoxure (_Paradoxurus niger_), an adenocarcinoma involving the head
of the organ, enlarging it to twice its normal size; there were no
metastases. The animal suffered also with an infective hepatic cirrhosis
of recent origin, chronic nephritis of the arteriosclerotic type,
chronic fibroid splenitis. No obstruction to the biliary channels
existed.
SECTION VII
THE ALIMENTARY TRACT, PART 4.
THE PERITONEUM
This visceral envelope is principally important because of the fatal
character of its acute inflammations. In man peritonitis of acute origin
and type is commonly secondary to a focus of progressive inflammation in
some abdominal organ and usually speaks for the virulence of the primary
disease and for the low resistance of the serous membrane. Because of
this vulnerability, greater foresight is attempted to prevent the
extension of acute intra-abdominal inflammations and under operative
conditions punctilious care is used to avoid contamination of the
general peritoneal cavity. Involvement of the peritoneum in septicemic
states is relatively uncommon in man, but seemingly more frequent in the
lower mammal. This surface seems more resistant to infection at
operation in the lower animals since post-operative peritonitis after
castration and experimental procedure is certainly infrequent; our data
will permit no percentage figures of vulnerability under such
conditions. Judging, however, from the number of times at which the
diagnosis of acute peritonitis has been made, the lower animal has a
decidedly low percentage resistance although its pathological states are
primary or secondary to conditions unusual in man. Among the 5365
autopsies acute peritonitis appears in the diagnoses 137 times or 2.4
per cent.; mammals, 57 or 3 per cent.; birds, 80 or 2.3 per cent.
The exact causes are usually obvious, practically always so in human
medicine, but a number of cases escape adequate explanation. From a
practical standpoint two origins are important to zoological
collections, trauma and intestinal perforations by sharp objects.
Ungulata frequently suffer abdominal injuries in fighting, as do
rodents. Peritonitis sometimes supervenes even in the absence of
penetrating wounds, probably by reason of damage to the intestine
whereby its permeability is increased. Pointed objects are frequently
swallowed by animals and perforation occurs. The danger of feeding split
bone to carnivores is well known; some years ago we lost two tigers and
a lion in this manner.
Ileus, in one of the several forms, has been an occasional cause of
peritonitis in primates and ungulates. The extension of purulent
inflammation, abscesses and the like is easy to understand, but we have
seen several cases of apparent extension from enteritis without
perforation. The reason for this is probably in the kind of enteritis.
Monkeys with amœbiasis and gallinaceous birds with enterohepatitis have
supplied most of the cases, these infestations of the gut wall being
deep and spreading so that a chance is afforded to penetrate the serosa
along blood and lymph vessels. One case in a deer seemed to originate
from a simple catarrhal colitis; trichocephalus in the colon may have
helped. Parasites are not very potent in causing an acute peritonitis,
but aggravate the action of other agents. Septicemic states are at the
bottom of 24 per cent. of our cases of peritonitis. This is particularly
true of birds, it being recognized that their acute general infections
frequently have such an effect, but the primates and carnivores also
have a vulnerable peritoneum when septicemia exists. The principal
outstanding visceral lesions in the mammalian cases is pneumonia; in
birds it is cholera and plague. The rupture of eggs in birds lays the
foundation of a peritonitis, while bacteria from the oviduct or cloaca
complete the process. Chronic peritonitis is not common. It is usually
due to parasites or to tuberculosis. There has been observed, however,
no complete general involvement of the peritoneal cavity including the
liver and spleen, sometimes called “sugar-icing,” and believed to be
tuberculous in origin. The only tumor found in very close association
with the peritoneum occurred in a Chapman’s Zebra (_Equus burchelli
chapmani_) in which animal a fibromyoma seemed to spring from a loop of
intestine and grow away from the gut wall. It was undergoing myxoid
change.
SECTION VIII
THE URINARY TRACT
THE KIDNEY.
The kidneys, ureters, bladder and urethra remain comparable in all
mammals excepting the monotremes where there is no urinary passage
through genital openings, the urine being ejected through the vesicoanal
pouch, a sort of cloaca. In the bird the first two parts remain as in
mammals while the ureters terminate in a hernia-like pouch of the rear
wall of the cloaca. It would seem from this arrangement that ureteral
transmission of infection from the anal area to the kidneys would be
facilitated in the lowest mammals and in the Aves. Variations in size,
shape and position exist to a minor extent in the higher orders but in
all forms, the system remains a post-peritoneal structure.
Differences in construction are to be seen for example, in the single
pyramidal kidneys of marsupials and certain rodents, in the lobulated
organ of bears, cattle and seals, in the twisted viscus of horses, but
these gross appearances do not destroy the uniform scheme upon which the
functionating unit is built. The single-lobed kidney discharges all its
collecting tubules into one calyx while the multiple pyramids of the
lobulated organ are fitted with individual calices which in turn empty
into the pelvis proper; this is true whether the lobulations are
retained, as in the bear, or are smoothed out in the course of
development as in man. The secretory tubule remains in essentially the
same form in all kidneys; the modern idea of its anatomy may be found in
the work of Huber[32].
The most decided example of the lobulated kidney is to be found in the
class Aves, wherein the organ consists of two or three large lobes lying
in concavities of the sacrum, each lobe being made up of tiny lobules.
The latter appear to the unaided eye as fairly distinct divisions
whether viewed on the exterior or by cross section. There is a cortex
and a medulla to each, the separation being clear in a large specimen,
vague in a small one. These lobulations are quite well observed when the
kidney is full of urates, a common finding in birds. Magnification of
the avian kidney reveals an apparently simpler tubular arrangement than
is found for mammals[33][34], yet the relation of vascular plexuses and
secreting tubules remains similar.
From the standpoint of comparative pathology attention can be drawn to
the glomerulus, to the interstitial tissue, and to the character of the
epithelium. The tuft of intricately wound capillaries called the
glomerulus has always been viewed as the part of the secretory unit
chiefly concerned in urine production whether one accept the older idea
that it excretes only fluid or the modern belief of many observers that
all parts of the urine go out through it. In the mammal the tuft is
closely wound, is surrounded by a distinct space and a limiting membrane
of appreciable width called Bowman’s capsule; all this so-called
Malpighian body has a breadth varying from 120 to 300 micra. There is
however great variation in the size of this body when seen in the
peripheral and deeper zones of the same organ, amounting at times to
seventy per cent. of the diameter. The capillary congeries forming the
avian tuft is by no means so delicate and one can see individual
capillaries with more ease. It may be impossible to discover a space
between the tuft and its exceedingly delicate capsule, the latter being
usually applied closely to the vascular corpuscle. The whole breadth
varies from 70 to 140 micra with an average of 110. There is more
uniformity in size than in the mammalian organ.
Supporting tissues between the tubules seem less definitely nuclear in
the bird than in the mammal, at least in so far as connective tissue is
concerned, there being in the former only a few groups of mononuclears
to be seen in the cortex. Perivascular tissues are reasonably rich. The
epithelium of proximal and distal tubules is not easily fixed by our
customary laboratory techniques, the best results being obtained by
Zenker’s fluid. As seen in a routine specimen of a normal organ it is
vacuolated or very palely stained. The individual cells stand out
clearly and many present a pointed end to the tubular lumen.
KIDNEY WEIGHTS.
According to the work of Mangan[35] and of Alezais[36], the bird has an
average kidney-to-body weight of 6.9 grams per kilo while man has a
ratio of 4.3 grams, dog 5.9 grams and guinea-pig 8.5 grams. The first
author would show that the fish-eating birds have the heaviest and
vegetarian birds the lightest organ. Our own figures are limited to the
weights of apparently normal organs in thirty-one mammals and five
birds; they are as follows:
│per kilo of body weight
Primates (5)│ 7.7 grams│
Carnivora (6)│ 7.6 grams│
Rodentia (2)│ 15. grams│
Hyracoidea (1)│ 7.5 grams│
Ungulata (9)│ 3.5 grams│
Edentata (1)│ 5.6 grams│
Marsupialia (7)│ 7.6 grams│
Monotremata (1)│ 11.2 grams│
│ │Average 7.
Steganopodes (1)│ 9.1 grams│
Anseres (1)│ 3.9 grams│
Struthiones (3)│ 7. grams│
│ │Average 6.7
────────────────┴───────────┴───────────
This to be sure is not a very exhaustive list but is the result of our
routine observations and subject to all limitations of such work.
Grossly diseased organs are naturally excluded. More avian weights are
not available because of the difficulty of removing the organ from its
bed, in a manner assuring us of completeness. I am inclined to view our
mammalian records as fairly representative. Figures to be found in text-
books of human and veterinary anatomy correspond to those given by the
authors just quoted and in our own list. The values for rodents,
hyraces, edentates and monotremes may be modified by more figures.
There is however one point which does not appear in the list. Small
animals have relatively larger kidneys than large animals. This is
perhaps most strikingly illustrated among the ungulates which have the
lowest value quoted. A small deer had a kidney-to-body index of 5.9
grams per kilo while a camel had only 2.8. Judging by the work of Magnan
the avian kidney should be larger than the mammalian, a conclusion with
which I am inclined to coincide, even though the weights cited do not
bear this out.
In so far as the function and chemistry of the kidney and its excretion
are concerned this study can supply little. The general metabolism is
known for most animals, it being dependent upon diet and
gastrointestinal discharge of excrement. What lessons can be learned
will be discussed by Dr. Corson-White in the section on diet. Our
observations upon the ability of the kidney to excrete normal urine are
limited to the examination of vesical contents at death or of the
occasional specimen obtained in cages in the quarantine room. Renal
disease was formerly considered of little or no importance in veterinary
medicine or at least was studied only as a specific separate and
occasional occurrence. Kitt[37] systematized the knowledge of the
subject at the time he wrote but it remained for Hutyra and Marek in
their text-book to emphasize its general importance and to clarify
diagnostic measures. Breindl[38] pointed out that nephritis occurs more
often in acute general diseases, notably the specific infections, than
was customarily thought, thus placing the subject for the lower animal
where it is in human medicine.
Renal disease is quite common among wild animals albeit there are
certain orders in which the lesions are less conspicuous. Clinical
diagnoses of nephritis, and this is the only diagnosis attempted, have
been made on monkeys by examination of urine which shows the same
characters as in the human disease. In ungulates more attention is to be
placed upon the cellular contents of the urine since renal epithelium is
apparently shed more readily and casts less often formed. Signs and
symptoms of renal disease are limited to edema and uremia; cases of the
latter are rare enough to discuss separately at the proper place.
ABSENCE OF ABNORMALITIES.
Abnormalities of size, shape and position of the kidney are frequently
reported in literature of veterinary medicine and aplasia has been
described. Our material has failed to present cases of horse-shoe kidney
well known to occur in horses, cows, sheep and dogs. Wandering kidneys
are also known but have not been seen in our wild animals. Shall these
abnormalities be considered as due to degenerative changes in cross bred
animals or as the result of the strain of domestication? To such a
speculative question our material affords no answer.
HYPERTROPHY.
That the kidney has the power of hypertrophy in a compensatory manner is
illustrated by two cases. A Japanese Macaque (_Macacus fuscatus_) ♂
apparently had suffered with a unilateral nephritis which had gone into
a contracted stage. At all events much functionating tissue was gone,
the organ irregular and small, being half or less of the size of the
other organ which was larger than is considered normal for the species.
Histologically the large organ was practically normal. A common opossum
(_Didelphys virginiana_) suffered with a complete suppurative nephritis
of the right side which completely destroyed the organ; the origin of
this is not clear as no ascending disease could be determined and no
certain acute infection had existed; decomposition precluded
satisfactory bacteriology. The left kidney was nearly twice its normal
size and involved in an early diffuse nephritis, with miliary abscesses,
in which the glomeruli did not participate. There were in these sections
evidences of regeneration, swollen reduplicated epithelial coverings
presenting a picture similar to those seen in so-called chronic
nephritis secondary to interstitial change.
INFILTRATIONS.
Pathological infiltrations of the renal structures are exceedingly
uncommon. Early in our experience we were often perplexed at the
appearance of certain organs, notably in carnivores and marsupials to
which we were inclined to apply the term fat infiltration. However the
absence of reasons for considering this picture pathological seemed
sufficient cause to ignore the finding, and later Pfeiffer[39] called
attention to the apparent inability of these kidneys to emulsify fat or
at least to combine it in an invisible form, an ability possessed by the
herbivorous organ. A monkey and a passerine bird only showed sufficient
fat visible in the renal epithelium to warrant a denomination of fatty
infiltration; these were both obese specimens. Amyloid infiltration
occurred in four mammals and six birds, being a sequel of its usual
causes, tuberculosis, chronic suppuration and osseous system disease. It
is perhaps well to emphasize the fact that every organ the seat of
amyloid deposit need not be enlarged. This teaching is common but I have
seen human cases without enlargement and only two of the ten cases in
these animals are noted as bulkier than normal.
DEGENERATIONS.
Degenerations represent the reaction of the kidney to toxic or
infectious agents and might be considered as indicating the
vulnerability of the organ. Their incidence does not coincide with that
of nephritis as we shall see later. Any discussion of degenerative
phenomena, and especially in the kidney, should be limited by a
definition of what they are believed to be and their separation from
inflammations. Degenerations are swellings, granularities,
vacuolizations or infiltrations of tubular epithelium, changes which
destroy the outline and internal structure, perhaps including the
nucleus. No changes of the glomerular tuft or interstitial tissue are
necessary for this conception since when these occur the picture becomes
that of nephritis. In border-line cases it is safer to include the case
under the latter heading since then the physiology is apt to be
disturbed, albumen and casts appearing in the urine. Degenerations
appear in various pathological states—toxemia, infection, prolonged
congestion and others. The first named cause seems to be the most
important in our records and the seat of the toxine production seems to
be the intestine. Enteritis stands very high in the list of accompanying
factors, especially in Carnivora, Primates and in Aves. Perhaps the most
instructive cases are to be found in the Ungulata with toxic duodenitis.
The kidney in these animals is deep red or purple, with a spanned
capsule. The section surface bulges slightly, is of an opaque, dull
purple color and shows a congested zone between cortex and medulla.
Tubular epithelium may be found, under the microscope, sufficiently
swollen to fill the lumina, in places being like ground glass, in others
distinctly vacuolated. It cannot be stated absolutely which part of the
tubule is usually affected; it seems more often the distal convoluted
portions than other subdivisions. Glomeruli may be full of blood but
there is no increase in cells nor any material in the capsular space.
The urine is dark and may or may not show albumen. The kidney of
kangaroos with streptothricosis is similar to the picture just given.
Mammals have shown a percentage incidence of renal degenerations of 4.8
per cent. while Aves show only 3. per cent. In order of incidence the
carnivores head the list followed by Lemures, Accipitres, Rodentia,
Primates and Marsupialia; the remaining groups show but a few cases. A
form of degeneration is sometimes seen in the avian kidney the seat of
excess urate collections, especially when these are arranged as so-
called uratic infarcts. This last term has been applied to the streaking
and mottling of human kidneys by the accumulations of these salts in a
manner believed by some to be related to the formation of uratic
calculi. The epithelium of such a kidney may show granularity and
collections of acids and salts have been found in the lumina. In the
bird on the other hand one frequently sees masses of urates in one
lobule, or a part thereof, arranged to simulate closely the common
infarct shape. Secretory cells in the affected area are hydropic, with
absent or dislocated nucleus, or again they present a densely basic
staining protoplasm. This form of kidney is well seen in what has been
called here an uratic serositis, a coating of all somatic free membranes
with a thin, white, granular film. We have tried with many techniques to
preserve one of these cases but the deposit either dissolves or the
whole specimen becomes opaque. Although the term infarct is applied to
these lesions, they are of course not infarcts in the customary use of
the term. True infarcts are exceedingly uncommon and, with the exception
of one case which became infected and suppurated, have been negligible
in our material.
HEMORRHAGES.
Hemorrhages into the kidney are found in acute infections and certain
diseases like leucemia; they are of little moment. Perirenal hemorrhage
is a somewhat striking and unusual affair. Recently I saw at a human
autopsy of a young subject a subcapsular hemorrhage from the renal
substance probably due to vascular rupture in an acute nephritis; there
was no history of injury. There have been three cases of subcapsular
hemorrhage in our records and as two of them represented the immediate
cause of death, are interesting enough to record. An armadillo suffered
an acute diffuse nephritis with much congestion but not enough to call
it hemorrhagic. There was a large hemorrhage around the left organ,
probably from a vessel near the hilum, sufficient to compress the kidney
and cause it to atrophy. A lion presented an acute vegetative
endocarditis with all its usual complications. The right renal capsule
was distended with recent clot to a size which reached to the pelvic
brim. Presumably an embolism caused thrombosis, ulceration and rupture
of some middle size vessel. A dormouse suffering with an acute general
infection probably emanating from the intestine, had several small
recent clots separating the kidney from its capsule.
NEPHRITIS.
Nephritis, whether one begin its conception with the clinicopathological
picture originally given by Bright, with the purely pathological
classification of Weigert and Virchow or the modern tendency to
subordinate all physical changes to clinical phenomena, is nevertheless
a process of degeneration and inflammation affecting the secreting and
supporting structures of the kidney and leading to some degree of
impaired function. The disease is bilateral in so nearly every case that
for practical purposes unilateral cases may be ignored. This implies
that for some reason the renal tissues are generally susceptible to
etiological agents so that when one side is affected its fellow seems
always to participate or to follow. It seems desirable in studying
nephritis to evaluate fully the mutual relations of functionating and
supporting tissues and of the various sections of the first named. It is
taught in many places that inflammations of one or another of these
parts may occur independently, as for example a tubular nephritis, a
glomerulonephritis and an interstitial nephritis. If however one reflect
upon the dependence of the tubular function upon the glomerulus and
_vice versa_ or upon the effect of inflammatory exudates in the
supporting tissues upon the blood supply of the tubule, it becomes
evident that only the most trivial or evanescent pathological changes in
one can be without effect upon the others. It is difficult to see how,
for examples, a glomerulus could remain normal if its associated tubule
were destroyed or how if round cell infiltration or pus surround a
capsule for any length of time, this structure could fail to be doomed.
All this is by way of directing attention to the progress of physical
damage in a kidney which has received injury sufficient to cause
nephritis, but of course it does not explain the cause.
In classification of nephritis different commentators have employed
different standards according as they viewed the acuteness or chronicity
of the process, or as the principal functionating structures,
glomerulus, tubular epithelium, blood vessels, or supporting connective
tissues, presented the most conspicuous changes. To these, clinicians
have added phenomena of constitutional complication or of direct renal
insufficiency. These latter being unavailable for us, we must fall back
upon a classification based upon physical changes and to this end we
have always used a slight modification of the Weigert method. This
classification offers little in the direction of etiology except that
toxins are believed to cause tubular changes, bacteria to produce
glomerular lesions and vascular deficiencies to lie at the root of
chronic interstitial nephritis.
The origin of acute nephritis of chiefly degenerative character seems
best explained by reference to some form of toxemia, whereas exudative
processes, be they in glomerulus or supporting structures, seem to
depend upon the direct action of bacteria. The origin of a chronic
nephritis cannot be explained quite so readily. No one has answered with
complete satisfaction whether a chronic process always begins with and
proceeds from a single attack of acute disease, whether many acute
attacks succeed upon one another or whether many small crops of agents
successively attack the organ over a long time. Nor has an adequate
explanation of the rôle of damaged blood vessels been given. It is
reasonably easy in man to discover the existence of nephritis and of a
possible cause; this is only true of acute cases in wild animals. Focal
infections, those which might be the point of mobilization for bacteria
sent to the kidneys, are frequently found in man but with exception of
an occasional carious tooth, or a chronic osteitis are to be localized
with difficulty in lower animals. In so far as the rôle of a single
acute attack in the causation of chronic disease is concerned our
material offers nothing, but some collateral or presumptive evidence may
be mustered in regard to multiple infections.
Wild animals do not give evidence of repeated attacks of acute disease
and indeed it would seem that they more often die of an acute infection
than live to have it repeated. Evidences of chronic infection, not
focal, are reasonably definite in forty-eight per cent. of the cases of
chronic nephritis encountered here. This suggests strongly that in this
material protracted infectious states offer opportunities for renal
damage of progressive character. Vascular disease has been found twenty-
eight times (see also section on arteries), in twenty-six of which the
nephritis seemed due to or advanced by the damage to the vessels. This
means further that only 14.3 per cent. of the chronic forms and 4 per
cent. of the total seem closely related to disease of blood vessels.
Nephritis has been found in 12.2 per cent. of our total autopsies.
Mammals show an incidence of 20.6 per cent., birds 7.7 per cent. Only
the orders upon which more than one hundred autopsies have been held are
subjected to separate analysis. Some of the remaining orders give very
high figures which may indicate great renal vulnerability but it is
deemed unfair to make statements upon them. Carnivorous mammals and
birds lead their respective classes, the succeeding order of renal
vulnerability being marsupials, ungulates, rodents, Primates, Galli,
Striges, anserine birds, parrots, and doves. The leaders of this list,
Carnivora and Accipitres, occupy a definite position in the analysis of
acute and chronic lesions. Their kidneys show the smallest percentages
of acute lesions and the highest percentages of chronic lesions. This
would seem to indicate a resistance to acute injuries but susceptibility
to prolongated or repeated infections or intoxications. The relation of
chronic infection of some sort to chronic renal disease is not as clear
as the influence of acute infection to acute nephritis. Taking Carnivora
for example with 34.2 per cent. of chronic nephritis we find 22.4 per
cent. with evident chronic inflammation while in the 55 per cent. of
acute forms 40 per cent. are of acute infectious origin—the relation is
as 64 is to 74.
While the relation of infection to nephritis is a consistent and
perfectly acceptable one, the frequency of this disease in the
carnivorous orders obliges one to think of high protein diet as a
favoring factor. Renal disease is common enough in other orders, some
strictly herbivorous, and it is fair only to emphasize which are the
leaders in incidence. In so far as anatomy or habits are concerned no
generalizations seem permissible. There is no relation of nephritis to
the size of the kidney as given on a previous page, to the length of the
alimentary tract, or to the expected longevity.
Toxic nephritis is a term applied when the kidney is the seat of
epithelial degeneration, much congestion, perhaps leading to tiny
hemorrhages, and definite swelling of the tuft without exudation into
the capsular space. It is a severe grade of the degenerations already
mentioned and is exemplified by the organ in cases of acute duodenitis
of ungulates and in some monkeys dying after tuberculin injection. It
seems especially to follow gastrointestinal diseases believed to be due
to food intoxications. It seems important in monkeys and wild rodents.
No adequate explanation is at hand for the latter.
As has already been stated vascular disease was present in twenty-six
cases in a manner suggesting some relation to the cardiorenal complex
but the only organ to which the term renal sclerosis of arteriosclerotic
origin could be applied is that of an eagle; the autopsy is cited.
Bald Eagle (_Haliæetus leucocephalus_). ♀ General obliterating
endoarteritis. Chronic interstitial nephritis. Passive congestion of
liver. Chronic localized myocarditis. Near the apex of the heart the
muscle shows a slight opacity. The kidney is enlarged, firm, section
surface glistening. Both section and surface show a mottled brown and
white appearance, following particularly on section the division into
cortices and medullæ. Digestive system apparently normal. Microscopic
section of heart muscle from the wall of the ventricle shows well
preserved muscle fibres with a slightly unusual degree of
pigmentation. Section from valve base shows a definite interfascicular
and intrafascicular fibrosis which is co-extensive with a similar
thickening of the endo- and pericardium. The new tissue under the
latter is edematous. The valve itself is thickened the fibres swollen
and hyaline. There is no reduplication of the endothelium. One artery
in the muscle is obliterated. This is not associated with any
degeneration of the muscle in the section. Section of kidney shows the
pale areas noted grossly to be made up of groups of arteries with
their extensive coalescing adventitiæ. The changes in the arteries are
precisely the same as those seen in the liver but are more extensive.
Connective tissue goes out from the arteries into the parenchyma
distorting the tubules and enclosing the glomeruli so that the capsule
of the latter is much thickened. Epithelium is granular, in some
places absent, nearly always low. Section of liver shows general
parenchyma practically normal with slight granularity in places and
moderate passive congestion. Veins are negative but arteries show a
general arteritis. The picture varies somewhat in different arteries
ranging from a simple thickening of the adventitia to a change
involving all three layers. There is hyaline change in the media in
many sections. Lumen is in all cases reduced and in some there is
active intimal proliferation in excess of what would be expected in
connection with the medial change. A few of the arteries have their
lumen completely obliterated.
This is meant to illustrate the picture of vascular disease in the
kidney in the absence of satisfactory evidence that nephritis _per se_
antedated or accompanied changes in the vessels. In such cases vascular
disease dominates, renal parenchymatous damage being relatively
inconspicuous. Two old carnivores, a paradoxure and a skunk, presented
shrunken kidneys with prominent wide-walled vessels but in these some
definite evidence of old nephritis was at hand.
In so far as the relation of senility to nephritis is concerned the data
at hand are not conclusive. In many old animals some degree of fibrosis
is present without the existence of truly destructive changes in the
parenchyma. Plimmer of London writes that there is increased nephritis
in old age but from our material I would be inclined to put in that in
many cases the nephritis was the reason for old age rather than that old
age brought on a nephritis. However the exact length of life and of
captivity is known in too few specimens to make a conclusion justified.
ASCENDING NEPHRITIS.
There is some difference of opinion as to the definition of the term
ascending nephritis, a confusion arising partly from the intended
meaning of the participial adjective, partly from the frequency with
which infections or obstructions of the urinary outlets antedate or
accompany suppurative nephritis. Perhaps our records may help to
straighten out this matter.
Ascending nephritis means for our study an infection which passes from
the pelvic surfaces of the pyramids outward toward the renal capsule.
Thus it is immaterial whether there be or be not an obstruction lower
down. Such forms of nephritis are infiltrative, frequently purulent and
are dependent upon pyelitis or the settling of bacteria in the deepest
parts of the medulla.
Three explanations are given in human medicine for the origin of this
lesion. Some observers assume a direct transmission of bacteria up the
ureter from an infected bladder or urethra, in a direction contrary to
the urinary current. This, it is believed by some can occur only in the
presence of physical obstruction, stone, kink, or pressure of adjacent
masses upon the ureter, whereby its blood supply is damaged and
infection facilitated. Others would explain the path of infection as the
lymphatics of the ureteral wall which are infected at the opening in the
bladder by a deep seated cystitis or by infection from a periproctitis
or from the female genitalia. Still another explanation is offered by
those who do not credit ascending infections. They would have it that
pyelitis arises from bacteria in the blood stream and only in the
presence of injury (_calculus_), ureteral dilation (slowly progressive
stenosis, or kinks, floating kidney, pressure by pregnant uterus) and
similarly operative factors. There should be excluded from this category
cases of chronic nephrolithiasis, and of stone only in the pelvis. Under
such conditions it is inevitable that a low grade of fibrosis with
damage to the secretory structures should exist, even in the absence of
active bacterial invasion. The cases are only important for our present
subject when active bacterial infection is implanted upon them.
Among our autopsies there have been found fourteen cases of ascending
nephritis and seven cases of pyelitis; the most instructive examples are
mentioned briefly as follows: Five of this twenty-one were associated
with general infectious diseases (three septicemias) and presented no
evidence of ascending obstruction. Two of this five were a bear and a
fox, the former suffering with streptothricosis septicemia, the latter
with distemper; one was a fox whose pelvic and renal lesion seemed
entirely primary for no apparent focus was detected; two were birds with
acute general infection. These cases seem therefore to be instances of
primary pyelitis. The following group includes cases with inflammation
low in the urinary tract. A fox had a cystitis, urethritis and colitis,
a distinct edema and congestion being found in the pelvis around the
rectum. Two opossums had cystitis, one due to a traumatic urethritis,
the other secondary to a prostatitis of undetermined causation. A
raccoon had a chronic cystitis with swelling and edema of the first
parts of ureter. A parrakeet showed ureteritis, pyelitis and nephritis
from simple cloacitis.
Where obstruction was more definite the following cases were observed.
Suppurative nephritis succeeded upon gangrenous cystitis after uterine
prolapse in a deer. The following cases of pyelitis and nephritis were
associated with calculus, only in the renal pelvis—an armadillo,
Tasmanian devil, a deer and a goose. A cockatoo had a stone in the
cloaca which seemed to cause a definite obstruction to both ureters and
a catarrhal inflammation of the wall. Pyelitis and interstitial
nephritis can also follow excessive urate collections in birds. At a
later time this will be discussed more fully, but at this place two
cases of distinct abscess formation in a renal lobule based upon urate
collections may be mentioned since in a measure the lesions were
dependent upon obstruction.
It is therefore evident that all the theories of the causation of
pyelitis with resultant nephritis seem acceptable. It has been claimed
that bacteria may be found in the blood stream before evidences of
pyelitis present themselves. Concerning this our records offer no
information, but it is worthy of note that five of twenty-one instances
gave a picture of septicemia. It is, however, fair to state that, while
mild cases of pyelitis occurred where there was, judging from the
protocol and histological sections, obvious opportunity for its ascent,
in ten other cases of cystitis and urethritis no pelvic or renal disease
is recorded; two of these were acute exudative cystitis and one was a
tumor. It seems that wild animals seldom live long enough to have
obstructions exert back pressure of urine to the extent which one is
accustomed to see in human medicine. Hydroureter and hydronephrosis have
not been seen.
Abscess of the kidney has occurred occasionally in the metastatic form
and only twice as the large destructive process such as is seen in the
human being (surgical kidney). One massive abscess was seen involving
about one-third of the organ, and this seems to have had a tuberculous
basis. Another destructive purulent nephritis was quoted on page 268
when illustrating compensatory hypertrophy.
Examination of records and preserved specimens of nephritis reveals few
striking differences which might be considered characteristic for the
various orders. This is possibly due to the fact that the lesions have
been classified under the same system, a method which has proven
convenient and consistent. In support of this one might refer to that
form of nephritis which gives the most definite clinical and
pathological picture of renal disease, namely the chronic
parenchymatous. This is fairly well represented in Primates, Carnivora
and Ungulata. In one-fourth of the cases one finds distinct edema,
especially in the body cavities, cervical and mediastinal tissues, and
in one-fifth an appreciable grade of anemia; uremia was the terminal
picture in one animal of each order.
HISTOLOGY OF NEPHRITIS.
An attempt to discover minute lesions peculiar to the various groups
gives results that are far from satisfactory. With reserve it may be
said that carnivorous animals show a tendency to greater interstitial
and glomerular lesions than do herbivorous ones, and that casts are more
often found, in all kinds of nephritis, in the former varieties. Rodents
are conspicuous exceptions to this statement, since they frequently have
glomerular lesions and casts in abundance; this exception exemplifies
the unwisdom of drawing definite conclusions in this respect.
Birds as contrasted with mammals show very prominent tubular and
inconspicuous glomerular lesions. The principal alterations seen in the
avian kidney are round cell infiltrations of the deep cortical and outer
medullary zones, and cloudy or hydropic swelling of the convoluted
tubules. In chronic cases intertubular fibrosis is clear but not so
definite as the perivascular, while the glomerular tufts are
occasionally wholly normal. When these are destroyed it seems to have
occurred by compression rather than by inflammation. A form of nephritis
peculiar to birds might be termed local necrotizing. It seems to be due
to local urate deposits and to have its origin like that form already
mentioned under acute interstitial nephritis. It has been seen in avian
gout, a condition in which the kidneys may or may not have visible
masses of hardened urates in them. The gross picture is of a spotty pale
organ of a gray-brown color. Minutely studied the medulla, adjacent
cortical tubules and perhaps the pelvic tissues will present an opaque
condition taking a diffuse basic dye. Crystals have not been seen. This
form is especially common in Columbæ, Psittaci and Herodiones.
GENERAL EFFECTS OF NEPHRITIS.
The results of nephritis generally speaking are edema, anemia, cardiac
hypertrophy, inflammations of the serous surfaces and uremia. Aside from
the cases of chronic parenchymatous nephritis cited above, edema has
been decidedly inconspicuous. It may be found in avian cases of acute
and subacute nephritis, about the flanks and in the thoracic areolar
tissues, but is only exceptionally perceptible before the body is
opened. Anemia is almost never extreme. The bone marrow although
mentioned in but few histories, seems unchanged. Cardiac hypertrophy was
observed ten times in 652 cases of nephritis, twice in 460 acute and
subacute cases, eight in 192 chronic cases. In the former no myocarditis
was found, in six of the latter it was found. Clinical and pathological
experience teaches that serous surfaces are frequently inflamed during a
nephritis. Observations on our material coincide with this statement,
but do not offer an explanation of it. The figures should be examined
for mammals and for birds separately, since the serous cavities of the
former are closed, separated, and protected, whereas a close apposition
exists between the serous membranes and the lungs in birds, an
arrangement facilitating infection from without. Nevertheless the bird
has definitely less serositis accompanying nephritis than does the
mammal—4.4 per cent., _versus_ 8.6 per cent. In the former class 70 per
cent. of these accompany acute nephritis associated with acute general
disease while only 45 per cent. of the 8.6 per cent. of mammals had
serositis, acute nephritis and general infection. This indicates clearly
that mammalian renal disease has some effect upon serous membranes other
than the simple participating coincidence of the two types of changes
during an acute general infectious disease. No one kind of nephritis was
especially characterized by this complication.
Uremia, except under the best clinical conditions, is a term to use with
caution. I have seen several monkeys, a few marsupials and carnivores
and an occasional bird in a dazed ataxic condition, sometimes exhibiting
an atypical clonic or tonic convulsion, with fixed, rather small pupils.
To this picture I have applied the name uremia, and upon several
occasions have found a severe grade of nephritis. I must admit having
failed to find renal change, however, with this clinical picture,
especially in the carnivores and parrots, animals which “throw fits” at
times without apparent good reason. In so far as the monkey is
concerned, I am satisfied that the picture is similar to that seen in
the human being. The London Garden reports in 1917 the occurrence of
uremia in a Mandrill (_Papio maimon_).
CALCULI.
Calculi are well known in the renal system of the domesticated animals
so that it is not surprising to find them well represented all through
the lower orders. Their structure, composition and effects do not
differ, however, and it remains only to point out their distribution.
One of the frequent results of renal and pelvic lithiasis is, however,
missing in our records, namely hydronephrosis, and indeed a pressure
dilatation of the ureter and pelvis has not been observed in all our
experience. This would seem to be explained first upon the infrequency
of stone, of obstructive new growths and inflammatory strictures and
second by the fact that lower animals do not long survive conditions
which would occasion back pressure upon the kidneys.
Definite renal and pelvic calculi have occurred in five Ungulata, one
each in Edentata and Steganopodes. To these might be added cases of
uratic sand in one Carnivora, one Marsupialia, and uratic stones of
large size in the cloaca of two Passeres and one Accipitres. Uratic
collections within the avian kidney have been mentioned and will be
discussed later.
According to written descriptions and three preserved examples the
calculi in four of the ungulates are mixed urates and carbonates,
although one in a deer was said to be “mulberry” in surface. The
specimens at hand are moderately hard with rough irregularly
crystallized outer shells like carbonate deposits. Incomplete moulding
to the calyx is found. The pelvic cavity while seeming to be enlarged is
not distended nor do the stones assume the “antler” character and
distort the pyramid. All the animals showing these stones have but a
single pyramid in the kidney. The fifth example in the ungulate had
early stones forming in the apex of the pyramid and not yet discharged
into the pelvis. Four of these cases showed stones on both sides, one
only in the left kidney.
The case among the Edentata concerned an Armadillo (_Tatu
novemcinctus_), in the kidney of which there were definite smooth,
round, hard pebbles in the right pyramid and several fine grains in the
pelvis. There was a recent hemorrhage in the pelvis which, from local
appearances and autopsy survey, was due to the lithiasis.
A Gannet (_Sula bassana_) represents the only avian true calculus. In
this case many small, hard, yellow stones occupied the right pelves,
which contained also loose urates. The lobules were much distorted and
showed a mild interstitial change. This accumulation was confined to the
left side. These well developed cases having been mentioned the next
most important may be quoted:
Tasmanian Devil (_Sarcophilus ursinus_). Inactive and rather on the
decline for several months. Chronic diffuse nephritis with acute
interstitial exacerbation. Calculi in kidney pelvis. The kidney size
is normal, shape irregular, capsule smooth, strips easily leaving a
rough mottled green-brown surface. Consistency is soft, tough,
resilient. Cortex slightly wide, medulla normal. On removal of capsule
the surface is found very irregular and elevations from the surface
are pale red gray-green color. These elevations do not correspond with
any change in cortex on section. Section is smooth, solid, markings
not clear but glomeruli are distincter than striæ. Line between cortex
and medulla obscure. The left kidney contains sand-like calculi,
possibly uratic, as there are some pale areas near point of pyramid
which are firmer than rest of tissue and rather gritty. Microscopic
section of kidney shows the architecture much disturbed by connective
tissue overgrowth in outer layers of medulla and inner layers of
cortex and following the medullary rays to the capsule. Tubules are
compressed and distorted in the vicinity mentioned. Epithelium is
elsewhere low, opaque and granular. The connective tissue about the
glomeruli is thickened and hyaline as it is in most other places.
Tufts are not yet compressed. Following medullary rays there is a
recent round and polynuclear infiltrate both around and in tubules.
A Golden Cat (_Felis temminicki_) presented sand in the urethra, which
had caused a traumatic urethritis and distention of the bladder. There
was no evidence of renal urate collections, but a low grade prostatitis
existed so that the bladder might have been distended before the urethra
became inflamed, thereby giving opportunity for sand to form or to have
arisen in the prostatic ducts.
Three birds, a Bunting (_Passerina ciris_), a Bulbul (_Chloropsis
aurifrons_), and a Buzzard (_Buteo albicaudatus_), had large cloacal
urate calculi which could obstruct the ureter but had failed to do so;
one had an acute ascending pyelonephritis, however.
Excessive urate collections in ureters and kidneys occur all through the
avian orders and in about the same percentages; meat and fish-eating
birds have practically no cases, however. The condition seems at times
the only finding at autopsy, or it may be associated with uratic
serositis. Gout of birds is commonly accompanied by it, but need not be
since two of the best examples of this disease had practically normal
kidneys.
From these records it would seem that renal and pelvic calculi occur
almost exclusively in herbivorous animals. At least true stones forming
in the renal pyramid and pelvis are found most characteristically
developed in the Ungulata, the typically herbivorous mammal. Judging by
the bilateral distribution of stones and uratic collections, local
processes, inflammation especially, have less to do with their
production than the availability of precipitable inorganic salts in the
urine.
TUMORS.
Tumors of the kidney have been observed sixteen times, fourteen of which
were primary and two secondary. The latter two concerned an
epitheliomatous metastasis from a malignant papilloma in the stomach of
a Kangaroo (_Macropus rufus_) and a sarcoma growing like an infarct
secondary to a mediastinal tumor in a Dorcas Goat (_Capra hircus_). The
only important primary tumor of the kidney in a mammal was found in a
Gray Squirrel (_Sciurus carolinensis pennsylvanicus_), a solid gray
nodule composed histologically of large and small deeply staining cells,
many containing large vacuoles and fitted with a small dark nucleus. The
arrangement of the elements was in irregular acini or bundles and
thereby suggested the tumor known as hypernephroma. A small nodular
adenoma was found at the upper end of the right kidney in a common
opossum (_Didelphys virginiana_) and seemed to be purely of renal
construction in that an attempt to retain tubular arrangement was
evident.
[Illustration:
FIG. 21.—CALCULI FROM RENAL PELVIS TO END OF URETHRA. COMMON RACCOON
(PROCYON LOTOR). THESE STONES WERE PALE YELLOW-GRAY. THEY CONSISTED
OF A URATIC BASE, BUT SOME PHOSPHATES AND CARBONATES WERE FOUND. THE
RIGHT KIDNEY WAS NOT AFFECTED. THERE WAS ONE IRREGULAR CALCULUS AND
THIRTY-SEVEN SMOOTH MASSES FROM BLADDER TO END OF PENIS. THIS CASE
IS NOT INCLUDED IN STATISTICS. OCCURRING AFTER THEIR COLLECTION HAD
CEASED.
]
Twelve primary tumors occurred in birds, and of these five were found
among parrakeets, they being curiously enough all of the same type.
These cases were all discovered in the undulated grass variety
(_Melopsittacus undulatus_ ♂ ♂ ♂ ♂ ♂ ) and, because of this fact and
their histological similarity, have excited interest. Grossly they are
irregularly nodular or lobulated tumors usually springing distinctly
from one lobe, but sometimes destroying the whole organ; they are soft,
resilient and hold their place well during manipulation. Sometimes one
may detect the topography of the renal lobes on cross section while at
other times the mass is homogeneous. Microscopically one finds the
structure of papillary adenoma with cystic formations or the production
of atypical solid nests of epithelia which would have to be called
cancerous, for they certainly make no attempts to retain acinus or duct
groupings. Carcinomatous areas have been discovered in two of these
cases, not in the other three, which have been called papillary adenoma.
One of the tumors was subjected to many sectionings and different
stainings techniques to discover, if possible, animal and vegetable
parasites; this search failed. One of these tumors produced hemorrhage
by rupture of a pyramid but extension to adjacent tissue and metastases
have not been seen. Pathologically these must be classified with the
tumors but because of the number of closely similar growths in the same
avian species housed in the same enclosure, the possibility of a
parasitic cause will not be forgotten.
The remaining seven renal neoplasms are made up of two adenomata in a
Jungle Babbler, (_Crateropus canorus_) and a red headed duck (_Fulligula
ferina americana_), two adenocarcinomata in a saffron finch ♀ (_Sycalis
flaveola_), and a chestnut-eared finch, ♂ (_Amadina castanotis_), two
hypernephromata in an American robin, ♀ (_Planesticus migratorius_) and
a European blackbird, ♀ (_Merula merula_), and a spindle celled sarcoma
on a scaly ground dove ♀ (_Scardapella squamosa_). One adenocarcinoma
sent out metastases to the lung, one hypernephroma had secondary growths
in the lungs, the other in the liver. The sarcoma case presented a
metastasis in the tibia.
Diseases of the lower parts of the urinary tract are not numerous and of
incidental interest only; many are associated with or due to lesions in
the genital organs, and will be referred to later. Cystitis is uncommon,
only being observed some four times unrelated to prostatitis and
vesiculitis. Two of these cases were secondary to a traumatic
urethritis. No stones have been seen. A mixed cell sarcoma was found
springing from the bladder wall in a Richardson’s Kangaroo Rat
(_Perodipus richardsoni_). The written record has unfortunately been
lost, but the preserved slide confirms the original diagnosis. Rupture
of the bladder occurred in a Gray Fox with stenosis of the end of the
penile urethra causing retention and secondary cystitis. Another
stricture of the urethra in an Ocelot (_Felis chibigonazon_) caused
great dilatation of the bladder. This animal is thought to have chewed
off all the external genitalia because of lice, with the result that the
stump of the urethra became involved in a contracting cicatrix.
Opossums, raccoons and wild dogs have shown light cases of urethritis
seemingly traumatic in origin, and two dogs had cystitis and urethritis
associated with what was believed to be distemper.
SECTION IX
THE FEMALE REPRODUCTIVE ORGANS
The mechanism and organs of reproduction differ so widely in the classes
under discussion that it will be necessary to describe separately the
alterations in mammals and in birds. Examples of abnormality and disease
are not very numerous and I shall cite cases for many of the conditions
rather than prepare comparative lists as has been possible in many
foregoing sections. Some years ago Dr. Edward A. Schumann[40] studied
the comparative anatomy and physiology of the mammalian female
generative organs, and I shall condense and paraphrase his work. (The
complete articles may be found as in the references below.) This
gentleman, because of his gynecological experience and broad interest in
comparative biology, has been consulted whenever unusual material from
this tract has presented itself so that many of the descriptions that I
shall employ are due to him. I take this opportunity to acknowledge with
thanks his interest and helpfulness.
COMPARATIVE ANATOMY IN EXPLANATION OF HUMAN UTERINE ANOMALIES.
The development of the genital tract seems to be essentially the same
through all orders in that the genital ridge forms the ovary and its
attachments while the Mullerian ducts supply the tubes, uterus and
vagina. Early in fetal life these two longitudinal ducts begin to
approach one another, and by the end of the third month should be in the
position which they are to retain for the full development of their end
result. In the human being this position is complete union and fusion,
with the production of a single tube from the uterine fundus to the
exterior, while in the lowest mammals, edentates and marsupials, the two
Mullerian ducts retain their lateral position, and upon completion of
embryonal life a double tube from the ovaries to the exterior is found.
If the normal fusion of the ducts does not take place, and if for any
reason their proper relation is not reached, an abnormality will result
varying according to the stage of development that has been reached.
Thus in man instead of a single uterus of triangular shape and a single
cervix, a double set of tubes may be found. It can be shown that the
abnormalities of the human uterus are of definite and fixed types
corresponding to an arrest of fusion or completion of the developmental
cycle as given for the Mullerian ducts and further that these very
deformities are comparable to normal organs of lower orders. In other
words abnormalities in arrest of development in the human uterus
represent normal types of lower uteri at various evolutionary stages. In
monotremes there are two ovaries, tubes, uteri, cervices, a urogenital
passage and a clitoris. This corresponds with Uterus didelphys with a
single vagina. This abnormality while occurring in the lowest mammal,
does not represent the most marked deformity known for the human being—
that in which the double tube remains to the vaginal outlet, a condition
found in the marsupials. In this order the uteri are entirely separate,
and each is fitted with its own vagina. The next higher order, Edentata,
seems somewhat out of place if it be judged by its female genitalia
since it is possessed of a triangular uterus and single vagina but
without distinct cervical segment; the tract is very similar to that of
the Primates.
Rodents, in the various families, present no uniform uterine
construction, there being four kinds corresponding to as many degrees of
Mullerian duct fusion and differentiation. The lowest forms simulate the
marsupials, another group is like the monotremes, a third shows a
complete fusion with a single cordiform uterine body, while the last
resembles somewhat the first, but the uterine divisions are bound
together and the vagina is divided only half way down. The Insectivora
occupy a transitional position resembling higher and lower groups in
having a long uterovaginal canal, without distinct cervix, extending
upward into long curved cornua. Cetacea (whales) have a highly rugous
single vagina, a distinct, short uterine segment divided into two
separate horns. The genitalia of Sirenia resemble those of the last
group, but the cervix is better developed. In the last three orders the
clitoris begins to be well developed and to present externally.
Proboscidea have a single vagina separated from the short uterine body
by three transverse folds corresponding to the cervix; the two cornua
are long and wide.
“The foregoing orders present in their uteri all the essential
characteristics of uterus bicornis unicollis with single vagina and are
therefore the homologues of this anomaly in man.”
In the Perissodactyla, the bicornate uterus has a body of a little less
than half the whole length; there is a sphincter at the lower end of the
body but no projecting cervix. The cornua are longer still in the
Artiodactyla and are coiled in a manner suggesting spiral sheep’s horns;
there is a differentiated projecting cervix. In cats the length of the
uterine body and of the cornua are almost equal and both are flat tubes;
the cervix is prominent and the vagina long and rather smooth. The dog’s
uterus is similar but the two cornua are bound together or fused before
the point at which their termini enter that of the uterine body; the
cervix is not very prominent, but well formed and the vagina is rugous.
These types correspond to the uterus cordiformis. Lemurs have a common
uterovaginal cavity like the Edentata. The lower monkeys possess a long
slender uterus with definite superior lateral angles, the last vestiges
of the cornua, a prominent cervix and a short rugous vagina. The higher
apes have a uterine construction almost identical with that of man at
the stage of infantile development.
“From the foregoing study it is clearly shown that every anomaly of the
female genitalia in Man is in reality the result of atavism and hence, a
degenerative change, and inasmuch as every special form of anomaly finds
its counterpart in the normal anatomical arrangement of the analogous
structures in one or another of the great mammalian groups, one
additional item of proof is offered in support of that greatest of
biological doctrines, the descent of Man from the lower forms of life.”
ANATOMY OF LABOR.
In a second article Schumann reviews the comparative anatomy of labor,
demonstrating that the basic principles are essentially the same,
alterations only being in the direction of accommodation to the pelvic
construction. In order to make the analysis comparable with human
conditions the pelvis is studied as if the animal were standing erect
upon the hind limbs.
The salient points of difference between the quadruped pelvis and the
biped, human type may be epitomized as follows: (a) The entire pelvis
lies (with the animal in its normal station) in a generally horizontal
position with a slight slope downward anteriorly. (b) The false pelvis
is almost entirely wanting, there being practically no bony structures
above the brim with the exception of the small upper portions of the
ilia. (c) The pelvis in quadrupeds is never basin-shaped, the lateral
walls from the iliac crests to the tuberosities of the ischia lying
roughly parallel to each other and enclosing a pelvic cavity rectangular
in outline. Only in the highest apes does the basin-shaped pelvis
appear. (d) The angle of the axis from the promontory of the sacrum to
the symphysis is always greater in the quadrupeds than in man, averaging
in the former from 70 to 80 degrees, in the latter about 55 degrees, (e)
The symphysis pubis is an extremely long joint, being frequently greater
than half the length of the entire pelvis, (f) The sacroiliac joint is
more or less movable in all quadrupeds, especially in young animals. The
rotation of the sacrum on the ilia increases the anteroposterior
(dorsoventral) diameter of the outlet and at the same time wedges apart
the ilia, thus increasing the lateral diameter.
In regard to the forces of labor it is to be pointed out that in the
lower mammals the pregnant uterus hangs below the pubic arch so that the
fetus must rise at an angle of about 45 degrees to pass over the pelvic
brim. In so doing it meets the narrowest part of the triangular bony
pelvic inlet, the anterior pubic angle. Since the sacrum is above and
out of the way, the lateral diameter is the one which must be suitable
to the passage of the presenting part. This is the head in homo, the
largest part of the fetus, but in lower animals either head or breech
often accompanied by one or more extremities, may present; the head is
not the largest part in lower mammalian fetuses. The uterine contraction
proceeds as in man, the fundus and cornua acting alone until the cervix
contains the fetus, at which time all parts contract. In the bicornate
organ both sides must contract or the fetus might be forced from the
gravid to the empty side. In multiparous animals with both uterine horns
occupied, the fetuses lie head to head, breech to breech and are
expelled alternately from each side.
In uniparous animals rotation is in the nature of an accommodation of
the greatest diameter of the fetal body in cross section to greater axis
of the mother—the dorsoventral. Uterine contractions cause the fetus to
unfold from its elliptical form and to assume an extended position,
permitting head or breech to enter the lower pelvis. The pubic angle
having been passed and the extension of the presenting part being
successfully accomplished, there is no striking difference in the manner
of external expulsion of the fetus.
DYSTOCIA.
Dystocia in domesticated animals is a well studied subject, and its
general clinical phases are fairly well known. Several cases have been
observed, details of which are worthy of note since some of them are
entirely complete.
Inertia uteri as a single non-obstructive condition seems not to have
been observed here, although well enough known to veterinarians. Nor has
a case of dystocia been seen as the result of excessive expulsive force.
Obstruction to natural passage by bony deformities or malformations is a
common occurrence in man but not so in lower animals. There may also be
dystocia by reason of a normally formed but too small pelvis when the
female has been impregnated by a much larger male, or if the female
conceived before the pelvis has achieved its full growth.
Deformities may be due to irregularities of bony development, exostoses,
fracture or diseases of the osseous system. A most interesting case of
this type occurred in a Barbary ape (_Macacus innuus_) which had been in
the collection for two years and was apparently in good health when
discovered in labor.
No progress being made and the animal becoming shocked, an ineffectual
attempt was made to deliver by version, the monkey dying during the
operation. Upon autopsy the uterus contained a fetus apparently at
term. The head was extended so that the face presented, but the head
was not engaged. The cervix was fully dilated but the uterine muscle
was relaxed and flaccid. The fetus was dead when the animal was first
examined. The uterus contained two placentæ as is normal for these
apes, the left placenta being the place of attachment of the fetus
while the right one was somewhat smaller and presented no umbilical
cord. The fetus was normal in size and form, the face was extended and
its lower portion far advanced in a caput succedaneum. The
measurements of the fetal were as follows: bitemporal 5.5 cm.,
biparietal 6 cm., occipitomental 8.5 cm., occipitofrontal 7.5 cm. The
pelvis (dried specimen) presents a most interesting condition. The
sacrum is bent sharply forward, carrying with it the border of the
ilia, which are bent upon themselves forward and downward. The lateral
walls of the pelvis are greatly narrowed, the ischia drawn inward. The
pubes and the symphysis are fairly normal. The pelvic measurements
are: diagonal conjugate 6 cm., true conjugate 4 cm., greatest
transverse 4 cm.
It is apparent at a glance that here was an impossible labor, since the
head of the fetus could not possibly enter the pelvis, the size of
which, _intra vitam_, must have been less than the above measurements by
reason of the soft parts. “This is in the experience of the writer a
unique case of a complete obstetric history, plus the specimens, of
labor with an osteomalacic pelvis in a wild animal.”
Another case may be added to those already reported by Dr. Schumann, as
follows:
Hairy rumped Agouti (_Dasyprocta prymnolopha_). Dystocia. An
apparently normal fetus occupies the left uterine horn. The nose was
engaged in the pelvis and has been moulded in a curve pointing to the
right. The fetus measures—bitemporal 30 mm., cervical-coronal 31 mm.,
length of fetus 17 cm. Pelvic inlet in the fresh state measures 18 mm.
transversely and about 17 mm. anteroposteriorly. The umbilical cord is
10 cm. long and appears normal as do the membranes. Placenta presents
as a spherical mass of hard dense consistency, 35 mm. in diameter and
with apparently normal placental tissue occupying the lower border of
this spherical mass. On section the mass shows areas of alternating
soft red tissue separated by communicating trabeculæ of dense white
fibroid tissue. This mass is distinctly encapsulated, but the nature
of the enclosing membrane is indeterminate. The pelvis in dry state
shows evidences of malformation due to trauma. The right ileum is
pushed forward and inward carrying the acetabulum a short distance
inward and backward. There is a marked thickening about the right
acetabulum. At the upper portion of the symphysis there is marked
bending backward toward the sacrum with thickening of the bone. The
last sacral vertebra is sharply bent and anchylosed, forming an angle
of sixty degrees. The pelvic measurements in the dry state—at superior
strait-transverse 24 mm., right oblique 23 mm., left oblique 26 mm.,
true conjugate 22 mm., outlet 17 mm., between the ischiatic spines.
This is obviously a traumatic malformation and forms a relatively
contracted pelvis. The delivery of an adult fetus is impossible.
Cape Hyrax (_Hyrax capensis_). Impossible labor due to malformation of
the pelvis. This animal died as the result of shock and exhaustion of
labor. She was pregnant of two fetuses, one of which was extracted
manually by the keeper but was dead at birth. Twenty-four hours later
the animal was found dead. On autopsy there was present a fully
developed fetus in the right cornu, the head just above the pelvic
inlet. The left cornu was large and boggy. The myometrium of the right
side was so thin as to be almost transparent. On examining the bony
pelvis the reason for the dystocia is at once apparent. The sacrum is
tilted to the right, and the body of the left ileum is bent sharply to
the right, the pelvic inlet being obliquely contracted, the right
oblique diameter being 16 mm. while the left is 23 mm.
The pelvic obliquity made the birth of a full sized fetus impossible,
the one delivered being under developed. The myometrium was evidently
stretched almost to the point of rupture when death occurred.
Obstruction to the birth canal by abnormalities in the soft parts, such
as muscular rigidity, edema, or inflammation, tumors, atresia or
developmental defects are occasionally seen by veterinarians but have
not been encountered here.
Dystocia from uterine displacements are uncommon except such as may
depend upon the failure of support by the abdominal wall, since this is
the principal support of the organ especially when gravid. Hernia or
hysterocele is known and anteflexion has been seen. Torsion, a rare
human condition, is not uncommon in lower animals probably due to the
loose dependent position of the pregnant cornua, attached only to the
pelvic walls by slender inactive suspensory ligaments. A case may be
reported, not originally described.
Canada Porcupine (_Erethizon dorsatus dorsatus_). Obstructed labor.
This animal died from exhaustion due to an impossible labor. On
autopsy the abdomen contained a moderate amount of clear serous fluid
with one small blood clot. The right uterine cornu was distended with
a fetus to about the same diameter as the uterine body. This cornu was
congested and edematous and its walls very thin. The cornu was twisted
one-half full turn from right to left, so that the pregnant portion
overlaid the uterine body anteriorly. The torsion produced a
compression of the vessels on the right side to the point of violent
congestion of the cornu. There was no apparent rupture of the uterine
walls, death having occurred from exhaustion. The fetus and its
membranes were normal.
Many forms of abnormalities in position are recognized for domesticated
animals, but since we know so little of the early stage in the wild
specimens no data can be given.
Complicated labor in lower varieties of animals will follow lines
similar to those for man and domesticated animals. Hemorrhage from
trauma is not common at term, but several cases of abortion following
injury have been seen. Postpartum hemorrhage might be expected in the
higher apes which have a large discoid placenta similar to the human
form, but when the placenta is more loosely attached and is subdivided
as in lower forms, such bleeding is of no danger; when a cotyledon is
torn from the ungulate uterine wall, a free hemorrhage sometimes occurs.
Geoffroy’s Marmoset (_Leontocebus geoffroyi_). Puerperal relaxation of
the uterus with fatal hemorrhage. The uterus is 4 cm. long, 15 mm.
wide at intertubal line. Uterine wall averages 2 mm. in thickness.
Peritoneal surface is smooth, glistening and intact. Uterine
musculature is soft and relaxed. Entire organ is intensely congested
and on section uterine cavity contains a large firm blood clot
completely filling it. Mucosa is of deep purple color, shows many
fragments of decidua and is the seat of profuse hemorrhage.
Placenta previa is very rare. A row of cotyledons may form near the
internal os, therefore like a placenta previa, but it appears to be of
no consequence. Premature separation of the placenta is known to
veterinarians, and is exemplified by the following case in our records:
Black Lemur (_Lemur macaco_) was found dead in its cage. Upon autopsy
the uterus contained a small fetus with one leg and the tail
protruding from the vulva. The fetus was normal in size. There was a
large amount of free blood in the uterine cavity and extensive
extravasation into the myometrium. The placenta was completely
detached.
Rupture of the uterus and cervix have not been seen, but a traumatism of
the vagina gave occasion for the following death:
Bactrian Camel (_Camelus bactrianus_) died of shock in labor. Upon
autopsy the animal was found to have hydatid disease of the liver,
lungs, and spleen, cirrhosis of the liver, and nephrolithiasis.
Protruding from the vulva was a portion of the fetal membranes, the
whole vaginal wall and several coils of intestine which had escaped
through a large rent in the posterior vaginal wall. The anterior wall
was swollen and edematous, the whole region surrounded by clotted
blood. The cervix was obliterated, the membranes unruptured, the fetus
in the normal extended head presentation. The veil-like placenta was
somewhat injected but otherwise normal. There was some hemorrhage
about the rectum but none in the free peritoneum.
This animal had broken her hind leg just above the fetlock three weeks
before falling into labor, and was unable to stand. It is evident that
the difficulty of delivery associated with an unnatural and forced
posture due to the fractured leg was sufficient cause for the rupture of
the vagina where the tissues were degenerated as a result of the
coincident general disease.
Inversion of the uterus is one of the common accidents of labor among
all animals, most frequently seen in ruminants. It is a condition more
to be expected in lower animals than in man because of the long slender
relaxed suspensory ligaments, the length of the uterus and the rigor of
the contractions. The immediate causes are those operative for human
beings. Three cases are recorded—one in an axis deer, one in an opossum,
one in a mouse, the last being detailed in the following notes:
A Japanese Waltzing Mouse (_Mus wagnerii rotans_) died a few hours
after an uneventful labor. On autopsy the entire uterus was found
inverted and prolapsed, the organ the seat of a violent congestion,
the animal having died of shock.
[Illustration:
FIG. 22.—INVERTED AND PROLAPSED UTERUS. JAPANESE WALTZING MOUSE (MUS
WAGNERII ROTANS). UTERUS SHOWN LYING ON CARD.
]
THE PELVIS.
A study of the dynamics of the female pelvis from an evolutionary
standpoint may explain some of the difficulties attending parturition.
Starting from the biological law that morphology follows function and
that the anatomy of a part alters to suit a changed physiology with such
modifications as are necessary to fit each part properly to interact
with other structures comprising the entire animal, it is evident that
two great changes have occurred in the evolution of homo—the assumption
of the upright posture and an increase of intellectual power
necessitating a larger cranium of modified form. To this end also the
pelvis would have to change both for support and to allow the passage of
the enlarged head. The functions of the pelvis are (1) to attach the
legs or hinder limbs to the trunk; (2) to furnish points of attachment
and fulcra for the great muscles which move the limbs, and in the case
of man, hold the trunk erect; (3) to provide egress and support for the
terminal canals of the intestinal and urinary systems; (4) to provide
for a birth passage; (5) to act as a shelf and support for the abdominal
viscera. In quadrupeds the first four functions being perfectly served,
there are fewer abnormalities of reproduction (and in the positions of
viscera as well—ED.). In man natural selection weeded out narrow pelves,
but the present product is as yet an imperfect structure for one of its
main uses, parturition. It should be a funnel-shaped basin of the shape
of the fetal head and of the same height at all points—that is not
oblique, there should be no promontory, the pelvic symphysis should be
short and the sacrum of the same height. This would obviate internal
rotation now necessitated by the oblique pelvis; this does not occur in
quadrupeds.
Tracing the evolution of the pelvis, it is to be found first in fishes
where it is a loose disjointed, variable structure not attached to the
spine; in some it consists merely of ischia. In reptiles the box assumes
a form suggesting higher types. Passing from the toads to turtles and to
the crocodiles, the elements which go to make up the pelvis assume a
more and more osseous character and become more and more definitely
articulated with the spine or with the differentiated sacrum. Its
purpose in these low forms is mostly as a support for the muscles of the
legs and back. Birds present an advance in pelvic construction but with
a great preponderance of the vertebral column since thirteen to
seventeen bones may fuse to form a sacral “roof.” The ilia, ischia and
pubis are firmly combined. The box is long and narrow with a heavy part
for the acetabulum and broad surfaces for muscular insertions. The
pelvis of birds differs from that of cold-blooded vertebrates in the
greater number of vertebral segments entering into its composition, and
in their bony confluence. It differs from that of mammals by being
unclosed by an anterior symphysis and by a widely perforate acetabulum.
The ossification of the pelvic bones is to afford a support for the
legs, and the open pelvis allows passage of the large brittle egg. The
shape of the pelvis is of little importance in parturition in the
foregoing animals, except for birds which bear large eggs when the pubis
anteriorly is open for that purpose.
In monotremes one finds the reptilian type of pelvis with the three
divisions of the innominate bone remaining separate. The pelvis is
short, heavy and flat and is fitted with marsupial bones. The marsupial
pelvis, possessing parallel walls made by the ilia and ischia and a long
symphysis, resembles roughly a triangular prism. The sacrum is wedge-
shaped, without a promontory and has a considerable movability. The
marsupial bones are quite long. The triangular outlet is many times the
size necessary for the passage of the fetus.
The rodent pelvis is difficult to summarize morphologically by reason of
the great diversity of form occurring in the many genera of the order,
but it may be said that here the pelvis is usually of a type rather
higher in the scale than the other structural characteristics of the
order would indicate. The outlet is more commonly ovate than
rectangular, the ischia and ilia lie at a more marked angle to each
other, and the true conjugate forms a lesser angle than is common in
quadrupeds. The sacroiliac joint is, in general, freely movable.
The female insectivorous pelvis is relatively large, the sacroiliac
junction usually being long and well knit while the pubes are slender,
wide of angle as to their descending rami and there may be no symphysis,
as in bats. Edentates have distinct bony unions of the elements of the
innominate bone and of this to the sacrum which increases in width
downward permitting a long synostosis with ischia and pubes; these
joints are not movable. The pubes are slender and the symphysis short.
The sacrosymphyseal angle is 80 degrees in the armadillo. The inlet is
roughly triangular to almost round. Cetacea have no clearly developed
pelvis, its place being represented by two long bones, larger in males,
which seem to be the insertion of the genital erector muscles. There is
no junction to form a pelvis nor is there an acetabulum. A pelvic box is
absent in the Sirenia, but lateral processes from the lumbar vertebræ
form a sort of ileum between which an ischium is located.
Proboscidea have a massive pelvis lying vertical to the spine. The iliac
alæ are wide and deeply concave; the ischia are short, heavy and
parallel to the ilia; the pubes are short and combined in a heavy
symphysis; the sacroiliac joint is short, heavy and slightly movable;
the outlet is ovate. In one specimen examined the length was 4 feet,
symphysis 18 inches, true conjugate 19 inches, transverse diameter 17.5
inches; crests of iliac were 28 inches long.
Perissodactylic animals throughout this suborder have similar pelves
except in so far as the obliquity is concerned. In the rhinoceros it is
90° with the spinal column, in the horse 135°; the angle of the true
conjugate is 10° in the former, 50° in the latter. The lateral halves of
the box are heavy and parallel; the symphysis is short in the
rhinoceros, large in the horse; the outlet is ovoid. Artiodactyla,
including pachyderms and ruminants, show a variety of shapes and
constructions. Hippopotami have a short massive box tilted at about 150°
from the spine, with widely flaring ilia and ischia; the pubes are
slender but not combined in a strong symphysis. In ruminants the sacrum
consists of four fused units; the sacroiliac joint is fairly movable;
the obliquity is about 145°; ilia are long and slender and flaring; the
ischia are broad and parallel with the ilia; pubes are slender but form
a symphysis about two-fifths the total pelvic length; the infrapelvic
angle is wide; the outlet of the pelvis is almost rectangular.
The general characteristics of the carnivorous pelvis may be summarized
as consisting of a long strong symphysis, parallel lateral pelvic walls,
a great sacrosymphyseal angle, and a marked separation of the bodies of
the ischia. The sacroiliac joint is in general moderately movable.
The pelvis of lemurs is narrow, attached lightly to the slender sacrum,
tilted at an angle of 140° and is possessed of a short weak symphysis;
it resembles the structure in bats. In macaques the box is long, the
sacrum wide, with a short iliac synostosis, the ilia long, narrow and
curved out sharply, the ischia are continuous with the ilia and widely
separated; the symphysis is short, about one-sixth the pelvic length;
the angle of the superior strait is about 60°; the outlet is oval, the
transverse diameter being short. The chimpanzee pelvis is made up of a
wedge-shaped sacrum composed of three vertebræ, wide, flaring, concave
ilia, stout well separated ischia with flattened tuberosities and a
short symphysis parallel to the sacrum; the outlet is ovoid; true
conjugate angle is 65°; the sacroiliac junction has little motility. In
the gorillas the following points differ from the last described
structure. Five vertebræ comprise the sacrum and the anterior surface is
distinctly concave; the pelvic contour while still ovoid, has the two
diameters more nearly equal; the pelvic angle is obtuse; the true
conjugate is at an angle of 70°.
In man the salient features of the pelvis are—a broad, wedge-shaped
sacrum, concave anteriorly, with wide articular surfaces and a limited
motility; widely flaring ilia including the concave curvature of the
body of the bone whereby the lateral diameter of the pelvic inlet
becomes wider than in lower orders; short stout pubes with a narrowed
angle beneath them; heavy blunt ischia with large tuberosities; true
conjugate is at an angle of 55°. The human fetal pelvis resembles that
of quadrupeds.
Study of these data indicates that the quadruped pelvis retains many
things in common through all the orders especially in being a roughly
rectangular structure lying chiefly horizontally, with a poorly
developed false pelvis, straight ischia and a long symphysis pubis; the
angle of the true conjugate is greater than in man and may be up to 80°.
The long pubic synostosis changes the relation of the true and diagonal
conjugate, but the former is no indicator of pelvic capacity, since in
lower mammals the promontory of the sacrum lies anterior to the
symphysis; the vertical diameter is a better measure of pelvic size and
form. Sacral movement seems greater in lower animals especially in
youth. The shape of the pelvic inlet is triangular in the lowest forms,
the posterior base of this becoming wide as one ascends in a zoological
line; the concavity of the ilia also increases so that the higher the
animal the more curved are the lateral borders. In quadrupeds the
anteroposterior diameter is greater than the lateral; the reverse is
true in man. The long straight-sided quadruped pelvis is retained
because of the direction of the forces from the legs, which is as much
or more upon the anterior or pubic arch as upon the sacroiliac junction.
In the semiupright position of the monkey the force is directed backward
and downward upon the sacrum, this aiming to widen the pelvis by forcing
the ilia apart. The effect of the upward force from the femora is to
throw the pelvis upward and anteriorly by directing the line of action
through the acetabula more toward the ventral surface. The sacroiliac
ligaments hold the ilia firmly, their alæ being spread outward by the
force from above. Elevation of the pubes shortens their symphysis and
the true conjugate. By these changes the birth canal is shorter,
entirely bony, with the upper inlet on the same plane, and promontory
and symphysis are near enough the same level to be met at the same time
by the engaging head. In these pelves the anteroposterior diameter is
still long and superior rotation is not necessary.
In Man the force exerted on the pelvis from above is greatest among all
animals and is greater when he is in active motion. The force is
directed from above to the sacroiliac joint, the iliac bodies and the
acetabular region while from below the pressure is directly exerted upon
the last named. The force from above rotates the sacrum downward at its
upper end, the attached sacroiliac ligaments at the same time pulling
the alæ inward and throwing outward the lower end, the acetabular part.
This tends to widen the pelvic box and to reduce its anteroposterior
diameter. But the force acting from the legs and the adductors of the
thigh push the lower parts of the ilia and the ischia and pubes apart,
thus counterbalancing the effort of the force from above. The combined
forces tend to bend the iliac bodies, thereby producing the curved
lateral margins of the superior strait and making the lateral axis long.
As between these two forces that from above is certainly the greater.
The effect of these forces can be followed by comparing a quadruped
pelvis, a human fetal pelvis and an adult human one. The first two are
similar chiefly in the shape of the inlet and the flat character of the
ilia. This is strongly corroborative of the evolutionary development of
the pelvis to meet the demand of the upright position. The effects of
this evolution are as follows: First, to develop a forward inclination
of the sacrum and a concavity in its surface anteriorly, second to
increase greatly the iliopubic and ilioischiatic angles, third to cause
the acetabula to move forward of the lumbosacral axis, fourth to shorten
the bodies of the ilia and to develop in them a regularly curved
surface, the concavity of which faces forward and inward, fifth to
decrease the interpubic angle and accordingly to remove the triangular
quality of the pelvic contour, sixth to increase the transverse diameter
at the expense of the anteroposterior, and seventh to decrease greatly
the sacrosymphyseal angle with the result that the entire pelvic cavity
lies in one plane.
The effect of forces in alterations of the pelvic architecture may be
seen in their several stages by the observation of the mammalian pelvis
in the course of its evolution and development. The transitions in form
are very gradual, but their gradations are well shown in the
characteristic forms which have been described; the quadruped, monkey,
anthropoid ape, human fetal and adult human type.
By an examination of the adult pelvis and fetal skulls it will be seen
that the shape of the quadruped birth canal accommodates the fetal head
nicely when in extension since there is no large posterior cranial
development, the head and neck being of nearly the same thickness. In
the monkey, where the facial angle increases, the head does not advance
as a pointed presentation but as an irregular surface—the chin, forehead
or occiput. It is only when the head has assumed a high facial angle and
a well developed occipital lobe and the pelvic inlet has become
transversely wide, that internal rotation is necessary.
Resuming a discussion of our records I shall at this place introduce
additional cases of pathology in the parturient genital organ and then
discuss the general system. Beside the cases of dystocia discussed in
preceding pages there occurred in a deer a complete eversion of the
uterus, which was incompletely involuted, accompanying prolapse of the
rectum and bladder due to straining after severe injuries, probably
inflicted by a male. The animal lived long enough to develop a purulent
cystitis which spread to the vagina, uterus and pelvic soft parts. The
left uterine cornu of an American bison was found to contain a
decomposing fetus at about half term; general sepsis had supervened
which led to the animal’s death in about a week, according to the
keeper’s observations. The history of a monkey, followed through two
pregnancies and finally dying of tuberculosis and sepsis is interesting.
Pigtailed Macaque (_Macacus nemestrinus_). Received March 5, 1903,
died October 29, 1904. This animal gave birth on December 28, 1903 to
a young one which appeared feet first; the arms appeared to have
penetrated the septum between the vagina and rectum and protruded
through the anus. Had to be cut off before delivery. She had a second
young one October 21, 1904, which was properly delivered but was weak
and lived two days, having received little attention from the mother.
The mother since has been weak in the hind legs, eaten almost nothing
and several times has passed a little blood in the stool. Lungs are
partially collapsed; contain scattered small pinhead tubercles; right
lower lobe contains a caseous nodule about the size of a cherry. Both
pleuræ contain clear fluid. Abdomen contains a half pint of cloudy
fluid. Omentum adherent along lower border and region of spleen and
contains pinhead tubercles. Surface of the liver is studded with
numerous pinpoint, pinhead and (old) pea sized tubercles. Some places
in the liver seem to be the result of two invasions. Spleen presents
small cherry sized tubercles thickly grouped together leaving small
amount of splenic tissue to be seen. Kidneys contain pinhead to barley
grain tubercles. Uterus is somewhat enlarged. External surface smooth.
Section shows wall to be about one-quarter inch thick. Uterine cavity
enlarged. Considerable bloody pus in uterine cavity. No communication
can be found between the bladder and the vaginal wall or between the
vaginal wall and the rectum. The intestines are negative. Mesenteric
glands enlarged and caseous.
Abortion and miscarriage are occasionally seen in the monkeys, rodents
and ungulates. The underlying reason for this can seldom be determined.
A few cases seem to depend upon annoyance or abuse by cage-mates, a few
to immaturity of the mother and some others seem the result of bone
diseases such as osteomalacia. It does not occur regularly in any group
or enclosure and appears to have no comparative pathological value.
Injuries of the external genitalia of the nature of lacerated wounds are
occasionally seen in ungulates and carnivores, but never in monkeys.
Acute vaginitis, sometimes localized into an abscess of the wall has
been known to follow these traumata. Chronic changes have been met but
once, which example will be detailed under another heading.
INFLAMMATIONS.
Endometritis has been observed sixteen times, as follows: Carnivora 10,
Rodentia 3, Ungulata 2, Edentata 1. In searching for causes it was found
that the association with a recent delivery of young, an abortion or the
retention of a fetus, was responsible five times. Association with
tumors of the uterus was noted four times. Injury preceded the condition
on two occasions, while one instance seemed to be hematogenic, being
secondary to a septic pneumonia. On four occasions the actual cause
could not be established with satisfaction. Pathologically the traumatic
and parturient cases were purulent while tumors seemed to produce a more
exfoliative or hypertrophic inflammation.
Inflammation of the Fallopian tube has been observed but five times, and
only in one of these did the uterine wall fail to participate in the
disease. The animals affected were three carnivores, one rodent and one
marsupial.
No particularly important association of this salpingitis and other
pathology was noted, and indeed the only noteworthy lesion of the organ
under discussion is now to be cited.
Nylghaie (_Boselaphus tragocamelus_). Chronic vaginitis, fibroma
uteri, chronic tuberculous salpingitis. The vulva and lower half of
the vagina are covered by a thin coating of yellowish mucus. Mucosa is
mottled purple, irregular, in some places smooth and flat, and in
others showing clear cysts with yellowish fluid contents. The upper
part of the vagina shows a pedunculated fibroid extending from the
cervix. This tumor measures 32 × 20 mm., and is attached to the
posterior cervical wall by a broad pedicle and is of smooth surface.
The right uterine wall shows a large fibroid which twists the uterine
lumen to the left. The tumor in the right uterine cornu is nodular,
measures 11 × 9 × 7 cm., shows many dilated veins coursing over the
surface and one section shows a soft central necrotic area. The left
uterine cornu shows a small fibroid at the lower end. There is a
chronic endometritis present. The outer half of the right tube is the
seat of firm nodular swellings, one of which proves to be a purulent
salpingitis (tuberculous), the others calcareocaseous salpingitis.
Both ovaries are fibroid and cystic. Microscopic section shows some
exfoliation of the epithelium of the vagina. The uterine cornu is
thickened and the fibrous tissue is greatly increased. The tube is the
seat of a purulent salpingitis with an occasional broken down tubercle
present. The ovaries show a mild degree of oöphoritis (Fig. 23).
OBSTRUCTIONS TO CONTINUITY OF BIRTH CANAL.
Obstruction to the lumen of the genital canal was observed in three
mammals.
An American Bison (_Bison bison_), five years old and known to have
been in captivity three years died of a chronic gastroenteritis and
pulmonary parasites after many weeks of failing health. At autopsy a
double hydrosalpinx, and probably unilateral hydrometra, with low
grade cystic oöphoritis were found. A picture is reproduced. The notes
are not perfectly clear as to the anatomy but from the gross specimen
in preservative it would seem that the left uterine cornu was involved
in the dilatation (Fig. 24).
[Illustration:
FIG. 23.—PEDUNCULATED FIBROMA OF CERVIX; INTRAMURAL FIBROMA OF UTERINE
BODY; FIBROMA OF LEFT UTERINE CORNU; TUBERCULOUS SALPINGITIS AND
MURAL METRITIS RIGHT SIDE. NYLGHAIE (BOSELAPHUS TRAGOCAMELUS).
]
[Illustration:
FIG. 24.—DOUBLE HYDROSALPINX AND UNILATERAL HYDROMETRA. BISON (BISON
BISON).
]
Lion cub (_Felis leo_) had congenital cystic uterus. The only
abnormality found is in connection with the internal genitalia. The
vagina is 50 mm. long, uterus 23 mm. long, horns of uterus each 90 mm.
long. The diameter of the uterus measures 10 mm. in both body and
cornua, the latter being distended by clear watery fluid. They are
symmetrically curved downward. They show no adhesions or obliteration
of the os uteri to account for fluid retention. The probe is readily
passed from the vagina to the end of the uterine horns. Vagina is
patulous through its whole course. Ovary and tube normal.
An Axis Deer (_Cervus axis_) showed congenital hydrometra. This
specimen is from a day old animal, consists of the genitalia in which
the entire body of the uterus and both uterine cornua have been
transformed into a thin-walled translucent cystic cavity containing
clear fluid. The body of the uterus measures 15 mm. diameter, each
cornu reaching the diameter of 5 mm. The cornua are curled not unlike
ram’s horns, and are united by a line of adhesions above the body in
the midline. From the ends of the convoluted and cystic uterus and
cornua spring the normal tubes each with its ovary.
CYSTS.
Cysts have not been noticed in the lower genital canal, but it is true
that this region is not exhaustively studied in routine autopsies;
however, no large cysts have occurred there. Cysts of the ovary have
been limited to the so-called cystic disease of this organ; one
parovarian cyst has been found. These animals, two ungulates, two
carnivores and a rodent, are noted as being young adults, only one of
which was known to have borne young. In only one, the rodent, was there
evidence of chronic peritoneal disease. The notes of the parovarian cyst
case are as follows:
An Aoudad (_Ovis tragelaphus_) showed a ruptured parovarian cyst with
normal right side pregnancy. The fetus, its placenta and membranes
show no change. The right broad ligament and ovary are negative, the
latter containing a red and gray corpus luteum. The left ovary is
fibrotic and the left ligament is the seat of a large hematoma, which
on section is found to contain thin sheets of gray translucent
membrane, like walls of a cyst. The vessels are all distended.
Arteries have stiff walls and are empty. Veins have well formed clot.
The whole uterus and adnexa were slightly turned to the right, but the
twist does not seem to have been sufficient to cause rupture of a
broad ligament vessel. Microscopic section of the broad ligament shows
a parovarian cyst into which there has been hemorrhage. The cyst is
separated from the ovary proper by a short band of tissue which
apparently consists of thinnedout ovarian cortex.
TUMORS.
Tumors of this tract in the mammals have been confined to the uterus
proper, none having been found in the vagina, tubes or ovaries; in birds
one oviductal growth and two ovarian tumors are recorded. These tumors
are reported briefly according to their histological structures, a brief
summary being added at the end.
A Black Lemur (_Lemur macaco_) showed a local leiomyofibromatous
nodule on the lateral aspect of the uterine body near the cornu.
A nine banded Armadillo (_Tatu novemcinctus_) gave an interesting
specimen which can be described as follows: The uterus is enlarged so
that it measures 90 mm. from external os to fundus. Tubes and ovaries
apparently normal. There is considerable grumous blood in the vagina
and cervix; the former is normal. The cervix is pale and opaque in its
lower half; upper half is slightly congested and mucosa decidedly
rugous. The uterus itself shows an attenuated muscular wall with a
thickened irregular mucosa which is the seat of pseudomembranous tabs
of a dull red color, while the mucous membrane itself is irregularly
red and yellow; also some grumous blood in the cavity. The size of the
uterus is due to a large fibroma attached to the left lateral wall
near the cornu. The mucous membrane of this is irregularly disturbed
in some places, the tumor being partly bare. Here and there the mucous
membrane shows the same degenerating hypertrophic character as seen on
uterine wall. The tumor is attached to the wall by a narrow peduncle
(Fig. 25).
A nylghaie with multiple fibromata has already been described.
A Jaguar (_Felis onca_) presented in the middle of the right uterine
cornu a cystic resilient tumor 3 × 4 cm., which proved to be a
fibroadenoma.
A lioness (_Felis leo_) presented a penetrating malignant adenoma of
the uterine cervix upon which an active endometritis was implanted.
The tumor penetrated the uterine wall, which gave way, an acute fatal
peritonitis resulting. Metastases had occurred to the lung.
A Wild Boar (_Sus scrofa_) had a generalized ulcerating carcinoma of
the uterine body.
An instance of chorionepithelioma in a Canada porcupine is worthy of
separate description.
[Illustration:
FIG. 25.—PEDUNCULATED FIBROMA UTERI. NINE BANDED ARMADILLO (TATU
NOVEMCINCTUS).
]
[Illustration:
FIG. 26.—FIBROMYOMA OF UTERUS. CORNUA AND TUBES. INDIAN ELEPHANT
(ELEPHAS INDICUS). WHOLE MASS AS MOUNTED ON BOARD. IT MEASURED WHEN
FRESH ABOUT SIX FEET ACROSS.
FIG. 27.—CROSS SECTION OF CORNU OF Fig. 26 AT HIGHER POWER. A PIECE
CUT OFF WHERE THE PALE AREA SHOWS ON THE RIGHT CORNU OF THE OTHER
FIGURE.
]
Canada Porcupine (_Erethizon dorsatus dorsatus_). Acute suppurative
catarrhal endometritis, hemorrhage in myometrium, chorionepithelioma.
In anterior abdominal wall a short quill was found imbedded. A very
small quill was imbedded in the retrocervical muscles. A quill about 2
cm. long lies free in the peritoneal cavity attached by recent plastic
adhesions to peritoneum over left pubic ramus. A fourth quill was
adherent by recent fibrous lesions to anterior wall of cecum.
Peritoneum contains a moderate excess of thin watery fluid. Liver and
spleen are negative. Kidney is large, greenish yellow, firm, smooth
and glistening. The right uterine cornu is subinvoluted (the animal
was delivered of a fetus before arrival at the Garden, which was
sixteen days before death). Its walls are thick and distinctly
congested, the congestion being of inflammatory type. Microscopic
section of uterus shows a regular, not ulcerated serosa. Subjacent
fibrous tissue is loose and contains a granular precipitate together
with a few red blood cells. Muscular bundles under this are widely
separated evidently partly by trauma, but certainly also by edematous
interstitial tissue in which fibrillæ are widely separated and between
which free red blood cells and plasma cells are seen. Capillaries
ramifying through muscular bundles are greatly distended and
congested. Numerous large arteries are present in addition. Some of
these contain pink granular material within their walls together with
diffuse collection of red blood cells. Fibroblasts extend into this
necrotic mass from other sections of the walls. Lumen of such arteries
is diminished and in places quite obliterated by recent organization
tissue. At many places in muscularis are large cells of irregular
rounded form and some cytoplasms incline toward the basic tint with
one or several large hyperchromatic nuclei. They are especially likely
to occur close to a capillary. There is an especially large
accumulation of these cells at that point of section farthest from
fundus. Here these cells occur in chord-like masses which infiltrate
the muscularis both internally and externally. This particular mass
lies in the muscularis internal to great arteries and well removed
from mucosa. In this mass are giant cells with multiple nuclei
scattered through the whole cytoplasm together with smaller cells with
exceptionally large hyperchromatic nuclei. Subepithelial tissue is
especially congested and contains numerous fibroblasts together with a
few well formed glandular acini. Lining epithelium is discontinuous,
of simple tall columnar type, in places becoming flattened or even
lost. Lumen of organ is practically completely occupied by pus.
The Indian Elephant “Empress” (_Elephas indicus_) showed calcified
fibroids of the fimbriæ; gross and microscopic notes and a photograph
are given. The uterus is bicornate in type. In its body there are
numerous fibrous nodules 1 to 4 cm. diameter. They can be traced from
the cervix to the ends of both horns and tubes. At the end of each
tube there is a great mass of calcified partly conglomerate tumors
some of which are partly, others quite, pedunculated. One specimen
measuring 2 × 1 × 1½ cm. has a peduncle 15 cm. long. The mass on the
right side weighs 3,926 grams, that on the left side about the same.
Section of tumor from uterine cornu shows the classical appearance of
a leiomyoma with usual whorling and interlacing bundles of involuntary
muscle fibres. Degenerative and vascular changes not seen nor is there
any notable addition of fibrous tissue. This latter tissue is shown
only in small amounts at one end of section.
The preceding data record the discovery of three fibromata of the uterus
and one of the fimbriæ; one fibroadenomata of the cystic type, one
malignant adenoma, one adenocarcinoma, and one chorionepithelioma. They
were found in Lemures 1, Carnivora 2, Ungulata 2, Proboscidea 1,
Rodentia 1, and Edentata 1. Metastases occurred but once, to the lung.
No secondary tumors were found in the uterus.
While upon the subject of neoplasms of the female genitalia, it may be
well to describe the three instances found in the avian organs. A very
definite case of adenocarcinoma occurred in the oviduct of an Undulated
Grass Parrakeet (_Melopsittacus undulatus_), a variety of bird very
susceptible to neoplasms. The notes in an abbreviated form are given:
Immediately under the ovary is an irregular mass measuring 2 cm. long,
1 cm. wide, 1 cm. deep. The lower part of the tumor thus comes to
press against the cloaca. It is adherent anteriorly to the peritoneum.
It apparently consists of two parts, an upper rounded larger, and a
lower spherical smaller. Both parts are well encapsulated and
separated from each other by a well defined constriction. The upper
part has a pale opalescent appearance. It cut easily with moderate
resistance. The lower portion externally has an egg-yellow color
streaked with red. Upon section it has the same general appearance but
contains in addition numerous small, irregular, yellow areas which
mask the general opalescent appearance. The centre of this node
contains an empty space (cyst) 1 × 2 mm. Microscopic section consists
of an oval or elliptical mass showing over one convexity a depression
simulating a constriction. A thin fibrous capsule extends over most of
the section which is extra thick at the point of constriction.
Constriction roughly divides the section into two. The upper portion
consists of one or two coarse septa of fibrous tissue. From these
central areas a delicate connective tissue framework extends
peripherally. In this framework are great numbers of irregular gland
spaces. These gland spaces are so closely placed in most cases that
room is afforded for but one nucleus of the bundle. The gland spaces
vary in size, some large, some small, and show grotesque shapes. The
larger gland spaces here contain granular debris and pyknotic nuclei.
Compound granule cells suggesting colostrum corpuscles may be seen in
this debris. The epithelium of the gland spaces consists of a single
layer of columnar epithelium of low cuboidal type. In places it is
heaped up so as to present several layers. In places too it is not
applied in a regular manner to the basement membrane but breaks
through and then the cells extend in most disorderly fashion into the
lymphatics of the stroma. At these points the nuclei are
hyperchromatic. The lower portion follows closely the description
given above save that the glandular spaces are much larger. They
contain pink glandular material with admixture of compound granule
cells. At the convexity of the tumor the acini are especially large.
Here they contain a pink granular material which stains more intensely
than the other granular contents and, too, inside of this intense pink
material are sharply circumscribed areas of yet more intensely pink
staining material. This latter substance has a streaming appearance
under the high power. This streaming appearance is due to elongated
areas of less dense material which are placed with their long axes
parallel. This lower portion shows, furthermore, even with the naked
eye, two large cysts which are lined by epithelium and contain a very
small number of compound granule cells. The capsule at the lower pole
is worthy of note from the extreme dilatation of its capillaries.
[Illustration:
FIG. 28.—PAPILLARY ADENOMA OF OVARY. WILD TURKEY (MELLEAGRIS
GALLOPAVO).
]
A papillary adenoma was found in a wild turkey (Fig. 26) and a mixed
cell sarcoma in a King parrakeet (_Apromictus cyanopygius_). None of
these tumors sent out metastases.
Interest in the avian reproductive tract from a pathological standpoint
centres around the tumors as already given, and abnormalities in egg-
bearing. Among our specimens there have been many cases of soft shelled
eggs apparently blocked in the oviduct, of “egg-binding” and of the
inspissated-egg-remains in the abdominal cavity. These conditions are
well known to veterinarians and are explained on the basis of improper
food, immaturity of the bearing fowl, injury and inflammations of the
cloaca and oviduct. I made an attempt to associate these conditions with
infectious disease incidence and with the normal egg size. The results
are not harmonious. No relation existed between general or local
infection and any of these conditions. Gallinaceous birds with their
large eggs show the highest percentage (2.3 per cent.), but Anseres with
a somewhat larger relative egg size show 1.6 per cent. Passeres, with
eggs of very variable size but relatively large pelves, have an
incidence of .6 per cent. Struthiones’ eggs are relatively small; their
incidence is 1.5 per cent.
Salpingitis occurred in seven cases, but there have been no evidences of
an acute infectious disease such as is responsible for gleet.
THE MAMMARY GLAND.
This structure has been the seat of three inflammatory conditions and
four tumors. The former occurred twice in nursing animals, one of which
seemed to be suffering with distemper, another from puerperal sepsis,
while the third case was probably traumatic. The animals were in order,
a raccoon, a coati and a skunk. Four cancers of the breast have been
observed, all richly cellular or glandular in type; none of the
scirrhous variety has been encountered. Two of them were ulcerating and
one was about to become so. One gave extension to the axilla and lung,
one had penetrated the abdominal wall and grown around the kidney; the
remainder had not yet extended. The animals were Black Bear (_Ursus
americanus_) (thoracic mamma with extension), Common Opossum (_Didelphys
virginiana_) (two sections of breast in pouch), two White footed Mice
(_Peromyscus leucopus_) (posterior abdominal right gland and whole
side). These animals were all adult but not old.
[Illustration:
FIG. 29.—ADENOCARCINOMA OF MAMMARY GLAND (TWO SECTIONS WITHIN POUCH).
COMMON OPOSSUM (DIDELPHYS VIRGINIANA).
]
SECTION X
THE MALE GENITALIA
Affections of the penis are limited to phimosis and occasional
inflammations on a traumatic basis. The latter is best seen in
carnivorous animals like raccoons and coatis, but has little
pathological interest. Two cases of phimosis have been seen at the
autopsy table and one in an animal (hyena) still living. The last was
operated upon some years ago and has given no trouble since. The prepuce
of this beast is seldom retracted, but no swelling or retention of urine
has occurred. A Red River Hog (_Potamochœrus porous_) dying of a variety
of lesions, was found to have contracted preputial opening, the edges of
which were tight and adherent to the glans penis at various spots. The
prepuce had been dilated with urine to a large size from which
collection the fluid could be pressed dropwise only by considerable
pressure. Opening the sac revealed forty to fifty gray white sand
granules about the size of millet seeds. A gray fox (_Canis cinereo
argenteus_) had a mild grade of phimosis; in this case probably
traumatism had some etiological relation, for it is the one referred to
before in which a terminal urethral stricture was followed by rupture of
the bladder.
The testes have been peculiarly free of disease, only a small number of
lesions having been found. A raccoon had an acute inflammation,
traumatic in origin, and a few passerine birds were noted as showing
involvement of this organ in the presence of some general infectious
diseases. Two tumors were found in birds, none in mammals. The avian
cases both occurred in Red shouldered Parrakeets (_Palæornis eupatrius_)
and were round cell sarcomata, without metastases.
Acute inflammations of the prostate and Cowper’s glands occurred only
once as secondary to pelvic infection. Chronic change was observed in
these bodies on two occasions, and prostatic hyperplasia, commonly
called hypertrophy, was seen thrice. The mammalian prostatic area is
known to become overfilled with secretion and to be affected by
inflammation when it is not discharged. This occurred in a wood rat
(_Neotoma pennsylvanica_) and a wild boar (_Sus scrofa_), the former
having the condition so marked that prostate and seminal vesicles were
swollen backward into the pelvis like a tumor. Histologically one finds
in these conditions an engorgement of the glandular and ductal spaces
with a mucoid substance and a mild round and plasma cell infiltrate in
the connective tissue; there are no marked evidences of active
inflammation. The testes were not abnormal in these cases.
The three cases of “hypertrophy” of the prostate are worthy of separate
record.
Indian Paradoxure (_Paradoxurus niger_) the prostate is greatly
enlarged, of pale orange color, soft and does not exude pus on section
or pressure.
Common Opossum (_Didelphys virginiana_) The prostate is enlarged,
soft, gray-yellow. Urethra contains a little gray mucus but seems
patulous. Seminal vesicles negative.
Rhesus Macaque (_Macacus rhesus_). Glandular hyperplasia of prostate.
The bladder is collapsed. The opening of the urethra is occupied by a
firm, friable yellow-white cast of matter apparently inspissated
semen. Urethral mucous membrane normal. Prostate is 7 × 4.5 × 3 cm.
firm, resilient, dull purple-gray, capsule negative. Section shows
normal lobulations containing apparently normal secretion. Vasa
negative. Testes negative. Microscopic section of prostate shows acini
of various sizes lined by a single layer of tall vacuolated cells with
nucleus at the bottom. Cells probably nowhere reduplicated. Acini
nowhere grossly atypical but everywhere hyperplastic and dilated
irregularly. Mass is adenomatous in general increase but no part is
truly neoplastic. Interstitial tissue rather less than normal
proportionately. No “amyloid” bodies.
[Illustration:
FIG. 30.—PAPILLARY ADENOMATOUS HYPERPLASIA OF THE PROSTATE GLAND. RING
TAILED LEMUR (LEMUR CATTA).
]
Still another case of accessory sex gland enlargement was found in a
Ring tailed Lemur (_Lemur catta_), this time, however, with more
suggestion of a neoplastic change. The prostate of the lemur is normally
large, pale gray-pink and rather firm. Histologically it is about
equally glandular and fibrous. In this case the cellular activity is
undoubted, and one must consider it adenomatous. The cause of death was
enteritis, being perhaps more serious in the presence of the urethral
obstruction.
The seminal vesicles are distended to 7 × 2 cm. with a thick boiled-
starch-like material. Wall and mucosa are negative. Prostate large,
tense and injected. Its cut surface is pale purple, homogeneous;
character of fluid is normal although excessive. Urethra is occupied
by a cast of rather tenacious starch-like matter which begins at neck
of bladder and runs almost to meatus. Openings of excretory ducts are
prominent. Mucosa and submucosa of urethra are deep purple and the
former seems to be slightly opaque as if covered with desquamated
epithelium. Testes and epididymes seem normal. Vasa deferentia are
slightly distended with excess of normally turbid fluid. Microscopical
section shows hyperplastic epithelial condition with accumulation of
droplets of hyaline matter but there is no amyloid deposit. In places
it is possible to see a hyperplastic and loosened epithelium with
nuclei becoming vacuolated, and the whole being cast off. Less
granular free globules suggest that this is the method of origin of
the hyaline globules free in the acini. The picture is one of
papillary adenoma. In some places there is surely reduplication of the
lining cells. Connective tissue is deeply staining, compact and with
adult nuclei. Growth is not very vascular. There are no corpora
amylacea.
A case of tuberculous prostatitis and seminal vesiculitis was seen in a
Japanese Macaque (_Macacus fuscatus_). Judging by the advanced stage of
these lesions and their more recent character in other viscera, the
disease was suspected as pelvic in origin, possibly due to infection by
a thermometer. Whether or not such be the case cannot be established,
but at all events, separate thermometers kept in carbolated vaseline
were employed after this death. The females caged with this animal did
not develop tuberculosis of the pelvic organs.
SECTION XI
THE DUCTLESS GLANDS
THE THYROID BODIES.
The ductless glands occupying the anterior cervical regions, known as
the thyroids and parathyroids are structures to be found in some form in
all vertebrates, but increase in distinctness of outline and
construction upward in the zoological scale. In the bird they present
themselves as discrete rounded bodies lying well to the side of the
midline resting usually upon the carotid artery or jugular vein or both.
As one removes the skin reddish brown globular masses will be exposed to
view, sometimes showing an irregular lobular outline, a variation due to
separate but attached masses of parathyroid glandules; the latter may be
yellowish or even white. For the most part, however, distinct thyroid
and parathyroid bodies are separated with difficulty, and one must
discover the latter by microscopical section. In the mammal these organs
are by no means so readily found when removing the cervical integument,
for they are usually buried beside the trachea and covered by
sternohyoid and sternothyroid muscles. Their position, relative to the
larynx and upper end of the sternum, varies considerably but this seems
to have little importance in the enlargements to which the gland is
liable. It is, however, lower, that is more posterior, than in the human
being, rarely rising as high as the lateral thyroid cartilages. The
principal lobes are elliptical or roughly triangular masses with their
long axis corresponding to that of the animal’s body and apposed
mesially to the trachea. When enlargement occurs it develops in the
anterior or ventral direction, pushing through the cleft between the
muscles and the trachea to present under the cervical skin. In
quadrupeds it may become dependent and the swelling is nearer the
sternum than is the case in man. The isthmus is a very variable
structure, and its presence or absence cannot be said to be a constant
character in any order, or indeed in any family. I have seen in old
animals a fibrous band extending over the face of the trachea connecting
the capsule of the lateral lobes, which might have been an isthmus at
one time. From these few observations the idea of atrophic fibrosis
occurred to me. Such may be the reason for the absence of this
transverse link in some adult specimens.
The amount of thyroid tissue possessed by an animal might be judged by
measurement or weight. The former is misleading since the density might
vary, as it certainly does in the two classes and between certain orders
in mammals. Actual weights would afford little comparison, whereas the
weight in terms of total body weight may supply a guide to the amount of
gland normal to an animal. There are given in Table 15 the grams-per-
kilogram-body-weights of the thyroid bodies (thyroid and parathyroids
both sides combined) of twenty animals whose gland seemed entirely
normal at autopsy. They are all adult specimens, free of cretinoid
characters and of bone or heart diseases, conditions which might reflect
abnormalities to these glands. The list is too small to warrant any
conclusions, but in one respect confirms Murray’s[41] observation and
certain experimental work, notably of Vincent and Jolly[42] and Carlson,
Rooks and McKie[43]. The carnivores have more thyroid than ungulates
(averages .55 gm. _vs._ .18 gm.), but the marsupials on our list have
nearly as high an average as the former, namely .44 gm. To these figures
might be added others which I have worked out from the list given by
Murray; it is only possible to compute the gram-perkilogram value for a
few of his examples since the body weights are not given in all. Using
2.2 pounds as equal to one kilogram, the seal of 432 kilos had .03 gm.
of thyroid, lion had .18 gm., leopard had .46 gm., a serval .36 gm., a
skunk 2.35 gm., (was this normal?) while a single herbivore with the
weight given was a porcupine having .25 gm. per kilo. The average of
Murray’s carnivores is therefore .67 gm. per kilo of body weight,
whereas our figure is .55 gm. That the incidence of thyroid
abnormalities stands in direct relation to carnivorous character has
been recognized before, and is abundantly borne out by our statistics,
as will appear at a later place.
TABLE 15
_Showing Weights of Animals, of Their Thyroid Bodies and the Relation
of These Weights Per Kilogram._
═════════════════════════════╤═════════════╤═════════════╤═════════════
│Grams of Body│ Grams of │ Grams of
│ │ Thyroid │ Thyroid per
│ │ │Kilo of Body
─────────────────────────────┼─────────────┼─────────────┼─────────────
Primates: │ │ │
Woolly Monkey │ 2,370│ 2.│ .84
Lagothrix lagotricha │ │ │
Carnivora: │ │ │
Wild Cat │ 8,180│ 2.│ .24
Felis ruffus │ │ │
Silver Fox │ 3,325│ 4.│ 1.2
Canis chama │ │ │
Kamchatkan Bear │ 31,800│ 22.│ .63
Ursus beringiana │ │ │
Lynx │ 9,500│ 1.│ .1
Felis canadensis │ │ │
Jaguar │ 29,500│ 16.│ .54
Felis onca │ │ │
Rodentia: │ │ │
Ground Squirrel │ 550│ 2.│ 3.6
Xerus capensis │ │ │
Ungulata: │ │ │
Zebra │ 340,000│ 64.│ .19
Equus burchelli │ │ │
Giraffe │ 384,000│ 45.│ .12
Giraffa camelopardalis │ │ │
Barasingha Deer │ 56,800│ 8.│ .14
Cervus duvanceli │ │ │
Kashmir Deer │ 56,800│ 20.│ .35
Cervus cashmirianus │ │ │
Urial │ 22,700│ 2.5│ .11
Ovis vignei │ │ │
Marsupialia: │ │ │
Kangaroo │ 18,000│ 10.│ .55
Macropus robustus (?) │ │ │
Tasmanian Devil │ 3,120│ 4.│ .13
Sarcophilus ursinus │ │ │
Wombat │ 26,000│ 7.│ .27
Phascolomys mitchelli │ │ │
Wallaby │ 3,360│ 3.│ .9
Genus and species (?) │ │ │
Edentata: │ │ │
Anteater │ 3,300│ 2.│ .6
Myrmecophaga tetradactyla│ │ │
Accipitres: │ │ │
Wedgetailed Eagle │ 2,300│ 1.│ .43
Aquila audax │ │ │
Struthiones: │ │ │
Rhea │ 18,000│ 5.│ .27
Rhea americana │ │ │
Emu │ 36,300│ 23.│ .63
Dromæus novæ-hollandiæ │ │ │
─────────────────────────────┴─────────────┴─────────────┴─────────────
ANATOMY.
The minute anatomy of the normal thyroid is fully given in text-books,
and is doubtless pictured in the minds of all but students of the
subject as a fixed and definite affair. Such is not the case. There is
certainly a variation in gross size under conditions of seasonal and
sexual activity, and it would seem acceptably demonstrated that changes
in diet, especially where meat is concerned, are associated with
swellings or shrinkage of the glands. These gross changes must be due to
alterations in histology. In youth also the bulk is larger, a condition
due to cellular activity, while as middle age advances the thyroid
becomes smaller and more balanced in its colloid and cellular
proportions. I need not detail the ultimate constituents of the gland,
but it is well to emphasize a few points which must be taken into
consideration in microscopical diagnosis. In the first place, the
lobules or acini are not all of the same size in normal organs. This is
especially true in the normal adult gland but may be so in youth. The
cells which form the inner lining of the acinus are low cuboidal in
shape but the elements which lie under them are oval and do not change
with hyperplasia of the former. The colloid which fills the glandular
spaces is very susceptible to mechanical and chemical agencies. In
material preserved in alcohol it may be shrunken away from the cells or
heavily vacuolated, while in tissue preserved a long while in any liquid
it may be found contracted or broken. Large vacuolated or vesicular
cells are characteristic of the human parathyroid; this type is by no
means so prominent in the lower animals, and in the few examples studied
closely the arrangement is less definitely glandular than in man.
The avian thyroid is distinct from the mammalian in the delicacy of its
fibrous framework and the flatter character of its epithelia. Acini are
usually of more uniform size. Capsular vessels are prominent but
internal vascularity is less in birds than in mammals and their goitres
are not solid.
PHYSIOLOGY.
The physiological value of the thyroid-parathyroid complex has been the
subject of extensive study and voluminous literature without exhaustion
of the possibilities, but with the result that we are possessed of
knowledge explaining certain phases of abnormality, even if the normal
functions be not unexceptionally demonstrated. The accepted alterations
of functions are hypothyroidism—inadequate physiology, and
hyperthyroidism—excessive activity. Absence or atrophy of the thyroid
bodies is usual in hypothyroidism, while enlargements, collectively
called goitre, commonly accompany excessive function. Exemplifying the
former, cretinism is the result of failure of normal function and
development during fetal life while myxedema is the expression of the
disappearance of thyroid secretion after it has once been operative; the
latter may occur in infancy after nursing has ceased, or at any time
that the thyroid may atrophy, during some of the forms of goitre for
example. Hyperthyroidism may express itself, with or without visible
enlargement of the thyroid body, in nervousness, gastrointestinal
disturbances, tachycardia, loss of weight and exophthalmos. The first
group, which might be called athyroidism, is often associated with
alterations in the bony skeleton in the form of chondrodystrophy or of
rickets, while some degree of osseous change is observed with myxedema.
Goitre, be it simple or exophthalmic, may be followed by cardiac
enlargement or by myocarditis.
The character of the thyroid secretion is not known except that it is
influenced by the availability of iodine in the diet, but there are some
other as yet unexplained features. The normal thyroid fed to cretins or
persons suffering with myxedema, has the power to improve the condition
apparently by supplying iodine and the other essential elements. Iodine
is an important constituent of the gland, being present in combination
with protein. Its quality varies indirectly with the amount of colloid
and of hyperplasia (Marine). The administration of this element is
beneficial in colloid goitre but is harmful in the toxic variety. Even
though the administration of thyroid extract may relieve athyroidism,
this procedure in normal animals fails to produce typical pictures of
hyperthyroidism. Carnivora fed thyroid gland do not show toxic symptoms
until excessive amounts are given, whereas herbivorous varieties are
much more sensitive to this feeding.[44] Tachycardia, nervousness and
exophthalmos are not produced by these experiments, an interesting
observation since these signs are not recorded in wild animals, and only
vaguely reported by veterinarians. Man is apparently very sensitive to
thyroid dysfunction.
On the other hand, meat-eating animals are more sensitive to excision of
the thyroid body than are grain eaters.[45] Chemical studies have shown
that the thyroid is concerned in basal metabolism since this is
increased in hyperthyroidism and decreased in myxedema; nitrogen output
is much elevated.
Thyroid physiology stands probably in some relation to the cardiac
mechanism since in simple colloid or simple hyperplastic goitre if of
long duration, cardiac enlargement and disease may be greater than the
excess work occasioned by the mere physical bulk of the enlarged gland
in the neck would seem to warrant. A detoxicating function has been
ascribed to the gland, but Murray discredits this on the ground that
congestion occurs in infectious disease of warm blooded animals but not
in snakes. He thinks the gland more likely stands in some connection
with the thermoregulatory mechanism.
It is evident from the foregoing that the thyroid is closely related to
protein metabolism, and that this is in some way connected with the
ability the body possesses to use iodine in the food if it can get it.
Feeding of meat to fish was found by Marine to increase the size of the
thyroid. With all this in mind it is not astonishing that two-thirds of
our cases of thyroid abnormalities were found in the order Carnivora.
The anatomical changes of the human thyroid that precede or accompany
the various clinical pictures cannot be said to be uniform to a degree
that one can even approximately predict in every case what will be found
at operation, at autopsy or by the microscope. Furthermore, much
discussion has existed upon the importance of the several changes, the
association with clinical phenomena and the nomenclature. I shall not
enter the academic discussion with our material because so much has
depended, in human medicine, upon symptoms, signs and chemistry—data
that we cannot adduce. Upon many occasions I have seen animals with very
evident goitres, but have not been able to detect bulging of the eyes or
especial nervousness. One striped hyena carried his mass for several
years. It swelled up occasionally and seemed to cause dyspnœa. At one
examination of the beast, to see if anything could be done for him, a
large cyst broke under the examining hand, whereupon a deep inspiration
was heard and relief was apparent. This handling was repeated twice,
these times with the purpose of breaking cysts and when this was
successful disappearance of the dyspnœa was observed. However, a similar
attempt upon another hyena and a wolf failed possibly because no large
thin-walled cyst was present. These and the case of the lion cub (page
170) are the only instances in which the enlarged thyroid seemed to have
given serious difficulty, and the symptoms were probably due to
pressure. Many, indeed most, enlarged thyroids have been found at
autopsy, when the Garden personnel was unaware of their existence.
Interesting notes of familial cretinism will be found under the
appropriate heading.
PATHOLOGICAL ANATOMY. CLASSIFICATION.
And now to return to the question of morbid anatomy of the thyroid
gland, I shall begin by outlining briefly the classification to be used
in analyzing our cases, a system which combines those of many
pathologists, yet which I believe contains the essentials of all. The
changes in the gland being hyperplastic and recessive, at times to a
stage of atrophy, no clear cut definite line of demarcation separates
all these pictures; instead they must be thought of as merging into one
another. When the thyroid enlarges more or less continuously with a
maintenance of considerable colloid, the picture is that of COLLOID
GOITRE. The gland is pale, gelatinous, tense but resilient and may show
large cystic areas with fluid contents. Microscopically studied the
acini are overfilled with colloid yet the lining cells are retained but
flattened. The cysts may show the ruptured septa of the original acini.
Enlarged soft reddish glands are found at times to contain much colloid,
nearly every acinus being distended with it, but in such organs the
epithelia are high or even reduplicated; the amount of contents is the
striking feature. These are termed HYPERPLASIA WITH COLLOID. Hyperplasia
may go on with the absorption of colloid, HYPERPLASIA WITHOUT COLLOID.
The gland is then a darker body of more solid character, red, dull
purple or uniformly pale pink, somewhat dependent upon the blood
content. By magnification one sees smaller acini with prominent high
cuboidal or cylindrical epithelia and little or no colloid. The increase
of cells seems to be due both to an increase in their size and number.
As the proliferation increases the lining layer must be accommodated so
that it bulges out into the lumen as a bud or papilla which, if it be
extensive or universal in the thyroid, gives rise to the ADENOMATOID
GOITRE OF PAPILLOMATOUS type. This growth is accompanied by much
congestion and small or large hemorrhages may occur, forming cysts
containing a blood stained fluid. Grossly such a gland has solid and
cystic areas, is mottled red and gray or brown from old pigmentation and
is usually of very irregular shape. These forms are more or less uniform
and general, but in certain instances the hyperplasia tends to remain in
isolated areas or nodules, and in these develop solid masses of thyroid
epithelium, sometimes with a small lumen usually devoid of colloid, and
a rather rich but loose fibrous supporting tissue, the whole picture
resembling the microanatomy of the fetal gland; to these the name fetal
adenoma has been given, but since they are not fetal in origin and do
not behave like tumors I have called them NODULAR ADENOMATOID
HYPERPLASIAS. The next step in hyperplasia would remove it from benign
to malignant in pathological character, and the term NEOPLASTIC
HYPERPLASIA is used; this must of course be limited to the epithelial
growths, since sarcomata, while they occur in the gland, come from other
cells.
The changes in atrophy consist in irregular distortion of the gland by
fibrous tissue to which may be added large colloid or fluid cysts. There
is no uniform finding in the thyroid for the diseases believed to be due
to its atrophy, functionally at least, namely cretinism and myxedema. In
the former there may be no thyroid, or it may rather closely resemble
the normal organ while in the latter definite scarring and distortion is
the rule. The gland acini are compressed, the cells vacuolated or
crushed out of existence or there may be colloid cysts.
Inflammations occur as swellings of the interstitial tissues and of the
acinus cells during many acute infections. Repetitions of this may leave
a definite increase of connective tissue with large cells in the acini,
a lesion which many observers have looked upon as underlying certain
goitres and myxedema.
HYPERPLASIAS.
The cause of progressive hyperplasias has been ascribed to infection, to
chemical substances in water and food, endogenous toxins, heredity and
many other factors. While we can add nothing definite in this matter it
is worthy of notice that all our animals are exposed to the same general
climatic conditions, receive the same water, are fed from the same
stocks and many varieties may be in charge of the same keeper. The
influence of preëxisting infections cannot of course be measured.
Inbreeding or captive breeding seems to have a very definite effect upon
thyroid insufficiency as is well known and so sharply emphasized by
McCarrison in his reference to intermarriage among certain Moslems; I
shall cite the history of a wolf bitch which gave birth to three cretin
litters while apparently well but mated to a goitrous male. These facts
concerning the etiology are given merely to emphasize the high degree of
probability that the distribution of the lesions of the thyroid gland
among our specimens indicates the susceptibility of the various orders.
This perhaps needs no emphasis for the carnivores, but it does for the
marsupials. The literature contains many references to goitre in
domesticated ungulates; this would give the impression that they are
common among them, and so they may be, but this is not the case for wild
ungulates. There being no doubt that the Carnivora have the highest
incidence of thyroid enlargement, man being especially prone to it, and
since goitre may be induced in fish by feeding meat, the inference is
direct that high protein diet stands in some relation to this condition.
Thirty-nine of our sixty thyroid lesions occurred in the order
Carnivora; all the families of land varieties are represented; 8.1 per
cent. of the specimens coming to autopsy showed definite thyroid
alterations. However, marsupials have also a decided thyroid
vulnerability as indicated by 4 per cent. of the specimens presenting
abnormalities at death. Four of the seven cases were among the
carnivorous opossums and “devils,” the remaining three being in
herbivorous kangaroos. The influence of high protein diet is not evident
in birds.
A discussion of the essential pathology can be based upon the
accompanying table. In making a diagnosis care was used to exclude mild
swelling of the gland seen in acute infectious disease and under
conditions of sexual activity. The gross diagnosis was checked by
microscopical section, and all but a very few have been reëxamined for
the purpose of making the table.
TABLE 16.
_Showing Distribution of Lesions in the Thyroid Body by Giving the
Number of Cases Met in the Autopsies upon
the Various Orders, According to the Classification Given in the Text._
═══════════╤═══════╤═══════╤═══════════╤═══════════╤═══════════
Order │ Cases │Colloid│Hyperplasia│Hyperplasia│ Papillary
│ of │Goitre │ with │ without │Adenomatoid
│Thyroid│ │ Colloid │ Colloid │Hyperplasia
│Disease│ │ │ │
───────────┼───────┼───────┼───────────┼───────────┼───────────
Carnivora │ 39│ 7│ 6│ 5│ 4
Rodentia │ 1│ │ │ │
Ungulata │ 2│ 1│ │ │
Marsupialia│ 7│ 1│ 1│ 1│ 1
Passeres │ 2│ 2│ │ │
Psittaci │ 2│ │ │ │ 1
Accipitres │ 1│ │ 1│ │
Galli │ 2│ 1│ │ 1│
Alectorides│ 1│ │ 1│ │
Anseres │ 3│ │ 2│ │
───────────┼───────┼───────┼───────────┼───────────┼───────────
Total │ 60│ 12│ 11│ 7│ 6
───────────┴───────┴───────┴───────────┴───────────┴───────────
═══════════╤═══════════╤═══════════╤══════╤═══════╤═══════
Order │ Nodular │ Malignant │Mixed │Sarcoma│Atrophy
│Adenomatoid│Hyperplasia│Tumors│ │
│Hyperplasia│ │ │ │
│ │ │ │ │
───────────┼───────────┼───────────┼──────┼───────┼───────
Carnivora │ 9│ 1│ 1│ 1│ 7
Rodentia │ │ │ │ 1│
Ungulata │ │ │ │ │ 1
Marsupialia│ 3│ │ │ │
Passeres │ │ │ │ │
Psittaci │ │ 1│ │ │
Accipitres │ │ │ │ │
Galli │ │ │ │ │
Alectorides│ │ │ │ │
Anseres │ │ │ │ │
───────────┼───────────┼───────────┼──────┼───────┼───────
Total │ 12│ 2│ 1│ 2│ 8
───────────┴───────────┴───────────┴──────┴───────┴───────
[Illustration:
FIG. 31.—HYPERPLASIA WITH COLLOID. AMERICAN BADGER (TAXIDEA TAXUS).
MEASUREMENTS; 3 × 1.5 CM.; 3 × 1.5 × 1½ CM.
]
[Illustration:
FIG. 32.—ADENOMATOID GOITRE. RACCOON-LIKE DOG (CANIS PROCYONOIDES).
]
This rather diversified group of pathological lesions would warrant one
to expect a notable number of instances of disease observed during life,
suggesting that the thyroid was at fault; such, however, is not the
case. In the first place, no case of exophthalmic goitre, as the symptom
complex is known in man, has been observed, yet the anatomical
alterations, hyperplasia without colloid, and with papillary or solid
adenomatoid character, are abundantly represented. For the pathologist
to accept a case as toxic goitre I would ask evidence of enlargement of
the heart and perhaps in addition degeneration of the myocardium. The
animal showing the closest resemblance to the disease in man was a
Raccoon-like Dog (_Canis procyonoides_) whose history and notes are
given in brief.
Raccoon-like dog (_Canis procyonoides_) ♀ . Acute hemorrhagic
splenitis. Acute fermentative gastritis. Subacute catarrhal enteritis.
Acute general infection. Hypertrophic cirrhosis of liver. Chronic
interstitial nephritis. Hypertrophy of heart with acute myocarditis-
infiltrative and parenchymatous. Chronic lymphadenitis with acute
exacerbation. Epigastritic and gastric venous stasis. Nodular
adenomatous goitre. The right thyroid is lower, both measure 4 × 3 × 2
cm., are soft, resilient with dense gray capsule. Section shows cysts
filled with blood separated by pale septa of soft tissue of varying
thickness. One similar mass under angle of jaw seemed like a lymph
node but on section is like thyroid. Parathyroids not found. Pleuræ
negative. Lungs are gray, collapsed except lower half of lower lobes
which are slightly emphysematous and edematous. No consolidations.
Pericardium contains about 3 cc. clear, colorless fluid. Epicardium is
glistening, transparent and pale. Heart muscle is soft flaccid, pale
mottled gray-brown. All chambers are distended with mixed clot. The
coronary muscles and columnæ are mottled brown and gray. The tips at
insertion of chordæ are pale. Streaks of gray run through muscles. One
area 1 × 2 cm. of softening found in middle of left auricular muscle.
Aorta negative. The liver is enlarged, surface rough and irregular,
edges rounded and uneven, consistency firm and tough, color mottled
deep red-brown. Section surface glistening, moist, granular, opaque.
Lobular markings not lost but obscured. Connective tissue lines not
clear but surely diffuse in lobules. Scars on surface leading to
definite connective tissue strands about vessels and irregularly
placed. Gall-duct patulous with limpid bile. Spleen is well forward in
front and below stomach. It is much enlarged, soft, tough, has a
smooth, tense capsule. Section surface shows homogeneous purple pulp
with faint, narrow but tough trabeculæ. Follicles distinctly outlined,
slightly large but merely of a slightly paler purple than pulp. On
surface are many round 2–5 mm. sharply outlined gray thickenings of
the capsule and immediately subjacent pulp. The right kidney’s lower
half has been replaced by a thin-walled clear cyst 3 × 2.5 × 2 cm. The
left kidney is small, capsule strips with difficulty tearing surface
slightly. Surface and section are mottled pink and gray, glistening
and opaque. It is firm, dense and tough, cortex narrow, medulla wide.
Cortex has obscure, irregular markings with few small cysts, striæ and
glomeruli, faintly visible, margin between layers irregular. Veins are
distended over surfaces of stomach, under surface of diaphragm, in
peritoneum over liver but not in abdominal wall. Stomach contains sour
gas and water. Mucosa especially near cardia is deep purple. Rugæ are
large and permanent but mucosa and submucosa are soft and on section
congestion does not extend deep. The tips of the rugæ near pylorus are
infiltrated and the infiltration is surrounded by a zone of
congestion. Mucosa seems about to slough but has not separated. At
pylorus mucosa becomes deep brown-red, dense, swollen, opaque and
covered with a slimy, soft brown mucus. Folds are prominent but
temporary. In jejunum and ileum mucosa is still swollen and opaque and
rugæ are still larger than normal and temporary with a dense sensation
on compressing them. The color is not brown but deep pink and yellow
with areas of submucous injection. Follicles not visible. Colon is
negative except for slight thickening of mucosa unaccompanied by
congestion or opacity. Lymph glands of small omentum are small, firm,
yellow, homogeneous; those of the mesentery are large, edematous,
yellow brown and tense with lymph which escapes on section. Lymph
channels up to mesenteric stalk can be traced.
HISTOLOGICAL NOTES.—Liver architecture much altered by passively
dilated hepatic capillaries chiefly toward the centre of the distorted
lobules. This distortion is in the form of irregular liver columns
separated by irregular vessels and interlobular connective tissue.
This latter is increased everywhere but is abnormal in distribution
within the lobules. The connective tissue at the portal spaces is not
so much increased but it shows most around arteries. Bile ducts seem
not increased in numbers. Much bile pigment in large, coarse, dark
brown masses chiefly settled within portal spaces. The cells show
slight fatty infiltration. No multinucleation. Organ is not seriously
robbed of functionating tissue. Alterations are not equally
distributed over section. Spleen shows enormous congestion with edema
of the few chords and perifollicular tissue left unengorged with
blood. Follicles are negative. No connective tissue increase. Blood
destruction not now active but there are many hemosiderotic masses
irregularly scattered. The subcapsular areas are loose edematous
follicles. Heart muscle fibres have lost all transverse striations,
some are hyaline while others are fibrillar. The nuclei are decreased
in number but there is no increase of connective tissue nuclei. No
pigmentation. There are several areas of round and polynuclear cell
infiltration and one distinct abscess in section. The perivascular
tissues are edematous. Muscle fibres are large and wide. Thyroid made
up largely of slightly enlarged acini in most of which a slightly
eosin-stained hyaline collection is found. There are a few cysts
containing a thrombus and hemorrhage. There are no typical colloid
cysts. Some scars from old hemorrhages may be seen. There is much free
blood in and between acini. Blood pigment free and in granule cells is
abundant. Some acinus cells show fat droplets. Lung shows old
interstitial tissue increase especially about vessels and a few scars,
some of which are forming cartilage. These are deeply encapsulated.
Mesenteric lymph nodes show trabecular thickening with active
connective tissue formation which is also present about follicles and
along edges of chords. Follicles lack germ centres, solidly lymphatic.
About them and in and along chords are many tissue cells some of
Maximov type and a few eosinophiles. Many of these and endothelial
cells are phagocytic of red blood cells. (Fig. 32.)
Just at the time of completing this book another case strongly
resembling exophthalmic goitre in man was encountered in a Gray wolf
(_Canis lupus_). This animal had a history of enlarged neck and
enlarging abdomen for about six months. His appetite and discharges
remained about normal but weight was lost and activity reduced to a
minimum. Attempts at removing the fluid believed to be in the
peritoneum, by the use of diuretics, failing and the beast being in such
poor shape, he was killed. An enormous adenomatoid goitre, concentric
hypertrophy of the heart, passive dilatation of all cervical and
thoracic veins, passive congestion of the liver and congestion of the
portal area were autopsy diagnoses. It will be noted that no
exophthalmos and nervousness were observed during life.
Bone disease and atheroma are at times associated with thyroid
insufficiency in man. The former, aside from osteogenesis imperfecta of
cretinism, occurred only once in a carnivore and once in a marsupial.
There is but one case of atheroma among the sixty cases of thyroid
disease.
The reaction of the avian thyroid in its hyperplasias is somewhat
different from that of the mammalian. The delicacy of the septa and the
relative paucity of vessels is perhaps the reason that the gross and
microscopic pictures differ from those found in mammals. It should be
emphasized, however, that while one can perceive a hyperplasia of the
gland of both classes when the testes or ovaries are active, there
appears less participation of the thyroid in birds in infectious
diseases than is the case for mammals. In simple functional hyperplasia
the capsular vessels are prominent, but the cross section need show no
change. In the continued hyperplasias the organ remains more solid,
being less apt to develop cysts; large cysts are occasionally seen,
however, and in one case the entire gland was composed of them.
Microscopically the differences are largely of degree in that the
process is less frank in development, but the essential changes of
swollen epithelia and condensed colloid remain the same.
ATROPHIES.
The thyroid gland in its functional capacity, may be considered to
undergo hyperplasia and then atrophy of the parenchyma cells. Normally
this would leave the colloid, the epithelia and the supporting tissue in
proper balance, but in the presence of low grade inflammation or where
an abnormally hyperplastic process retrogresses, the connective tissues
may exceed their norm, the epithelia may be shed or remain high and the
colloid be irregular in distribution. Such a state of atrophy may exist
in fetal life, arise from unknown cause during a course of toxic goitre,
or perhaps insidiously in chronic toxic conditions. When this occurs in
fetal life cretinism or myxedema arises, when in later life, only the
latter appears. Judged entirely by microscopic findings, eight instances
of atrophic changes in the thyroid have been found. Three of these were
in Carnivora and were secondary to definite goitres, but were not
followed by myxedema; one of these three was a cretin. A brother of this
cretin but not himself a cretin, died at the age of five months from
acute dilatation of the heart, and with a decidedly atrophic thyroid
gland. A lion showed a distorted gland, the result of chronic
inflammation, a condition also present in a leopard, in the latter
possibly in association with a general infection of the heart, vessels
and kidneys of long standing. A case in a bear can only be explained on
the basis of chronic intestinal toxemia. A camel is the only other
variety of animal to show this regressive change. The beast suffered
with a marked anemia with marrow atrophy and hydatid disease;
calcification was found in the thyroid.
[Illustration:
FIG. 33.—COLLOID GOITRE WITH HEMORRHAGE FROM LEFT GLAND WHICH KILLED
THE BIRD. BLACK AREA IS CLOTTED BLOOD. MUTE SWAN (CYGNUS OLOR ♂ ).
]
[Illustration:
FIG. 34.—AT THE LEFT, THE INSIDE OF THE CALVARIUM SHOWING HEMORRHAGIC
PACHYMENINGITIS. AT THE RIGHT IS A FEMUR, SHORT AND HEAVY BUT WITH
THIN CORTEX; CONSTRUCTION IS ORDERLY. CRETIN GRAY WOLF PUP (CANIS
MEXICANUS).
]
As has been repeatedly stated, myxedema has not been seen, but
hypothyroidism has expressed itself in these animals as cretinism. The
most interesting pathological fact concerning the relation of the
thyroid to this maldevelopment is that there is absolutely no uniform
gross or microscopical change constantly present in the typical cases.
This will become more evident as the following records of our cases are
perused. In 1914 an apparently normal Gray Wolf bitch threw two normal
young ones which died of lack of maternal care; they were not posted.
The father of this litter died shortly and was found to have a
sarcomatous hyperplasia of the thyroid. A year after the first lot a
second litter was born of an apparently perfect father which still
lives. This animal was purchased in the same lot with the mother, and
the two could be related. The first father was not related to the
female. This litter consisted of seven, two dying almost at once and
burned, the other five not being especially good specimens. They died at
ages ranging from two to five months and were all cretins or cretinoid.
Two showed hemorrhagic pachymeningitis, one external, one internal, and
the usual bulky skeleton of cretinism (Fig. 34). The bones were
constructed in a rather orderly and somewhat graceful manner, the
uncalcified epiphyses being only occasionally distorted. The same two
animals, mated again in 1916, had as offspring seven pups. One evident
cretin was killed while another runt was sacrificed and found to have
fractures of both femora around which no trace of callus was
discoverable (Fig. 35). Two other cubs were apparently normal, while the
remaining three did not develop and soon showed the cretin characters.
When this group was about three months old they were fed chopped horse
thyroid; one improved decidedly, one slightly, the third not at all, but
it might have been too weak to get its share. These animals lived from
eight months to three years; the two good ones remain alive. In 1919 the
mother was killed by her cubs, probably because she was weakened by long
sickness. A papillary adenomatoid goitre, endocarditis, nephritis and
chronic enteritis were found. The pathological changes in the thyroids
of the cretins were as follows: In the second litter two cubs had
hyperplasia with colloid, one had nodular adenomatoid change and the
fourth showed distinct atrophy secondary to colloid increase. In the
third group two had distinct colloid changes, once pure and once as a
secondary process with some evidence of atrophy to alter the fibrous
tissue and shape of the acini. The remaining four seem to be all colloid
in character, but I am not satisfied with the description or sections so
that I shall not offer an unqualified diagnosis. The adrenals of these
animals all showed some medullary congestion but no change in the
chromaffin or lipoidal content.
The deformative lesions of bones are frequently associated with lesions
in the pituitary body. Several of our thyroid cases have been studied
for such changes without their discovery. Indeed no gross alterations
have been noted among many hundreds of hypophyses seen in removing the
brain nor in a small number studied histologically. Those examined under
the microscope have seemed to correspond to the descriptions given by
Stendell in Oppel’s _Handbook of Comparative Microscopic Anatomy_.
[Illustration:
FIG. 35.—PATHOLOGICAL FRACTURE OF FEMUR. CRETIN GRAY WOLF PUP.
]
[Illustration:
FIG. 36.—ADENOCARCINOMA SARCOMATODES. ADENOMATOUS PORTION ATTACKING
CAPSULE. RACCOON-LIKE DOG (CANIS PROCYONOIDES).
]
TUMORS.
True malignant hyperplasias of the thyroid epithelium in man are being
more thoroughly studied in recent times so that similar lesions in the
lower animals gain interest. The notes given below are of value as
individual observations only, but since three were in carnivores,
another indication is at hand of the vulnerability of this order. One of
the cases is admitted upon diagnosis alone, the slides and records
having been lost, but since the determination was made by Dr. C. Y.
White, I am satisfied to accept it. The four of which notes are at hand
are as follows:
Raccoon-like Dog (_Canis procyonoides_) ♂ . Adenocarcinoma
sarcomatodes. Metastases to liver and lungs. Fatty degeneration of
liver and kidney. Acute diffuse splenitis. Submucous hemorrhages in
stomach. At level of thyroid cartilage on each side and removed 1 cm.
from same is a rounded encapsulated nodule measuring 2.5 × 2 × 1 cm.
Portions are hard, others fluctuate suggesting cystic degeneration.
Below these nodules are two bodies also bilateral, evidently lobes of
thyroid, each measuring 5 × 2.5 × 2.5 cm. They are firm with some foci
of cystic softening. From a ruptured cyst of the right lobe grumous,
red, malodorous material exudes. Peripheries of such cyst show
greenish discoloration. Bodies as a whole are greenish black in color.
They are well encapsulated, do not meet in midline but are joined at
lower pole by firm, apparently colloid, material. All through lung
especially under pleura there are dark red, rounded, firm, well
circumscribed foci measuring 2–8 mm. diameter. They project markedly
on pleural surface. No capsule can be made out. Upon incising they
have lighter red centres and deeper peripheries. They cut with
resistance and have no inclination toward a wedge shape. Surface is
for most part smooth except where tumors are present. Organ is soft
and distinctly yellow. All portions of liver contain rounded and
irregular nodules, some deep, others superficial. They vary in size
from 2 mm. to 3.5 cm. diameter. No capsule can be made out, yet they
are circumscribed. The central portions of larger nodules are dirty
gray and friable. Peripheral parts dark red. Smaller lesions are solid
red and of fleshy consistency. Spleen is deep dark red, homogeneous.
Histological section of thyroid shows firm, old, dense capsule very
irregular in thickness seemingly on account of the penetration of the
enclosed tumor cells. Such infiltration gives the inner outline of
capsule a very irregular, bizarre appearance, and at times thins the
capsule until it is reduced to nil. In one place the tumor elements
appear outside the capsule at a point where a large vessel is apposed
to outside capsule. The appearances within this capsule vary; in
places the picture is that of a carcinoma. Small, round, interspersed
with larger irregularly shaped acini are seen lined by a single layer
of low cuboidal epithelium. Very frequently indeed the lining cells
contain fine granules of golden brown pigment even where their lumina
contain no blood. Some of the larger acini contain altered blood cells
and a smooth, pink material, knife streaked and vacuolated
peripherally. In some parts of section these acini are regular and
well formed, in others they are very irregular and appear to be
eroding the capsule. A second appearance concerns the connective
tissue. Appearing in almost any part of the section and bearing no
regular relation to the epithelial elements or the section in general
are areas of closely packed large spindle cells with hyperchromatic
nuclei. In another place such spindle cells are arranged purposefully
to form irregular capillaries containing blood. A third appearance
results from a combination of the first two. Here there are acini,
between which run blood capillaries with remarkably rich and numerous
embryonic lining cells. A section stained by Van Gieson stain proves
that part of the pink intra-alveolar material is colloid. Every
gradation can be made out in tint of this material from pink to salmon
to orange. It is often very difficult or impossible to state whether a
given blood-filled space is a blood vessel or an acinus with
hemorrhage. In both structures the lining consists of flattened cells.
In one there is the possibility of colloid, in the other of
hematogeneous hyaline, both with peripheral vacuolization. Lung shows
walls of alveoli thickened by young type of cells. Nuclei of cells
lining bronchi are prominent, in good condition. Much coal pigment
through whole section. Air sacs empty. There are several rounded nodes
through section consisting of closely packed spindle and round cells.
Blood is abundant in such nodules both in small lined spaces like
capillaries and in larger necrotic foci where there is abundant blood
pigment. In one place an irregular, large acinus is seen containing a
smooth pink material. A large part of the interstitial tissue is
diffusely infiltrated by the large, round cells with hyperchromatic
nuclei (Figs. 36 and 37).
Prairie Wolf (_Canis latrans_) ♂ . Mixed tumor of thyroid. Metastases
to lungs. The neck of the animal is enormously enlarged, the diameter
exceeding that of the body. Thyroid is enormously enlarged to about
the size of a child’s head, rather firm before incision. When incised
about 300 cc. blood stained fluid drained. It is rather soft and quite
friable looking as if made up of fatty and hemorrhagic matter. The
lung is of mottled deep red color with here and there on surface small
hemispherical areas about the color of the surrounding tissue but of
slightly increased resistance. They are raised above the surface and
measure 2–7 mm. in diameter. Histological section of thyroid shows a
mixed tumor. It is not possible to say that it is a pure thyroid gland
tumor. It is largely sarcomatous, the round cell alveolar arrangement
dominant at one place, at another the short spindle cell but not
typical, so-called spindle celled type. There are many areas of small
and a few of large hemorrhage. Cartilaginous deposit is occurring at
some places in the field showing the latter type of sarcoma. Section
of lung contains a large sarcoma nodule. The cells consist of round
cells without the large cartilage-like cells found in the original
tumor mass.
[Illustration:
FIG. 37.—ADENOCARCINOMA SARCOMATODES. SARCOMATOUS PORTION. RACCOON-
LIKE DOG (CANIS PROCYONOIDES).
]
[Illustration:
FIG. 38.—ADENOPAPILLOMATOUS HYPERPLASTIC PORTION OF THYROID. UNDULATED
GRASS PARRAKEET (MELOPSITTACUS UNDULATUS).
]
Coypu (_Myocastor coypus_) ♂ . Sarcoma of right thyroid. The thyroids
occupy a position deep in the neck upon the anterior vertebral
muscles, the left higher than right, being up to level of top of
thyroid cartilage. Only a half-inch of lower pole of right remains and
it is like the left which is soft, deep brown-red, delicately
lobulated, closely bound to trachea but movable in fascia. It is
30 × 10 × 3 mm. The upper part of the right organ is occupied by, or
at least within the same capsule as a 25 × 15 × 10 mm. encapsulated,
pink mass with many small vessels on its exterior. It is soft and on
section the surface is mushy, of gray-pink-yellow, and seems to have
an exceedingly delicate trabecular network. Posterior and superior to
this, lying near the salivary glands but back of them is a similar
mass 15 × 12 × 5 mm. Still another lies anterior to what remains of
the right thyroid and is about 8 × 5 × 4 mm. The adrenals are
30 × 13 × 8 mm. slightly hard and not unlike a long kidney in
arrangement. The cortex is wide, regular, brown or tawny, the medulla
rich in vessels and deep brown. Histological section of thyroid is an
almost completely cellular mass with here and there delicate and
incomplete trabeculations. Small blood vessels are numerous and
consist of a delicate line with a cell nucleus here and there, that is
no true wall. It seems as if the blood channels were simply regular
spaces through the cell mass. The cell type is mononuclear with
definitely acidophilic “granuloid” somewhat vacuolated protoplasm. The
nucleus is almost without exception eccentric, rather poor in
chromatin but in places diffusely staining. Mostly, however, the
nuclear skein is in spots or threads and fairly dense around margins,
therefore not unlike a thyroid cell and a plasma cell. Here and there
one finds compressed remains of thyroid acini. There is decided
irregularity of size and shape in these cells. Its origin is not clear
but this seems like a sarcoma of the thyroid.
Undulated Grass Parrakeet (_Melopsittacus undulatus_) ♂ . Medullary
carcinoma of thyroid. On opening the body a mass 10 × 6 × 4 mm. is
found in the upper thoracic region on the right side. A similar mass
measuring 5 × 3 × 2 mm. lies in similar position on the left side.
They are identified as thyroid glands only from their position and
from the numerous large vessels which radiate from them. An especially
large vessel leads directly to the heart. Long axes extend
anteroposteriorly. The masses are of a firm gelatinous consistency,
the color of carpenters glue in lower portions, shading off to a dirty
canary yellow above. They have a translucent appearance in lower
portions. The surface is fairly smooth, adherent latterly and
posteriorly. They are well circumscribed. At one end of the
histological section thyroid tissue is easily identified. It varies
from normal in that its spaces are often very large, contain villus
projections or may be completely filled by large compound granule
cells with no colloid. Other acini are atypical and contain typical
colloid. Continuous to such thyroid tissue is a very large, rounded
tumor. It consists of round cells with round nuclei in which many
mitotic figures may be seen. An arrangement into acini cannot be made
out nor is colloid material abundant. In one or two places an
irregular collection of such material may be seen with peripheral
vacuolization but its confines are always indefinite. As far as
section goes the mass is well encapsulated but the lymphatics are
infiltrated by the tumor cells. The tumor, too, is sharply separated
from the relatively normal thyroid. Irregularly scattered through
section are remarkable cells with nuclei three or four times the size
of other nuclei. They may be hyperchromatic or normally staining.
(Figs. 38 and 39.)
The THYMUS BODY is a structure encountered in our specimens with greater
regularity than is the case in human autopsy experience. However, no
great size of the gland is observed, and there is no record or
recollection of anything which could resemble an enlargement suggesting
status thymicolymphaticus nor has a tumor with this organ as its origin
been observed. In one case only did the thymus present what was believed
to be an unusual size. An adult Gray Lagothrix (_Lagothrix lagotricha_)
died with an acute intestinal infection. Its thymus was a large, soft,
deep pink body lying in the anterior mediastinum, running up to the
clavicular joints and down along the sternum. The death had ample
explanation without any state of this organ. The thymus body has not
been found enlarged in association with thyroid disease.
[Illustration:
FIG. 39.—MEDULLARY CARCINOMATOUS PORTION OF THYROID. UNDULATED GRASS
PARRAKEET (MELOPSITTACUS UNDULATUS).
]
The SUPRARENAL or ADRENAL BODY is an organ of essentially the same
general construction in the two classes here studied except that in
birds the cortical portion may be imperfectly developed and in some of
the lower groups is decidedly narrow. This outer zone may indeed be
entirely missing since tissue comparable to it is distributed elsewhere
in the body, notably with ganglia along the vertebral column. The organ
is infrequently the seat of alterations, detectable either grossly or
microscopically. Congestion and small hemorrhages are rather common in
acute infectious disease especially when the respiratory system is
involved, but these rarely destroy tissue or materially reduce the
chromophilic cells. These circulatory disturbances have, however, been
predominatingly among the mammals although birds have suffered with
infections to a high percentage. The medulla is much more often the seat
of congestion while, when hemorrhage has occurred, the cortex is
apparently always involved. Lipoidal reduction has been seen in a few
mammals, Primates and Carnivora, once to a state of complete exhaustion.
More serious lesions have occurred eleven times, and since the cause and
meaning of disease in this body are so vague it seems well to recite
briefly each one.
A Weeper Cebus (_Cebus capucinus_) suffered for several months with
constantly but slowly increasing skeletal deformity of the osteomalacic
variety. He died after moving him to a new cage, his end being hurried
by a scalp wound. At autopsy the skeletal condition was determined to be
of the above named kind. The organs were in good condition. The adrenals
were decidedly enlarged for a monkey of this size, measuring 1.8 cm. in
length. The medulla was a solid, brownish, homogeneous portion covered
with a very narrow, barely discernible cortical zone. This was
apparently due to a uniform hypertrophy of the cells of the medulla. The
testes were slightly atrophied and fibrotic. A Black Spider Monkey
(_Ateles ater_) had a history of stiffness of legs for six months. This
was probably a sign of osteomalacia since at autopsy this condition was
found together with a secondary anemia, chronic gastritis, acute
enteritis and brown atrophy of heart. The adrenal was knob-shaped, the
cortex was wide, brown, regular, the medulla small gray-purple.
“Histologically the capsule of the adrenal is thicker than is commonly
seen in Primates and connective tissue bands between the units of the
zona glomerulosa are somewhat stouter than common. The cells of this
layer take the stain a little more deeply than usual, but are otherwise
negative. The layer separating cortex and medulla is occupied by a band
of well formed connective tissue which is not proceeding inward but
outward and so encroaching upon the zona reticularis as to remove it
completely in places, in others to make isolated islands of its cell
groups. Fine lines of connective tissue are penetrating from this into
the middle layer but not disturbing it as yet. The connective tissue
septa penetrating the medulla are somewhat wider than one would expect
but show no activity in their growth. The medulla is somewhat broken up,
vacuolated and the chromophilic cells are not especially prominent,
indeed some of them seeming to have undergone necrosis.” A puma (_Felis
concolor_) died after a sickness of two weeks from acute gastroenteritis
with its usual visceral associations, including acute nephritis, and
with calcifications in the adrenals. These structures were quite firm
and nodular, on section tough and resilient. “The cortex is irregular,
brown, with paler brown medulla. Areas of calcifications appear as small
dots, as linear formations and in some places seemingly around blood
vessels. Histological section shows marked vacuolization of cells,
particularly of cortex. There is a diffuse overgrowth of connective
tissue which has become hyaline. Here and there small calcareous
deposits may be seen but no massive areas as mentioned above.”
A Himalayan Thar (_Hemitragus jemlaicus_) came to his end, after a
history of convulsions, from nephritis, which had resulted in general
edema including the serous sacs, and an associated cardiac dilatation.
His adrenal was egg-shape, of normal size, with a wide, irregular dull
brown cortex and a homogeneous opaque, darker brown medulla.
“Histologically the cellular structure of the cortex is partly
destroyed, partly dropped out and partly disturbed by overgrowth of
connective tissue. This connective tissue is quite prominent in the
medulla where it is surely increased although it is made more prominent
by absence of cells, some of which have been degenerated and some
dislodged.” A Japanese Macaque (_Macacus fuscatus_) after drooping three
weeks presented at autopsy the following numerous lesions: anemia,
chronic atrophic gastritis, atrophy of heart muscle with regeneration,
hemosiderin pigmentation of liver, perilobular fibrosis of liver,
chronic diffuse nephritis (subcapsular type), congestion of spleen,
fibrillar fibrosis of spleen, hemosiderin pigmentation of spleen, local
amyloid infiltration of spleen, calcareous infiltration in medulla of
adrenal. Grossly the adrenal showed a thick, orange yellow cortex and
small solid, brown medulla. “Histologically the organ appears normal in
all respects save for the presence of a few small irregular areas of
calcification in the medulla. These occur apart from any recognizable
necrotic or fibrous areas. In one place one appears to lie within the
lumen of a blood vessel. No fibroses or special congestions found
anywhere in the organ and cells show normal details and normal numbers
of vacuoles.”
A California hair seal (_Zalophus californianus_) which had been
refusing food and having loose stools for about ten days presented after
death the following diagnosis: Hypernephroma of adrenal, chronic
hypertrophic enteritis with acute exacerbation, hemorrhagic splenitis,
passive congestion of liver, congestion and edema of lungs with
catarrhal pneumonia, acute fibrinous pericarditis, chronic
lymphadenitis, chronic interstitial nephritis. His right adrenal seemed
about normal, being 5 × 2 × 1 cm. with a narrow, dull yellow cortex and
a large mottled gray-brown medulla. The left one was 5 × 3 × 1 cm. The
upper pole is swollen and contains in its centre a spherical tumefaction
which is red, mottled, sharply outlined, with a suggestion of a capsule
and slightly firmer than surrounding organ. “Histological section shows
a capsule of very noticeable thickness but possibly not much in excess
of normal. The cortex particularly in its deeper layers is much injected
and in some places there has been hemorrhagic diffusion. In many places
in the zona fasciculata, more especially near the periphery, there is
breaking up of the cell tubes with an infiltration of large round cells
and some chromatophilic cells. In other places this seems to have gone
on to fibrous tissue increase and necrosis of the cortical fibrous cell
types. The connective tissue layer below the cortex is wide and the
spaces filled with blood. This connective tissue also surrounds islets
of medullary cells which are not specially chromatophilic. The mass in
the medulla is made up of varying sized alveoli surrounded by rather
rare, highly vascularized connective tissue and enclosing islets of
medullary cells. These alveoli may be subdivided by septa. Hemorrhage
has occurred into many of them. The individual cell masses are made up
of groups of rather large cells with illy defined margin, a granular,
opaque but not vacuolated protoplasm. They have a bladder-like nucleus
in which the centrosome is large and prominent. Definite mitotic figures
could not be found, but mitosis is probably present. A few cells with
double nuclei were seen and one with four. In many of these large
islands the centre has gone to pieces from hemorrhage or necrosis. Some
of the vessels are thrombotic and one shows a very pronounced
periarteritis.” A brown cebus (_Cebus fatuellus_) was killed because of
a poor tuberculin test chart. His organs were negative except the right
adrenal body which was 3 × 1.5 cm., or four times the size of its
fellow. It was a tense body with a smooth, mottled, deep yellow surface.
On section there were deep yellow islands separated by pale brownish
septa; the structure did not resemble adrenal. Histological section
showed a hypernephroma of vacuolated cell type, roughly alveolar. Two
other cases, which because of their microanatomy are to be called
hypernephroma can be added to those just cited. One occurred in an
undulated grass parrakeet (_Melopsittacus undulatus_), the other in a
black duck (_Anas obscura_). As illustrative of this tumor the former
will be cited in brief. “Hypernephroma of adrenal with hemorrhage into
body cavity. A tumor approximating in size the head of the host extends
from the region of the internal genitalia and adrenals lying more on the
right than on the left side extending fully to cloaca and shoving all
abdominal viscera forward. It has a pedicle springing from between the
two upper lobes of the kidney where adrenals and internal genitalia are
not distinguishable. Tumor is coarsely lobulated, well encapsulated,
nowhere adherent. It has a pale, dirty yellow color, richly marked by
red lines of congested vessels. It is fairly soft, _i.e._, about
consistency of normal liver. Upon incising, the cut surface bulges
markedly, is a dirty gray-yellow, blotched with darker gray areas, shows
no internal hemorrhages or markings of special import. No metastases
noted to any other organ. Microscopic section shows a light capsule
surrounding the tissue of the tumor. The latter has a very scanty
fibrous reticular framework showing no orderly or purposeful
arrangement. Upon and between the reticulum, irregular and for the most
part elongated collections of cells are placed. At times these present
an elongated fascicular form, but this is not by any means a prominent
feature. The cells themselves are large, rounded or polygonal, have
coarsely granular cytoplasm which only in rare cases contains vacuoles.
Nuclei of these cells stain very poorly, but it can be made out that
they are of large epithelial type and of vacuolar appearance.”
A somewhat unusual tumor was encountered in a Polar bear (_Ursus
maritimus_), an adenocarcinoma of the adrenal, when judged purely by its
histology but a secondary tumor in the lung displayed the more familiar
picture of large vacuolated cells as seen in hypernephroma. The
diagnosis follows: “Scirrhous adenocarcinoma of adrenals, secondary
carcinoma of lymph glands, secondary hypernephroma of lung, secondary
carcinoma of diaphragm, acute mucopurulent bronchitis, acute catarrhal
enteritis, chronic diffuse fibrous cholecystitis, cholelithiasis, slight
acute interstitial pancreatitis, follicular hyperplasia of spleen with
fibrosis, hydrothorax, hydropericardium, chronic hypertrophic
osteoperiostitis, encysted trichina in diaphragm, fatty infiltration of
diaphragm, chronic diffuse nephritis, chronic productive lymphadenitis,
pigmentation of lymph gland. Both adrenals are smaller than normal, of
woodeny consistency, the pale cortex and medulla are poorly separated
from each other. The cut surface shows gray white and tawny mottling and
occasional calcareous points. Histological section shows an extra
capsule of fibrous tissue containing highly distended veins; the lining
contains masses of tumor cells, many of which are necrotic. It is
distinctly denser in type than normal and more abundant in places
showing a proceeding fibrosis. Parenchyma shows but few irregular
islands containing non-neoplastic cells, some of which are highly
vacuolated, others are not. Interstitial tissues in peripheral parts are
often grown together with the deeper portion where are intermixed tumor
areas. The latter consist of small round acini of variable size lined by
cells of active type. Nuclei are large and hyperchromatic, cytoplasm
broad and disintegrating. Parts show necrosis and hemorrhage. Upon
search transitionals from non-neoplastic to neoplastic cells can be
discovered in same fasciculus.”
SECTION XII
THE SKELETON AND ITS JOINTS
The bones with their articulations have been the subject of extensive
study and research by zoologists in the direction of classification and
evolution. Adaptation of the osseous construction to the needs of the
animal is well appreciated biological knowledge. For example, the keel
of the sternum in birds affords broad origins for the flying muscles,
the pectorals, which also insert on the alæ of this bone and on the
clavicle, and in addition use these latter formations as fulcra. So too
the extremities of quadrupeds are angular in their upper two segments
for the purpose of supplying a direct action of the flexors employed in
running and leaping. The thick masseter muscle of carnivores is
accommodated in the deep zygomatic fossa. Many other examples might be
cited, but these serve to direct attention to the adaptation of function
and construction. Pathological changes in our materials are however too
few to permit conclusions as to possible relation of zoological position
and development except such as may refer to deformity incident to the
degenerative processes—rickets, osteomalacia and osteogenesis
imperfecta, and in these conditions the alterations are merely passive
accommodations to weakened support in order to obtain comfort. To put
the matter in other words, it would seem that, aside from the diseases
just named, there is no outstanding change in the skeletal tissues
peculiar to zoological orders that might indicate vulnerability of the
system or the methods of response to injury or disease.
EFFECTS OF TRAUMA.
There must be considerable reserve or reconstructive power in the bones
of animals since it is a common thing at autopsy to see unmistakable
evidences of repair of fractures, dislocations and inflammations. Some
illustrations are introduced to exemplify this healing ability, one of
which was found in an animal shot by a hunter, the other an incidental
autopsy discovery. Even though there be no definite relationship between
the zoological order and osseous disease, it is interesting to record a
very simple observation. Animals with long extremities, especially when
the bones are quite near the skin, have a rather high incidence of
fractures and inflammations. Thus the ungulates have of all orders the
highest percentage of these traumatic and infective lesions; herons and
gallinaceous birds follow the ungulates. Marsupials, primates and
carnivores, in this order, are susceptible to inflammations but not to
fractures. Bones are often broken, among the Cervidæ, Bovidæ and
Camelidæ, when as they are chased by mates, they fall upon the slippery
floor of the cages; or again the mounting of a small animal by a large
buck may crush the former to the earth. Two cases of fractured pelvis
have been seen in antelopes from a fall with extended hind legs.
It would seem that repair is usually satisfactory if the animal has a
quiet retreat where callus may form and union occur. A heron is known to
have broken both bones of the leg; at autopsy a very insignificant
circumferential callus remained, the member being as straight and strong
as normal. Figure 40 shows the femur of a deer shot by a hunter; the
shortening was considerable, but function was doubtless good because the
hunter could perceive no limping as the animal ran. The most interesting
fracture among our records was an intracapsular fracture of the hip in a
Huanaco (_Lama huanacos_) shown in Figure 41. This animal slipped on the
ice in December and was thought to have broken something near the hip,
but it limped around without any great show of pain until the following
May, when it died of meningitis secondary to an _otitis media et
interna_. At autopsy an unhealed, complete fracture of the neck of the
right femur was found, apparently separating the head from the neck, the
former being dislocated to the upper angle of the obturator foramen.
Everywhere about the joint callus had been thrown out, but not in a
manner to effect a junction of the broken ends nor to seal the edge of
the acetabulum to the femoral neck. This was probably due in part to the
irregularity of the line of fracture and to the interposition of the
upper part of the dislocated head between the lower rim of the
acetabulum and the surgical neck of the bone. When the specimen was
fresh traces of capsule were found over the upper half of the
acetabulum. While it is usually difficult to decide the manner in which
these injuries effect their damage and deformity, it might be ventured
to explain this case as due to extreme posterolateral extension of the
leg driving the head of the femur downward and inward, rupturing the
capsule and the ligament bridging the acetabular notch, to rest on the
pubis at the upper edge of the obturator foramen where it could find a
sort of joint cavity made by the pubic and ischial segments of the old
acetabulum, but about an inch and a half below its normal location.
[Illustration:
FIG. 40.—HEALED FRACTURE OF FEMUR. FROM A DEER SHOT BY A HUNTER.
]
[Illustration:
FIG. 41.—PARTIALLY HEALED INTRACAPSULAR FRACTURE OF HEAD OF RIGHT
FEMUR. HUANACO (LAMA HUANACOS).
]
Another injury to the hip joint was noted in a Livingstone’s eland
(_Taurotragus oryx livingstonii_). This beast was not positively known
to have fallen, although it was suspected that such an accident had
occurred by reason of sudden inability to rise. At autopsy, death having
succeeded on signs of shock, a complete upward and backward dislocation
of the right femoral head was found; there was also an intracapsular
rupture of the left round ligament, but on this side the femoral head
had not left the acetabular cavity.
Many other fractures have been observed but generally without
interesting features. The conclusions which may be drawn from our
experience are that animals with long bones, and liable to chase have
the greatest liability to fractures, and that the healthy beast, given
seclusion and quietude, possesses great ability to heal its broken
bones. Pathological fractures are occasionally seen. (Consult notes on
cretin wolves.)
Before entering upon a discussion of the most important of osseous
lesions, rickets and osteomalacia, certain inflammatory states may be
appropriately described.
INFLAMMATIONS.
Hypertrophic osteoperiosteitis: A male lion (_Felis leo_) at the Garden
three years died, after being out of condition for a long time, from
chronic ulcerative pulmonary tuberculosis with terminal pneumonia,
nephritis and enteritis. Both hind feet had been observed as enlarged
and apparently painful for some weeks before death. Upon dissection the
bones of both hind feet are the seat of extensive hypertrophy, and the
periosseous fibrous tissues are thickened. A large mass about the size
of a small orange lies attached to the outer side of each ankle. The
hypertrophic periosteitis extends up the tibia a distance of about three
inches and the fibula for about the same distance. These two bones are
adherent to each other for about 1½ inches. The joint between them and
the tarsal bones is apparently perfectly free. The calcaneum is the bone
most severely involved; on this is a large rounded mass which extends on
the bone for a distance of about 2½ inches. The small bones of the foot
are more or less severely involved but are not bound together, the
joints being practically free. The terminal and next phalanges are
entirely free from disease while the metatarsals are severely involved
and grown together into one large mass. On section this appears as a
mass of spongy bone lying on top of the cortex. In the dried specimen
this looks very like old pumice stone. Histological section shows the
periosteum raised from the bone by mononuclear infiltration. The bone
marrow spaces are filled by a very delicate gelatinous material. The
lamellæ are thickened. A photograph of the foot with a normal example is
given. (Fig. 42.) (See also Tuberculosis section—Carnivora.)
[Illustration:
FIG. 42.—HYPERTROPHIC PERIOSTEITIS. RIGHT HIND FOOT WITH A NORMAL
LEFT. LION (FELIS LEO). THIS CONDITION WAS ASSOCIATED WITH CHRONIC
PULMONARY TUBERCULOSIS.
]
[Illustration:
FIG. 43.—MARKED SCOLIOSIS IN A COCKATOO.
]
A cockatoo died from acute miliary tuberculosis; the upper thoracic and
lower cervical vertebræ are involved in an S-shaped scoliosis which
reduces the height of the thorax by perhaps a centimetre. Thorough
dissection was not made, the trunk being kept as a museum specimen and
for study in event another avian scoliosis occurred; but from palpation,
separation of the muscles and stretching of the spinal column it does
not appear that a tuberculous osteitis of the vertebra existed. It seems
that this may be due to congenital deformity or old injury.
A white-nosed coati (_Nasua narica_) suffered with generalized
tuberculosis which also affected the wrist joint with a caseous and
ulcerative arthritis.
Gouty arthritis has been recorded but three times, although on several
occasions small uratic deposits in tendon sheaths have been observed in
birds; gout has not been seen in mammals. An illustrative case in a
Boat-billed Heron (_Cancroma cochlearia_) will be given in the section
on gout.
Arthritis as an acute infectious disease such as rheumatism of the human
being, has not been observed, but copious examples of acute, subacute or
chronic monoarticular inflammation are recorded. Nearly all of these
have a definite explanation—traumatism or acute general disease, and
there are a few cases of polyarthritis with chronic disease. Notable
among the last are two instances of chronic dry ossifying arthritis and
synovitis, one with tuberculosis, the other with actinomycosis, both
occurring in ungulates. A third case similar in character deserves
special mention. The Indian elephant “Bolivar” (_Elephas indicus_) died
from pulmonary tuberculosis, myocarditis, nephritis and hepatic
cirrhosis. The joints of all extremities showed atrophic arthritis with
fluid, the synovial membranes being ulcerated or retracted and fibrotic.
The articulating surfaces where not roughened by erosion, were
flattened. It is perhaps worthy of mention that this old and familiar
animal was the occupant of the same enclosure, floored with cement, for
over thirty years, conditions which might be partly instrumental in the
arthritic changes as well as in the flattening of articular surfaces.
The Ungulata frequently suffer with wounds, ulcers and abscesses about
the lips, nose, and soft tissues of the jaws which may at times be
confusingly like actinomycosis. This disease we have seen in gazelles
and tapirs but have had to exclude it in several other members of this
order. A number have come to autopsy with osteitis of the lower
mandible, some evidently traumatic in origin, others probably due to
infection _via_ the teeth. Figure 44 represents the jaw bone of an
Isabelline gazelle (_Gazella isabella_) suffering with a rarefying
osteitis from a root abscess, and illustrates well the possibility of
focal infection from this source.
DEGENERATIVE SKELETAL DISEASES.
While the foregoing instances of disease in the osseous system are
interesting examples of individual pathological lesions, they are
insignificant in comparison with the forms of bony change known under
the names of rickets, osteomalacia, osteogenesis imperfecta and the
like—systemic conditions which are chiefly degenerative but have certain
evidences of inflammation in addition. The modern knowledge of the first
two named is so far from complete that it cannot be said that there is
any certainty of their identity. Indeed there seem to be some reasons to
think that there is more than one variety of rickets, that all cases are
not dependent upon the same cause, and that in essence it is the same
process as osteomalacia, the latter, however, occurring at a later age.
We shall show that in the same order, Primates, both diseases may occur
in animals fed upon the same diet, and that one family tends to have one
disease, another family the other.
[Illustration:
FIG. 44.—DENTAL ROOT ABSCESS AND OSTEITIS OF JAW BONE. ISABELLINE
GAZELLE (GAZELLA ISABELLA).
]
RICKETS.
Since the two conditions are diagnosed separately in veterinary practice
and each seems to have a distinct place in medical ideas, it may be well
to outline upon what criteria the two diagnoses have been made in this
Garden. Rickets is essentially a disease of early life. The animal is
noted as having a large head, squatty station, heavy extremities and a
prominent belly. Death occurs as the result of enteritis or pneumonia.
Occasionally such a young specimen seems to recover from the disease but
retains the distortion of his skeleton; this is important, for we
believe that osteomalacia, except the variety confined to periods of
pregnancy, rarely ends in recovery when once thoroughly established. At
autopsy the cranial bones are the seat of osteotabes, the face is broad,
the epiphyseal junctions are swollen by irregular osteogenesis and
granulation tissue, the periosteum shows an irregular fibrous tissue
overgrowth—the last two processes producing bones of irregular contour
and thickness. Section through the osteogenetic ends of the long bones
shows actively congested marrow up to the articular cartilages with very
tortuous strands of spongy bone or cartilage, and when considered
transversely, there is a bone-forming layer of many times the normal
thickness but bloody red instead of pink.
OSTEOMALACIA.
Osteomalacia appears in mature animals or at least those well able to
care for their own nourishment. The earliest observations are not
referable to the skeleton but to the change in the activity of the
beast. He will be noted as less active in running, jumping or searching
for his food. The customary position is a sitting or lying one. No
change is noted in the head or face. As the disease progresses, the
animal becomes quite inactive, seeks solitude but will eat well if the
food be conveniently available and he does not have to fight for it. The
movements are stiff and seem painful. About this time definite
alteration in the shape of the chest is perceptible, and in some cases
there is anterior curvature of the legs. Movement becomes so difficult,
probably from weakness and pain, that it seems as if paraplegia actually
existed. The inability of affected monkeys to climb has given rise to
the term “cage paralysis,” but this term should not be restricted to
weakness, the result of osteomalacia since it is used by dealers and
keepers to imply the cramped station and gait of an animal long housed
in quarters too small for it, an appropriate application because it
suggests cause and effect. However, the appellation is widely and
loosely used insuring its employment in diagnosis for entirely different
conditions such as degenerative bone disease and hind-quarter laming
from enteric intoxications; for these affections one might use the term
in an adjectival or descriptive sense.
Our Primate collection has suffered considerably with osteomalacia, and
we have devoted much time to the study of its cause and treatment.
However, the Garden is not alone in this experience, for wherever
certain species are kept the disease appears. The description of cases
in the New York Garden by Blair and Brooks[46] is excellent, and with
the exception of data concerning the nervous system, almost exactly
parallels our own observations. They lay much stress upon the changes in
the brain, cord and ganglia as constant in well developed cases but as
probably secondary to the osseous, hemic and metabolic disturbances. We
have been unable to find any pathological lesions in four thoroughly
studied brains and cords from well developed cases. As will appear
later, our most satisfactory findings were in the dietary and metabolic
chemistry and in the osseous pathology. The cases recorded by Campbell
and Cleland[47] would seem to be undoubted instances of myelitis, but
the osseous changes are not sufficiently discussed. In many cases it
would seem, therefore, that there is some change in the nervous system,
but there may be some examples without this and with predominant osseous
lesions. We are inclined to think that these two groups differ
qualitatively, and we look upon the confusion as demanding for its
ultimate solution the use of exact nomenclature, especially the
exclusion of “cage paralysis” as a diagnostic term. The only division we
can understand at the present time depends upon the gross changes in the
bones, those with and those without definite irregularities in contour
due to periosteal overgrowth. Certain of the former may show no
unevennesses at all, the deformity being due to softness of the
skeleton. The other group has shafts of irregular thickness, swellings
around the joints and much beading of the middle of the ribs.
Whether or not there be true paralysis is difficult to settle, but in
our cases we have decided always in the negative because of the ability
of the monkeys to grasp firmly with the hind digits. The animals tend to
lie in one position, determined probably by comfort, the result being
that they develop sores at the points of contact with their cage floor,
and deformities of the skeleton (see Fig. 45). These deformities are
especially well exhibited by the chest, the vertebræ and the pelvis and
are referable to the almost constant squatting of the animal; the long
bones may be bowed but not as much as in rickets, nor is the epiphyseal
junction so knobby as in that disease.
The foregoing description is based chiefly upon observations on monkeys
but may be closely paralleled in carnivores and rodents. These latter,
however, lie rather than sit during the development of the disease, so
that thoracic and pelvic deformity is relatively less than in monkeys.
Death is due to enteritis, anemia, shock from fractures and respiratory
inflammation.
In so far as the deformities of the skeleton may serve to distinguish
between rickets and osteomalacia, I can only point to the preponderance
of changes in the skull and extremities in the former and of the trunk
bones in the latter. Deformity of the chest, barrel-shape shortening and
pigeon breast, is due more to posture than to the essentially osseous
changes. “Rachitic rosary” may occur in both, but it is always better
exhibited in rickets; in this disease the swellings occur at the
costochondral junction, while in osteomalacia rosary-like nodules may
develop anywhere along the ribs.
Examination of the anatomical lesions is, however, somewhat more
helpful, and the following description for osteomalacia may be
contrasted with that already given for rickets. The peculiar change is a
thinning of the shaft of long bones and reduction of the subperiosteal
plates of flat bones.
In mammals the long bones are more affected than in birds whose sternum,
ribs and beak show the severest changes. The skull is frequently not
affected to a serious degree, but may, however, show advanced lesions,
the cranial plates being thinned in places so that they may be bent in,
or occasionally a periosteal thickening may be found; the head as a
whole is not misshapen. The ribs are softened and may be of paper
thickness although there may be found a periosteal overgrowth, perhaps a
kind of splinting, which makes the diameter variable. At costochondral
junctions, beading may be found, but without the active congestion seen
in rickets. Similar alterations may be found in the long bones, here in
characteristic degree in that the shaft walls are thin, by removal of
the endosteal and periosteal layers sometimes with definite retraction
of the marrow. Occasionally subperiosteal thickenings, made of
osteofibrous tissue are encountered. At the epiphyses there are strands
of gelatinous tissue, fibrous and cartilaginous, separating pink or
blood-red areas of marrow. These strands may contain calcareous matter
and are probably the remains of the cancellated tissue. Despite all this
activity at the ends of the long bones there is not the extreme
prominence of articulations so characteristic of rickets. Gelatinous or
cartilaginous islands may be seen in the deep red shaft marrow.
[Illustration:
FIG. 45.—OSTEOMALACIA. MODERATELY ADVANCED CASE WITH HOWEVER WELL
ESTABLISHED DEFORMITY OF THORAX AND PELVIS. THIS POSITION WAS
CONSTANT FOR THREE MONTHS BEFORE DEATH. BLACK HANDED SPIDER MONKEY
(ATELES GEOFFROYI).
]
Fractures may be found and around them may form a blood clot or loose
fibrous tissue entirely devoid of bone salts. If a break has existed for
some time a very pronounced fibrous overgrowth from the periosteum is
apt to occur, indeed an excessive fibrosis may exist, but this is
ineffective for healing of the fracture or splinting of the shaft.
Certain cases, notably in Carnivora, seem to have especial activity in
and around joints so that when the member is dissected one gets the
impression of osteoarthritis. In such cases the synovia may be fibrotic
and the articular surfaces dry. The pelvic deformities are similar to
those in the human being—lateral contraction with bending in of the
superior rami of the pubis with the production of a beak, to which the
name “duckbill” has been given. The anterior curvature of the lumbar
spine makes an acute angle at the upper end of the sacrum.
Histological examination of a number of our cases of osteomalacia and
rickets have failed to show any lesion different from those known for
the human being and for domesticated animals. It is noteworthy that not
all bones of a given case will show the changes to the same degree even
though grossly they may seem comparably affected. So too there is no
certain relation between the degree of deformity as shown by the body as
a whole and the advancement of osteoporosis as seen under the
microscope. These observations are in accord with those of Brooks and
Blair. Just why this is cannot be stated, but as the cause of these two
bone diseases may not always be the same, variations in gross and minute
anatomy are not remarkable.
Analysis of the bones shows a loss of calcium and an excess of sulphur
and magnesium. The loss of the first is chiefly _via_ the intestinal
discharges but also _via_ the urine. The metabolism of one monkey showed
a high calcium and phosphorus loss with moderate retention of sulphur
and magnesium.
Because of the importance of osteomalacia and rickets in cebus monkeys
and certain other animals, Dr. E. P. Corson-White has been investigating
its etiology. I shall refer briefly to her results as they affect our
present subject but shall leave for discussion in the chapter on diet,
which she has written, the broader question of food and systemic
disease.
It must be understood that the instances included in this general
discussion of degenerative osseous disease are cases of definite
character and development. There may have been, in addition to the
numbers cited in the list on page 357, many more animals at autopsy with
early or unrecognized constructive or destructive abnormalities, and we
are thoroughly familiar with the imperfect skeletal development of
specimens, inbred or reared in captivity or even those adult when caught
yet under Park conditions for many years. In these latter groups the
changes vary from incomplete construction (an example of atrophy was
quoted on page 24) to actual degeneration as in osteomalacia. Inbreeding
seems to be a potent factor in many cases, a well known fact in human
and veterinary medicine. The importance of inactivity in the causation
of degenerative bone disease, the unused muscles giving the bones
nothing to do, is certainly admitted but it is immeasurable. It is
probably not great in a cage of mixed varieties of monkeys. The effect
of the absence of sunlight in osseous degeneration is no factor in our
material. The exhibition house is well lighted and many animals are out
of doors all year around.
The ductless glands have repeatedly been accused of responsibility for
these disorders. In our seventy-nine cases of osteomalacia and thirty-
four of rickets, no abnormality has been observed in ovary, testes or
adrenals except for moderate congestions. Two cases were associated with
pancreatic disease, once acute, once chronic. The thyroid body has been
found to have been definitely abnormal only once—secondary hyperplasia
with colloid in a carnivore. In the Primates this body was frequently
congested and has shown small colloid cysts but was not uniformly
enlarged or atrophic. As a therapeutic measure I have administered
adrenalin to two monkeys, one for a few weeks, one for nearly six
months; this treatment was without any perceptible effect upon the
process.
Dr. Corson-White has, by the study of some cases during the life of the
monkey, confirmed the decreased alkalinity of the blood in connection
with the increased output of calcium in the feces and urine.
Since the explanation of the disease by blaming the ductless glands has
failed, Dr. Corson-White has undertaken a study of the diet given our
monkeys to see if any fault in it were a part of the etiology. Analysis
of this diet (see list page 426) computed from Atwater’s table, and by
actual analysis of the amounts of food consumed by the animal in four
four-day periods, gave:
1. Protein—low in quantity and poor in quality; especially low in
phosphorus content.
2. Fat—very low.
3. Carbohydrate—very high, almost eleven times the value of all other
ingredients.
4. Ash—decidedly low and predominatingly acid. Further analysis of this
ash showed a trace only of calcium and phosphorus and iron and only a
small amount of sodium; potassium, sulphur and magnesium were slightly
higher.
5. Vitamines A, B, C, were present in extremely small amounts—A was
exceptionally deficient, and in the rations of some days was entirely
lacking.
There are in this monkey diet several factors of importance. 1. Low
vitamine contents—especially Vitamine A—factors which are essential for
life and growth. 2. A high carbohydrate diet—which in oxidation yields
an acid ash and which favors the growth of intestinal bacteria producing
acid and gas. The acid from these two sources must be neutralized either
by the alkali derived from food, or from the body storage. This diet,
however, is abnormally low in ash and especially in the alkaline salts
of the ash, therefore making it an ideal diet for the production of
osteomalacia.
The following table shows the additions necessary for corrections of the
separate ingredients of the diet:
Monkey diet Corrected by
Rice Casein, Salt mixture, Carrots, or Lettuce.
Bread Casein, Butter fat, Salt mixture, especially Phosphorus.
Potato Salt mixture, especially NaCl and CaCO_{3}.
Raw peanuts Salt mixture.
Bananas Casein, Yeast, or Carrots.
Corn Casein, Tryptophan, Lacto-albumin.
Apple Casein, Gelatin, Butter fat.
Onion Casein, Gelatin, Butter fat.
The complete diet may therefore be rendered adequate by the addition
of fresh, whole milk and leafy vegetables, or by butter fat, salt
mixtures and leafy vegetables.
It would seem from these data that in this inefficient diet we have, if
not the cause of osteomalacia, at least a very potent factor in its
production. The disturbance of the calcium and phosphorus metabolism may
be due primarily to the deprivation of the alkaline salts from the diet
(famine osteomalacia) or to a drain from the alkaline storage of the
body, associated with a deficient diet (as in the cases of osteomalacia
of pregnancy and lactation) or in the combined action of a diet faulty
in more than its salt content, which by the production of acid in its
oxidation and by favoring the development of acid-forming bacteria,
causes the drain of the body alkali for the neutralization of this acid,
or it is due to the combination of all these factors acting through
their influence on the ductless glands.
It is important also that while this disease is very common among the
Cebidæ it has never been found among the macaques. This may be due to
the fact that, owing to the storage sacs in the mouth of the macaques,
more food proportional to body weight is consumed, or there may be an
essential difference in the basal metabolism of the families and
individuals. All the factors enumerated do tax the metabolic resources
of the body and depress the functions of the endocrine glands. Only
detailed and accurate quantitative studies of normal metabolism and the
effect of alterations of it on the ductless glands will give a more
definite answer to the problem.
This work indicates clearly the alterations to be made in the diets to
meet the requirements of the Cebidæ and is to be followed by
investigations along similar lines for other families.
TABLE 17.
_A List of the Orders Exhibiting Definite Lesions of Osteomalacia and
Rachitis._
═══════════════════════╤═══════════════════════╤═══════════════════════
│ Osteomalacia │ Rachitis
───────────────────────┼───────────────────────┼───────────────────────
Primates │ 29 │ 10
Lemures │ 4 │ 2
Carnivora │ 3 │ 8
Hyracoidea │ 2 │ 1
Rodentia │ 5 │ 3
Marsupialia │ 1 │ 10
│ 44 │ 34
Passeres │ 3 │
Psittaci │ 9 │
Accipitres │ 2 │
Columbæ │ 12 │
Galli │ 9 │
│ 35 │
───────────────────────┼───────────────────────┼───────────────────────
│ 79 │ 34 = 113
───────────────────────┴───────────────────────┴───────────────────────
Having discussed the nature of these diseases and some of the factors in
their causation, analysis of their distribution may be appropriately
added. The accompanying list (Table 17) illustrates the orders in which
the two diseases have been found. Veterinarians are familiar with
systemic osseous diseases in all the domesticated herbivores, but Hutyra
and Marek note them as uncommon in dogs and birds. Among the Primates,
osteomalacia occurs almost exclusively in New World monkeys, Cebidæ and
Hapalidæ, whereas rickets is much more common among macaques
(Cercopithecidæ). Eight of the ten cases of rickets in monkeys seem to
have arrived at the Garden with evidences of this disease. Half of the
cases were arrested, or at least not florid, when the beast came to
autopsy. All of the osteomalacic lemurs belonged to the ring tailed
species, born in the Garden and dying at ages from three to seven years.
The cases of rickets among the Carnivora were four Felidæ, three Canidæ
and one Procyonidæ while all the osteomalacia cases were in the last
family. Six of the eight cases among the rodents affected squirrels. The
large number of cases of rickets among the marsupials is due to a litter
of small opossums thrown by an apparently healthy mother and dying in
from six weeks to three months.
The avian varieties which show the most definite osteomalacic changes
are the pigeons and pheasants, with the parrakeets presenting nearly as
characteristic lesions. Birds when affected with this disease, may come
to autopsy in fairly good plumage and without any very marked
emaciation. This is remarkable, for when the _cresta sterni_ is palpated
this ridge may sometimes be bent enough laterally to touch the _alæ
sterni_. How the bird can sit upon a perch when it is possible to bend
the femora almost double, is difficult to understand. Deformity is by no
means so frank as in mammals although periosteal overgrowth may be quite
marked at times. Anemia is undoubted in nearly every instance, the
pallor of the muscles seeming to be as great as if the specimen were
intentionally bled to death.
OSTEITIS DEFORMANS.
Dr. Corson-White was fortunate enough, during the course of her work
upon osteomalacia of monkeys, to detect a specimen which did not show
the usual excessive excretion of calcium but on the other hand retained
this element and evinced alkali hunger. The general appearance of the
specimen was similar to that of monkeys having osteomalacia but at
autopsy a definite picture of Paget’s disease or osteitis deformans was
discovered. This led to a search for cases in the literature and to the
following study, which I paraphrase and condense from Doctor Corson-
White’s notes.
Osteitis deformans is a chronic constitutional affection characterized
by the absorption of compact bone, chiefly in the cranium and long
bones, and the laying down of fibro-osteoid tissue in such an excess as
to enlarge the affected bones. This material, which is soft and cuts
with reasonable ease, has calcareous matter in it as shown by Röntgen-
ray examination. Paget described it in a classical article in 1876[48]
since which time the reported cases have mounted to three hundred and
fifty. Because it has only been recognized in its best developed stages,
it may be that early mild or arrested cases have been overlooked.
Judging by the instances claimed to have been found in museum
collections of bones, it is probably an affection dating to antiquity.
So far these remarks apply only to man but in lower animals the reports
are very few and those are not available in the original. The abstracts
and references show considerable confusion. The names osteitis
deformans, osteoporosis, osteitis fibrocystica, osteodystrophia
deformans and osteosarcoma, leontiasis ossei, etc., are used almost
interchangeably. In 1901 Barthelemy[49] described a condition (_Maladie
du Son_) in horses in which there was a marked enlargement of the head
and of the epiphyses of the long bones. His cases were more allied to
osteitis fibrosa cystica. Paget’s disease always attacks the diaphyses
of the bones and not the epiphyses. Goldman[50] described typical
examples of this condition in fowls. Jöst[51], in one communication,
described a case in a horse which he says was identical with that
condition described by Paget as osteitis deformans and by Virchow as
leontiasis ossei; he also refers to similar cases in goats and monkeys.
Rossweg[52] found it in goats. In wild animals the only suggestive
article found was by Jöst but the description was probably of an
osteoporosis and a craniosclerosis which occurred in a young lion and a
monkey. All the communications deal with either domesticated animals or
those in captivity.
The etiology of this condition is as obscure to-day as it was at the
time of Paget’s first description. Prince thought it might be due to a
defect in some peripheral nerve or nerve centre or to a tract
degeneration. Cases have been reported in conjunction with a myelitis.
There has been however little on which to base these suppositions. Paget
felt that the process was at least upon an inflammatory basis and
deduced this from the enlargement and the excessive production of an
imperfectly developed structure with increased blood supply. Many felt
that rickets, osteomalacia and osteitis deformans were all
manifestations of the same disease. A bacterial cause was proposed by
Arcangelli who claimed the discovery of diplococci and improvement from
a vaccine. Lancereaux[53] and Richards felt that focal infection played
a profound rôle in the etiology. However all other observers fail to
isolate an organism from the bones or to get improvement from removal of
infectious foci. Heredity has been held responsible in seven per cent.
of the cases in human beings.
That some inflammatory factor is partly responsible seems plausible when
one considers the active growth of fibrocellular tissue in the endo- and
periosteum. The more interesting theories go back to perversions of
internal secretions, pituitary, parathyroid etc., (Macallum & Vogtlein).
Higbee and Ellis[54] say in relation to the neurotrophic theory that if
the neurotrophic mechanism governs metabolism and is influenced by the
activity of the ductless glands, there is considerable likelihood that
its disturbance may possibly be found to be the cause.
Da Costa[55] believed the disease to be a disorder of bone metabolism
probably dependent on the absence or perversion of some internal
secretion. There is much evidence on hand to indicate that disorders of
the ductless glands do influence bone metabolism, and changes in these
glands have been reported in cases of Paget’s disease, although the
findings and lesions have been far from uniform or distinctive or even
confined to one gland. Eight cases were reported as possibly due to a
hypothyroid condition; pituitary changes were found in three; adrenal
changes in one; parathyroid reported missing in two; three had sclerotic
thyroids. Many case reports make no mention whatever of the glands of
internal secretion.
Da Costa interprets the retention of calcium, phosphorus and magnesium,
with the sulphur loss found in these cases, as indicating a stimulated
osseous or osseoid formation accompanying the resorption of a highly
sulphurized organic matrix. In the course of this calcification
procedure we suppose a certain quota of the sulphur of the matrix is
replaced by other elements, a process which must entail retention of
calcium, phosphorus and magnesium and increased elimination of sulphur.
He shows the close parallelism between the mineral metabolism of a
growing boy, a case after parathyroidectomy and a case of osteitis
deformans, and suggests that this depends in some way either on the
absence or perversion of some internal secretion, possibly of the
parathyroids, which controls calcium exchange in the body. Substances
from some cause arise which have the power to abstract calcium from the
body tissues, the abstraction of these salts being the first step in the
production of the disease.
The example which is reported in full was the first to be encountered in
our 5,365 autopsies but shortly after this series was concluded two more
came to autopsy and Dr. Corson-White’s studies were made to embrace
these.
A reddish woolly monkey (_Lagothrix infumatus_) received November 25,
1919, was a particularly active specimen and as far as we could
determine a perfectly healthy adult animal. He passed the tuberculin
test and was placed on exhibition. In April, 1920, he was first reported
as crippled and was removed to the laboratory in June, 1920. At that
time the long bones of the legs and arms were bowed anteriorly and
laterally, the degree of curvature making the hands and feet seem
disconnected. The monkey could stand but made no voluntary effort to do
so. There was evidently some pain although it could not have been at all
severe. He resented handling, especially of his arms and legs. The head
was rounded, resembling that of a baby, and the eyes were protuberant
suggesting an exophthalmos. The maxillary bones were so excessively
thick that the mouth could not close and the monkey drooled saliva. His
blood on admission to the infirmary in May was—Hg eighty-nine per cent.,
R. B. C. 4,370,000, W. B. C. 5,800; one week before death it was Hg
fifty-four per cent., R. B. C. 2,860,000, W. B. C. 6,000. Routine urine
examination showed a constant trace of albumin, hyaline and granular
casts. There was at no time a Bence-Jones protein reaction, excess of
indican, indol, or diacetic acid. He had a constant slight diarrhœa with
some flatulence, the semifluid, constantly acid feces presenting a
preponderance of Gram-positive coccoid organisms. His appetite was fair
and he showed marked craving for lime, eating plaster from the walls
when he could get it. Because of this desire for lime he was given a
salt mixture to see if it would have any effect on the bone condition.
The mixture used was the following:
[Illustration:
FIG. 46.—OSTEITIS DEFORMANS. SKELETON SHOWING GENERAL THICKENING OF
ALL BONES, BUT ESPECIALLY OF THE SKULL, JAWS AND LONG BONES. NOTE
THICKNESS OF CALVARIUM, 10 mm.; NORMAL IS ABOUT 3–4 mm. THE HUMERUS
IS TWICE NORMAL SIZE. THE WIDTH OF THE ULNAR CORTEX IS SHOWN BY A
TRANSVERSE SECTION NEAR THE ELBOW JOINT. REDDISH WOOLLY MONKEY
(LAGOTHRIX INFUMATUS).
]
NaCl 0.874 grams
KCl 0.548 grams
CaH(PO) H_{2}O 3.608 grams
Ca lactate 0.386 grams
Mg citrate 0.848 grams
K citrate 1.953 grams
This mixture the animal ate with avidity and seemed more comfortable;
other than that no change was noted.
An inorganic metabolism examination was attempted on the ordinary diet
and the diet plus the salt mixture. Under the circumstances at our
disposal this was not entirely accurate but showed such marked variation
from the control animals examined—normal and osteomalacic—and such
marked correspondence on the four separate four-day periods of each
intake that it seemed acceptable. The result of this investigation on
the first series of four four-day periods was:
═══════════╤═════════╤═══════════════════╤═════════════════════════════
│ Intake │ Output │ Total
───────────┼─────────┼─────────┬─────────┼─────────────────────────────
„ │ „ │ Feces │ Urine │ „
───────────┼─────────┼─────────┼─────────┼─────────────────────────────
Calcium │0.0280 │0.014 │0.0022 │0.0162 = 0.0118 retention
Magnesium │0.0640 │0.034 │0.0123 │0.0463 = 0.0177 retention
Phosphorus │0.1540 │0.027 │0.0430 │0.07 = 0.084 retention
Sulphur │0.1440 │0.002 │0.1680 │0.17 = 0.026 loss
───────────┴─────────┴─────────┴─────────┴─────────────────────────────
The result on the higher salt content was practically the same, the
retention being in proportion slightly less. The diet for these small
monkeys is two apples, two bananas, six small sweet potatoes, with a
lump of boiled rice about the size of an egg. The content of this diet
has been found very low in calcium, phosphorus, sodium, chlorine and
iron, while potassium, magnesium and sulphur were high. To this diet
lime water was added to increase its inorganic content.
This Reddish Woolly Monkey died August 20, 1920, and was immediately
posted. There was marked thickening of the frontal, occipital and
parietal bones, upper and lower jaws. The increase in the size of the
alveolar margins prevented the closing of the mouth; only the last four
teeth could be brought into apposition. The enlargement of the mandibles
reduced the capacity of the mouth cavity. The skull while decidedly
thickened did not enlarge at the expense of the cranial cavity. There
was a cervical and dorsal kyphosis. The chest was increased
anteroposteriorly and contracted laterally. The long bones were thick,
bulky and deformed. (Fig. 46.)
A Black Spider Monkey (_Ateles ater_) showed a general hyperplasia of
the whole shaft of the long bones. She was much deformed by curvatures
and swellings of the skeleton—head enlarged, face deformed by the
swelling of the upper and lower alveolar processes, jaws do not close
and the palatal bones were flattened, skull irregularly thickened,
elastic but not soft, slight subperiosteal growth. Thickening of the
long bones was largely due to subperiosteal growth; section of the ulna
showed a subperiosteal osseoid layer surrounding the old shaft. This
tissue seemed to be very poor in lime salts, cutting without any grit.
Marrow cavity was filled with a fairly firm, deep red marrow which did
not bleed on section. The third monkey, a Brown cebus (_Cebus
fatuellus_) showed exactly the same general picture but was less
severely affected than the other two.
“The more minute study of the bones of these monkeys shows a variety of
pictures while preserving one general form. The skull was smooth,
mottled by irregularly placed areas of congestion; it was asymmetrically
thickened; differentiation between cortex and diploe, internal and
external tables was lost; calcareous matter was absorbed and the
resultant bone was soft, elastic and porous; lacunæ enlarged and lined
with bone corpuscles and giant cells. Other areas show more dense bone,
the reparative processes being more active in that the lamellæ are wide
and the vascular spaces narrower. As a rule the compact bone is
absorbed, the Haversian canals are more or less confluent and there is
generally a marked increase of newly formed osseoid tissue. The
ossifying periosteitis obliterates the depressions for the cranial
arteries and the sutures. The skull cap becomes finely porous,
cancellous and even cavernous. The spaces are filled with a soft, red
marrow-like material. The bones at the base of the skull are much less
involved; the pericranium, dura and brain are normal.
“The long bones show interlacing narrow strands which are in some
regions wide, in others narrow or thin as in spongy bone. Large
irregular cavities are present and there is a disappearance of the
compact bone and an encroachment on the medullary canal of a relatively
dense new bone with small irregular trabeculæ surrounded by osteoblasts
and a fibrous connective tissue which fills the outer trabecular spaces.
The new bone is often both subperiosteal and subendosteal, the latter
often gaining on the former. It is always soft and irregularly
calcified. The general arrangement of the strands in the deep layers is
longitudinal but in the subperiosteal bone they are very irregular and
almost at right angles with the central strands. In this new osseoid
tissue cysts are frequent, varying in size from very small to rather
large cavities filled with a cloudy gelatinous material. The picture
here is very like osteitis fibrosa cystica. Endosteal cells proliferate
and may fill up the marrow spaces so that solid masses of fibrous tissue
result. Frequently the osteoid material shows fibrillæ. The compact bone
may be irregular with well marked Haversian systems. Toward the
periosteum the cells may become scanty, the bone dense in structure
while toward the interior the cells are more numerous and in the more
cancellous portions, the trabeculæ become slender and far apart; here
they may be covered by a single row of osteoblastic cells. The
intertrabecular spaces are large, irregular and filled with a delicate
alveolar tissue containing only a minimal number of normal bone marrow
cells, large capillaries and no giant cells. Periosteum may be of usual
thickness; the bone immediately beneath is spongy. The sclerosis of the
bone in its densest areas is entirely due to the ossification of spindle
cells which have remained in the place of the original marrow of the
bone. As a whole the bone is nowhere normal in amount or proportion but
the small Haversian systems are properly made, the abnormality being
chiefly due to cellular and fibrous growth around the large lamellæ
which at times is normal in amount but usually much in excess. In places
this consists wholly of fibroblasts, at others of giant and round cells
very suggestive of sarcoma. All histologists apparently agree that
Paget’s disease starts as a resorption of already calcified bone.”
These data seem to supply ample evidence that the autopsy diagnosis of
Paget’s osteitis deformans was correct. While the anatomy and course and
chemical changes presented by these monkeys do not settle the causation
of the disease, they offer very definite suggestions which Dr. Corson-
White summarizes in the following cautious conclusions.
“Many of the cases of Paget’s disease first came under the observation
for fractures, accidents common in osteomalacia but very rare in
developed cases of osteitis deformans. Early cases all presented
diarrhœa, which was present in all the early human cases seen, and in
all the cases reported in monkeys. This symptom was mentioned in
fourteen of the cases from the literature. It was also a constant
symptom in primate osteomalacia. The diet of these monkeys was
exceedingly low in those substances essential to bone development, and
Sherman has shown that the calcium balance is regulated to a certain
extent by the calcium ingested, and that when the diet was poor in this
element, the output materially exceeds the intake, a fact which is
immediately changed where the animal is put on a diet high in calcium.
So far as we could find there are no studies on the mineral metabolism
of beginning cases of Paget’s disease. It seems possible from the
osteomalacic animals previously studied, that the low mineral and
otherwise faulty content of the diet might so disturb the chemical
equilibrium directly, through the neurotrophic mechanism or through the
perversion of the ductless glands, that the mere addition of lime water
might entirely change the pathological picture. This is in accord with
the histology. The initial histological picture is always resorption of
bone, a general decalcification which later presents an irregular
proliferation. The disease then progresses along different lines ending
as osteitis fibrosa cystica, Paget’s or Von Recklinghausen’s diseases,
etc., dependent upon the strength of the reparative stimulus and the
organism upon which it acts.
“These cases are of interest (1) because they are typical examples of
Paget’s disease as it has been described in man both clinically and
pathologically, (2) because the disease shows the same general type of
inorganic metabolism that was exhibited in man, (3) because of the
alkali hunger shown by one monkey, and by two human cases, a hunger
which was severe, which preceded the deformity and disappeared after the
deformity was established, (4) because the disease developed in animals
fed on a diet insufficient in its inorganic and vitamine content to
which an excess of calcium was added.
“From this study it seems possible that Paget’s disease may be just one
stage in a deficiency disease, a reparative response through a
neurotrophic mechanism or through the perversion of the glands governing
calcium metabolism which has been perverted by an improperly balanced
diet.”
TUMORS.
Neoplastic diseases of the bones have yet to be classified to everyone’s
satisfaction. All gradations of hyperplasia of osteogenetic cells and
fibres and of the marrow elements, from simple inflammation to true
sarcoma, are recognized. As one reviews a large series of lesions,
clearly defined types may be found, but there are transition stages to
which an exact name is difficult or impossible to apply. Nor does the
pathological diagnosis always fit with the clinical course. Thus, for
example, the giant cell tumor of bones looks malignant, and is not, and
its structure may be simulated in such diseases as fibrous osteitis and
Paget’s disease. As we have seen in the discussion of the latter of
these two, abnormalities of fibre and cell growth simulate neoplasms
very closely. In addition it might be mentioned here that actinomycosis
may produce bony growths resembling sarcoma. When osteitis deformans
affects the facial bones especially, it has been called leontiasis
ossium, and it is then a more nodular, tumor-forming process, the
enlargement consisting of fleshy masses occupying the whole bone, but
especially the marrow cavity. Histologically the lesion is
fibrocellular, frequently with numerous giant cells; accumulations of
small sarcoma-like alveoli may be found. We have encountered four cases
among common opossums (_Didelphys virginiana_) and one in an Isabelline
Gazelle (_Gazella isabella_) and, because of the localization and fleshy
consistency of the tumor, we have called them osteosarcomata for
descriptive purpose, but not for classification among neoplasms (where
they will not be found). Two of the opossums had osteoporosis and
gelatinous marrow in the ribs. All these animals had been in the
exhibition under a year, and as far as known are not related. Figure 47
shows the gross character, while the following is the description from
one protocol.
[Illustration:
FIG. 47.—EXAMPLES OF LOCAL OSTEOMATA RESEMBLING OSTEOSARCOMA AND
FIBROUS OSTEITIS; THEY PROBABLY BELONG TO THE DISEASE KNOWN AS
LEONTIASIS OSSIUM.
]
[Illustration:
FIG. 47B. A AND B, OPOSSUMS (DIDELPHYS VIRGINIANA).
]
[Illustration:
FIG. 47C. C, ISABELLINE GAZELLE (GAZELLA ISABELLA).
]
[Illustration:
FIG. 48.—FIBRO-OSTEOMA, A LOCAL SINGLE TUMOR OF THE UPPER JAW. THIS
DID NOT RESEMBLE THE CHANGES IN ACTINOMYCOSIS, BUT THE INFECTION WAS
NEVERTHELESS EXCLUDED BY BACTERIOLOGICAL SEARCH. ISABELLINE GAZELLE
(GAZELLA ISABELLA).
]
Common Opossum (_Didelphys virginiana_) ♀ . Osteosarcoma of alveolus,
rarefying osteitis deformans of skull, hypertrophy of thyroid, acute
catarrhal enteritis, acute hyperplasia of spleen. About the middle of
both lower rami and involving the posterior half of each upper maxilla
is a uniform elliptical growth apparently emanating from alveolus.
Teeth not loose, but can be moved in tumor to be described. On section
a white glistening homogeneous growth is seen apparently originating
in the body of the alveolus and around the teeth. The shaft of bone is
soft and easily broken. What remains of marrow is irregularly
injected. In upper jaw there is a distinct porosis of facial bones;
they and the enclosed sinuses are deeply injected. Lower four ribs on
both sides show distinct nodulations of pale color along a bluish
bone. All ribs are very soft and section shows osteoporosis of shaft
with injected marrow and distinct cartilaginous periosteal bone
formation. The skull is everywhere soft and the bone is apparently
increased in thickness, rich in blood, but porotic. Rest of skeleton
seems well calcified. Microscopic section of tumor shows practically
the same picture. Bone is nowhere normal in amount and proportion but
the Haversian systems seem properly made, the abnormality consisting
chiefly of cellular and fibrous growth around larger lamellæ, which at
times is normal in amount but usually much in excess. In places this
consists wholly of fibroblasts, at others of giant and round cells
very suggestive of sarcoma; indeed all areas must be called giant cell
sarcoma. There is an attempt to lay down osteoid tissue at places
particularly beneath periosteum. The giant cells are in great numbers
and some seem osteoclastic. As the lamellæ disappear young connective
tissue seems to take their place but giant cells do not remain
numerous at such places. Despite its atypical nature it must probably
be looked upon as an osteosarcoma. The tooth socket is not much
involved save for hyalinization of root matrix immediately about
dentinal zone.
In another Isabelline Gazelle (_Gazella isabella_) there was a fibro-
osteoma localized to one side of the superior maxilla (Fig. 48); this
has been included among the tumors, while the above mentioned cases have
not been so grouped.
True osteosarcoma seems not to have occurred. One tumor was seen upon
the wing of a Cuvier’s Toucan (_Rhamphastos cuvieri_) which was formerly
diagnosed as sarcoma, but later examination reveals some giant cells in
arrangement suggestive of tuberculous osteitis; since this is the only
case and not unequivocally a tumor its record is hardly warranted.
Osteomata of the hard variety have been seen on the ribs of a pigeon and
a pheasant as small rounded compact well outlined tumors. It is thought
that they represent products of healing after osteomalacia or rickets.
An osteochondroma growing from the nasal cartilage was found in a
caracal (_Felis caracal_), a fibro-osteoma was found on the vertebra and
clavicle of a Beechy’s spermophile (_Citellus grammurus beecheyi_) and a
fibroma occurred on the clavicle of a lesser snow goose (_Chen
hyperboreus hyperboreus_). The only other tumor from a bone was an
endothelioma from the periosteum of the clavicle in a moorhen
(_Gallinula chloropus_). It corresponds to the usual idea of this tumor.
It probably caused death by cachexia, and by its size, interference with
respiration. The only secondary tumor was a metastasis in the tibia from
a spindle cell sarcoma of the kidney in a scaly ground dove
(_Scardapella squamosa_).
THE MUSCLES.
The skeletal muscles of the wild animals of our collection have been
quite free of pathological lesions such as atrophies and dystrophies and
indeed seem relatively seldom affected by disease. Occasionally
hyalinization will accompany infectious disease or local suppurations
will spread into the muscles. Much more often filaria, sarcocystis,
flukes and larval insects will be found resident within or between
muscle bundles; this will be discussed at a later time. Six tumors have
been found, three of which certainly developed in a muscle, while for a
fourth case no primary growth was discovered. This last one, to dispose
of it at once because of its peculiarity, was an adenocarcinoma found as
a firm, conglomerate, encapsulated mass in the sheath of the gluteal
muscles of a waltzing mouse (_Mus wagneri rotans_). No other growth was
discovered although it must be admitted the body was not exhaustively
searched for some tiny nodule to which primary focus this muscle mass
could have been secondary. That metastases may be larger than original
growths is well known. The gross diagnosis was sarcoma. If this be an
original tumor it might be explained as arising from ectopic mammary
tissue.
The five other tumors were sarcomata, one of large cells almost
syncytial in size, shape and number of nuclei, two definite spindle cell
growths and two of fibrosarcoma type. The first occurred in an all green
parrakeet (_Brotogerys tirica_), the second in an undulated grass
parrakeet (_Melopsittacus undulatus_), the third in a larger Egyptian
gerbille (_Gerbillus pyramidum_), the fourth in a white-footed mouse
(_Peromyscus leucopus_), and the last in a bean goose (_Anser fabalis_).
SECTION XIII
THE CENTRAL NERVOUS SYSTEM AND THE SPECIAL SENSES
Diseases of this system and its specialized end organs of sense in the
eye, ear and nose are recognized by veterinarians as occurring among
domesticated animals, in which however they are by no means so common as
in human beings. Because of the natural reserve of wild beasts and
because their habits and manners are not so familiar to the observer, it
would seem that clinical evidences of disease of the nervous system are
rarest among them. The brain, cord and nerves of our specimens have not
been studied with the minuteness accorded to the examination of other
viscera since we have not had the personnel to devote the time to this
really colossal undertaking, our work with these tissues being directed
toward the accumulation and preservation of apparently normal brains
from every species; there are now some nine hundred brains on the
shelves. However, whenever the history of the animal before death has
suggested that disturbance in the nerve organs might exist, they have
been dissected grossly and examined microscopically. Had we subjected
all our material to microscopic study it is quite possible that we might
have discovered more lesions. This is still possible by reason of our
gross material and autopsy protocols.
We have been fortunate in having Dr. W. B. Cadwalader, Secretary of the
Society, and Dr. J. H. W. Rhein with their broad experience in
neurology, take interest in this phase of the subject and study our
material. The number of cases in which definite lesions have been found
is surprisingly small, so that no generalizations can be attempted
except perhaps in a negative sense. After the study of thirty-nine
brains and cords from animals in whose history some suggestion of
nervous system disease existed, Doctor Cadwalader could find
abnormalities in only twenty-two cases, mostly however of a very
indefinite character. This observer further points out that in his
experience with our material, his observations of our animals and a
review of the literature, he is unable to find satisfactory instances of
the so-called system or tract diseases such as tabes and lateral
sclerosis. This he suggests is due to the absence of arterial sclerosis
in the lower types of brain, intimating further that perhaps the
relation of syphilis to human arteriosclerosis and degenerative nervous
system disease is thereby strengthened. These facts being true it is not
astonishing that massive cerebral apoplexy and cerebral softening do not
occur[56]. The lesions that have been found were either definitely
infectious, as encephalitis or acute septicemia, tuberculosis,
poliomyelitis, meningitis, or the minute hemorrhages and vague
granularities or vacuolizations of nerve cells in toxemic conditions.
The material being limited and broad statements being impossible, the
important cases will be cited individually or in small groups.
CONVULSIONS.
Before entering upon the special subjects, a word might be added
concerning the clinical evidences of neurologic conditions as seen in
the Garden. Perhaps the most common and certainly the most definite
clinical sign of nervous disturbance is the convulsion. General spasms
or fits are fairly common among the carnivores and monkeys, in the
former most often associated with intestinal parasitism, in the latter
with no especial relationship unless it be renal disease. The
convulsions have been general, with and without the preservation of
consciousness. No cases of focal or Jacksonian spasms are recorded
although we shall cite two instances of tuberculoma reasonably near the
motor area in the cerebrum. The exact cause of many cases cannot be set
down since intracranial disease does not often exist.
Intoxication from chemical products of disturbed digestion or from worms
themselves is the usual explanation of spasms associated with intestinal
parasitism; if this be true, intoxication in the absence of demonstrable
parasites may also be the cause in certain cases of enteritis. However
we have seen fits when enteritis, parasites and renal disease were not
found. If these were true epilepsy, they are instances of perhaps the
rarest disease of animals, which I do not presume to diagnose.
Convulsive seizures in herbivorous animals are exceedingly rare although
I have seen clonic movements of a spasmodic character in antelopes and
deer shortly before death from gastroenteritis. Ataxia and
incoördination are much more common. Birds, notably parrots and soft-
billed insectivorous varieties, are not uncommonly afflicted with fits
but as they are rarely observed except by the keeper the exact nature is
difficult to describe. Those seen by the writer have been of two kinds.
The first and more common consists of falling from the perch in a dazed
and stiff condition, with dilated fixed eyes, stiffened and spread-out
legs and wings. Recovery follows shortly and the bird resumes its perch
either in excitement, or slowly and uncertainly, perhaps to have another
attack in a few minutes. These cases, in the few instances in which they
could be followed, were due to faulty feeding and enteritis and showed
either nothing or a mild congestion of the brain. The other variety of
fit is epileptiform, a rapidly developing clonic spasm of all parts of
the body with a tendency to opisthotonos. In one case of this character,
a parrot, no lesions were found in the brain, an enteritis existing
however. Another case concerned a pet Indian Shama I had at my home. He
had been doing well and singing loudly, until one evening he was allowed
to remain in a tobacco-smoke-filled room whereupon next morning he
stopped eating and singing. Later that day the clonic form of
convulsions appeared, growing worse for thirty-six hours or until death.
At autopsy no food was found in the alimentary tract. The brain and cord
were congested grossly, while minutely, perivascular hemorrhages and
marked vacuolization and diffuseness of staining were found in ganglion
cells of the bulb, pons, anterior spinal horns and in the pyramidal
cells of the cerebellum. Happening so promptly after exposure to tobacco
smoke, when the bird was doing well, I venture to associate the two.
ATAXIA.
Incoördination and ataxia are so often observed and under so many
conditions that it is well nigh impossible in any individual case to
give an adequate explanation before death. They are in all probability
the expression of sickness and nothing more in the vast majority of
instances. When they are observed in such cases as the tyromata of the
cerebrum or in certain of the ungulates, they may mean something
definite. In this latter order and to a less extent in carnivores, one
frequently sees weakness and uncertainty of gait in the hind quarters,
the legs being usually coördinate but tending to give way under the
weight of the body.
From a study of veterinary literature and our own material it would seem
that this may have many explanations. In the first place, it may simply
indicate weakness expressing itself in the heaviest part of the body,
the animal inclining its femora forward to assist in supporting the
heavy abdomen. It may be an expression of abdominal pain, the recti
becoming rigid and the quadriceps of the thigh participating in the
protection of the belly. Almost any of the intra-abdominal conditions,
gastroenteritis, mesenteric thrombosis, peritonitis, or diseases of the
psoas muscle and lumbar vertebra, might occasion this attempt at
support. Disease of gluteal muscles, as hemoglobinuric fever, may
produce a palsy of the whole pelvic girdle with weakness of the hind
legs. There may be associated with the weakness of the hind legs a
humped-up condition of the lumbar spine and retraction of the abdomen,
sometimes called “tucked in;” in two definite cases of this last sort we
have found renal pelvic stones and once intestinal sand. Some instances
are undoubtedly due to meningomyelitis or to poliomyelitis and at the
place for this subject a few cases will be discussed. Meningitis has not
been found in the ungulates showing this weakness. There have been
however cases of ataxia in the hind legs of deer and antelopes, which
did not have a ready explanation fitting in with the foregoing. Two of
these we thought might be due to certain grasses in the enclosures and
have changed the exhibition spaces. No conclusion can be drawn from this
as yet. No enterocolic disease could be found nor any lesion of the
sciatic nerve and lumbar enlargement of the cord. We have however
discovered sciatic neuritis in a case like hemoglobinuric fever in a
Burchell’s zebra. The history of the animal is similar to that of this
disease in domestic animals in so far as symptomatology is concerned; in
so far as confinement in a stall is concerned no data is at hand but
death occurred on December 26th in the zebra house whereas he had been
accustomed to go out into the yard all summer and autumn.
MENINGITIS.
The coverings of the brain and cord have not been the seat of the well
known acute inflammations seen in domestic horses and cattle. Eleven
instances of disease in the meninges are recorded but, with very few
exceptions, have been accompanied by other lesions offering a ready
etiological explanation. These cases are however not very instructive
except perhaps three in monkeys where the meningitis seemed to be
secondary to gastroenterocolitis. In one case a colon bacillus was
apparently responsible, in a second no bacteriology was undertaken and a
third was too rotten for the results to be dependable. A focus of
infection aside from the intestinal area could not be found. The only
noteworthy finding was the scantiness of the cerebrospinal fluid and the
almost exclusive subpial exudate; these facts would seem to strengthen
the thought that the virus came through the blood stream. Another case
was due to extension, through the temporal bone to the lateral sinus, of
a necrotizing process beginning in the buccal muscles or parotid gland;
the necrosis bacillus and a host of Gram-positive cocci were found. A
Canadian porcupine suffered with a mucopurulent nasopharyngitis which
involved the deep sinuses, the middle ear and the temporal bone; smears
from the pus over the corresponding cerebral hemisphere and from the
nasal pus showed pneumococcus forms; the lungs were not affected. The
llama which showed the intracapsular fracture of the femur (page 344)
had also hemorrhage into a fibrinous exudate in the mastoid cells with
deep opaque congestion and edema of the pia above the petrous portion of
the temporal bone. Decomposition precluded satisfactory bacteriology but
it is suggested that probably injury in falling started a hemorrhage in
the ear upon which a secondary infection was implanted. What seems a
true meningitis secondary to otitis media and mastoid suppuration was
seen in a marmoset.
A case of the well known but obscure condition known as chronic
productive pachymeningitis was observed in a badger. Although it cannot
be explained it is cited as a matter of record and interest.
American Badger (_Taxidea taxus_). Pachymeningitis externa. The dura
is fast to the skull and cannot be removed. Scattered irregularly over
the entire inner surface of the skull are pale pinhead sized hard
nodules. It is impossible to tell if they are in the dura or the bone.
The brain shows engorged vessels but is otherwise negative.
Two instances of hemorrhagic pachymeningitis associated with cretinism
were seen in wolf cubs. The following notes illustrate both cases.
American Gray Wolf (_Canis mexicanus_). Cretinism. Hemorrhagic
external pachymeningitis with craniotabes. Upon removing the calvarium
a marked craniotabes of the under surface is found and with it a deep
red and purple staining of outside of dura and inner table of skull.
These changes are most marked along the longitudinal sinus at internal
occipital protuberance and along left parietal region. Dura on left
side is distinctly congested. This is also true of pia. The brain and
its base seem normal.
Cyst of the brain. A sooty mangabey (_Cercocebus fuliginosus_) had been
in the Garden for about four months and was apparently an adult normal
animal. It died rather suddenly after a distinct convulsion with
semiconsciousness. At autopsy in addition to a nephritis, a large cyst
was found to occupy the posterior third of the left hemisphere. Its
walls were composed of a thin (one-sixteenth inch) rim of cerebral
substance and the meninges; its contents were clear. The notes do not
record any examination for parasites. This monkey showed no localizing
signs.
TUBERCULOSIS.
Gross tuberculous lesions have been found in the brain in several
specimens with generalized disease but only two cases are of special
interest. A Rhesus macaque (_Macacus rhesus_) suffering with generalized
but chiefly lymphatic tuberculosis, showed a large plaque on the
external surface of the dura over the vertex where it was adherent to a
yellow, fairly firm nodule about ten mm. across. This nodule was deeply
imbedded in the brain substance, barely projecting above the surface,
generally spherical and not encapsulated. There was no peripheral
reactive zone. The meninges were not altered anywhere except as above.
The blood vessels were not especially congested. The pia arachnoid
contained no excess of fluid but the summits of the convolutions were
flattened. The mass was located in the posterior frontal convolution,
near the longitudinal fissure, occupying nearly its whole breadth and
penetrating about one centimetre. It did not enter the fornicate gyrus.
There was a completely degenerated core about two mm. across. The
adjacent bone was beginning to erode. No localizing signs were reported.
The other case, that of a young Drill baboon (_Papio leucophæus_), was
studied with Dr. J. H. W. Rhein and can be reported in the following
condensed notes.
The baboon appeared to be perfectly well until October 18, 1906, when
some lameness in the anterior and posterior extremities on the right
side was observed. This gradually increased, and was associated with
general convulsions. On November 30th, I made an examination and found
the following condition: The right upper and lower extremities were
weaker than on the left side. On the left side the power seemed to be
fair. He was able to hold on to an iron bar with the fingers of the
upper and lower extremities on the right side but in withdrawing the
bar it was not difficult to overcome his grasp and the power on this
side was distinctly less than on the left. The movements of the right
arm were somewhat ataxic, as observed when he made efforts to grasp
the bar. The knee jerks were increased on both sides and appeared to
be equally so. There was no evidence of facial palsy. He moved both
sides of the face equally well at times when he expressed anger or
fear in the facial expression. The tongue seemed to be retracted
equally well on both sides. Tests for hemianopsia were, of course,
unsatisfactory, but he seemed to recognize readily the approach of the
iron bar from both sides. There was no disturbance of the rectal or
bladder functions, although at autopsy the bladder was full. Death
occurred on December 2, 1906. At the autopsy the brain and spinal
cord, with the other organs were examined. The dura was adherent to
the left side of the brain, in the prefrontal region, in the upper
third and when the brain was removed it was observed that an area of
softening lay beneath this point. A small caseous mass was also
observed at the base of the right lung, and beneath the diaphragm on
the right side was a large abscess, partly involving the liver. The
tubercle bacillus was found in the pus removed from the area of
softening beneath the left cortex. A study of the brain revealed the
presence of three foci of softening. The largest one was situated in
the left hemisphere in the prefrontal region, and extended from just
beneath the cortex in the upper third of the region, downward almost
to the base of the brain. This area was cylindrical in shape and
measured 2.5 cm. in its greatest diameter. The area of softening
consisted of caseated material and pus, in which the tubercle bacillus
was found present. The second area of softening was found on the right
side of the brain, much smaller in extent and measuring 1.5 cm.
diameter. There was no pus present in this area, but it consisted of a
circumscribed mass of caseous material. The apex of this area of
softening was just beneath the cortex in the prefrontal region on the
right side, and in the removal of the brain the cortex was torn just
above this area of caseation. This point was .5 cm. in front of the
central fissure and about 1 cm. below the superior surface of the
brain. A third area of softening was observed posteriorly, in the
white substance, in the parieto-occipital region, and measured about 6
mm. in diameter. A study of the sections of the brain shows
beautifully the extent of the destruction of the brain tissue. The
optic thalamus and the lenticular nucleus, and the posterior limb of
the internal capsule, on the left side, are destroyed in part. The
anterior limb of the internal capsule in one section, is preserved,
notwithstanding the fact that the optic thalamus on the same side has
been in large part destroyed. In spite of the fact that the posterior
limb of the internal capsule has been destroyed at some levels, it is
interesting to note that the degeneration of the pyramidal tracts of
the pons and medulla on the opposite side and the lateral columns of
the spinal cord are not intensely—although distinctly—degenerated. It
is very interesting to note that in view of the severe damage to the
posterior limb of the internal capsule on the left side, there was not
more paralysis, for it will be remembered that there was considerable
power of prehension in the right upper and lower extremities.
ENCEPHALOMYELITIS, POLIOMYELITIS.
While, as has been stated, no well defined cases of the recognized
meningocephalic infectious diseases have been observed in the Garden,
there have been several animals in whose cord and brain changes were
found comparable to the infections disease known in man as
poliomyelitis. On several occasions since this disease was recognized as
occurring in epidemic form it has been observed that domestic mammals
and fowls suffered from a similar condition. The general vicinity of
Philadelphia had a low grade epidemic among children during the years
from 1907 to 1912 and it is during this time that most of the cases of a
comparable character were observed among our animals. It is to be
emphasized that attacks were entirely sporadic and the cases did not
appear to bear a relation to one another. This character is quite in
accord with certain of the outbreaks in man. However we cannot state
that the disease is exactly the same as seen in the human being for, as
will be noted in the cited examples, all the pathological features were
not fulfilled.
It is not always possible to differentiate between myelitic disease and
polyneuritis of man or animals. Studied symptomatically the cases in our
records which proved to have degenerative and infiltrative lesions
comparable to poliomyelitis showed gradual but progressive paralysis
expressed by inability to move rather than disinclination—in other words
loss of power rather than restriction because of pain. None of the
animals in which poliomyelitis was demonstrated have exhibited the
ataxia of the hind legs discussed on a previous page nor have we found
myelitic lesions in the few cords from animals suffering with this
weakness. The nearest approach to a cerebrospinal explanation for
weakness and palsy was in a zebra which died with constipation, acute
nephritis, and hepatic perilobular fibrosis. In this animal a pronounced
subpial mononuclear infiltrate was observed, in places involving the
superficial parts of the cerebral gray matter, especially about the
congested vessels of this area. This condition was present to a slight
degree in the cord. There was then a low grade meningoencephalitis but
no nerve cell changes. So far as is known to me no animal showing a
definite local paresis or paraplegia recovered from the attack; had this
occurred we might have observed residual palsies.
In so far as lesions are concerned they are perhaps best illustrated by
the appended cases, but since even in them there is a lack of
uniformity, it may be well to discuss the basic changes of all. The
outstanding abnormality in the microscopic anatomy is the richness of
small mononuclear cells beneath the pia, both spinal and cerebral,
around the smaller blood vessels and to a lesser extent around the
multipolar cells of the gray matter. These do not present the dense
colonization often seen in the acute cases of infantile paralysis in man
but are prominent in comparison to normal nervous tissue. Hemorrhages or
at least small groups of erythrocytes outside of blood vessels are seen
here and there. Vacuolization of ganglion cells is variable, being
prominent in some, trifling or absent in others. Glial proliferation is
often quite marked, and in one case to be cited seems the prominent
lesion.
The animals in which meningopoliomyelitis has been found were three
monkeys, two Canadian lynx, a bear and a raccoon; about a score of cords
from other animals with some kind of palsy have been studied
microscopically without discovering it. The following cases illustrate
our material. The only instance of two cases in close relation concerns
the lynx (_Felis canadensis_). They occupied the same cage and died
twelve days apart. No symptoms were recorded until a few days before
death when a general paralysis appeared, deepening to completeness on
the day of death. No case occurred in neighboring cages. Doctor Rhein
studied all these cases, and his notes are used for these records.
Portions of the lumbar and cervical enlargements and of the thoracic
regions of the cord were stained with hemalum and acid fuchsin and with
thionin. The pia was slightly infiltrated. There was some cellular
infiltration of the anterior septum, and the vessels here showed an
increase in the nuclei of the walls and a slight perivascular
infiltration. The pial infiltration seemed to be equally distributed in
the entire circumference of the cord, although perhaps a little more
marked over the anterior and posterior septa. The vessels of the gray
matter were congested and the walls of the vessels in most part showed a
proliferation of the nuclei. There were a few small hemorrhages into the
gray matter, probably agonal. As compared with the human cord and the
cords of monkeys, antelopes and dogs, there was an unusually large
number of glia nuclei, which, if found in the human cord, would be
looked upon as a proliferation process. In some cases these nuclei were
heaped together in masses, and were evidently pathological. There was
also, about the ganglion cells, some pericellular round cell
infiltration, and this was more marked around a few cells which were
almost entirely destroyed. The ganglion cells themselves were swollen.
Some showed eccentric nuclei, and many of them stained poorly, while one
or two showed distinct vacuolization. In one field a ganglion cell was
partly destroyed by a recent hemorrhage. There were, however, a number
of cells which appeared normal. This process seemed to be fairly
distinct in the lumbar and cervical enlargements, but was not clearly
demonstrated in the sections from the dorsal region. The cellular
infiltration of the horns was evidently not leucocytic, but presented
the appearance of a connective tissue proliferation. Although these are
not the exact lesions found in poliomyelitis in the human animal, they
are at least suggestive of the same process since the infiltrating cells
are of the lymphatic or connective tissue types. There is no acute
inflammatory leucocytic infiltrate.
A weeper cebus (_Cebus capucinus_) ever since he was received acted in
such a peculiar manner, seeming to have only partial control of his
movements, that he was known as the “Crazy Monkey.” There was no history
of illness before death. Pathological diagnosis: Chronic enterocolitis,
chronic adhesive pericarditis, early interstitial change in kidney,
edema of lungs, meningitis and poliomyelitis. The pia of the paracentral
cortex was thickened and was the seat of a round cell infiltration of
moderate degree, the cells being of the mononuclear type. The blood
vessels of the cortex were congested and the nuclei of the walls were
increased. The round cell infiltration of the pia had in some places
extended into the cortical layers. The pia surrounding the medulla
oblongata was also the seat of a slight round cell infiltration. The pia
of the spinal cord, however, did not show any cellular infiltration. The
cells of the anterior horns of the spinal gray matter were extensively
diseased, being swollen in places, some surrounded by a glia
proliferation and many with marked vacuolization.
A common raccoon (_Procyon lotor_) was observed in the laboratory to
have complete paralysis of the anterior and partial paralysis of the
posterior extremities. This latter was almost complete in muscles
controlling the feet, while the thigh and hip muscles showed some
irregular incoördinate movements. Respiration shallow but regular.
History shows that the power of the extremities began to fail about a
month before death and was absolutely lost in the fore extremities three
days before the animal was killed. Diagnosis: Poliomyelitis. Examination
of the central nervous system showed the presence of marked round cell
infiltration of pia of cortex and of spinal cord, more particularly in
the lower thoracic and lumbar regions. Ganglion cells in the lumbar
region were markedly diseased. There were numerous old and fresh
hemorrhages and a moderate degree of round cell infiltration in the
anterior horns. Two young of this animal, born three months before its
death, showed weakness and gradual increasing paralysis of their
extremities beginning when three months old (that is at the time of the
death of their mother), and lasting until their death, one in the
seventh and one in the eighth month of life. These were found not to
have changes in the central nervous system, but there was sufficient
rachitis to account for this paralysis.
The only tumor of the central nervous system found among these animals
occurred in an Undulated Grass Parrakeet (_Melopsittacus undulatus_).
The gross notes are very vague but the microscopy is suggestive of a
glioma. The growth in the brain consists of large irregular masses of
large cells with vesicular nuclei and pale homogeneous protoplasm.
“Scattered between these accumulations are irregular strands of spindle
cells, with spindle-shaped nuclei, taking the hematoxylin very deeply.
The supporting tissue is almost without cells, taking the eosin faintly,
and is quite loosely arranged. No fibrils are seen among the cells. The
blood vessels are congested, and at one place there is a small
hemorrhage. The vessel walls are the same as the rest of the connective
tissue. There is a slightly atypical metastasis in the liver.”
A case, the identity of which is still undecided, was observed in a
Green Monkey (_Cercopithecus callitrichus_); it may belong among the
gliomata or glioses. There was in the middle of this monkey’s cerebrum a
gray area about 3 × 2 × 1 cm. with a softened centre, the more solid
parts being found under the microscope to consist of glia tissue, blood
vessels and degenerated cells. No true gliomatous formations could be
discovered. Because of the indefiniteness of the lesion, it is not
included in the tumors or inflammations. Clinically the effect of the
change was to cause blindness and ataxia but motor power was not greatly
impaired.
A very small number of tumors of the brain in wild animals is on record
in the English and German literature, perhaps the most interesting being
what resembles in description a subdural neurocytoma reported by Wilson
in the _Proceedings of the London Zoological Society_, 1908. The mass
was separate from the cerebellum, but had hollowed out a place for
itself in this part of the hind-brain.
BRAIN WEIGHTS.
The policy of preserving the brain of all species enables us to record
in the accompanying list the weights of a large number of specimens. In
order that the figures may have a representative and comparative value
only those are given where the total body weight of the animal is also
known. The specimens were removed by the laboratory staff, most of them
by one person, and by the same technique. All brains were weighed
immediately upon removal from the body, no preservative being near the
organ. The brains were themselves externally normal. Our technician is
skillful in removing the organ, practically always getting the pituitary
body, and cutting off the brain stem at the foramen magnum, the pia
remaining but the dura removed. Because the specimens were taken, in
practically all cases, from animals that died in the Park, and because
of the shortness of the list (196), it seems wise not to attempt
conclusions referable to comparative weights of the different orders and
families. However, the data seem worthy of record because it is doubtful
if anywhere one can find so many weights taken under comparable
conditions by the same personnel. One can find a considerable list of
brain weights and values in many publications throughout the literature,
notably in an article by Ziehen in Bardeleben’s _Handbuch der Anatomie_
(Vol. IV, Abt. III 363), but from no single source are there so many
varieties or so long a list. Ziehen’s tables are compiled from the
literature and therefore represent data collected under different
conditions, many of which were probably pathological. The appended
figures are to be considered as raw material collected under uniform
conditions.
Examination of the figures bears out in a measure some of the remarks
made by Ziehen, notably those which indicate that between large and
small varieties of the same general group, the smaller has the greater
brain weight value and that the youthful animal has more brain than the
adult.
The brains at the museum are fixed in saline-formaldehyde—sufficient
strength of the former to suspend the organ in the container and four
percentage of the latter. When fixation is complete, as indicated by
density, preservation is done in one per cent. formaldehyde, the organ,
usually bound in gauze, being laid in cotton. A list of important
references is added to the weight tables—some antedating Ziehen’s
articles, but principally those that have appeared since the publication
of his monograph.
PRINCIPAL REFERENCES TO THE RELATIVE WEIGHT OF THE BRAIN
ZIEHEN: In _Bardeleben’s Handbuch der Anatomie des Menschen_, Vol. 4,
pt. 3.
ZIEHEN: _Handbuch der Anatomie des Nervensystems_, Jena, 1903.
GIRARD: _Bulletin de l’Institut Gen. Psychologie_, Vol. 7, p. 53.
VON BUSCHAU: _Real Encyclopedie der Gesamten Heilkunde 3. Aufl._
VON BUSCHAU: _Neurologisches Zentralbl._, 1897, March.
BRANDT: _Bull. de la Soc. Imperial des Naturalistes de Moscow_, 1867,
40, pt. 2, 525.
MIES: _Verhandl. der Gesellsch. deutscher Naturforsch und Arzte_, 1898,
353.
DHERE ET LAPICQUE: _Archives de la Physiologie_, October, 1898.
LAPICQUE ET GIRARD: _C. R. des Sceances de l’Academie de Science_,
Paris, 1905, 140, 1057.
LAPICQUE: _Bulletin de Museum d’Histoire Naturelle_, 1909, No. 7, 408.
LAPICQUE: _Revue du Mois_, Paris, April, 1908, 445.
LAPICQUE: _Bulletin et Memoires de la Société d’Anthropologie de Paris_,
1907, 5, Vol. 8, No. 3, 261.
LAPICQUE: _Biologica_, Vol. 2, 1912, p. 257.
FUNK: _Inaug. Dissert. Wurzburg_, 1911.
POYNTER: _Cerebral Anthropology_, Lincoln, 1913.
MOLLISON: _Arch. für Anthropologie_, 1914, XIII, 388.
HULTGREN: _Das Hirngewicht des Menschen_, Upsala, 1912.
WEBER: _Festschrift für Karl Gegenbauer_, 1898.
DUBOIS: _Bulletin de la Soc. Anthropologie_, Paris, 1897, 337.
DUBOIS: _Archiv. für Anthropologie_, Vol. 25, 1898.
DUBOIS: _Proc. Sci. K. Acad. Wet., Amsterdam_, 1914, 16, 647.
DUBOIS: _Zeitschrift für Morph. und Anthropologie_, 1914, Vol. 18, 323.
MARCHAND: _Hirngewicht des Menschen_, Leipsig, 1902.
RUDOLPH: _Beiträge zur Path. Anatomie_, Jena, 58, 1914, 48.
KRAEMER: _Mitt. der Deutsch. Landwehrgesell_, 29, 1914, 55.
TABLE 18.—_Giving the Actual Weight of the Brain and the Relation of this to that
of the Body in 196 Animals._
════════════════════╤═══╤══════╤═══════════╤══════╤═════════╤════════╤══════╤══════
Order Family │Sex│Known │Development│ Time │Condition│ Body │Brain │Grams
│ │Age at│ │ in │ │ Weight │Weight│Brain
│ │Death │ │Garden│ │in Grams│ in │ Per
│ │ │ │ │ │ │Grams │ Kilo
│ │ │ │ │ │ │ │ of
│ │ │ │ │ │ │ │ Body
│ │ │ │ │ │ │ │Weight
Genus Species │ „ │ „ │ „ │ „ │ „ │ „ │ „ │ „
Common Name │ „ │ „ │ „ │ „ │ „ │ „ │ „ │ „
────────────────────┼───┼──────┼───────────┼──────┼─────────┼────────┼──────┼──────
PRIMATESA: │ │ │ │ │ │ │ │
SIMIADÆ: │ │ │ │ │ │ │ │
Simia satyrus, │ │ │ │ │ │ │ │
Orang utan │ ♂ │ │Immature │4 yrs.│Good │ 15,500.│ 405.│ 26.1
│ │ │ │6 mo. │ │ │ │
Orang utan │ ♀ │ │Immature │4 yrs.│Thin │ 22,178.│ 300.│ 13.4
│ │ │ │2 mo. │ │ │ │
Hylobates │ │ │ │ │ │ │ │
hainanus, │ │ │ │ │ │ │ │
Hainan Gibbon │ ♂ │ │Mature │4 yrs.│Good │ 5,900.│ 115.│ 19.4
│ │ │ │3 mo. │ │ │ │
Hylobates │ │ │ │ │ │ │ │
leuciscus, │ │ │ │ │ │ │ │
Silver Gibbon │ ♀ │ │Mature │14 │Very thin│ 3,030.│ 75.│ 24.7
│ │ │ │days │ │ │ │
│ │ │ │ │ │ │ │
CERCOPITHECIDÆ: │ │ │ │ │ │ │ │
Presbytis │ │ │ │ │ │ │ │
cephalopterus, │ │ │ │ │ │ │ │
Ceylon Entellus │ ♂ │ │Mature │1 mo. │Good │ 4,080.│ 58.│ 14.2
Cercopithecus │ │ │ │ │ │ │ │
sabæus, │ │ │ │ │ │ │ │
Grivet Monkey │ ♀ │ │Mature │14 │Good │ 3,530.│ 65.│ 18.4
│ │ │ │yrs. │ │ │ │
Cercopithecus │ │ │ │ │ │ │ │
patas, │ │ │ │ │ │ │ │
Red Monkey │ ♂ │ │Mature │2 yrs.│Good │ 5,060.│ 105.│ 20.7
│ │ │ │9 mo. │ │ │ │
Cercocebus │ │ │ │ │ │ │ │
fuliginosus, │ │ │ │ │ │ │ │
Sooty Mangabey │ ♀ │ │ │3 mo. │Good │ 3,342.│ 105.│ 31.4
Macacus arctoides,│ │ │ │ │ │ │ │
Brown Macaque │ ♂ │ │ │3 yrs.│Good │ 3,161.│ 100.│ 31.7
│ │ │ │6 mo. │ │ │ │
Macacus │ │ │ │ │ │ │ │
nemestrinus, │ │ │ │ │ │ │ │
Pigtailed │ ♀ │ │ │4 yrs │Very Thin│ 4,560.│ 100.│ 21.9
Macaque │ │ │ │3 mo. │ │ │ │
Pigtailed │ ♀ │10 mo.│Baby │10 mo.│Good │ 1,390.│ 67.│ 48.2
Macaque │ │ │ │ │ │ │ │
Macacus rhesus, │ │ │ │ │ │ │ │
Rhesus Macaque │ ♂ │6 mo. │Baby │6 mo. │Good │ 462.│ 67.│ 145.
Papio porcarius, │ │ │ │ │ │ │ │
Chacma Baboon │ ♂ │ │Mature │1 wk. │Thin │ 12,300.│ 180.│ 14.6
Papio │ │ │ │ │ │ │ │
cynocephalus, │ │ │ │ │ │ │ │
Yellow Baboon │ ♂ │ │Mature │4 yrs.│ │ 8,942.│ 140.│ 15.6
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
CEBIDÆ: │ │ │ │ │ │ │ │
Ateles ater, │ │ │ │ │ │ │ │
Black Spider │ ♀ │ │ │1 mo. │Good │ 1,790.│ 125.│ 70.
Monkey │ │ │ │ │ │ │ │
Black Spider │ ♀ │ │ │2 mo. │Good │ 2,475.│ 105.│ 42.5
Monkey │ │ │ │ │ │ │ │
Black Spider │ ♂ │ │ │2 mo. │Good │ 3,630.│ 125.│ 34.4
Monkey │ │ │ │ │ │ │ │
Lagothrix │ │ │ │ │ │ │ │
lagotricha, │ │ │ │ │ │ │ │
Woolly Monkey │ ♀ │ │ │9 mo. │Thin │ 1,634.│ 82.│ 50.3
Cebus fatuellus, │ │ │ │ │ │ │ │
Brown Cebus │ ♀ │ │ │2 yrs.│Thin │ 1,500.│ 60.│ 40.
Cebus albifrons, │ │ │ │ │ │ │ │
White fronted │ ♂ │ │ │ │ │ 1,750.│ 61.│ 34.8
Cebus │ │ │ │ │ │ │ │
Aotes vociferans, │ │ │ │ │ │ │ │
Noisy │ ♂ │ │ │2 wks.│Good │ 480.│ 20.│ 41.7
Douroucouli │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
CALLITRICHIDÆ: │ │ │ │ │ │ │ │
Callithrix │ │ │ │ │ │ │ │
pencillata, │ │ │ │ │ │ │ │
Black eared │ ♂ │ │ │1 yr. │Good │ 135.│ 10.│ 73.
Marmoset │ │ │ │ │ │ │ │
Black eared │ ♂ │ │ │6 mo. │Good │ 250.│ 15.│ 60.
Marmoset │ │ │ │ │ │ │ │
Leontocebus │ │ │ │ │ │ │ │
œdipus, │ │ │ │ │ │ │ │
Pinche Marmoset │ ♂ │ │ │1 wk. │Good │ 167.│ 14.│ 84.
│ │ │ │ │ │ │ │
LEMURES: │ │ │ │ │ │ │ │
LEMURIDÆ: │ │ │ │ │ │ │ │
Lemur catta, │ │ │ │ │ │ │ │
Ring tailed │ ♀ │Mature│ │7 yrs.│Good │ 1,470.│ 30.│ 20.4
Lemur │ │ │ │ │ │ │ │
Ring tailed │ ♀ │ │ │1 yr. │Good │ 1,240.│ 20.│ 16.
Lemur │ │ │ │3 mo. │ │ │ │
Lemur mongoz, │ │ │ │ │ │ │ │
Mongoose Lemur │ ♀ │ │ │2 yrs.│Good │ 1,457.│ 20.│ 13.8
Galago maholi, │ │ │ │ │ │ │ │
Maholi Galago │ ♂ │5 yrs.│Mature │5 yrs.│Good │ 100.│ 4.│ 40.
│ │3 mo. │ │3 mo. │ │ │ │
│ │ │ │ │ │ │ │
CARNIVORA: │ │ │ │ │ │ │ │
FELIDÆ: │ │ │ │ │ │ │ │
Felis viverrina, │ │ │ │ │ │ │ │
Fishing Cat │ ♂ │ │ │10 mo.│Good │ 7,000.│ 60.│ 8.5
Felis chaus, │ │ │ │ │ │ │ │
Jungle Cat │ ♀ │ │Mature │5 yrs.│Good │ 3,640.│ 45.│ 12.2
│ │ │ │3 mo. │ │ │ │
Felis ruffus, │ │ │ │ │ │ │ │
American Wild │ ♀ │ │ │4 yrs.│Thin │ 4,402.│ 50.│ 11.1
Cat │ │ │ │ │ │ │ │
Felis onca, │ │ │ │ │ │ │ │
Jaguar │ ♀ │20 │Mature │15 │Very thin│ 29,500.│ 170.│ 5.7
│ │yrs. │ │yrs. │ │ │ │
Felis eyra, │ │ │ │ │ │ │ │
Eyra │ ♂ │ │ │3 mo. │Good │ 5,000.│ 44.│ 8.8
Felis canadensis, │ │ │ │ │ │ │ │
Canada Lynx │ ♀ │ │Mature │4 yrs.│Very thin│ 7,270.│ 80.│ 11.
│ │ │ │6 mo. │ │ │ │
Felis │ │ │ │ │ │ │ │
chibigonazon, │ │ │ │ │ │ │ │
Brazilian Ocelot│ ♀ │ │Young │1 mo. │Thin │ 1,350.│ 35.│ 26.
Felis pardalis, │ │ │ │ │ │ │ │
Common Ocelot │ ♀ │ │ │10 mo.│Good │ 5,800.│ 50.│ 8.6
Common Ocelot │ ♂ │ │Young │2 mo. │Thin │ 2,700.│ 45.│ 16.6
Felis concolor, │ │ │ │ │ │ │ │
Puma │ ♂ │ │ │ │Good │ 52,700.│ 150.│ 2.8
Puma │ ♀ │ │Mature │8 yrs.│Very thin│ 29,500.│ 50.│ 1.69
│ │ │ │6 mo. │ │ │ │
Puma │ ♂ │ │Baby │ │Good │ 1,067.│ 55.│ 51.5
Puma │ ♀ │ │Baby │ │Good │ 998.│ 55.│ 55.
Felis tigris, │ │ │ │ │ │ │ │
Bengal Tiger │ ♀ │ │Mature │12 │Fair │ 66,000.│ 250.│ 3.8
│ │ │ │yrs. │ │ │ │
Bengal Tiger │ ♂ │ │Mature │12 │Very thin│ 91,000.│ 240.│ 2.6
│ │ │ │yrs. │ │ │ │
Felis uncia, │ │ │ │ │ │ │ │
Snow Leopard │ ♀ │ │Mature │8 yrs.│Good │ 22,700.│ 120.│ 5.3
│ │ │ │ │ │ │ │
HYÆNIDÆ: │ │ │ │ │ │ │ │
Hyæna hyæna, │ │ │ │ │ │ │ │
Striped Hyæna │ ♂ │ │Mature │4 yrs.│Poor │ 27,200.│ 92.│ 3.3
│ │ │ │ 3 mo.│ │ │ │
Striped Hyæna │ ♂ │ │Mature │8 yrs.│Good │ 36,300.│ 90.│ 2.4
│ │ │ │10 mo.│ │ │ │
│ │ │ │ │ │ │ │
CANIDÆ: │ │ │ │ │ │ │ │
Canis │ │ │ │ │ │ │ │
procyonoides, │ │ │ │ │ │ │ │
Raccoon-like Dog│ ♀ │ │Mature │3 yrs.│Good │ 4,770.│ 25.│ 5.2
Raccoon-like Dog│ ♀ │ │ │ │Good │ 4,900.│ 35.│ 7.1
Canis familiaris, │ │ │ │ │ │ │ │
Eskimo Dog │ ♂ │ │Mature │ │Very thin│ 36,300.│ 100.│ 2.7
Canis cinereo │ │ │ │ │ │ │ │
argenteus, │ │ │ │ │ │ │ │
Gray Fox │ ♀ │ │Mature │3 yrs.│Good │ 2,652.│ 40.│ 15.
Canis cinereus │ │ │ │ │ │ │ │
argenteus scotti, │ │ │ │ │ │ │ │
Scott’s Gray Fox│ ♀ │ │Mature │2 yrs.│Good │ 2,200.│ 53.│ 25.
│ │ │ │6 mo. │ │ │ │
Canis chama, │ │ │ │ │ │ │ │
Silver Fox │ ♂ │ │ │7 mo. │Good │ 3,325.│ 40.│ 12.
Canis mesomelas, │ │ │ │ │ │ │ │
Blackbacked │ ♂ │ │ │2 yrs.│Good │ 6,000.│ 60.│ 10.
Jackal. │ │ │ │6 mo. │ │ │ │
Blackbacked │ ♀ │ │ │ │ │ 3,500.│ 70.│ 20.
Jackal │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
MUSTELIDÆ: │ │ │ │ │ │ │ │
Mustela foina, │ │ │ │ │ │ │ │
Beech Marten │ ♀ │ │Mature │3 yrs.│Good │ 810.│ 15.│ 18.3
Mustela americana,│ │ │ │ │ │ │ │
Pine Marten │ ♂ │ │Mature │4 yrs.│Good │ 680.│ 13.│ 19.
Gulo gulo, │ │ │ │ │ │ │ │
Wolverine │ ♀ │ │ │3 yrs.│Good │ 5,700.│ 75.│ 13.1
│ │ │ │3 mo. │ │ │ │
Galictis barbara, │ │ │ │ │ │ │ │
Tayra. │ ♂ │ │ │7 mo. │Good │ 1,480.│ 55.│ 37.
Mephitis │ │ │ │ │ │ │ │
mephitica, │ │ │ │ │ │ │ │
Common Skunk │ ♀ │ │ │6 mo. │Good │ 1,755.│ 6.│ 3.4
Common Skunk │ ♀ │ │ │2 wks.│Good │ 1,700.│ 7.│ 4.1
Meles meles, │ │ │ │ │ │ │ │
European Badger │ ♂ │ │ │3 yrs.│Good │ 7,473.│ 46.│ 6.
│ │ │ │ │ │ │ │
PROCYONIDÆ: │ │ │ │ │ │ │ │
Procyon lotor, │ │ │ │ │ │ │ │
Common Raccoon │ ♂ │ │Mature │7 yrs.│Good │ 9,000.│ 42.│ 4.6
│ │ │ │3 mo. │ │ │ │
Common Raccoon │ ♀ │ │Mature │9 yrs.│Good │ 5,450.│ 37.│ 6.9
│ │ │ │2 mo. │ │ │ │
Procyon lotor │ │ │ │ │ │ │ │
hernandezi, │ │ │ │ │ │ │ │
Mexican Raccoon │ ♀ │ │ │2 yrs.│Good │ 6,130.│ 40.│ 6.5
Nasua nasua, │ │ │ │ │ │ │ │
Ring tailed │ ♂ │ │ │1 yr. │Good │ 1,600.│ 40.│ 25.
Coati │ │ │ │4 mo. │ │ │ │
Ring tailed │ ♂ │ │ │10 mo.│Good │ 1,600.│ 35.│ 24.3
Coati │ │ │ │ │ │ │ │
Nasua narica, │ │ │ │ │ │ │ │
White nosed │ ♂ │Mature│ │8 yrs.│Very thin│ 5,000.│ 44.│ 8.8
Coati │ │ │ │ │ │ │ │
Potos │ │ │ │ │ │ │ │
caudivolvulus, │ │ │ │ │ │ │ │
Kinkajou │ │Mature│ │3 yrs.│Good │ 1,440.│ 35.│ 24.2
│ │ │ │2 mo. │ │ │ │
│ │ │ │ │ │ │ │
URSIDÆ: │ │ │ │ │ │ │ │
Ursus malayanus, │ │ │ │ │ │ │ │
Sun Bear │ │ │ │1 yr. │Good │ 41,000.│ 125.│ 3.5
│ │ │ │9 mo. │ │ │ │
Ursus beringiana, │ │ │ │ │ │ │ │
Kamchatkan Bear │ ♀ │ │ │ │Very thin│ 31,800.│ 315.│ 9.9
│ │ │ │ │ │ │ │
PINNIPEDIA: │ │ │ │ │ │ │ │
OTARIIDÆ: │ │ │ │ │ │ │ │
Eumetopias │ │ │ │ │ │ │ │
stelleri, │ │ │ │ │ │ │ │
Steller’s Sea │ ♂ │ │ │4 yrs.│Very thin│120,400.│ 515.│ 4.27
Lion │ │ │ │ │ │ │ │
Zalophus │ │ │ │ │ │ │ │
californianus, │ │ │ │ │ │ │ │
California Hair │ ♂ │ │Mature │6 yrs.│Very good│ 94,000.│ 420.│ 4.46
Seal │ │ │ │9 mo. │ │ │ │
│ │ │ │ │ │ │ │
RODENTIA: │ │ │ │ │ │ │ │
MURIDÆ: │ │ │ │ │ │ │ │
Peromyscus │ │ │ │ │ │ │ │
leucopus, │ │ │ │ │ │ │ │
White footed Mouse│ ♀ │5 yrs.│Mature │5 yrs.│Good │ 39.│ 1.│ 25.6
│ │ │ │ │ │ │ │
CASTORIDÆ: │ │ │ │ │ │ │ │
Castor canadensis,│ │ │ │ │ │ │ │
American Beaver │ ♀ │ │ │8 yrs.│Good │ 10,000.│ 40.│ 4.
│ │ │ │2 mo. │ │ │ │
│ │ │ │ │ │ │ │
OCTODONTIDÆ: │ │ │ │ │ │ │ │
Myocastor coypus, │ │ │ │ │ │ │ │
Coypu │ ♀ │ │ │ │Good │ 2,000.│ 20.│ 10.
│ │ │ │ │ │ │ │
HYSTRICIDÆ: │ │ │ │ │ │ │ │
Hystrix │ │ │ │ │ │ │ │
longicauda, │ │ │ │ │ │ │ │
Malaccan │ ♀ │ │Mature │18 │Thin │ 6,000.│ 26.│ 4.3
Porcupine │ │ │ │yrs. │ │ │ │
Erethizon dorsatus│ │ │ │ │ │ │ │
dorsatus, │ │ │ │ │ │ │ │
Canada Porcupine│ ♀ │ │ │2 mo. │Good │ 4,065.│ 20.│ 4.9
Coendon │ │ │ │ │ │ │ │
prehensilis, │ │ │ │ │ │ │ │
Brazilian Tree │ ♀ │ │ │1 wk. │Good │ 480.│ 14.│ 29.1
Porcupine │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
CAVIIDÆ: │ │ │ │ │ │ │ │
Cavia porcella, │ │ │ │ │ │ │ │
Wild Guinea-Pig │ ♂ │ │Mature │6 yrs.│Good │ 320.│ 4.│ 12.5
│ │ │ │2 mo. │ │ │ │
Hydrochœrus │ │ │ │ │ │ │ │
hydrochœrus, │ │ │ │ │ │ │ │
Capybara │ ♂ │ │ │1 mo. │Good │ 19,000.│ 50.│ 2.63
│ │ │ │ │ │ │ │
PROBOSCIDEA: │ │ │ │ │ │ │ │
Elephas maximus, │ │ │ │ │ │ │ │
Asiatic Elephant│ ♂ │3 yrs.│Young │1 mo. │Good │241,000.│3,432.│ 14.1
│ │ │ │ │ │ │ │
HYRACOIDEA: │ │ │ │ │ │ │ │
HYRACIDÆ: │ │ │ │ │ │ │ │
Procaria capensis,│ │ │ │ │ │ │ │
Cape Hyrax │ ♂ │ │ │8 mo. │Good │ 1,800.│ 15.│ 8.3
Cape Hyrax │ ♀ │ │ │1 yr. │Good │ 2,170.│ 20.│ 9.2
│ │ │ │9 mo. │ │ │ │
│ │ │ │ │ │ │ │
UNGULATA: │ │ │ │ │ │ │ │
TAPIRIDÆ: │ │ │ │ │ │ │ │
Tapirus indicus, │ │ │ │ │ │ │ │
Malayan Tapir │ ♀ │ │Mature │7 yrs.│Thin │250,000.│ 300.│ 1.2
│ │ │ │4 mo. │ │ │ │
Malayan Tapir │ ♂ │ │Young │3 mo. │Good │ 80,000.│ 225.│ 2.8
│ │ │ │ │ │ │ │
EQUIDÆ: │ │ │ │ │ │ │ │
Equus prjivalskii,│ │ │ │ │ │ │ │
Wild Horse │ ♀ │1 wk. │Baby │1 wk. │Good │ 22,700.│ 330.│ 14.
Equus burchelli, │ │ │ │ │ │ │ │
Burchell’s Zebra│ ♂ │ │Mature │6 yrs.│Good │341,000.│ 645.│ 1.9
│ │ │ │ │ │ │ │
BOVIDÆ: │ │ │ │ │ │ │ │
Strepsiceros │ │ │ │ │ │ │ │
capensis, │ │ │ │ │ │ │ │
Greater Kudu │ ♂ │ │ │4 mo. │Thin │285,000.│ 290.│ 2.2
Cobus leche, │ │ │ │ │ │ │ │
Leche Antelope │ ♀ │ │Mature │10 │Good │ 52,700.│ 200.│ 3.8
│ │ │ │yrs. 6│ │ │ │
│ │ │ │mo. │ │ │ │
Damaliscus │ │ │ │ │ │ │ │
albifrons, │ │ │ │ │ │ │ │
Blessbok │ ♂ │ │Mature │11 │Good │ 58,100.│ 245.│ 4.2
│ │ │ │yrs. │ │ │ │
Boselaphus │ │ │ │ │ │ │ │
tragocamelus, │ │ │ │ │ │ │ │
Nylghaie │ ♀ │ │ │2 yrs.│Good │136,300.│ 310.│ 2.3
│ │ │ │2 mo. │ │ │ │
Poephagus │ │ │ │ │ │ │ │
grunniens, │ │ │ │ │ │ │ │
Yak │ ♂ │3 yrs.│Young runt │3 yrs.│Runt │114,000.│ 290.│ 2.5
│ │6 mo. │ │6 mo. │ │ │ │
Yak │ ♀ │ │Mature │5 yrs.│Thin │177,000.│ 385.│ 2.2
Taurotragus oryx │ │ │ │ │ │ │ │
livingstonii, │ │ │ │ │ │ │ │
Livingstone’s │ ♀ │ │Old │13 │Good │327,000.│ 415.│ 1.3
Eland │ │ │ │yrs. │ │ │ │
Hemitragus │ │ │ │ │ │ │ │
jemlaicus, │ │ │ │ │ │ │ │
Himalayan Thar │ ♂ │ │ │2 yrs.│Good │ 31,800.│ 165.│ 5.2
│ │ │ │2 mo. │ │ │ │
Himalayan Thar │ ♂ │9 mo. │Young │9 mo. │Good │ 9,100.│ 130.│ 16.
Ovis tragelaphus, │ │ │ │ │ │ │ │
Aoudad │ ♂ │ │ │3 yrs.│Good │ 77,200.│ 233.│ 3.
│ │ │ │2 mo. │ │ │ │
Aoudad │ ♀ │ │Old │3 yrs.│Good │ 41,000.│ 195.│ 4.8
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
GIRAFFIDÆ: │ │ │ │ │ │ │ │
Giraffa │ │ │ │ │ │ │ │
camelopardalis, │ │ │ │ │ │ │ │
Giraffe │ ♀ │ │ │5 yrs.│Good │500,000.│ 630.│ 1.2
│ │ │ │8 mo. │ │ │ │
Giraffa capensis, │ │ │ │ │ │ │ │
Giraffe │ ♂ │ │Old │7 mo. │ │383,000.│ 670.│ 1.7
(Southern) │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
CERVIDÆ: │ │ │ │ │ │ │ │
Cervus duvanceli, │ │ │ │ │ │ │ │
Barasingha Deer │ ♀ │1 mo. │Baby │1 mo. │Good │ 9,500.│ 121.│ 13.
Cervus eldi, │ │ │ │ │ │ │ │
Eld’s Deer │ ♂ │ │ │ │Good │ 59,000.│ 225.│ 3.8
Cervus elaphus, │ │ │ │ │ │ │ │
Red Deer │ ♀ │ │ │ │Good │ 72,700.│ 310.│ 4.4
Cervus porcinus, │ │ │ │ │ │ │ │
Hog Deer │ ♂ │11 mo.│Young │11 mo.│Good │ 25,000.│ 130.│ 5.2
Hog Deer │ ♂ │ │ │3 yrs.│Good │ 41,000.│ 125.│ 3.
│ │ │ │4 mo. │ │ │ │
Cervus sika │ │ │ │ │ │ │ │
manchuricus, │ │ │ │ │ │ │ │
Manchurian Sika │ ♂ │ │Mature │6 yrs.│Good │ 56,800.│ 265.│ 4.6
Deer │ │ │ │3 mo. │ │ │ │
Cervus │ │ │ │ │ │ │ │
cashmirianus, │ │ │ │ │ │ │ │
Kashmir Deer │ ♂ │ │ │3 yrs.│Fair │ 56,800.│ 275.│ 4.6
│ │ │ │4 mo. │ │ │ │
│ │ │ │ │ │ │ │
CAMELIDÆ: │ │ │ │ │ │ │ │
Camelus │ │ │ │ │ │ │ │
bactrianus, │ │ │ │ │ │ │ │
Bactrian Camel │ ♂ │ │Mature │11 │Fair │430,000.│ 610.│ 1.4
│ │ │ │yrs. │ │ │ │
Camelus │ │ │ │ │ │ │ │
dromidarius, │ │ │ │ │ │ │ │
Common Camel │ ♀ │ │Mature │5 yrs.│Fair │472,700.│ 465.│ .98
│ │ │ │ │ │ │ │
HIPPOPOTAMIDÆ: │ │ │ │ │ │ │ │
Hippopotamus │ │ │ │ │ │ │ │
amphibius, │ │ │ │ │ │ │ │
Hippopotamus │ ♂ │1 mo. │Baby │1 mo. │Good │ 40,000.│ 195.│ 4.87
│ │ │ │ │ │ │ │
SUIDÆ: │ │ │ │ │ │ │ │
Macrocephalus │ │ │ │ │ │ │ │
africanus, │ │ │ │ │ │ │ │
Wart Hog │ ♀ │ │Mature │7 yrs.│Good │ 59,000.│ 151.│ 2.5
│ │ │ │9 mo. │ │ │ │
Wart Hog │ ♂ │ │ │2 yrs.│Good │ 82,700.│ 150.│ 1.8
│ │ │ │9 mo. │ │ │ │
Wart Hog. │ ♂ │ │ │ │Good │ 90,000.│ 158.│ 1.7
│ │ │ │ │ │ │ │
TAYASSUIDÆ: │ │ │ │ │ │ │ │
Tayassu tajacu, │ │ │ │ │ │ │ │
Peccary │ ♀ │ │Mature │6 yrs.│Good │ 19,650.│ 95.│ 4.8
│ │ │ │6 mo. │ │ │ │
Peccary │ ♂ │ │ │3 yrs.│Good │ 22,700.│ 75.│ 3.3
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
ENDENTATA: │ │ │ │ │ │ │ │
DASYPODIDÆ: │ │ │ │ │ │ │ │
Tatu novemcinctus,│ │ │ │ │ │ │ │
Nine banded │ ♀ │ │ │2 yrs.│Good │ 1,840.│ 10.│ 5.4
Armadillo │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
MYRMECOPHAGIDÆ: │ │ │ │ │ │ │ │
Myrmecophaga │ │ │ │ │ │ │ │
tetradactyla, │ │ │ │ │ │ │ │
Tamandua Anteater │ ♀ │ │ │1 wk. │Good │ 3,300.│ 24.│ 7.3
│ │ │ │ │ │ │ │
MARSUPIALIA: │ │ │ │ │ │ │ │
DIDELPHYIDÆ: │ │ │ │ │ │ │ │
Didelphys │ │ │ │ │ │ │ │
virginiana, │ │ │ │ │ │ │ │
Common Opossum │ ♂ │ │ │2 wks.│Good │ 2,500.│ 6.5│ 2.6
Common Opossum │ │ │Young │3 mo. │Good │ 351.│ 6.│ 17.
│ │ │ │ │ │ │ │
DASYURIDÆ: │ │ │ │ │ │ │ │
Sarcophilus │ │ │ │ │ │ │ │
ursinus, │ │ │ │ │ │ │ │
Tasmanian Devil │ ♂ │ │Mature │4 yrs.│Thin │ 2,950.│ 8.│ 2.7
│ │ │ │6 mo. │ │ │ │
Dasyurus │ │ │ │ │ │ │ │
viverrinus, │ │ │ │ │ │ │ │
Common Dasyure │ ♀ │ │ │2 yrs.│Good │ 680.│ 4.5│ 6.6
│ │ │ │2 mo. │ │ │ │
Common Dasyure │ ♂ │ │ │8 mo. │Good │ 1,130.│ 5.5│ 4.8
Common Dasyure │ ♂ │ │ │1 yr. │Good │ 1,430.│ 7.│ 4.9
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
PHASCOLOMYIDÆ: │ │ │ │ │ │ │ │
Phascolomys │ │ │ │ │ │ │ │
mitchelli, │ │ │ │ │ │ │ │
Wombat. │ ♂ │ │Mature │9 yrs.│Excellent│ 25,900.│ 70.│ 2.7
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
MACROPODIDÆ: │ │ │ │ │ │ │ │
Macropus │ │ │ │ │ │ │ │
giganteus, │ │ │ │ │ │ │ │
Great Gray │ ♂ │ │Mature │3 yrs.│Good │ 34,000.│ 65.│ 1.9
Kangaroo │ │ │ │2 mo. │ │ │ │
Macropus rufus, │ │ │ │ │ │ │ │
Red Kangaroo │ ♂ │ │Mature │5 yrs.│Good │ 63,600.│ 70.│ 1.1
│ │ │ │8 mo. │ │ │ │
Macropus unguifer,│ │ │ │ │ │ │ │
Nailtailed │ ♂ │ │ │2 wks.│Good │ 4,600.│ 12.│ 2.6
Wallaby │ │ │ │ │ │ │ │
Macropus thetidis,│ │ │ │ │ │ │ │
Thigh striped │ ♂ │ │ │2 wks.│Good │ 5,150.│ 25.│ 4.8
Wallaby │ │ │ │ │ │ │ │
Macropus │ │ │ │ │ │ │ │
ualabatus, │ │ │ │ │ │ │ │
Black Wallaby │ ♀ │ │ │1 yr. │Good │ 8,170.│ 35.│ 4.2
│ │ │ │6 mo. │ │ │ │
Aepyprymnus │ │ │ │ │ │ │ │
rufescens, │ │ │ │ │ │ │ │
Rufous Rat │ ♀ │3 yrs.│Mature │3 yrs.│Good │ 1,130.│ 15.│ 13.3
Kangaroo │ │1 mo. │ │ │ │ │ │
Rufous Rat │ ♀ │6 yrs.│Mature │6 yrs.│Good │ 1,485.│ 15.│ 10.+
Kangaroo │ │9 mo. │ │9 mo. │ │ │ │
│ │ │ │ │ │ │ │
PASSERES: │ │ │ │ │ │ │ │
ICTERIDÆ: │ │ │ │ │ │ │ │
Quisculus │ │ │ │ │ │ │ │
quiscula, │ │ │ │ │ │ │ │
Purple Grackle │ ♂ │ │ │2 yrs.│Good │ 115.│ 2.7│ 23.4
│ │ │ │7 mo. │ │ │ │
Icterus icterus, │ │ │ │ │ │ │ │
Common Troupial │ ♂ │ │ │2 yrs.│Good │ 53.│ 2.│ 27.7
│ │ │ │7 mo. │ │ │ │
Common Troupial │ ♂ │ │ │4 yrs.│Thin │ 68.│ 2.│ 29.4
│ │ │ │7 mo. │ │ │ │
│ │ │ │ │ │ │ │
PLOCEIDÆ: │ │ │ │ │ │ │ │
Amadina │ │ │ │ │ │ │ │
erythrocephala, │ │ │ │ │ │ │ │
Red headed Finch│ ♀ │ │ │4 yrs.│Good │ 25.│ 1.2│ 48.
Munia malacca, │ │ │ │ │ │ │ │
Black headed │ ♂ │ │ │3 yrs.│Good │ 13.│ .7│ 52.6
Finch │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
TANAGRIDÆ: │ │ │ │ │ │ │ │
Euphonia violacea,│ │ │ │ │ │ │ │
Violet Tanager │ ♀ │ │ │2 days│Good │ 15.│ 1.│ 66.6
Violet Tanager │ ♂ │ │ │2 days│Good │ 16.│ 1.│ 62.5
Tanagra cana, │ │ │ │ │ │ │ │
Silver blue │ ♂ │ │ │6 mo. │Good │ 29.│ 1.│ 34.5
Tanager │ │ │ │ │ │ │ │
Silver blue │ ♀ │ │ │1 yr. │Good │ 30.│ 1.│ 33.3
Tanager │ │ │ │2 mo. │ │ │ │
│ │ │ │ │ │ │ │
FRINGILLIDÆ: │ │ │ │ │ │ │ │
Zonotrichia │ │ │ │ │ │ │ │
albicollis, │ │ │ │ │ │ │ │
White throated │ ♂ │ │ │1 yr. │Good │ 35.│ 1.5│ 42.8
Sparrow │ │ │ │6 mo. │ │ │ │
White throated │ ♂ │ │ │6 mo. │Good │ 32.│ 1.5│ 46.9
Sparrow │ │ │ │ │ │ │ │
White throated │ ♂ │ │ │1 yr. │Good │ 23.│ 1.3│ 56.5
Sparrow │ │ │ │8 mo. │ │ │ │
Eophona melanura, │ │ │ │ │ │ │ │
Black tailed │ ♂ │ │ │2 mo. │Good │ 31.│ 2.│ 64.5
Hawfinch │ │ │ │ │ │ │ │
Black tailed │ ♂ │ │ │1 mo. │Good │ 30.│ 1.7│ 56.6
Hawfinch │ │ │ │ │ │ │ │
Java Sparrow │ ♂ │ │ │ │Good │ 28.│ 1.2│ 42.8
Passerina ciris, │ │ │ │ │ │ │ │
Nonpareil │ ♂ │ │ │9 mo. │Good │ 15.│ .5│ 33.3
Bunting │ │ │ │ │ │ │ │
Pipilo │ │ │ │ │ │ │ │
erythropthalmus, │ │ │ │ │ │ │ │
Towhee │ ♀ │ │ │1 yr. │Good │ 16.│ 1.2│ 75.
│ │ │ │2 mo. │ │ │ │
│ │ │ │ │ │ │ │
TURDIDÆ: │ │ │ │ │ │ │ │
Turdus iliacus, │ │ │ │ │ │ │ │
Red winged │ ♀ │ │ │5 yrs.│Good │ 55.│ 1.5│ 27.2
Thrush │ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
PITTIDÆ: │ │ │ │ │ │ │ │
Pitta strepitans, │ │ │ │ │ │ │ │
Noisy Pitta. │ │ │ │1 yr. │Good │ 92.│ 2.5│ 27.
│ │ │ │8 mo. │ │ │ │
│ │ │ │ │ │ │ │
CRATEROPODIDÆ: │ │ │ │ │ │ │ │
Garrulax │ │ │ │ │ │ │ │
leucolophus, │ │ │ │ │ │ │ │
White crested │ ♀ │ │ │2 yrs.│Good │ 105.│ 2.7│ 25.7
Jay Thrush │ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
PICARIÆ: │ │ │ │ │ │ │ │
RHAMPHASTIDÆ: │ │ │ │ │ │ │ │
Rhamphastos │ │ │ │ │ │ │ │
cuvieri, │ │ │ │ │ │ │ │
Cuvier’s Toucan │ ♀ │ │ │11 │Thin │ 356.│ 8.│ 22.4
│ │ │ │yrs. 9│ │ │ │
│ │ │ │mo. │ │ │ │
│ │ │ │ │ │ │ │
BUCEROTIDÆ: │ │ │ │ │ │ │ │
Lephoceros │ │ │ │ │ │ │ │
flavirostris, │ │ │ │ │ │ │ │
Yellow billed │ ♀ │ │ │1 yr. │Good │ 177.│ 6.│ 33.8
Hornbill │ │ │ │9 mo. │ │ │ │
│ │ │ │ │ │ │ │
STRIGES: │ │ │ │ │ │ │ │
ALUCONIDÆ: │ │ │ │ │ │ │ │
Aluco pratincola, │ │ │ │ │ │ │ │
Am. Barn Owl │ ♂ │ │ │1 mo. │Good │ 470.│ 11.│ 23.4
│ │ │ │ │ │ │ │
BUBONIDÆ: │ │ │ │ │ │ │ │
Bubo virginianus, │ │ │ │ │ │ │ │
Great Horned Owl│ ♀ │ │ │1 yr. │Good │ 1,415.│ 12.│ 8.4
Otus asio asio, │ │ │ │ │ │ │ │
Screech Owl │ ♂ │ │ │1 day │Good │ 122.│ 6.│ 49.
Strix varia varia,│ │ │ │ │ │ │ │
Barred Owl │ ♀ │ │ │11 │Good │ 1,022.│ 12.│ 11.6
│ │ │ │yrs. │ │ │ │
│ │ │ │ │ │ │ │
PSITTACI: │ │ │ │ │ │ │ │
PSITTACIDÆ: │ │ │ │ │ │ │ │
Conurus cactorum, │ │ │ │ │ │ │ │
Cactus conure │ ♀ │ │ │1 yr. │Good │ 64.│ 4.│ 62.5
│ │ │ │6 mo. │ │ │ │
Chrysotis │ │ │ │ │ │ │ │
leucocephala, │ │ │ │ │ │ │ │
White fronted │ │ │ │1 yr. │Good │ 251.│ 8.5│ 33.8
Amazon │ │ │ │ │ │ │ │
Chrysotis │ │ │ │ │ │ │ │
levaillanti, │ │ │ │ │ │ │ │
Levaillant’s │ │ │ │1 yr. │Good │ 300.│ 12.│ 40.
Amazon │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
ACCIPITRES: │ │ │ │ │ │ │ │
SERPENTARIIDÆ: │ │ │ │ │ │ │ │
Serpentarius │ │ │ │ │ │ │ │
serpentarius, │ │ │ │ │ │ │ │
Secretary │ ♂ │ │ │2 wks.│Good │ 3,768.│ 15.│ 4.
Vulture │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
FALCONIDÆ: │ │ │ │ │ │ │ │
Haliæetus │ │ │ │ │ │ │ │
leucocephalus, │ │ │ │ │ │ │ │
Bald Eagle │ ♀ │ │ │1 yr. │Good │ 2,860.│ 15.│ 5.2
│ │ │ │3 mo. │ │ │ │
│ │ │ │ │ │ │ │
COLUMBÆ: │ │ │ │ │ │ │ │
COLUMBIDÆ: │ │ │ │ │ │ │ │
Ocyphaps lophotes,│ │ │ │ │ │ │ │
Crested Pigeon │ │ │ │3 mo. │Thin │ 142.│ 2.│ 14.
Lophophaps │ │ │ │ │ │ │ │
leucogaster, │ │ │ │ │ │ │ │
Plumed Pigeon │ ♂ │ │ │ │Good │ 52.│ 1.2│ 23.
Phaps chalcoptera,│ │ │ │ │ │ │ │
Bronze winged │ ♀ │ │ │4 yrs.│Good │ 219.│ 1.5│ 6.8
Pigeon │ │ │ │2 mo. │ │ │ │
Columba phæonata, │ │ │ │ │ │ │ │
Dark backed │ ♂ │ │ │2 yrs.│Good │ 360.│ 2.│ 5.05
Pigeon │ │ │ │9 mo. │ │ │ │
Scardapella │ │ │ │ │ │ │ │
squamosa, │ │ │ │ │ │ │ │
Ground Dove │ ♀ │ │ │2 yrs.│Good │ 23.│ 1.7│ 64.
│ │ │ │9 mo. │ │ │ │
Zenaidura macroura│ │ │ │ │ │ │ │
carolinensis, │ │ │ │ │ │ │ │
Carolina Dove │ ♂ │ │ │2 yrs.│Thin │ 92.│ 1.│ 10.8
│ │ │ │9 mo. │ │ │ │
│ │ │ │ │ │ │ │
GALLI: │ │ │ │ │ │ │ │
PHASIANIDÆ: │ │ │ │ │ │ │ │
Coturnix │ │ │ │ │ │ │ │
pectoralis, │ │ │ │ │ │ │ │
Stubble Quail │ ♀ │ │ │2 yrs.│Good │ 70.│ .7│ 10.
Lophortyx │ │ │ │ │ │ │ │
californica │ │ │ │ │ │ │ │
californica, │ │ │ │ │ │ │ │
California Quail│ ♀ │ │ │1 yr. │Good │ 180.│ 1.5│ 8.33
│ │ │ │4 mo. │ │ │ │
Arboricola │ │ │ │ │ │ │ │
atrogularis, │ │ │ │ │ │ │ │
Black throated │ ♀ │ │ │1 yr. │Good │ 151.│ 2.5│ 16.
Hill Partridge │ │ │ │2 mo. │ │ │ │
Meleagris │ │ │ │ │ │ │ │
gallopavo │ │ │ │ │ │ │ │
silvestris, │ │ │ │ │ │ │ │
Eastern Wild │ ♂ │ │ │ │Good │ 6,340.│ 12.│ 1.9
Turkey │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
CRACIDÆ: │ │ │ │ │ │ │ │
Ortalis vetula, │ │ │ │ │ │ │ │
Mexican Guan │ ♀ │ │ │2 yrs.│Thin │ 442.│ 5.│ 11.3
│ │ │ │2 mo. │ │ │ │
│ │ │ │ │ │ │ │
MEGAPODIDÆ: │ │ │ │ │ │ │ │
Catheturus │ │ │ │ │ │ │ │
lathami, │ │ │ │ │ │ │ │
Brush Turkey │ ♂ │ │ │3 mo. │Good │ 1,487.│ 5.│ 3.37
│ │ │ │ │ │ │ │
ALECTORIDES: │ │ │ │ │ │ │ │
GRUIDÆ: │ │ │ │ │ │ │ │
Grus lilfordi, │ │ │ │ │ │ │ │
Lilford’s Crane │ ♂ │ │ │1 yr. │Good │ 3,790.│ 18.│ 4.7
│ │ │ │4 mo. │ │ │ │
Tetrapteryx │ │ │ │ │ │ │ │
paradisea, │ │ │ │ │ │ │ │
Stanley Crane │ ♂ │ │ │3 yrs.│Good │ 4,450.│ 13.│ 2.9
│ │ │ │3 mo. │ │ │ │
│ │ │ │ │ │ │ │
STEGANOPODES: │ │ │ │ │ │ │ │
ANHINGIDÆ: │ │ │ │ │ │ │ │
Anhinga anhinga, │ │ │ │ │ │ │ │
Darter │ ♂ │ │ │3 yrs.│Good │ 251.│ 8.5│ 33.8
Darter │ ♀ │ │ │7 yrs.│Good │ 998.│ 6.│ 6.
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
HERODIONES: │ │ │ │ │ │ │ │
ARDEIDÆ: │ │ │ │ │ │ │ │
Nycticorax │ │ │ │ │ │ │ │
nyctanassa, │ │ │ │ │ │ │ │
Yellow crowned │ ♂ │ │ │1 yr. │Good │ 620.│ 7.│ 11.3
Night Heron │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
CICONIIDÆ: │ │ │ │ │ │ │ │
Leptoptilus │ │ │ │ │ │ │ │
dubius, │ │ │ │ │ │ │ │
Adjutant Stork │ │ │ │ │ │ 7,873.│ 36.│ 4.5
Leptoptilus │ │ │ │ │ │ │ │
crumeniferus, │ │ │ │ │ │ │ │
Marabou Stork │ │ │ │ │ │ 4,580.│ 24.│ 5.2
│ │ │ │ │ │ │ │
PLATALEIDÆ: │ │ │ │ │ │ │ │
Carphibis │ │ │ │ │ │ │ │
spinicollis, │ │ │ │ │ │ │ │
Straw necked │ │ │ │ │ │ 1,665.│ 89.│ 4.8
Ibis │ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
PALAMEDES: │ │ │ │ │ │ │ │
Palmadea derbiana,│ │ │ │ │ │ │ │
Derbian Screamer│ ♂ │ │ │3 yrs.│Good │ 2,730.│ 10.│ 3.6
Derbian Screamer│ ♂ │ │ │1 wk. │Thin │ 1,700.│ 8.│ 4.7
│ │ │ │ │ │ │ │
ANSERES: │ │ │ │ │ │ │ │
ANATIDÆ: │ │ │ │ │ │ │ │
Cygnopsis │ │ │ │ │ │ │ │
cygnoides, │ │ │ │ │ │ │ │
Chinese Goose. │ ♂ │ │ │2 yrs.│Good │ 2,740.│ 15.│ 5.5
│ │ │ │6 mo. │ │ │ │
Plectropterus │ │ │ │ │ │ │ │
niger, │ │ │ │ │ │ │ │
Black Spurwinged│ ♂ │ │ │9 yrs.│Good │ 2,735.│ 13.│ 4.7
Goose │ │ │ │ │ │ │ │
Cereopsis novæ- │ │ │ │ │ │ │ │
hollandiæ, │ │ │ │ │ │ │ │
Cereopsis Goose │ ♀ │ │ │2 yrs.│Good │ 2,370.│ 9.│ 3.6
│ │ │ │3 mo. │ │ │ │
Cereopsis Goose │ ♂ │ │ │1 yr. │Good │ 2,748.│ 11.│ 4.
Anser domesticus, │ │ │ │ │ │ │ │
Sebastopol Goose│ ♂ │ │ │3 yrs.│Good │ 3,106.│ 19.│ 6.1
│ │ │ │2 mo. │ │ │ │
Anser fabalis, │ │ │ │ │ │ │ │
Bean Goose │ ♂ │ │ │12 │Good │ 2,640.│ 13.│ 4.9
│ │ │ │yrs. 6│ │ │ │
│ │ │ │mo. │ │ │ │
Chloephaga │ │ │ │ │ │ │ │
magellanica, │ │ │ │ │ │ │ │
Upland Goose │ ♂ │ │ │2 wks.│Thin │ 1,822.│ 8.│ 4.4
Coscoroba │ │ │ │ │ │ │ │
coscoroba, │ │ │ │ │ │ │ │
Coscoroba Swan │ ♂ │ │ │1 mo. │Good │ 1,915.│ 9.│ 4.7
Anas │ │ │ │ │ │ │ │
platyrhynchos, │ │ │ │ │ │ │ │
Mallard Duck │ ♀ │ │ │3 yrs.│Good │ 1,471.│ 8.│ 5.4
Mallard Duck. │ ♀ │ │ │3 yrs.│Good │ 525.│ 6.│ 11.4
Dafila acuta, │ │ │ │ │ │ │ │
Pintailed Duck. │ │ │ │3 yrs.│Good │ 489.│ 6.│ 12.2
Fuligula ferina, │ │ │ │ │ │ │ │
Pochard │ ♂ │ │ │4 yrs.│Good │ 600.│ 6.│ 10.
│ │ │ │6 mo. │ │ │ │
│ │ │ │ │ │ │ │
STRUTHIONES: │ │ │ │ │ │ │ │
STRUTHIONIDÆ: │ │ │ │ │ │ │ │
Struthio │ │ │ │ │ │ │ │
molybdophanes, │ │ │ │ │ │ │ │
Samoli Ostrich │ ♀ │ │ │9 yrs.│Thin │ 60,000.│ 37.│ .65
│ │ │ │3 mo. │ │ │ │
│ │ │ │ │ │ │ │
CASUARIIDÆ: │ │ │ │ │ │ │ │
Casuarius │ │ │ │ │ │ │ │
papuanus, │ │ │ │ │ │ │ │
Papuan Cassowary│ ♂ │ │ │8 yrs.│Good │ 24,000.│ 30.│ 1.3
────────────────────┴───┴──────┴───────────┴──────┴─────────┴────────┴──────┴──────
SECTION XIII-PART II
THE EYE
INFLAMMATIONS.
Conjunctivitis is rather rare but does occur in all varieties of
animals, seldom however, to the extent that the specimen has to be
sacrificed. So far as the daily reports can be relied upon we have had
no epidemic inflammations of the eye. The parrots and monkeys are the
only animals that can be handled enough for treatment, and in them the
applications have not seemed very efficacious. Two cases of
conjunctivitis and iritis have had a tuberculous basis and two other
specimens have had tuberculosis in the eye. Two parrots had, in
association with generalized tuberculosis, semisolid masses in the orbit
which dislocated the bulb, thickened the lids and presented as yellowish
granulating tumors under the conjunctiva; a Swainson’s long-tailed jay
(_Calocitta formosa_) had this lesion on both sides. The only case in a
mammal concerned an Anubis baboon (_Papio anubis_) in which one eye had
been enucleated, two weeks before death, for purulent ophthalmitis. The
other eye became affected shortly after the extraction and the animal
was killed; it was found to have caseous pneumonia. The tuberculous
process had probably begun in the region of the optic nerve and involved
the whole bulb. Secondary infection with pyogenic cocci had been
superimposed upon the original process. Keratomalacia, encountered on a
few occasions, will be discussed by Doctor White.
Iridocyclitis was found in a white browed guan (_Penelope
superciliaris_) the notes of which are condensed as follows:
The internal organs show nothing of value pathologically. The right
eye shows moderate conjunctivitis and a marked thickening of the
cornea with complete opacity. The lens is destroyed and the retina
infiltrated by gelatinous material. Humors are watery, non-
suppurative, but the fundal portion of the retina shows several poorly
circumscribed, yellowish white, gelatinous collections. Microscopical
section of cornea shows replacement of normal bundles by wavy ones
intermixed with small numbers of nuclei. These are never of
inflammatory type, but always of connective tissue type. Conjunctival
mucosa defective in centre, puckered but shows no subjacent
inflammatory features. Ciliary body richly infiltrated by lymphocytes
and vessels distinctly congested. This condition extends over whole
anterior surface of iris and for a short distance over posterior.
Sclera shows much bone formation. Chronic interstitial keratitis,
subacute interstitial iritis and cyclitis.
CATARACT.
Opacities of the cornea are quite common among our specimens, most often
due we believe, to local trauma; ungulates exhibit them more than other
varieties. Cataractous opacities of the lens are frequently observed in
senile animals but, while I have no figures for the statement, I believe
they are not as common among our specimens as can be observed in
domestic horses and dogs. No record has been made of streaky clouds or
spots in the lens but only of complete opacities. There are three only,
an aoudad (_Ovis tragelaphus_) a macaw (_Ara macao_) and a summer duck
(_Aix sponsa_) the last of which alone is interesting. This bird, a
fully developed adult female, was killed because of total blindness and
found to have a low grade chronic pancreatitis and a bilateral
Morgagnian cataract, the lens capsule containing a thin cloudy fluid
with the nucleus quite freely movable in it.
AMBLYOPIA.
A very interesting case of amblyopia in a young monkey was studied and
reported by Dr. H. M. Langdon and Doctor Cadwalader in the _Journal of
Comparative Pathology and Therapeutics_, Vol. XXVIII, Part 4. Because of
its unusual character and careful investigation, the report is
reproduced here:
Pigtailed macaque (_Macacus nemestrinus_) was born June 9, 1913, in
the monkey house, a well developed baby. He thrived and was as good as
any for his age. He was never known to have anything wrong with him
until on the morning of June 3, 1914, when he was found on the bottom
of the cage in the monkey house. He had clenched hands and feet, jaws
tightly closed, lips drawn back, eyes staring and glassy, with
convulsive shaking of the extremities. At intervals he would become
limp, with fists still clenched, and with only occasional jerks in the
extremities. This would last about a minute, and then convulsive
movements would be resumed. The entire “fit” lasted about ten minutes.
He was immediately removed from the large cage in the monkey house to
a small one in the back room of the laboratory. When put in the small
cage he staggered as if dazed, and groped about apparently blind. He
never recovered his sight entirely, but at times seemed to see better
than at others. He was not seen in a “fit” in the laboratory. On June
24th, a small piece of banana was offered by a person who stood
directly in the sunlight. The monkey came to the front of the cage,
reached out and grasped very firmly the thumb of the hand holding the
banana but did not take the banana although he very plainly wanted it.
The banana was thrown into the cage, hitting the monkey on the back.
He turned very quickly, then smelled over the floor of the cage until
he found the banana. On June 30th, he was examined by Doctor Langdon
and the following condition was noted:
“Pupils react to the light of the ophthalmoscope. Optic discs are
normal. Arteries possibly a little small. No other fundus changes.” On
July 1, a cloudy day, he was laid facing a window. A coat sleeve was
laid over his eyes for a minute and then quickly removed. His pupils
were seen to react slowly but distinctly to the light. His gaze would
not follow a finger moved in front of his eyes. When put back in the
cage he climbed up on the wire at the back and then tried to climb the
plain sheet-iron side. He groped and felt for a support and then fell.
This he did several times. About August 1, when the eyes were
examined, there seemed to be more visual perception and very
distinctly prompter pupillary reflex, which condition remained about
the same when examined October 1. He died October 10, 1914, of a
compound fracture of the right femur inflicted by a monkey in the
adjoining cage.
At autopsy the viscera appeared normal throughout. The animal was
fairly well nourished. There was about 5 cc. clear, pale yellow fluid
under the dura. It escaped upon removal of the brain. There were
adhesions of the dura over the temporal lobe (inferior surface),
posterior and external to the optic tract, so firm as to remove some
periosteum and superficial bone. Rest of dura seemed normal.
Examination of the brain. Sections were made from different parts of
the cerebral cortex, all of which were more or less alike. There was
swelling of the endothelium of the pial lymph spaces, with some
separation of the fibres of the pia itself which extended into the
sulci. The perivascular lymph spaces of the larger arteries of the
cortex were dilated, and the adjacent cerebral tissue was edematous. A
well marked endothelial swelling and hyperplasia affected a number of
the arteries and capillaries producing marked general or nodular
thickening in some places. Accompanying these hyperplastic changes
there was a marked calcification of some of the arteries. This was not
confined to one tunic, but in some instances it extended almost
completely through the vessel wall, and here and there the lumen of a
vessel was nearly obliterated. The main features were endothelial
hyperplasia, edema of the pia and of the subpial cortex with some
calcification of the vessels. It was perhaps less well marked in the
occipital lobes than in other parts. The optic nerve and other
portions of the brain appeared to be normal.
MOON BLINDNESS.
It seems also profitable to repeat here a report Dr. H. M. Langdon and I
made in 1911 upon a horse with periodic ophthalmia or “moon blindness,”
a widespread condition and one upon which there is even to-day little
known and much contradictory theorizing. It is worthy of record that Dr.
J. H. W. Eyre of Guy’s Hospital, had a case to study at the same time as
ours. He did not find the protozoön-like body discussed below, but laid
weight upon the isolation of St. aureus, an organism often mentioned in
the literature about this disease. I cite the whole report since our
publication in the 1911 Report of this Garden seems not to have been
quoted in any of the reference articles on “Moon blindness.” Those who
are interested in the clinical and pathological sides of the question
will find a good summary in _Veröff. aus der-Jahres. Vet. Berichten der
beamt. Tierärzte Preussens_, 1908, and the bacteriology of the equine
eye by Karsten, _Inaug. Disser._ Giessen, 1909.
“During the latter part of 1909 and first part of 1910 we had a horse
referred to us suffering with recurrent ophthalmia or moon blindness.
This affection, suggested by its name, is supposed to have some relation
to the lunar periods. Some points in our work showed that such may be
the case. Attacks appear not infrequently at the time of the full moon,
and in our only experimental infection twenty-eight days elapsed between
inoculation and a general ocular inflammation.
“This affection manifests itself as a conjunctivitis early in the
attack, but rapidly progresses to an iridocyclitis and lastly to a
panophthalmitis. After each attack the ball is smaller until it is so
shrunken as to be sightless from chronic thickening and opacities. The
causation is not known. The disease behaves not unlike an infectious
one, remaining in a stud for years at a time. Not every horse may be
affected. It has been connected with dampness, bad fodder, overwork and
the like. Again others have connected it with malaria or rheumatism.
Potapenke, Vigezzi, Koch and others have found various microörganisms,
no two of which seem to be the same. Even an animal organism like
malaria has been described. (Whether or not malaria has anything to do
with the disease, it must be said that our horse was favorably affected
in regard to temperature as well as to the eye condition by repeated
subcutaneous injections of Quinine Bisulphate, Grain xx daily.) The
attacks last five to nine days. One or both eyes may be attacked and not
uncommonly do they alternate. One eye may cease to have attacks while
the other continues. The experiments here recorded were made with the
idea of transmitting the disease to other horses. They were only
partially successful. During eight months the affected animal referred
to us had six attacks of ophthalmia. The attack was observed for study
on the first occasion, but during the second his anterior chamber was
entered by a needle attached to a syringe, the exudate aspirated and
injected into the eye of a horse with apparently healthy eyes. The
history of this second horse will be given later. The attacks of the
first horse ranged from six to twelve days. Five of the six affected the
left eye and one the right. In January, 1910, the left eye was used for
further inoculation, and following this traumatism complete recovery
never took place. The corneal scar left by the needle tract almost
disappeared, but an inferior anterior synechia formed and was followed
by a spreading opacity of the cornea, much wrinkling of the iris and
opacity of the depths. After the fourth attack in this eye it was
completely blind. Material was obtained from this eye during its last
attack, but it was merely serous fluid containing a few blood cells and
epithelium, but no bacteria.
“In transferring the affection from this animal, the conjunctival sac
was washed with 1–5000 bichloride of mercury solution and well rinsed
with salt solution. The anterior chamber was then entered with an
aspirating needle and the exudate removed. This consisted of 0.4 cc.
slightly turbid straw colored fluid containing a few shreds of lymph.
Bacteriological cultures, moist and dry preparations were made from a
part of this, while the remainder was introduced into the anterior
chamber of the second horse. This animal’s eye showed the effects of the
traumatism for eight days, and then was normal save for a small opaque
spot in the cornea left from needle puncture. After twenty-three days a
small patch of lymph collected in the pupil. This increased slowly
accompanied by lacrymation until the twenty-seventh day, when a sudden
and violent conjunctivitis arose. The lymph in the anterior chamber
likewise suddenly increased and rapidly became pus, forming a hypopyon.
The conjunctivitis became purulent. The violent stage lasted five days
and slowly subsided, leaving an ectropion with a densely injected bulbar
conjunctiva, almost complete corneal opacity and an irregular
contraction of iris, apparently due to several small synechiæ. The
depths could not be seen because of the corneal condition. This stage of
affairs remained during the rest of the animal’s life, two months. He
was permitted to live to see if an exacerbation of this chronic process
or involvement of the other eye would appear. Such not occurring in two
months, he was killed and the eyes removed. Fluid removed from the left
eye of the first horse when killed during the last attack was injected
into the anterior chamber of a third horse. This animal’s eye received
the operation well and the trauma had entirely disappeared when the
animal died on the eighth day.
“LABORATORY EXAMINATIONS.—From fluid removed from horse eye (No. 1)
anaerobic cultures made on milk and blood serum, blood agar, glycerine
agar; cultures were made directly from the fluid, while the coagula were
dried upon slides and stained as follows: Loeffler’s, Gram’s, Giemsa. In
all there are very few recognizable bodies. They are red blood cells,
polynuclears and a very few small mononuclear cells. In regard to
microörganisms three structures present themselves. A well staining
Gram-positive, rounded end rod of fairly uniform size but tending to
grow in pairs and stain rather irregularly with Loeffler and Giemsa.
These forms are sometimes called ‘dumbbell’ in that they are bipolar, or
even seem to have a constriction in their centre. Another form is
peculiar and cannot be said to be recognized as a bacterium. It is
circular, of fairly regular size and contour and in many places looks
like a very large coccus. In Loeffler’s stain it is colored deeply in
the centre with a paler marginal zone and an unstained halo about it,
which, however, is not like a capsule. In the Gram and Giemsa method it
is deeply blue or purple with a retractile centre and very sharply
outlined contour. These forms varied from 3 to 5 microns. The third form
is a wavy delicate short mycelium-like thread. Smears from the cultures
as made above showed chiefly a Gram-positive, rounded end rod but which
did not grow on planting out. It grew on aerobic media, but was not
found on anaerobic. The Gram-positive organism would not grow beyond the
fourth generation. It was not identified with any known species by the
characters manifested during the short time we were able to keep it
alive but could be placed in the Hog Cholera group. The mycelium was
found to be an aspergillus. In regard to the large coccus-like body,
little can be added to the above description. Further examination did
not reveal characters permitting us to place it among the protozoa. No
evidences of division were seen. The body is quite uniform in
appearance, varying only in size. Whatever this is it seems to be an
organized body.”
“Cultures from pus in the anterior chamber of the second horse showed
the palely staining rod, an aspergillus and Micrococcus aquatilis. The
first was planted on horse serum bouillon, but did not grow after the
first generation. These cultures were made after death, but the cultures
made during the acute attack direct from conjunctival sac contained such
a host of organisms that no judgment could be formed of their relative
importance. The polar staining rod was found in smears. No large coccus-
like bodies were observed in the second horse. Fluid taken from the
first horse’s eye at death was sterile.”
“These observations are at variance with those of others but such
results are not unique in this respect. It seems as if the polar
staining rod deserves some consideration, and we expect to devote some
attention to it if another horse suffering from recurrent ophthalmia
come to our notice. The large coccus-like bodies are very interesting
and may be protozoa. The finding of the amœba in the cases of Potapenke,
increases their importance. Before, during and after the fourth attack
of the first horse twenty grains of quinine bisulphate were given
hypodermically daily for twenty days. The attack was very mild. Before
the drug was given his temperature had ranged from 99° to 101° F.
Immediately after the first dose the temperature fell to below 99° F.,
and remained at a very regular level during the entire twenty days. No
malarial organisms were found in the blood.”
The ear is without special interest except as a place of localization of
sarcoptes, demodex and fly larvæ. A few cases of acute catarrhal otitis
media have been found in association with nasopharyngitis both of the
nonspecific variety and that which resembles distemper. One case which
led to meningitis has been mentioned.
SECTION XIV
CONSTITUTIONAL DISEASES
There is a long list of diseases including among others such conditions
as hyperthyroidism, osteodystrophies, diabetes and gout which are spoken
of as constitutional but which in reality are usually dependent upon
some lesion peculiar to a definite organ. Several have been discussed
under systemic diseases so that there remain for consideration in this
section only two, gout and diabetes.
Constitutional diseases are recognized in wild animals either not at all
or by some happy chance which permits of examination direct enough to
elicit diagnostic criteria. Gout has been discovered for example in some
parrots and herons because of their swollen feet and their movements. In
veterinary practice fairly accurate diagnoses are possible but in wild
collections they are nearly always hit or miss. Therapeutics naturally
follow this rule.
GOUT.
Gout in mammals has been observed in the London Zoological Garden but
has not been encountered here or we have overlooked it. Avian gout on
the other hand in one of its forms comes to our attention not
infrequently. It occurs most often in parrots, gallinaceous and anserine
birds and herons; occasionally accipitrine birds will suffer with it, an
observation more often recorded in European collections than with us.
The figures show no predominance of percentage for any order but the
records indicate that the most beautiful examples of internal uratic
deposits occur in the anserine birds and parrots, while the best
specimen of general gout, including the joints, was found in a boat-
billed heron (_Cancroma cochlearia_) quoted below.
In so far as etiology of this disease is concerned in domestic stock,
too rich food, especially in protein, and restriction of activity seem
to be credited with the greatest influence. These factors, while
doubtless of importance for birds as they are believed to be for man, do
not seem to fill all the requirements since all our specimens are
confined and, because of their lack of exercise, possibly receive too
much food. Judging by our observations and by publications from other
gardens, carnivorous birds are not conspicuous for the incidence of gout
whereas grain- seed- and fish-eaters suffer more often. This suggests
that these varieties cannot dispose of dietary protein which might be
excessive for their metabolism while in captivity, whereas carnivorous
species have a digestive and chemical reserve to take care of excess
protein. Some such accommodative power must exist in human beings since
not every large meat-eater develops gout. Heredity, often blamed for the
human disease cannot help us with these birds. Examination of the diet
list at the Garden does not reveal a great percentage of concentrated
protein in the feed of the grain- and seed-eaters. The disease occurs
too seldom to disturb the accepted dietary for its possible elimination.
Studies now going on may indicate appropriate changes in the dietaries
that might be responsible.
Arthritic gout appears usually in the pedal joints but may be found in
the wings. Irregular, sometimes very deforming swellings appear which
must be tender judging by the quietness of the bird and by its behavior
if the joints be touched. Most often the swelling seems greater upon the
flexor (palmar) surfaces of the toes or in the end of the tarsal
articulation. Aside from these few observations there is nothing
peculiar about the attack or the specimen during its sickness.
Chronicity seems to be the rule and little emaciation may be found.
Appetite is normal or excessive, provided the food can be reached.
Internal or serous membrane gout cannot be recognized during life so far
as I know. The bird may seem in its usual condition of feather,
activity, appetite and elimination, when suddenly it will fade in a day
or so and die. At autopsy the serous surfaces of the heart and
peritoneum will be white with uric acid crystals and the kidneys a pale
yellow brown with markings indicating that the pelves and tubules are
choked with urates.
The boat-billed heron (_Cancroma cochlearia_) had had bad feet for
three months. The general condition is poor as to plumage and flesh.
The tarsal and metatarsal joint areas of both legs are surrounded by
firm tough swellings involving skin and periarticular tissue. That on
left foot has ulcerated and bled. On section the swelling is found to
consist of reddened fibrous tissue around tendons, the latter
apparently running through smooth sheaths. At both ankles are urate
deposits clearly seen in this inflammatory tissue but at the lower end
of the tarsus there are no distinct deposits. The joint surfaces do
not seem to be involved. Knee, hip, and wing joints seem uninvolved.
Internally all surfaces are opaque by sprinkling of whitish or
yellowish dots like urates; this is especially marked over heart.
Pleuræ aside from urates are negative. Lungs very slightly uniformly
congested throughout. Aorta and branches are stiff, intima smooth. The
liver is soft, deep brown color, architecture seems normal. The kidney
has a smooth capsule and a smooth pale yellow surface. Organ is firm.
Section surface is glistening and opaque, every lobule clear, pelves
filled with pale yellow material, cortical areas irregular. Alimentary
tract negative. Microscopical section of kidney shows general
topography retained, vessels very much injected, some showing
thrombosis. Cortex slightly irregular probably by swelling of medulla.
Tubular epithelium swollen and granular or desquamating and
degenerating. Glomeruli vary in size and shape, mostly fill out the
capsule. Capillary cells show some vacuoles. Some urate collections in
tubules; practically all pelvic tubules have some urates. Interstitial
tissue not increased. Blood vessel walls somewhat loose. Endothelium
prominent. No areas of degeneration seen.
DIABETES.
Diabetes is an infrequent but well recognized disease among domestic
animals. Its detection depends on a rather vague chain of symptoms
confirmed by the discovery of sugar in the urine. For the suspicion that
a wild animal was suffering with diabetes one would have to rely upon
great thirst, loss of flesh, depression, excessive urination and
possibly cataractous opacity of the eye. Such a chain of symptoms has
not been detected. At every occasion at postmortem that the bladder is
full of urine, a routine examination is made. In this way we detected
one case which seems to have been diabetes, the diagnosis being based
upon the glucosuria and the lipemia. For some unknown reason a section
of the pancreas was not made, a regrettable matter since a definite
purulent gingivitis existed and may have lain at the basis of an
infective pancreatitis, well known to be the cause of certain cases of
diabetes. The case is recorded in full since it is unique, no other case
in a wild animal being fully reported.
The arctic fox (_Canis lagopus_) ate and appeared well the day before
it was found dead. Diagnosis—Diabetes mellitus. The animal was in good
condition. The left conjunctiva was reddened, congested, edematous,
with slight mucopurulent discharge in canthus. Muscles have a cloudy
appearance. Fat lacks rich yellow color. The general impression of
anemia is present. Lungs and pleura are normal throughout. Heart
muscle is pale, firm and tough. The tricuspid shows thickening of the
edge of posterior leaflet, the mitral shows slight sclerosis of edge
of mesial leaflet. The auricles are distended with clot. Left
ventricular wall is greatly thickened. Upon incising the heart the
surface of blood shows fine fat globules. Peritoneum is normal. Liver
is slightly increased, surface smooth, edges rounded, consistency
soft, color brownish red with yellow mottlings which are without
definite boundaries; the section surface is moist, granular and
opaque. The bile is fluid, green-yellow and the duct is patulous. The
spleen is slightly enlarged and soft. The kidney is slightly enlarged,
capsule strips easily leaving a smooth, purplish red surface; section
surface is glistening, moist and exudes blood; consistency is slightly
softened; cortical striæ very distinct. The bulging cut surface and
poor demarkation of cortex and medulla characteristic of acute
nephritis are present. The organ shows fat globules in the expressed
blood. The adrenals are very small, firm, brown, bean-shaped bodies
with a brownish medulla. The bladder is slightly distended with turbid
urine. Urine shows dark granular casts, compound granule cells,
spermatozoa and a positive Fehling’s test. Prostate is large and firm
and a turbid material exudes from external meatus. The mouth shows
several decayed teeth. In the neighborhood of last molars on left side
of upper jaw a bead of pus exudes; further pressure results in no
greater flow. The stomach is distended with a great quantity of
undigested food and gas; no worms. Serosa and wall normal but anemic.
Duodenum normal. Jejunum contains numerous worms about 1 to 1.5 cm.
long; it is distended with gas. The pancreas is large, soft, like fat,
white; it extends between the layers of mesentery along the course of
the duodenum; at first the pancreas was mistaken for fat.
HISTOLOGICAL NOTES.—Spleen shows a distinct overgrowth of trabeculæ.
Beyond this there is nothing pathological. Liver shows distended
portal venules in which there are chains of bacilli. There is no
especial fibrous overgrowth of capsule of Glisson; capillaries are
choked with shadow corpuscles and here too, long chains of bacilli may
be seen; parenchyma cells show postmortem change. Adrenal is the seat
of postmortem degeneration, not congested, nor is there any evidence
of bacterial invasion. The kidney shows no interstitial changes, in
fact the section seems to be entirely normal save for moderate
congestion. Vessels show no bacteria.
SECTION XV
THE RELATION OF DIET TO DISEASE
BY
DR. E. P. CORSON-WHITE
Food in the widest acceptation of the term, means every thing ingested
that goes, directly or indirectly, to growth, repair of the body, or
production of energy, all of which phenomena must continue when food is
withheld or supplied in insufficient quantities. Under the latter
condition the processes go on at the expense of the body tissues as
these are protected only when the diet is adequate in every way. A
proper diet, therefore, must be one on which an animal will attain
maximum development, maintain a normal weight curve, show a minimum
susceptibility to disease, live out a full term of life, breed normally,
and rear healthy offspring, capable of normal independent life after
they are weaned. It must fulfill the caloric needs of the body, and in
young animals it must also supply the growth impulse. In its physical
properties it must fit the morphological demands of each type of
gastrointestinal tract. In its chemical content it must supply all the
elements found in the body in usable form, and in amounts sufficient to
cover the needs of the body for growth, repair and waste. To evaluate
fully the influence of food on the individual animal it is necessary to
study its relation: (1) to the type of alimentary tract, (2) to the type
of bacterial flora and their metabolic processes, (3) to the chemical
needs of the body, (4) to the changes arising in the catabolism and
anabolism of all types of food, (5) to exercise or its lack, keeping in
mind always the constant interdependence of all factors. Our knowledge
of nutrition has to a very large extent paralleled the advances in
chemistry, especially the researches into the structural makeup of
living cells, the intermediate stages in their upbuilding and
degradation and the products resulting from their physiological
activities.
Incorrect feeding both qualitative and quantitative undoubtedly plays an
important rôle in producing disease. In the early works on nutrition,
the proportion of fats, carbohydrates and proteins was regarded as the
essential point of a normal diet. The researches on the composition of
foods marked the first real epoch in this history and Fischer’s[57]
studies on the variation in the composition of proteins from different
sources first introduced the idea of quality. Later Mendel and Osborne
investigated the biological values of purified proteins, while at the
same time McCollum and others were studying the value of the groups of
proteins occurring in a single natural food stuff, were calling
attention to the so-called vitamines, and were emphasizing the need of
balanced inorganic materials. These studies have practically
revolutionized our knowledge, particularly of the effects of badly
balanced foods. They have clearly demonstrated that dietary values can,
in all probability, be discovered only by careful biological study of
feeding experiments together with the finer analysis of the components
of the diet, especially of the protein and fat radicles. At the same
time a definite appreciation of the rôle of each element in metabolism
must be kept in mind.
These varied studies on nutrition have shown that the chemical
requirements of a diet are in their ultimate analysis essentially the
same for all species of the higher animals—that is all require
approximately the same amount of protein, fat, carbohydrate, etc., per
kilo of body weight, while the morphology of the tract decides the
physical properties of the diet.
RELATION OF FOOD TO ALIMENTARY TRACT.
Food derived from animal sources is high in protein, readily digested,
and highly putrefactive. This type of diet is suited to an alimentary
tract which permits rapid passage through its length, and is fitted with
sturdy walls. The gastric section is simple, the intestine short and
narrow with ill-defined separation of its parts into small gut, cecum
and colon. This type is found in all land Carnivora. The fish-eating
carnivores have a strong tubular stomach and an enormous length of
intestine, but no cecum. The omnivores occupy a middle place. In them
the alimentary tract consists of a simple stomach, a short wide
intestinal tube, and a more complex, although still comparatively
simple, cecum which is generally longer than that found in the
carnivores. This tract is too small to manipulate the bulky vegetable
masses necessary to provide their minimum protein requirement, and too
long and complicated to dispose quickly of the putrefactive animal
tissue. Among these animals colitis is common, due to the fact that the
shape and position of this part of the tract favors stasis, or at least
a sluggish movement of its contents at a point in the digestive scheme
where the food residue is rich in protein by-products, ready for
bacterial growth.
The herbivores with food derived from plants which requires a long
period of time for its digestion, have, on the other hand, voluminous
stomachs, or large ceca or both; and very long small intestine. In this
tract the concentrated food of the carnivores would provide an
enormously excessive protein intake or if only the protein requirement
is supplied would leave the tract so empty that it would be unable to
functionate.
All studies in comparative anatomy demonstrate the fact that while
neither a complex stomach nor a large cecum is essential to the
digestion of vegetable food, a capacious and complex alimentary canal,
as a whole, bears a relation to vegetable diet, particularly in the
mammals. Either a highly developed concentrated glandular apparatus is
added to the stomach, as in the wombats, beavers and dormice, or the
stomach is subdivided, sacculated, or otherwise amplified as in the
ruminants and herbivorous marsupials. Sometimes both complexities are
combined as in the case of the sloths. If the simple stomach is
retained, it is supplemented by a large sacculated colon or cecum, as in
the horse. In birds, the proventricle is larger in meat- and fish-
eaters, while the gizzard is more muscular in grain- and insect-feeders,
and the intestines are longer in those devouring coarse green grass and
leaves. The length of the ceca is related entirely to the diet, the long
ones corresponding to the diet which needs protracted periods of time to
exhaust its nutriment.
THE BACTERIAL FLORA.
The bacterial flora harbored in the intestinal tract is closely related
to the type of food and to the character of the alimentary tract.
Levin[58] found sterile intestinal tracts in white bears, seals,
reindeer, eider ducks and penguins when in the Arctic regions; but these
same animals when they are brought to a temperate climate rapidly
acquire intestinal bacteria. The function of the normal inhabitants of
the tract is, probably, to protect the body against invasions of
obnoxious species. Herter found in man that a few species adapt
themselves to the digestive tract and control the growth of newcomers
capable of doing injury. These common varieties become a source of
danger only when present in large numbers.
Bacteria which produce decomposition of food in the digestive tract are
of three types: (1) Pure putrefactive anaerobes, (2) organisms both
fermentative and putrefactive, but tending generally to antagonize the
putrefactive anaerobes, and (3) fermentative organisms. In the stomach,
fermentation of carbohydrates with the production of organic acids is a
frequent occurrence. Putrefactive types are very rare except with
pyloric stenosis, a condition which favors excessive fermentation by
diminishing the tone and motility of the stomach and the amount of
hydrochloric acid. This condition is further increased by excessive
carbohydrate food. In general the products of fermentation tend to
restrict putrefaction, yet both may be operative. In the small
intestines, bacteria are always present because of the protein richness
of secretions, the rapid digestion of food and the slight or ineffectual
antiseptic properties of intestinal juice, bile and pancreatic
secretions. The putrefactive bacteria rapidly increase and decompose any
protein that is unabsorbed—a process most marked in the colon because
its shape and position favor stasis or slow movement of its contents. In
general the greater the amount of unabsorbed and digestible protein and
the longer the material stays in the intestinal tract, the greater the
putrefaction. The meat-eating animals develop Gram-negative bacilli,
while the carbohydrate-eaters show a predominance of Gram-positive
types.
Ingested food never contains the enormous amount of bacteria found in
the feces. The alimentary tract with its contents forms a most
efficiently combined incubator and culture medium, in which bacterial
growth exceeds that of any known location both in intensity and
complexity. The range of reaction and composition of nutritive
substances at different levels of the intestinal tract is such that a
great variety of bacteria capable of growth at body temperature develop.
The prominent types that appear in the flora of each order of mammals
are fairly constant in their occurrence. They depend primarily on food
ingested, and show well marked seasonal variations, dependent again on
changes in food. Faulty feeding may itself give rise to a toxic
condition of the gastrointestinal tube, and thus often prepares this
soil for the development of organisms.
The intestinal flora also changes along rather definite lines as the
diet of the host changes from the monotony of the infant to the variety
of the adult. At birth the tract is sterile, but bacteria soon make
their entry through the mouth in food and water. The majority of these
organisms pass to the stomach where many are destroyed, but a number
travel to the intestines where they may gain a foothold. There is always
a mechanical transportation of intestinal bacteria from higher to lower
levels. A continued preponderance of protein in the diet of all animals
leads to a partial or complete suppression of the Gram-positive acid-
forming groups and an increase of the proteolytic Gram-negative types;
while on the other hand an excess of carbohydrate leads to diminution or
suppression of proteolytic activity and an increase in the fermentative
organisms. Therefore the most important normal factor in determining the
intestinal flora in health is the chemical composition of the ingested
foods.
The nature of the dominant organisms which develop in diets rich in
carbohydrates varies with the carbohydrate itself. In all ordinary diets
there are (1) starches—forms not readily fermentable, and (2) sugars—
which are largely absorbed from the higher levels of the small
intestine, leaving residual starches and proteins in relatively great
concentration in the lower levels. Therefore the obligate fermentative
organisms are prominent only in the higher levels, the facultative
appear in the intermediate places, and the obligate proteolytic
organisms in the lower intestines. This accounts in a measure for the
great increase of lower intestinal disturbances in omnivores. Complete
proteins resist putrefaction, but the products of protein digestion and
of the intestinal secretions constitute the main substrata for
putrefactive bacteria. Animal protein develops more active proteolytic
bacteria than vegetable protein, which accounts for the greater
predominance of putrefactive infections in carnivores than in omnivores.
There are two important factors to consider in discussing the influence
of diet on intestinal bacteria: (1) The substitution of types, which
frequently follows a monotonous diet, and (2) the change in metabolism
of existing types of bacteria when dietary conditions are such that the
intestinal medium at one or another level fluctuates in its content of
usable carbohydrate and other nutrient. The nature and extent of these
modifications and their effects upon the host vary greatly, not only
qualitatively but quantitatively. An invasion of the tract by exogenous
bacteria, as the dysentery bacillus, cholera, typhoid, etc., in food or
water may lead to a more or less pronounced replacement of some of the
normal intestinal types by these alien organisms, and to the production
of disease.
The importance of all the foregoing facts concerning the changes in the
food, in the intestinal cultural substrata and in the advent of new
kinds of organisms was emphatically demonstrated in the marked fall in
gastrointestinal diseases in carnivores after proper screening of meats.
The simple protection of the food given to these animals eliminated the
air bacteria which, entering from dust and flies, alter the chemistry of
the meat before consumption or change the flora of the intestine after
consumption. Normal organisms, or types indistinguishable from them, may
multiply, through unusual conditions, extend their normal habitat, and
eventually lead to abnormal reactions detrimental to the host. These
facts throw considerable light on the site and character of
gastrointestinal lesions found in various orders, a subject to be
discussed more fully later.
There are many intestinal disturbances of unknown causation, in some of
which bacteria presumably play a secondary part. The primary disturbance
is due to the products resulting from the action of bacteria upon food.
Many toxic bodies are produced either before or after ingestion by the
bacterial decomposition of carbohydrate, fat or protein, independent of
any actual infection. The symptoms arising from bacterial decomposition
of foods depend largely on the organism concerned and vary from a mild
intoxication to a severe toxemia.
RELATION OF DIETARY GROUPS TO AUTOPSY DIAGNOSES.
Analysis of the autopsies on file from sole point of view of dietary
habits of the animals gives rather interesting groupings of disease
states, which apparently and, in some cases definitely, emphasize the
relationship between food, metabolism and disease. (Table 19.)
From this table a few facts stand out prominently. It is definitely
shown that both birds and mammals on a diet of mixed animal and plant
tissue show a low percentage of disease in the gastrointestinal tube,
liver, pancreas and kidney. The mammals on this diet give the highest
figures for anemias and degenerative osseous conditions. Birds on this
diet show very little osteomalacia, but a fair amount of anemia.
Possibly this may be accounted for by the fact that all of them pick
gravel and may be able from this to supply some of the inorganic
deficiency. Carnivorous birds and mammals, on the other hand, show an
exceedingly large assortment of gastrointestinal disorders, diseases of
the accessory glands of digestion, and of the kidneys. Disorders of the
thyroid gland are almost entirely confined to carnivorous mammals—7.5
per cent., compared to 0.25 per cent. in all other orders. Gout, while
common among birds, was not present in any mammalian autopsy, while
arthritis in mammals reached its highest record among grass- and grain-
eating herbivora. The percentage of rickets was highest in the young
carnivores (2.6 carnivores as against .4 per cent. in all other
mammals), and was very rare among all birds.
The succulent vegetable diet was lowest in its relation to degenerative
visceral disorders and highest in acute gastritis; the latter fact was
probably due to the fermentation of soft moist food that requires rather
a long time for its primary digestion. This type of food has also a high
and easily available sugar content which makes it a very favorable
medium for many of the fermentative types of bacteria. Most of the
lesions in this group were around the pylorus and upper duodenum.
TABLE 19.
_An Analysis of the Pathological Findings Described in the 5,365 Autopsies from
the Point of View only of the Dietary Habits of the Animals. The Percentage
Results Represent the Proportionate Number of Cases of Each Pathological Lesion
Found in the Entire Group of Animals on Each Special Diet without Reference to
Zoological Orders._
═════════════════╤═══════════════════════════════╤═══════════════════════════════
Disease states │ Mammalia 1860 │ Aves 3505
─────────────────┼──────┬───────┬────────────────┼──────┬───────┬────────────────
„ │Omniv-│Carniv-│ Herbivora │Omniv-│Carniv-│ Herbivora
│ ora │ ora │ │ ora │ ora │
─────────────────┼──────┼───────┼──────────┬─────┼──────┼───────┼─────┬──────────
„ │ „ │ „ │Succulent │Grain│ „ │ „ │Seeds│Succulent
│ │ │Vegetables│ │ │ │ │Vegetables
─────────────────┼──────┼───────┼──────────┼─────┼──────┼───────┼─────┼──────────
Malnutrition │ .1│ 1.6│ .6│ 2.2│ .05│ .4│ .1│
Food Poisoning │ .3│ │ │ 2.5│ .05│ .2│ .08│
Acute Gastritis │ 3.2│ 6.3│ 9.3│ 3.1│ .9│ 2.│ 1.3│ 13.5
Acute Duodenitis │ .5│ .3│ │ .5│ .1│ 1.4│ 1.2│ 5.4
Acute Enteritis │ 2.5│ 3.4│ 3.│ 3.1│ 7.│ 1.│ 8.│ 5.4
Acute │ 26.3│ 53.2│ 19.9│ 29.2│ 25.3│ 38.6│ 35.6│ 64.8
Gastroenteritis│ │ │ │ │ │ │ │
Chronic Gastritis│ 1.1│ 6.│ 2.│ .8│ .2│ 1.4│ .3│ 5.4
Chronic Enteritis│ 2.│ 5.6│ 3.│ 2.2│ 1.1│ 3.3│ 1.3│ 13.5
Colitis │ 1.9│ │ │ │ │ │ │
Acute │ .1│ 2.2│ 1.│ 3.1│ .4│ .6│ .08│
Pancreatitis │ │ │ │ │ │ │ │
Chronic │ .5│ 1.7│ │ │ .2│ 1.2│ .5│
Pancreatitis │ │ │ │ │ │ │ │
Acute Liver │ .8│ 1.3│ .3│ 1.4│ 4.2│ 2.8│ 2.5│ 2.7
Disease │ │ │ │ │ │ │ │
Chronic Liver │ 3.│ 6.3│ 3.3│ 6.│ 1.1│ 2.5│ 1.6│ 13.5
Disease │ │ │ │ │ │ │ │
Acute Nephritis │ 9.1│ 12.2│ 12.7│ 12.4│ 5.1│ 6.7│ 4.1│ 8.1
Chronic Nephritis│ 4.5│ 11.6│ 6.7│ 7.8│ 2.9│ 6.7│ 2.1│ 13.5
Myocardial │ .1│ .34│ │ 1.1│ .3│ 2.│ .4│ 8.1
Degeneration │ │ │ │ │ │ │ │
Arterial Disease │ .1│ 3.1│ .3│ 2.2│ .3│ 3.1│ .66│ 1.8
Anemia pernicious│ .3│ .32│ │ │ │ │ │
Anemia secondary │ 4.2│ .32│ 1.2│ 1.5│ 1.1│ 2.5│ 1.5│
Thyroid Disease │ │ 7.5│ .3│ .7│ .3│ .2│ .3│
Adrenal Disease │ 1.6│ 1.3│ .3│ 1.5│ │ │ .08│
Diabetes │ │ .2│ │ │ │ │ │
Osteomalacia │ 5.2│ .4│ 2.3│ .2│ .1│ .6│ 2.8│
Osteitis │ .6│ │ │ │ │ │ │
deformans │ │ │ │ │ │ │ │
Arthritis │ │ .3│ .3│ 2.2│ │ .2│ .08│
Rickets │ .1│ 2.6│ .6│ .7│ │ │ .08│
Gout │ │ │ │ │ │ .4│ .08│
Sore Eyes │ │ .3│ │ .2│ .1│ │ .3│
Malignancy │ .05│ .9│ .6│ │ .05│ │ .6│
Tuberculosis │ 32.6│ 3.5│ 4.5│ 9.6│ 12.│ 1.7│ 17.2│ 5.7
─────────────────┴──────┴───────┴──────────┴─────┴──────┴───────┴─────┴──────────
Overeating is a factor that must be borne in mind when considering the
hay- and grass-eating herbivora. Packing of the rumen is a not
infrequent discovery. This condition is also found in certain seed-
eating birds. As a supply of food is constantly at the disposal of these
animals and exercise is prevented by captivity, continuous eating
becomes their principal diversion. In this group also food poisoning was
highest, a condition which may be due to (1) spoiled food, (2) poisonous
substances in the foods, (3) fermentation of grass foods (spoiled hay or
musty fodder). Malnutrition also, is higher than with any other diet,
due probably to the somewhat meagre nutritious value of the food. This
group also shows a high percentage of acute pancreatitis, degeneration
of the liver, myocardium and arteries. Arthritis was present in this
group 2.2 per cent., against 0.2 per cent. in all other groups.
A study of Table 19 demands a constant recollection of the morphology of
the tract involved and its main points of vulnerability, the bacteria
capable of living on the particular type of food or its constituents and
the by-products produced during the digestion and absorption of these
foods. Not one of these factors can be ignored in evaluating the
influence of diet, which to be correct must supply elements in
proportions that are chemically available for body needs (for instance,
Von Wendt[59] found that more iron was required if the diet was
deficient in calcium). These proportions must be worked out by carefully
combined chemical and biological experiments.
MALNUTRITION.
There was one omnivorous beast, a Hamadryas Baboon, which represented
the only true case of starvation, probably induced by nostalgia, as it
never ate after coming into the Garden. Thirty cases of partial
starvation or malnutrition are listed in our records, the majority among
the rarer specimens, ten carnivorous, seven herbivorous and one
omnivorous mammals, ten carnivorous and two seed-eating birds, due
possibly to inappropriate diet or to some unknown factor that rendered
the diet inadequate. At the autopsy nothing was found to account for
death except the draining of all storage supplies.
STARVATION.
The reports of studies conducted during long laboratory fasts have been
among the most valuable records for the understanding of the chemical
requirements of diet and of the close chemical interrelationship
existing between the different food factors. In absolute starvation life
is very short, primarily because water is necessary for respiration, for
dissolving products of metabolism and for preventing changes in
digestive intestinal secretions. The amount of water needed varies with
different species of animals. If the water is supplied, the organism is
enabled to maintain its energy for continued existence from the
destruction of its own tissues. The length of life depends upon the
amount of protein ingested before the fast commenced, and the amount of
stored fat and glycogen, especially that stored in the liver. The
mechanism of the results is similar. The animal body uses first its
available glucose, and when this is partially exhausted burns its stored
fat and protein. The fat combustion is usually defective, ketone bodies
appearing in the urine in large quantities. The change from fat to
protein metabolism accounts for the premortal rise in metabolism which
occurs usually a few days before death. The chemical composition and
corpuscular richness of the blood is tenaciously preserved; glucose and
protein concentration are practically normal up to the day of death.
There is at times a slight increase in globulins and always an increase
in fat due to its transportation from storage depots. The cause of death
is primarily due to loss of substance in organs necessary to life and to
an acid intoxication.
Wasting occurs first in stored substances, fat, glycogen, etc., then in
the least used organs. The bones usually show some rarefication. The
animal, as a rule, dies from acid intoxication before atrophy of the
organs is marked.
In the wild, when animals are forced to seek their food with the
expenditure of much energy and where feasts are often followed by fasts,
this using up of storage supplies cannot help being a factor in
preserving the integrity of the storage and eliminative organs. In
captivity this cannot occur. Food is supplied regularly, exercise is
lacking, consequently overloading and disease of storage and eliminative
organs is more or less constant—a situation very marked in the
Carnivora.
TABLE 20.
_Detailed Analysis of the Various Diets Used at the Philadelphia Garden
on Basis of 100 Grams of Mixed Food._
═════════════╤══════════════╤═════════════╤══════════════╤═════════════
│ Omnivora │ Carnivora │ Herbivora │ Herbivora
│ │ │ Succulent │ Coarse Food
│ │ │ Vegetables │
─────────────┼───────┬──────┼──────┬──────┼───────┬──────┼──────┬──────
„ │Mammals│Birds │ Meat │ Fish │Mammals│Birds │ Hay │ Seed
│ │ │ │ │ │ │ Food │ Food
─────────────┼───────┼──────┼──────┼──────┼───────┼──────┼──────┼──────
Protein │ 14.3│ 11.5│ 15.6│ 17.2│ 6.1│ 3.2│ 6.4│ 7.1
Fat │ 9.5│ 7.2│ 18.8│ .3│ 2.6│ .5│ 2.2│ 1.3
Carbohydrate │ 26.7│ 41.2│ │ │ 18.5│ 25.7│ 35.9│ 51.2
Calcium │ .034│ .068│ .058│ .109│ .067│ .025│ .071│ .044
Magnesium │ .058│ .093│ .118│ .133│ .164│ .119│ .289│ .16
Potassium │ .497│ .713│ 1.694│ 1.671│ .538│ .242│ .644│ .324
Sodium │ .103│ .284│ .421│ .373│ .08│ .291│ .089│ .261
Phosphorus │ .263│ .484│ 1.078│ 1.148│ .556│ .342│ .692│ .458
Chlorine │ .117│ .377│ .378│ .528│ .038│ .044│ .073│ .063
Sulphur │ .338│ .486│ 1.146│ 1.119│ .134│ .125│ .217│ .163
Iron │ .0032│ .0063│ .015│ .0055│ .0018│ .0012│ .0022│ .0012
─────────────┴───────┴──────┴──────┴──────┴───────┴──────┴──────┴──────
A further study of Table 19 in the light of the finer analysis of the
ingredients of the diets, shown in Table 20, explains, at least in part,
the high percentage of certain types of disease in relation to
particular diets.
In the food of the first group, the omnivorous mammals, there is a
moderately increased carbohydrate content and an unevenly balanced
inorganic content, the last being the factor most at fault. The calcium
and phosphorus are both so low that at the best the animal could only be
in equilibrium, while any drain of the fixed bases would sooner or later
have to be replenished from the calcium and phosphorus storage depots,
the bones. Osteomalacia is most marked in the Cebidæ, monkeys whose diet
is even lower in these same elements: calcium .025, phosphorus .116, and
iron .0008 per 100 grams of food. The inorganic composition of all
animals is grossly similar; the typical digestion developed from the
habitual diet of the animal explains the more apparent changes and
variations in their reactions to certain deprivations.
IRREGULARITIES OF INORGANIC METABOLISM.
Twelve essential elements are present in the body, namely: carbon,
nitrogen, hydrogen, oxygen, phosphorus, calcium, sulphur, sodium,
chlorine, potassium, iron, magnesium. Of these, five are furnished by
the protein molecule and three of the five are duplicated in the fats
and carbohydrates; the remaining seven must be present in the mineral
ash. These elements functionate in three ways, (1) as constituents of
bone, (2) as essential elements of organic compounds, (3) as soluble
salts in body fluids. Chlorine, sodium, sulphur are supplied in
sufficient quantity with most diets. In the case of chlorine, marked
differences exist between the herbivores and carnivores. The meat-eating
mammals easily acquire sufficient sodium chloride from the flesh and
blood of their victims, while the herbivores on the other hand, find in
their vegetable food large amounts of potassium and very little sodium
or chlorine which must therefore be acquired separately. Both omnivores
and herbivores crave salt, probably because this large potassium content
of vegetable food tends to increase the sodium elimination. A
deprivation of salt always leads to a distaste for foods rich in
potassium. So far as is known excessive sodium stimulates protein
catabolism, and through the overstimulation of the digestive tract, may
interfere with the absorption of food.
Sulphur is largely taken into the body in organic combination with the
protein, (a very little inorganic sulphur appears in the drinking water)
therefore if the protein requirements are adequate the sulphur will
usually be adequate.
Magnesium is abundant in meat and most plant tissues; so that except in
diets of highly refined foods, it is more often excessive than
deficient.
The other elements, calcium, phosphorus and iron are frequently
insufficient, especially for animals on omnivorous diet (cf. Table 20).
Phosphorus enters into every living cell, and in cases of starvation is
excreted up to the last. It is involved in practically all the cell
functions. In the body it is present (1) as an inorganic compound in the
bone tissues and blood where it helps to maintain neutrality, (2) as
phosphorus-containing protein, phosphatids and phosphoric esters of a
carbohydrate, all closely associated with the cell and its nucleus. In
foods, phosphorus occurs in the same positions, that is, inorganically
or combined with protein, fat or carbohydrate. It is not entirely proved
but is very probable that the phosphorus in organic combination has the
greater metabolic value, inasmuch as there is greater storage of
nitrogen and stimulation of tissue growth on foods containing
phosphorized proteins, fats, etc. It has been shown, however, that the
animal body can satisfactorily supply its phosphorus requirements by
inorganic phosphates. The omnivorous diet, even the widely varied diet
of man, is very often deficient in phosphorus, a fact which becomes very
important when we consider that the omnivorous diet produces many acid
residues which must be neutralized, and that phosphorus is largely
responsible for the maintenance of tissue neutrality. Voit showed that
the phosphates excreted during starvation were withdrawn from the bones;
and there is much proof that during the daily metabolism a certain
slight movement of phosphorus takes place. The metabolized phosphorus is
excreted by carnivores practically from the kidney alone; by herbivores
almost entirely through the intestinal wall, while in the omnivores it
is excreted by kidney and intestinal tract. Whether these facts have any
real influence on the phosphorus need of different types is not
altogether determined.
Calcium also enters into many of the essential functions of life,
coagulation of the blood, contractility of the heart, etc. Omnivorous
diet is usually deficient in this element, which is very irregularly
distributed both in animal bodies and plants. Insufficient amounts lead
to deprivation of body tissues and to the production of osteomalacia-
like conditions. Voit produced marked thinning of the skull bones and
sternum by a diet poor in calcium. Steenbok and his associates had the
same results in cattle by feeding “shorts” a diet rich in magnesium.
Etienne[60] showed that an excess of magnesium in an otherwise well
balanced food caused a continual loss of calcium. Adults stand a
deprivation of calcium much better than children or young animals. They
often show no symptoms and retain a normal blood content as the losses
from the blood and soft tissues are promptly replaced from the bones.
Sooner or later all these animals show weakness and flexibility of the
bones. Osteomalacia occurred in 5.2 per cent. of the animals on an
omnivorous diet, that is this number showed gross evidence of absorption
of bone salts. This condition occurring in man and the lower animals is
a generalized softening of adult bones that were at one time normally
calcified. Three clinical varieties are recognized in man: a mild form
seen in pregnant, puerperal and lactating women, a senile form in which
the lesions are usually limited to the pelvis, and a severe progressive
form encountered in both sexes and at any age. This last form ends in
marasmus. Its chemical characteristic is a loss of calcium and
phosphorus with retention of sulphur and magnesium.
The progressive type has occurred very frequently among the Cebidæ whose
diet on careful examination, showed a protein content low in quantity,
poor in quality, and especially deficient in the phosphorus-containing
proteins and total fat. The carbohydrate was high. The ash was small in
amount and predominatingly acid. The daily ration often showed only an
unweighable trace of calcium, phosphorus or iron. Sodium, potassium,
sulphur and magnesium, on the contrary, were present in amounts
sufficient for equilibrium or in excess. The Vitamines A.B.C. were
present but were not always correctly proportioned. The fat soluble A
was low and in some daily rations was entirely lacking.
Diet has at various times been proposed as at least one factor in the
production of this condition, a premise that has gained considerable
weight through the increase in the number of cases, both in man and in
the domesticated animals, reported from the war-famine district of
Central Europe where the dietary was restricted and unbalanced. It has
been shown that when calcium is low in the diet, the amount excreted
materially exceeds the intake. Benedict[61] has further shown that even
during absolute fasts calcium is excreted. The requirements of this
element for man have been fairly well worked out, but for animals we
have no standards. Still it seems certain from the foregoing
observations that storage supplies are called upon very early in cases
of deprivation, while in pregnancy and lactation when the calcium
requirements are greatly increased, a reason is found for a higher
incidence of osteomalacia, Steenbok and Hart[62] have shown that the
skeletons of cows and goats gave evidence of a drain of inorganic salts
during the production of milk unless the calcium and phosphorus of the
diet were liberally supplied. In osteomalacia it would seem that
inefficient diet, if not the cause, was at least a very potent factor in
pathogenesis. The disturbance of the calcium-phosphorus-metabolism may
be due to the deprivation of the alkaline salts as in the famine
osteomalacia, to a drain from the alkaline storage of the body
associated with an inefficient diet as in the osteomalacia of pregnancy
and lactation or to the combined action of a diet faulty in more than
its salt content, which by the production of acid in its oxidation and
by favoring the development of acid-forming bacteria, causes a drain of
the body alkali for neutralization of the acid; or it may possibly be
due to a combination of all these factors acting through their influence
on the ductless glands.
Paget’s disease or Osteitis Deformans is a chronic constitutional
process which usually involves all the bones of the adult skeleton.
DaCosta[63] believed it to be a disorder of bone metabolism probably
dependent upon absence or perversion of some internal secretion. We have
had the unique opportunity of observing three cases of this disease in
Cebidæ, the family of monkeys which has presented the highest incidence
of osteomalacia. The experience is all the more interesting because of
the typical picture presented by the specimens, and of the absence of
references in the literature on the subject, to the occurrence of the
malady in wild animals. The interesting point about these cases lies in
the fact that the disease appeared in all three only after lime water
was added to the diet to supply the deficiency of calcium.
Search for literary record of the disease brought to light a case in a
horse that Barthelemy[64] described, but this involved the epiphyses of
the bone while osteitis deformans is confined as a rule to the
diaphyses. This case was probably more closely allied to osteitis
fibrosa cystica. Goldman[65] described examples in fowls and Rossweg[66]
refers to specimens in domestic goats and monkeys. Many of these cases
first come under observation through fractures, an accident common to
osteomalacia, but very rare in well developed osteitis deformans. The
diet of our monkeys was exceeding low in those substances essential to
bone development. Sherman[67] has shown that the calcium balance is
regulated to a certain extent by the calcium ingested, and that when the
diet is poor in this element, the output materially exceeds the intake,
a condition which is definitely changed when the animal is put on a diet
high in calcium.
So far as we could find there are no recorded studies of the mineral
metabolism of beginning cases of Paget’s disease. It seems possible from
the study of osteomalacia that the low mineral and otherwise faulty
diet, added to the symptoms produced by that diet might so disturb the
chemical equilibrium, directly through the neurotrophic mechanism or
through the perversion of the ductless glands, that the mere addition of
the lime water might entirely change the pathological picture. This is
in accord with the histology where the initial lesion is resorption of
bone followed by irregular proliferation. It is also in accord with the
probable chemistry of calcification. These animals all showed a lowered
carbon-dioxide-carrying-power of the blood, and therefore lowered
ability to carry calcium in solution. It is possible that Paget’s
disease is but a stage in a deficiency disease, a faulty reparative
response through a disordered neurotrophic mechanism, or through a
perversion of the glands governing calcium metabolism. Such perversion
could be caused by an improperly balanced diet, or by the addition of an
excess of calcium to the diet of an animal whose body fluids were unable
by reason of previous faulty diet or other disorder, to hold it in
solution. In young animals the calcium demands are much higher than in
adults, a need met in the high calcium content of breast milk, a content
in excess of almost every other food, but apparently just sufficient to
maintain calcium equilibrium. After it is weaned the young animal
frequently shows disorders of its inorganic metabolism. Herter estimated
that a child should store at least 0.1 gram of calcium daily and he
described many cases of arrested bone development occurring during
infancy and early childhood, because of an inefficient assimilation of
calcium. One case, probably of this character, was found in a Hamadryas
Baboon (_Papio hamadryas_) a typical example of infantilism. The animal
was an adult male about half the size of an adult female. His skin was
fine and more delicate than normal, the bones were small and slender,
contour of body was that of a young animal, genitalia were imperfectly
developed, thyroid gland apparently normal, gastrointestinal tract
atrophic, associated was a slight arthritis, portal cirrhosis of liver
and diffuse nephritis.
First among the results of inorganic insufficiency in youth stands
Rickets. This disease occurs in children starting usually at about the
sixth month and continuing with irregular remissions for several years.
The bone changes, which are the most prominent, are always associated
with more or less severe anemia, a general lowered resistance and flabby
musculature. The excretion of calcium is very high in the feces and low
in the urine. There is a frequent negative calcium balance dependent
upon the great loss in the feces. Healing is preceded by a
hyperretention of calcium and a relative increase in the urinary
calcium. The excessive loss of calcium in the feces is not brought about
through the agency of fats because fat could only remove calcium as
insoluble soaps and these are not at all increased. This fact
contradicts the idea of fat starvation as a cause of rickets. Howland
and Kramer found that the blood in active rickets had a normal or
slightly lowered calcium content, but a regularly reduced phosphorus
content. The latter deficiency was extreme at times. They ascribe to
this deficiency the failure of the bones to calcify. It can be readily
understood that a decrease of phosphorus in the blood would render
difficult the precipitation of calcium phosphate.
Recently two series of studies, the first by Pappenheimer, Zucher and
McCann and the second by Shipley, McCollum, Park and Simonds have shown
that rats fed on a diet low in calcium but with a sufficient amount of
fat soluble vitamine and phosphorus develop a bone condition with many
fundamental resemblances to rickets. They were also able to produce the
condition with an excess of calcium and deficiency of phosphorus. On the
first diet, the condition differs from rickets in that the arrangement
of the proliferating zone of cartilage cells is maintained and the
evidence of bone resorption in the diaphyses is excessive. A diet
deficient in both calcium and phosphorus leads to an atypical rickets.
In the animals autopsied at this Garden rickets occurred very much more
frequently in the flesh-eaters than in any of the other dietary groups.
On closer analysis it was found that rickets in almost every case
appeared in the carnivores which did not receive bones as a part of the
food. Rickets occurred frequently in the omnivorous macaques which
however did not show osteomalacia, although they belong to the same
dietary group as the Cebidæ. The reason they did not suffer the latter
disease while adult but had rachitic young is probably due to the fact
that this monkey group, which breeds best in our Garden, receives in
addition to the diet given to Cebidæ one raw egg. This increased the
calcium content of their food more nearly to the requirements of these
mammals. These monkeys also have mouth sacs, which enable them to
acquire more food per kilo of body weight than the smaller Cebidæ which
are not so advantageously equipped. The food even in the amounts
consumed by the macaques is low in calcium, phosphorus and iron. It is
very possible that there are enough of these ingredients present as a
rule, to maintain the animal in organic equilibrium, during normal life,
and possibly even enough to supply the needs of the embryo but not
sufficient to maintain the young during the period of lactation. A few
macaques dying during the delivery of young showed slight osteomalacic
changes in the pelvis. This was notably present in one described in
detail by E. A. Schumann.
The calcium requirements of the female are always much increased during
pregnancy and lactation due to the withdrawal from the mother to meet
the needs of the embryo and nursling. Forbes and Beegle[68] found that
lactating animals made heavy drains on their storage calcium even when
the diet was liberal and the animal was storing nitrogen.
Iron is the essential element of hemoglobin and chromatin—the body
constituent most directly concerned with the process of oxidation,
secretion, reproduction and development. The iron of the food is
absorbed from the small intestines, enters the circulation through the
lymphatics, is deposited in the liver, spleen, and bone marrow and
eliminated through the intestinal walls. There is very little iron
reserve in the adult body; and as a result any failure of the intake to
equal the output causes an immediate reduction of the hemoglobin. Voit
found that the iron eliminated in the feces of starving dogs, or dogs on
a diet low in iron comes from the body through the intestinal walls.
Medicinal iron stimulates the production of hemoglobin and red blood
cells but whether it is directly employed in the production of
hemoglobins has not been proved. Undoubtedly most of the extra iron
given with the food passes through the alimentary tract without being
absorbed or metabolized. The greater the amount of iron in the food, the
greater the influence of the inorganic iron. Anemia occurred in all the
animals we examined at least four times as frequently in omnivorous as
in all the other dietary groups, a fact probably explained by the low
content of iron and calcium in this diet. Both Von Wendt[69] and
Sherman[70] demonstrated that larger amounts of iron were required to
maintain the iron equilibrium when the amount of calcium was low.
Herter has shown that many anemias are associated with intestinal
putrefaction. The carnivores, however, on a diet that putrefies very
easily and on one in which the iron content is apparently of distinctly
lower nutritive value than that of the iron found in milk, eggs and
vegetables, presented an anemic incidence of only 0.32 per cent. This is
probably due to the excellent hygienic care of the meat foods and to the
morphology of the carnivorous intestinal tract, which is short, straight
and fashioned for quick elimination. The cases of anemia steadily
increase among the animals as the conformation of the tract approaches
the omnivorous type with the longer and wider hind-gut.
Herbivora, obtaining their iron from vegetable sources, are much less
liable to blood disorders. The iron needs of the female are greater than
those of the male because of the drains of pregnancy and lactation.
Young animals demand more iron than adults. All exclusively breast-
feeding animals have a considerable storage of iron in the body at
birth, while those that eat food immediately have no such supply.
Bunge’s[71] experiments showed that breast-fed animals contained about
six times as much iron as the milk that nourished them. The iron content
of all these animals is highest at birth, remains constant during the
suckling period and then rapidly decreases to the adult standard. After
this level is reached the iron metabolized must be supplied from the
food if the hemoglobin is to be spared.
The functions of all these inorganic substances are intimately
interrelated and in places interchangeable. Calcium is capable of
correcting disturbances of inorganic equilibrium in the animal body
whatever the direction of the deviation from the normal may be. These
interrelationships are most involved in the maintenance of body
neutrality. The normal processes of metabolism involve a continual
production of carbonic, phosphoric and sulphuric acid which must be
immediately disposed of if the neutrality of the body is to be
permanent.
The factors involved in this are carbonates, phosphates, ammonia and
proteins. Carbon dioxide is the chief excretory product but is at the
same time a normal constituent of the blood and as such, is an important
factor in this physicochemical regulation. There is a tendency for the
respiratory mechanism to hold its carbon dioxide tension nearly
constant. Late investigations have shown that lowering of this tension
is an early sign of beginning acidosis. When food such as protein, is
taken in excess the strongly acid residues are neutralized by the sodium
and potassium carbonates which are eliminated with a corresponding loss
of sodium and potassium. The carbon dioxide tension diminishes, 37.2 per
cent. on a high protein as against 43.3 per cent. on a vegetable diet.
If this excess is long continued, the result may be, and often is, an
increased elimination of the base-forming elements which if not made
good tends to diminish the body’s reserve alkalinity. A diet with a
preponderance of basic elements leads to an alkaline urine with an
increased uric acid solvency and an increased carbon dioxide tension and
reserve alkalinity. A diet with a preponderance in the acid-forming
elements, on the contrary, leads to an increased urinary acidity and
urinary ammonia, decreased ability to dissolve uric acid and lowered
carbon dioxide tension and alkaline reserve.
DEFICIENCIES OF VITAMINES.
Recent investigations have shown that diets furnishing sufficient
amounts of protein, fat, carbohydrate and inorganic salts may yet prove
inadequate for growth or even for maintenance. Hopkins,[72] feeding rats
on purified food mixture was unable to obtain any growth until he added
small quantities of milk or of the ether-soluble portion of milk but
with this addition growth progressed in the normal manner, but it was
out of all proportion to the energy or protein value of the addition.
Five substances of this character, called by Funk[73] Vitamines, have
been described, two of which have definitely established a place as
essential food factors. According to him, pellagra, rickets, scurvy and
beriberi are the result of a lack of these unidentified but specific and
indispensable food complexes.
The first vitamine isolated was the fat soluble A, an adequate supply of
which is necessary, not only because of its stimulating growth
properties, but because its absence produces a serious condition of the
eyes and, at times, marasmus leading to death. Xerophthalmia is a common
condition in animals on experimental diets. The eyes are swollen, the
cornea inflamed and often opaque while blindness and death invariably
occur unless the dietary error is corrected. McCollum[74] rescued
animals almost at the point of death by butter or other fat rich in this
vitamine. Opacities of the cornea are often seen in the animals in this
and other gardens among ungulates—hay-eating mammals; four advanced
cases were found, three in seed-eating birds and one in a fox on a diet
made up solely of horse muscle. The quantity of vitamine A present in
muscle, hay and seeds is very small. It is supplied in largest amounts
in milk, eggs, glandular organs and leaves, substances which were very
low or absent in the diet of all the affected animals. This
xerophthalmia has been reported in man on several occasions, especially
by Hrdlicka[75] in American Indians, by Mori[76] in 1400 Japanese during
a period of food shortage (this epidemic was cured by the addition of
chicken livers to the diet), by Bloch[77] in forty-seven children of
Copenhagen fed on a fat free milk who were cured by the administration
of cod liver oil. The disease is not however a fat starvation, as it is
entirely uninfluenced by vegetable fats which do not contain this
vitamine.
Beriberi is an established deficiency disease, frequently seen among the
poorer classes of the Orient whose diet is limited to polished rice and
fish. It has appeared in Labrador coincident with the excessive use of
bolted flour. A similar condition has been induced in pigs and cattle by
a diet made up of an excess of cotton seed meal and tankage. Two forms
of the disease are described: (1) acute or wet, characterized by marked
edema, ascites, hydropericardium, hydrothorax, edema of the lungs, and a
congestion of the spleen, liver, kidney, and heart muscle, (2) chronic
or dry, characterized by polyneuritis. The disease was first produced
experimentally in pigeons by Eijkman[78] in 1897 by means of a diet of
polished rice. The paralysis appeared in 2–3 weeks after the diet was
initiated. Fraser and Stanton[79] in 1907, found that it could be cured
by an alcoholic extract of rice polishings. Funk[80] later determined
the vitamine character of this extract. In pigeons and fowls
experimental feeding usually results in the chronic or polyneuritic
form, expressed by a typical degenerative inflammatory condition of the
peripheral nerves. In pigs, on the contrary, Rommel and Vedder[81]
produced both types, though the acute or wet beriberi appeared more
frequently. In rats the same deficiency causes multiple hemorrhages in
the cerebellum and midbrain followed by a degeneration of the associated
nervous structures. It is possible that the pathology following a lack
of the vitamine B or in fact any of the vitamines will vary with the
different species or with varying demands of different individuals. This
antineuritic vitamine affects more than the nervous system, and it is
possible that all vitamines may have wider effects than are at present
described.
Scurvy was the first condition to call attention to diet as a cause of
disease. It occurs in man when deprived of fresh vegetables. That faulty
diet was in some way the cause of scurvy has been known for many years,
but only since 1905 has there been any systematic attempt to determine
the peculiar value of the curative foods. At this time Theobald
Smith[82] called attention to a disease suggestive of scurvy which
developed in guinea-pigs fed on a diet of oatmeal. This observation was
confirmed by Holst and Frölich[83] who stated that the disease could be
prevented by the addition of fresh milk or cabbage, because in these
foods there was present an antiscorbutic or C vitamine. This
unidentified substance was easily destroyed or diminished by heat or an
alkaline medium. It was found in rather large amounts in succulent
vegetables and fruits. McCollum[84] and his coworkers showed that the
oat kernel was low in inorganic salts and vitamine A and poor in the
quality of its protein; but with these faults corrected it proved to be
a complete food for rats. McCollum also found that scurvy developed more
readily in animals if the physical properties of the diet favored
constipation. He was able to delay the onset of the disease in guinea-
pigs for a considerable period by the addition of mineral oil which has
no food value, or phenolphthalein, a cathartic. At the same time,
Jackson and Moore,[85] found the cecum of all guinea-pigs dying of
scurvy, packed with putrefying feces. They were able to produce a mild
type of the disease by the injection of the diplococci isolated from the
swollen joints.
From these observations it seems safe to conclude that scurvy may not be
purely a deficiency disease, or even a simple dietary one, although the
presence of a vitamine influence is not excluded; but it is probably the
result of a bacterial invasion of tissues debilitated by a faulty diet
and by the toxins produced by the putrefactive bacteria developing in a
diet unsuited to the anatomical demands of the alimentary tract. This
theory receives support from the fact that pasteurization destroys all
aciduric bacteria, allowing only the spore-forming putrefactors to
develop; and from the fact that scurvy develops more frequently in
children on stale pasteurized than on stale raw or boiled milk. In this
Garden no suggestion of scurvy has been noted.
Pellagra is very definitely a disease of poverty endemic for years among
the poor, especially in the mountains of Northern Italy. It has been
under observation in the United States since 1907. So far as is known no
cases have been observed among animals. Opinions differ as to the rôle
of diet in the etiology but the results of recent studies seem to show
that uncomplicated cases of average severity clear up entirely on a diet
rich in animal protein. No vitamine deficiency has so far been
determined. Wilson’s careful studies of the diets known to have produced
the condition show that the etiological factor lies in a deficiency of
the protein molecule. The results of Goldberger[86] corroborate this
fact, and he concludes from his latest studies that “the dominating rôle
of diet in the prevention and causation of pellagra is referable
primarily to the character of the protein supply or to the specific
quality of the aminoacid makeup of the protein supply.” Just what
aminoacid or combination of aminoacids it is, has not been determined,
nor has the possibility of a vitamine alone or in combination with the
aminoacid factor been absolutely excluded.
The principal influence of the omnivorous diet is toward those
degenerations arising primarily from imbalances in the inorganic makeup,
or to insufficiencies of certain necessary factors. The vitamine
deficiencies are markedly less prevalent in animals than in man whose
food is less often consumed in its natural state. It is now known that
much of the injury and loss of nutritive value in foods is produced by
the processes involved in preparation, preservation, refinement and
storage. Whenever the choice of food is not restricted, vitamine
deficiencies do not occur. The vitamine requirements probably differ in
different species and in individuals from the same species according to
their environmental and individual variations. It is very possible that
if the diet is low in vitamine content there may arise conditions of
relative deficiencies; and McCarrison has shown that a vitamine
deficiency associated with a high fat or carbohydrate content may
disturb the balance of the endocrine glands. It is however to the
inorganic content of the omnivorous food that most of the disturbances
peculiar to this diet are to be assigned.
With the flesh eating animals and birds the records present a very
different picture. Disorders of the digestive tube, of the storage
organs, of the organs of elimination and of the endocrine glands
predominate. Their diet is low in carbohydrates and, at times, in fats
and very high in protein. Bone supplies the inorganic salts, which in
this Garden is fed only to the larger mammals. The carnivorous birds get
their inorganic supply from mice which are eaten entire. The carnivores
are as a rule large and are given to active fighting or to long flights.
In the wild, very probably there are long periods between feasts, while
in captivity the food is always plentiful and regularly supplied. This
regularity added to the lack of exercise, particularly among the larger
animals, must lead to excessive demands upon the storage and eliminating
organs. Storage is always promoted by rest and liberal diet, and cleared
away by exercise and starvation. The life of these birds and mammals,
moreover favors inactivity of the bowels, which, together with the
highly putrefactive diet adds another serious factor to a problem which
in gardens is almost insurmountable.
IRREGULARITIES OF CARBOHYDRATE METABOLISM.
The carbohydrates are derived from the glucose and glycogen of the meat
and from the protein molecule. They are absolutely less than in the diet
of herbivores but become a factor in the disorders of this group because
of the lack of exercise and the regularity of feeding. In digestion the
carbohydrate becomes available for absorption and bacterial growth in
the upper small intestine and appears on the other side of the
intestinal wall as blood glucose in which form it is burned for energy
or stored as glycogen for the future maintenance of the blood glucose.
The blood of different animals has a glucose concentration between
0.05–0.1 which for each species is quite constant, as it is regulated by
the coadaptation of four factors: combustion, fermentation of glycogen,
formation of fat, and elimination from the kidney. In excessive feeding
the amount needed for energy is burned, the remainder is stored in the
liver up to its capacity, then in the muscles and other cells, after
which fat is formed and all further excess is eliminated by the kidney.
Overfeeding causes an immediate overloading of the oxidative mechanism
with symptoms of gastric disorder, achylia, and at times acid
fermentation with irritation of the stomach walls and the development of
bacteria in the organ. This is frequently followed by glycosuria,
several types of which are described: (1) associated with an increased
concentration of glucose following excessive ingestion exceeding the
normal glycogenic function of the liver, a form common among the
Herbivora, (2) that due to a reduction of the glycogenic function of the
liver, (3) that associated with disease of the ductless glands in which
the resulting glycosuria probably depends upon the influence of these
glands upon the pancreas, (4) that dependent upon the defect of
glycolysis or to an overstocked liver seen in gout, obesity or
hypertrophic cirrhosis, and (5) renal glycosuria due to a lowering of
the renal threshold and usually associated with gout, arteriosclerosis
or chronic nephritis; this last is best explained on the ground of
increased renal permeability. Normally when the blood sugar
concentration rises above a certain level the elimination _via_ the
kidney begins and continues until the blood has again reached its normal
concentration. The relation of the kidney to glucose concentration is
not constant and variation is always toward the side of lesser
elimination while the kidneys become accustomed to the higher level.
Diabetes, a disease of the islands of Langerhans in the pancreas, is
essentially a disturbance of sugar metabolism always associated with an
exaggerated and defective fat and protein combustion. It is not only
that the diabetic has lost the faculty of combustion but these
abnormalities all establish states of intoxication to which the diabetic
must sooner or later succumb. Among lower animals the disease is rare.
Dogs are most frequently affected (about 1 in 12,000 deaths). It has
also been described in horses, cattle and monkeys. In our records there
was one case an Arctic fox (_Canis lagopus_) presenting a typical
picture. Degeneration of the islands of Langerhans was seen in three
other animals, but there was no other evidence of diabetes. This disease
is not due to diet but to the absence of a normal ferment
(pancreaticozymo-excitor) for one particular type of food.
IRREGULARITIES OF FAT METABOLISM.
Disorders of fat metabolism are very rare among lower animals
notwithstanding the fact that fat even in the carnivorous diet,
represents about 13 per cent. of the whole intake. It plays two
important rôles in the body, storage for energy reserve, and as a most
essential structure in cellular protoplasm, in which position it joins
with protein in complex combinations of still unknown composition which
present to a striking degree the phenomenon of absorption. Very marked
biological differences exist in the value of fats from different
sources, due to the presence or absence of vitamines. The body fat is
derived from the fat of the diet or is synthesized from glucose. The
former is specific to the fat consumed while the latter is specific to
the animal. In omnivores the type depends upon the varying extent to
which animal fats enter the diet, in carnivores it depends almost
entirely on the fat intake, while in the herbivores practically all the
fat is synthesized from the carbohydrate. On digestion, fat splits,
yielding a glycerol and fatty acid which are collected in the lymph
spaces of the intestinal mucosa, there changing to some complex
combination which is not only soluble but diffusible.
Fatty infiltration and fatty degeneration are conditions of much
pathological interest and of great frequency in captive animals. The
researches of Mansfield[87] have thrown considerable light upon these
conditions. He found that the total fat content in cases of most marked
degeneration was normal or reduced. The proportion of fat free from
protein was increased and the firmly bound fat decreased. This increase
is due to neutral fat brought from without the organ by the blood when
for any cause the oxidative powers are decreased, and setting free of
the previously invisible intercellular fat and lipoids, which are
normally present in the cells, by autolytic or physicochemical changes.
This condition is pretty evenly distributed among the dietary groups,
the liver being most commonly involved. The hepatic cells are easily
degenerated by the toxins or other harmful substances passing through
the organ and become passive and unable to throw off or to utilize the
deposited fat. In all probability the same general situation occurs in
the atheromatous changes in arteriosclerosis which on this diet shows a
high incidence. The causative agent is probably some poisonous
substance, possibly a protein degradation product, indol, pressor
substance, acting on the intima over long periods, or at irregular but
often repeated periods causing first destruction then fat accumulation.
It is also possible that it may be caused by repeated absorption of some
sensitizing protein. Arteriosclerosis in these animals is often closely
associated with nephritis.
Obesity may result from excessive ingestion of food in individuals whose
habits are sedentary and whose digestions are active or it may come from
an inherent abnormality of metabolism dependent upon ductless gland
disease. It is very common in castrated animals. The obesity of
overeating is always of milder type than that associated with endocrine
disturbance.
So far as is known there are two main disorders of fat metabolism—the
failure of the diabetic to form fat from glucose, and acidosis, the
inability of the organism to burn fat beyond betaoxybutyric acid,
acetoacetic acid, or acetone. The symptoms are unsteadiness of gait,
stupor, coma, air hunger, in all of which the essential features are due
to the impoverishment of the body in available bases. In infants this
frequently follows an excessive fat diet. It is also common in
starvation due to the deprivation of sugar. It is associated with
phosphorus poisoning, narcosis, carcinoma, liver disease, inanition,
etc. It has been produced experimentally by the administration of acids
or by foods deprived of their bases. The excess of acid in the body
whether produced in the body or introduced from without must be
neutralized in part by the ammonia manufactured in the ultimate
metabolic transformation of the protein and by the alkaline salts of the
blood and tissues. When alkali is reduced the carbon dioxide accumulates
in the tissues, blocking oxidation. The urine immediately shows an
increase of ammonium salts, a decrease of the urea and an increase in
the output of sodium, potassium, calcium and magnesium, which last two
are drawn from the bones.
Symptoms do not arise until the fixed alkalies are exhausted; and they
are immediately relieved by the administration of alkalies, except in
those cases of starvation where the administration of sugar and the
subsequent sparing of the fats relieves the situation. In herbivores,
acidosis does not follow starvation, but, on the other hand, it is
markedly easier to excite it in herbivores than in carnivores whose
heavy protein diet produces more ammonia, which better enables the
animals to protect their fixed alkalies. The acid intoxication of
infections arises from different causes and is dependent on the
intensity of the type of infection; but ultimately it also depends upon
the depletion of the fixed alkalies.
IRREGULARITIES OF PROTEIN METABOLISM.
Fat and carbohydrate disturbances are not infrequent in carnivores, but
it is with the protein fraction of the diet that most of the trouble is
connected. Natural foods contain several proteins or groups of proteins,
whose biological adequacy depends upon their yield of aminoacid.
Experiment has shown that many proteins are entirely lacking in one or
more of these essential radicles; and no food can be adequate unless it
contains at least all the aminoacids that the individual animal is
unable to manufacture for itself. So far as is known, no animal can
produce in itself either lysin or tryptophane. Gliadin, the principal
protein of wheat and lacking in lysin, is unable to support growth even
when given in amounts sufficient to insure the storage of nitrogen, and
is associated with a diet adequate in all other factors. Absence of
tryptophane prevents not only growth but maintenance. Any of the
aminoacids, whose radicles are contained in tissue proteins, may
contribute to the maintenance of adult equilibrium; but no growth occurs
unless all the necessary groups are present. Except in laboratories,
diets are never made up of isolated proteins, but they are often
composed of proteins derived from one plant and are often deficient.
McCollum and his associates in their studies showed that while there
were pronounced differences in the composition of many foods used by men
and animals not only in their protein content but in water, fats,
carbohydrates, etc., yet in the combinations found even in rather
restricted diets, the errors, as a rule, corrected each other.
During digestion the protein molecule is broken down into the component
aminoacids which are absorbed and synthesized in the intestinal walls,
and appear on the other side as the specific blood protein, which serves
as the substrate for the anabolism of all the special tissue proteins.
Excessive protein is stored to a slight extent as aminoacid for the
future maintenance of the blood protein, the integrity of which is
tenaciously protected during hibernations, sexual migrations, and even
during starvation. The animal body tends to adjust its nitrogen
metabolism to its nitrogen supply; the adjustment requires an
appreciable amount of time. A diet changed to a lower nitrogen level
results in a continued loss of nitrogen, increased combustion of fats
and carbohydrates. The animal makes no apparent effort to reëstablish
equilibrium, and sooner or later digestive disturbances and loss of
strength occur.
If, on the contrary, the protein is steadily increased after an animal
has established equilibrium, the nitrogen metabolism increases and the
level of nitrogen equilibrium rises to higher and higher levels. There
is, at the same time, a lowering of the fat combustion, an increase in
the respiratory quotient and in the heat production. The excess protein
must be split, deaminated, burned and eliminated. Fifty-five per cent.
of the intake is converted into glucose which is burned and the excess
stored as glycogen. The sulphuric acid formed during the protein
cleavage is neutralized by the body alkalies. In these cases the liver
is often congested and enlarged. The urine shows excess of urea and
ammonia. At times the excess, being so great that it cannot be absorbed,
undergoes chemical and bacterial decomposition which causes digestive
disturbances, torpor and constipation.
The organisms associated with protein food are usually the putrefactive
types which break the protein molecule into the aromatic bodies,
phenols, indolacetic acid, indolpropionic acid, skatol, etc. These
bodies on absorption are believed to give rise to hypertrophy of the
adrenal, interstitial changes in the kidney, and arteriosclerosis.
Another group of substances, pressor bases and amines, are manufactured
by certain anaerobes acting on proteins. These, when fed by mouth, are
detoxicated by the liver cells, but when formed below the portal
circulation, give rise to anaphylactic phenomena—urticaria, etc. Certain
other organisms give rise to soluble toxins as in botulism and
thyrotoxicon poisoning. All these types of toxins will destroy if they
act acutely in sufficient concentration; or as is more common, if they
act persistently over long periods, or at oft recurring intervals they
will cause serious injury to the tissues coming in contact with them,
and have a part in the production of cirrhosis of the liver, chronic
nephritis, myocarditis, arteriosclerosis, etc.
All foods have a limit beyond which they are excreted untouched or
imperfectly oxidized. Many of these partial oxidation products of
protein are in themselves toxic and may also be a source of these
degenerative organ conditions. The pathological material studied by us
showed a marked decrease in gastrointestinal diseases in close
association with the more hygienic care of the meat foods.
Always associated with the protein foods are the nucleoprotein
complexes, which are split by both bacteria and digestive juices into
globulins and nucleic acid, and then through the agency of a special
enzyme, into purin bases and uric acid, in which forms they are excreted
in the urine and feces. The oxidation of purins is never complete.
Gout, representing the pathology of purin metabolism, is a paroxysmal
inflammatory disturbance, due to the deposition of sodium urates in the
joints or in the internal organs, usually accompanied by a fibrosis
especially in the liver, kidney, arteries, etc. The disease occurs
almost exclusively in birds. Isolated cases have been described in dogs,
horses and hogs, but among lower animals it is undoubtedly very rare. In
birds it is most frequent in the carnivores—4 per cent., as against 0.02
per cent. in all other groups. It is higher in fish-eating birds than
among the flesh-eaters. The avian gout is usually of the visceral type
and was most marked in its distribution over the organs in the Anseres
and Psittaci, birds whose diet apparently is not unduly heavy in
nucleoproteins, but whose tract approaches the carnivorous type. The
only arthritic cases occurred in Boat-billed herons (_Cancroma
cochlearia_), fish-eaters. Our records show examples in Accipitres,
Galli and Columbæ, although the number of cases in the last order were
few and slight in extent. This disease stands in close relation to diet,
as it develops on generous protein food, high in nucleoprotein or
hypoxanthin, especially if this be associated with restricted activity.
The carnivorous mammals lead in the disease of the thyroid glands.
Thyroid disease occurs among the birds, but is equally distributed among
the dietary groups. Thyroid activity has a marked influence on
metabolism probably through the influence of the iodine-containing
protein of its secretion. There are some experimental evidences in favor
of a detoxicating function of the thyroid, of which the following are
quoted: (1) The effects of thyroidectomy are most marked in the
carnivores; Herbivora are often capable of several years of life without
thyroid tissue; (2) administration of meat to thyroidectomized omnivores
or herbivores caused a marked increase in all symptoms. The importance
of the relation of the meat diet, detoxication and thyroid disease
receives considerable confirmation from the fact that among the 1,860
mammalian postmortems thyroid disease occurred in 2.6 per cent. of all
mammals, 94.9 per cent. of which were found in flesh eating varieties.
Wells[88] suggested that possibly this could be interpreted as an
indication that toxic materials found in the meat in the intestinal
tract were, under normal conditions, detoxicated by the thyroid. Against
a local neutralization, however, is the improvement following the
administration of dried thyroid substance. The function is either
neutralization of toxic substances or the stimulating action on
intracellular metabolism, both of which might be called into play by an
excessive protein diet.
THE CARNIVOROUS DIET.
The pathology of the more prominent diseases developed in carnivores
points at least to diet as a predisposing or determining factor. This
diet is very high in a distinctly putrefactive protein and yields
products, chemical and bacterial, which are toxic and which give rise to
acute or more often chronic diseases of the alimentary tract and its
adnexa. By reason of the amount ingested, excessive because of lack of
exercise, there is a severe tax on the storage organs and on the
detoxicating glands, as the liver and thyroid. The constant absorption
of these toxic substances gives rise to chronic degenerative or fibrotic
changes in the organs through which they pass: liver, kidneys, arteries,
heart. In birds the degenerative diseases are even more marked than in
mammals on the same diet. The ultimate fault of this diet, especially
for mammals and birds with restricted activity, lies in the production
of toxic bodies, produced either in the incomplete degradation or
oxidation of the protein molecule or as the result of bacterial action
on the protein molecule, a poisonous quality which is probably enhanced
by the chemical changes occurring while the digested protein is passing
through the intestinal mucosa. Garden conditions are such that these
factors are almost unsurmountable unless the substitution of vegetable
protein could be accomplished. Failure is often caused by limited
feeding to carnivores of muscle and bones, whereas they should be
supplied with glandular organs and blood.
THE HERBIVOROUS DIET.
Herbivorous diet must be divided into two groups, (1) that composed of
succulent vegetables, and (2) of grasses, grains and seeds. In the first
group there is an apparent variation in the results found in mammals and
birds. In both there is a marked decrease in the chronic degenerative
pathology. In both, acute gastritis is more prominent, far outstripping
the incidence of this condition in other classes.
This diet yields a large and quickly available amount of carbohydrate
which in conjunction with the moisture, heat and bacteria which are
unavoidably associated with raw vegetables, makes an ideal situation for
infection. These foods carry many saprophytic bacteria, moulds, etc. In
birds the conditions are aggravated by the injuries that may occur from
the sharp objects picked up with the gravel. The incidence of acute
infection is higher among birds than among mammals of this group, and
often there is involvement of the whole tract. The explanation of the
other pathological findings occurring among birds must be found in the
frequently repeated low grade infections which result finally in the
production of chronic lesions in the digestive tract, liver, pancreas
and kidney. Toxins as an etiological factor cannot be altogether
excluded, but as a rule they are not important because the by-products
of vegetables are distinctly less toxic than those derived from animal
sources. Arteriosclerosis is much less frequent and less intensive in
herbivorous birds than among the carnivorous, probably because of
differences in the concentration and character of toxins in the two
groups.
SOFT HERBIVOROUS DIET.
The diet of succulent vegetables is composed of tubers, edible roots and
leaves. The tubers and edible roots are high in water and carbohydrate
and poor in the amount and quality of the protein, most of which is not
even a true protein but a mixture of aminoacids. The leaves, on the
contrary, are rich in organic ash, especially calcium, sodium, chlorine,
and fat soluble A vitamine, and as a rule contain a good quality of
protein. They often, however, contain injurious substances. This diet,
while measurably less nutritious than that of the carnivores, can
satisfactorily nourish many animals with an extensive intestinal tract
during growth and even throughout their entire life, but proves entirely
inadequate when fed to an omnivorous tract.
SEED DIET.
Closely allied in general character to the diet of succulent vegetables
are the seed diets, eaten only by birds and having no parallel among
mammalian foods. All seeds, in contradistinction to tubers, contain true
proteins which, however, are of poor quality because of the deficiencies
in the aminoacid content. They are as a rule low in the fat vitamines
and in the amount of calcium, sodium and chlorine carried. In three
pathological conditions only do these birds show any oversusceptibility:
(1) Sore eyes, (2) acute enteritis, (3) osteomalacia. Sore eyes were
frequently noted in this group. The lesions were very like those
described in animals deprived of the fat vitamine, which was present in
this food in very small amounts or entirely absent, thus giving a very
plausible explanation of this condition, especially as in some of the
cases no other cause could be found. Gastric disease of any type is rare
in this group because the food at the gastric stage is highly resistant
to bacterial action. In the duodenum, however, the conditions are early
changed because the bacteria carried with the food through the stomach
become active in the presence of available carbohydrate and protein
decomposition products.
Osteomalacia is confined almost as exclusively to the seed-eating birds
as it was to the omnivorous mammals, and it is also associated with the
same deficiencies, calcium and phosphorus (cf. Tables 19 and 20). It is
also interesting to note that these two diets, the omnivorous and seeds,
yield the greatest number of cases of tuberculosis. Mammals showed 32.6
per cent., as against 5.8 per cent. in all the other dietary groups, an
observation which becomes more striking when man is added to the
omnivorous group. Seed-eating birds showed 17.2 per cent., as against
6.4 per cent. in other groups. In both diets the fat, fat vitamine and
inorganic salts, especially the calcium, are deficient in amount. In the
wild, birds vary their diet of seeds with insects, worms, soft fruits
and the tender shoots of plants, and at the same time they increase
their inorganic intake by the minerals picked up with the gravel and
from the water which has penetrated the soil.
GRAIN AND GRASS DIET.
The hay-eating animals constitute a large and well studied group—
including practically all the domestic varieties. Table 19 shows that
these animals yield the greatest number of cases of malnutrition, food
poisoning, acute pancreatitis, acute degenerative conditions of liver
and myocardium.
Recent literature describes many cases of osteomalacia, especially among
horses and cows, in the famine districts of Europe. In our collection of
1,860 postmortems only one case was found, that of an Isabelline gazelle
(_Gazella isabella_), a hay-eating animal, and in this case it was
secondary to infection.
Arthritis, occurring in 3.4 per cent. of all the autopsies, was almost
entirely confined to the hay-eating animals. The literature describes
many cases of arthritis almost entirely confined to ungulates, of which
many were associated with calving and subsequent infection.
Bacteriological researches have found it most often associated with
streptococci, staphylococci, or Bact. perfringens, organisms that
require a certain amount of carbohydrate for their proper development.
The relation of diet to this condition probably lies only in the fact
that it provides an excessive carbohydrate substrate suitable for the
optimum development of these organisms. Folin and Bergland, noting
glycoresis in Herbivora, thought that it represented the absorption and
excretion of unusable carbohydrate, present in grains, vegetables,
fruits, etc., and that it was sharply separated from the main
carbohydrate metabolism. These products were absorbed from the blood
exactly as they were ingested like lactose, dextrose, etc., are
absorbed, but do not enter into the economy although they might cause
disorders, especially forms of arthritis.
The grain foods are composed largely of carbohydrates (principally in
the form of cellulose and starch) small amounts of protein and little or
no fat. They have a very low nutritive index so that large amounts must
be consumed to supply adequate calories. This food is constantly
present, and during the enforced idleness of captivity is almost
continuously eaten. Despite these facts, however, malnutrition is
present in 2.2 per cent. of the animals on this food. Associated with
the plentiful food and lack of exercise are overeating and pica.
Overfilled stomachs occurred thirty-four times. They were limited to
these mammals and to the seed-eating birds whose environmental
conditions are practically the same. Pica or excessive appetite for
abnormal food, is also more frequent in these groups, but is usually
associated with badly balanced diets, and thus represents an effort on
the part of the animal to supply its own deficiency. It is present in
osteomalacic monkeys and has been reported in cattle from regions where
osteomalacia is common and following crop failures where the rations are
restricted. In cattle it very often accompanies food poisoning,
especially that produced by ingestion of peat hay.
Disturbance of the alimentary tract and its adnexa occurs in two forms:
(1) Infection which is quite common and involves the duodenum, pancreas
and liver, and (2) toxic. Compared with other diets alimentary disorders
are not frequent among grain feeders, despite the ease with which grass
foods ferment and the great variety of organisms found in them such as
moulds (aspergillus), Bact. coli, paratyphosus, enteritidis,
suipestifer, oidium lactis, etc. Few bacteria can attack whole protein,
cellulose or starch, and the decomposition products, peptone, glucose,
etc., are not available in any quantity until the lower stomach and
duodenum are reached. The inflammation of the alimentary tracts of these
animals is confined to the fourth stomach and duodenum, with, in many
cases, extension to liver and pancreas.
Acute and chronic degenerative changes occur very frequently, and as a
rule are the result primarily of absorbed toxins. After ingestion of new
hay this often appears. The toxic substance probably is a terpinol
ester, cumarin, which is produced by an enzyme in the cut grass.
The result is a gastroenteritis with jaundice, thirst and marked
flatulence. It is very probable that many of the gastrointestinal and
degenerative lesions are the result of the combined action of toxin and
bacteria.
FOOD POISONING.
Food poisoning occurs in all diets, but especially among the grass-
eating mammals. To-day under the general heading of food poisoning are
included those cases due to (1) some injurious substance inherent in the
food itself, true food poisoning, (2) those due to toxic substances
liberated or produced in food contaminated by parasites or bacteria, (3)
those due to bacteria that are carried by food and develop into true
infection after ingestion. Most of the cases of meat poisoning described
in literature undoubtedly belong to this third class, _i.e._, flesh is
infected during the life of the animal or during its preparation for
food and the virus develops in the host after ingestion. A fourth and
more rare class of food poisoning is due to the condition of the
individual consuming the food-protein sensitization.
Injurious constituents of normal flesh foods are very uncommon. There
are a few poisonous fish, notably the balloon, puffer, and Fuga fish of
Japan, which when eaten give rise to cholera-like conditions ending in
convulsions and paralysis. A marked intoxication has been described in
dogs which have fed upon the Greenland shark. Some fish are poisonous at
certain periods as spawning season, the poison then being confined to
the roe. Still others are harmless unless rendered toxic by some
injurious food. This poisoning of muscle meats is seen in quail and
partridges fed on mountain laurel, in some fish after consuming certain
marine plants, and in cattle poisoned by amanita.
The most common sources of poisoning are spoiled meat and flesh of
diseased animals, both of which are serious factors in the production of
the gastrointestinal disorders of omnivores and carnivores. Practically
all the reports of meat poisoning from the literature have been traced
to the use of raw or insufficiently cooked flesh, and have yielded on
bacteriologic examination _Bact. paratyphosus_, _Bact. enteritidis_,
_Bact. suipestifer_, _Bact. coli_, or _Bact. proteus_.
The bacteria may produce toxin in the food previous to ingestion causing
in the host only a severe intoxication. This is the situation developed
after eating sturgeon infected with _Bact. piscidus agilis_, an organism
which manufactures a highly poisonous alkaloid. A similar intoxication
follows the ingestion of potatoes infected with _Bact. proteus_ or
containing the poisonous alkaloid, solanin, which is produced in
diseased and sprouting potatoes. Other examples of this are (1)
ergotism—due to an infection of rye and wild grasses with _Claviceps
purpurea_ which produces three poisonous bodies, ergotinic acid, which
is not poisonous when taken into the stomach, sphacetinic acid and
cornutin which act on the nervous system, brain, cord, vagus and
vasomotor centre giving rise to toxic polyneuritis, and (2) favus, an
acute febrile anemia with jaundice and hemoglobinuria probably due to a
bacterial infection or fungus growth of the bean. Infected food may also
produce soluble heatresisting toxins that produce immediate symptoms and
increase the animal’s susceptibility to infection. This is the more
common finding in cases of poisoning with milk and milk products. Non-
pathogenic saprophytes carried in milk produce (1) a poison closely
allied to tyrotoxicon, (2) a toxalbumin which in itself causes serious
disturbances. Botulism, also probably of this group, is a disease
initiated by a toxin elaborated by _Bact. botulinus_ acting on a
protein. There is, however, some evidence that _Bact. botulinus_ can
also establish a real infection.
The toxemias from food infected with bacteria may not occur until the
food is ingested or the bacteria implanted. This result occurs in
infections with _Bact. bovis morbificans_, Gärtner’s bacillus, etc., or
after the feeding of meat from animals infected with _Bact.
paratyphosus_ and _enteritidis_.
The plant poisons are more frequently due to inherent injurious
substances, although even among them, bacterial and fungus diseases play
an important rôle. Among the 16,673 plants indigenous to North America,
almost 500 are more or less poisonous and about 30 are of great economic
importance. The toxic factor may be confined to the leaf, seed or root,
but more often it is associated with all parts of the plant. Through the
efforts of the Department of Agriculture a more or less complete list of
the plants implicated in the poisoning of stock has been compiled. This
list includes the following: _Amanita muscaria_; _A. phalloides_;
_Veratrum viride_; _Phytolacca decandra_; _Agrostemma githago_;
_Delphinium_, 25 varieties; _Astragalus mollissimus_; _Aragallus
lambertii_; _Crotalaria sagittalis_; _Euphorbia lathyris_; _E.
marginata_; _Rhus radicans_; _R. diversiloba_; _R. vernix_; _Aesculus
pavia_; _A. hippocastanum_; _A. glabra_; _A. Californica_; _Cicuta
maculata_; _C. vagans_; _Conium maculatum_; _Kalmia latifolia_; _K.
augustifolia_; _Leucothöe catesbaei_; _Rhododendron maximum_; _Pieris
mariana_; _Datura stramonium_; _Solanum nigrum_; _S. dulcamara_;
_Helenium autumnale_; _Asclepias pumila_; _A. verticullata_; _A.
galoides_; _A. mexicana_; _A. eriocarpa_; _A. speciosa_; _A. fremonti_;
_Eupatorium agertoides_; _E. urticarfolium_; _Isocoma wrightii_;
_Daubentonia longifolia_; _Senecio jacobia burchelli latifolius_.[89]
Some of these as the Amanita are only occasional sources of disaster,
but as they frequently involve man they are important. The _Amanita
muscaria_ symptoms appear very soon after eating the fungus and consist
of a deepening stupor. _A. phalloides_, on the contrary, starts with
severe abdominal pain, cramps, discharges of blood and mucus and later
convulsions. The meat of animals dying from fungus poisoning is
distinctly poisonous. This transfer of poison to the muscles of the
animal partaking of these plants occurs also in poisoning with Kalmia.
The other plants of this list are closely associated with the grass
foods and are consumed usually when the food on a range is scarce. Some
groups as the Asclepias contain a distinct neurotoxin and give rise to a
condition known as trembles or staggers. It affects mostly cows and
sheep, causing staggering, trembling gait, bloating and salivation and
death with convulsions. There is marked congestion of alimentary tract,
liver and kidney. In the cerebrospinal axis there are marked changes in
the nerve cells of the medulla and spinal cord. The Purkinje cells show
the effect of extreme fatigue. Other plants causing stiffness or
weakness of the extremities, show on microscopic examination no definite
lesions in the cerebrospinal axis. Loco weed—_Astragalus mollissimus_
and _Aragallus lambertii_—causes maniacal disturbances but no gross
lesions. This weed in Colorado costs the state enormous amounts of money
yearly.
Helenium poisons domestic animals by means of a toxic glucoside,
dugaldin, which produces stiffness, salivation and nausea with mild
depression (“spewing sickness”). The alimentary tract shows severe
inflammation of the rumen and reticulum which may at times be
hemorrhagic. The liver usually presents an interstitial hepatitis. This
toxin is decidedly hemolytic. The effects of this plant are always
permanent, total recovery being very rare.
The larkspur (25 different varieties), on the contrary, shows prompt
recovery after treatment, but no establishment of toleration. These
plants give rise to nausea, vomiting and great agitation and destroy
many animals yearly. The poisons are included in four alkaloids, all
spinal cord depressants resembling aconite in general character.
These poisonous plants all produce more or less gastrointestinal
inflammation and practically all are destructive in their action on the
liver, pancreas and kidney. It is impossible to form even approximate
estimates of the damage done by them because of the general ignorance of
the subject. The Division of Botany has been collecting for the past few
years specific information concerning these plants, but the individual
plants are not equally poisonous, and all animals do not show the same
susceptibility to the poison. _Veratrum viride_, for instance, is eaten
with relish by sheep and elk and is decidedly toxic for the horse. In
many the toxic factor has not been isolated. Some, as Euphorbia, are
poisonous only when fed in honey derived from its flowers.
The influence of diet on the general health of animals is very far
reaching and very inclusive. Metabolic disturbances are undoubtedly at
times the result of unbalance—deficiencies on the one side, excesses on
the other, at times are probably much more the results of bacterial
invasions aided and abetted by the food administered, at still other
times are poisonous either in their own content or from the degradation
products resulting from digestion or bacterial decomposition.
SECTION XVI
NEOPLASMS
The occurrence of true neoplasms in domesticated animals has always been
well known and thoroughly studied while for beasts in the wild the data
has been fragmentary. That tumors exist in natural environment has been
accepted upon the testimony of hunters but there is an impression, and
nothing more, of their extreme scarcity probably because only younger
vigorous animals come to the attention of the sportsman or collector.
This matter will of course not be settled until some natural historian
with a knowledge of pathology, makes a survey of a large number of
specimens taken during a collecting expedition. Observations in
menageries are valuable to the extent that they show what tumors may
occur, the orders most commonly affected and the incidence under captive
conditions. It is unfortunate that too seldom do we know the history of
our specimens in regard to the age, manner of capture or breeding, data
which if at our disposal would permit of a very fair idea of the
probable incidence in the wild and of the effect of captivity. Some
observations in this direction are however possible by using the figures
of known captivity and breeding.
The facts gleaned from a study of neoplasms under captive conditions may
be of interest to the experimental pathologist, especially when
considering the relation of the origin from the embryological layers. I
have tabulated this with great care, using Jordan’s[90] table for the
source of the various tissues, and further have studied the destination
of metastatic emboli in terms of the blastoderm.
The following observations are based entirely upon our own data for
while it might be valuable to include the cases in the literature their
descriptions are often so meagre that they would not combine readily
with our records. Plimmer, Seligmann, and Murray have published in the
_Proceedings of the London Zoological Society_ since 1903, their annual
report of the pathological service in which they have recorded very many
interesting tumors. So too from time to time Harlow Brooks and W. R.
Blair in the _Annual Report of the New York Zoological Park_, have
presented cases occurring in their service. Joest [91] discusses tumors
in the lower animals in a broad way and analyzes their incidence and
characters. C. Y. White and I [92] have already published articles on
this subject. Numerous single references may be found in the _Jahresber.
der Veterinär-Medicin_.
In so far as the incidence of tumors in wild animals is concerned this
literature can scarcely give an adequate measurement but it would seem
that they are less than in domestic varieties. Exact figures for the
occurrence of tumors in the latter seem not available in the literature,
but one can find that in the Prussian army horses about one hundred are
observed each year. In our 5,365 specimens collected during nineteen
years, 94 tumors in 92 animals have been found, 1.7 per cent. or about
one in every sixty specimens, not at all a low figure. If one were to
include all fibromata of the feet and the blood collections to which the
name angioma might be applied, this incidence would be greater; they are
excluded because few in number and vague in history; only one true
angioma was seen.
The gross and microscopical appearances of tumors in the lower animals
are essentially the same as one encounters in human beings or at least
it is possible to apply the pathological nomenclature used in human
medicine to all the neoplasms we have discovered. There is appended a
list of all the animals and their tumors, a table of zoological orders,
tumors and organs (Table 21) and an analytical table of the histological
data. (Table 22)
TABLE 21.
_Table of Orders and Families Showing Type of Tumor and Principal Organ
of Origin._
═══════════════════╤═══════╤═══════╤═════════╤══════╤══════════╤══════
Order Family │Fibroma│Osteoma│Chondroma│Lipoma│Myoma and │Glioma
│ │ │ │ │Fibromyoma│
│ │ │ │ │ │
───────────────────┼───────┼───────┼─────────┼──────┼──────────┼──────
„ „ │ „ │ „ │ „ │ „ │ „ │ „
│ │ │ │ │ │
───────────────────┼───────┼───────┼─────────┼──────┼──────────┼──────
Primates, │ │ │ │ │ │
Cercopithecidæ │ │ │ │ │ │
Cebidæ │ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
Lemures, Lemuridæ │ │ │ │ │ │
│ │ │ │ │ │
Carnivora, Felidæ │ │ │ 1│ │ │
│ │ │ │ │ │
Viverridæ │ │ │ │ │ │
Canidæ │ │ │ │ │ │
Procyonidæ │ │ │ │ │ │
Ursidæ │ │ │ │ │ │
│ │ │ │ │ │
Phocidæ │ │ │ │ │ │
│ │ │ │ │ │
Rodentia, Sciuridæ │ │ 1│ │ │ │
Muridæ │ │ │ │ │ │
Heteromyidæ │ │ │ │ │ │
│ │ │ │ │ │
Octodontidæ │ │ │ │ │ │
Hystricidæ │ │ │ │ │ │
Dasyproctidæ │ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
Proboscidea │ │ │ │ │ 1│
Ungulata, Equidæ │ 1│ │ │ │ │
Bovidæ │ │ │ │ │ 1│
Cervidæ │ │ │ │ │ │
Camelidæ │ │ │ │ │ │
Suidæ │ │ │ │ │ │
Edentata, │ │ │ │ │ 1│
Dasypodidæ │ │ │ │ │ │
Marsupialia, │ │ │ │ │ │
Didelphyidæ │ │ │ │ │ │
Dasyuridæ │ │ │ │ │ │
Peramelidæ │ │ │ │ │ │
Macropodidæ │ │ │ │ │ │
Passeres, Turdidæ │ │ │ │ │ │
Crateropodidæ│ │ │ │ │ │
Tanagridæ │ │ │ │ 1│ │
Fringillidæ │ │ │ │ 1│ │
Icteridæ │ │ │ │ │ │
Striges, Bubonidæ │ │ │ │ │ │
Psittaci, Loridæ │ │ │ │ │ │
Cacatuidæ │ │ │ │ 2│ │
Psittacidæ │ │ │ │ 3│ │ 1
│ │ │ │ │ │
Accipitres, │ │ │ │ 1│ │
Falconidæ │ │ │ │ │ │
Columbæ, Columbidæ │ │ │ │ │ │
Galli, Phasianidæ │ │ │ │ │ │
Fulicariæ, Rallidæ │ │ │ │ │ │
Anseres, Anatidæ │ 1│ │ │ │ │
Struthiones, Rheidæ│ │ │ │ │ │
───────────────────┼───────┼───────┼─────────┼──────┼──────────┼──────
Total │ 2│ 1│ 1│ 8│ 3│ 1
───────────────────┴───────┴───────┴─────────┴──────┴──────────┴──────
═══════════════════╤═══════╤════════════╤═══════╤═════════╤═══════════
Order Family │Angioma│Endothelioma│Sarcoma│Papilloma│Epithelioma
│ │ │ │ │
│ │ │ │ │
───────────────────┼───────┼────────────┼───────┼─────────┼───────────
„ „ │ „ │ „ │ „ │ „ │ „
│ │ │ │ │
───────────────────┼───────┼────────────┼───────┼─────────┼───────────
Primates, │ │ │ │ │
Cercopithecidæ │ │ │ │ │
Cebidæ │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
Lemures, Lemuridæ │ │ │ │ │
│ │ │ │ │
Carnivora, Felidæ │ 1│ 1│ │ │
│ │ │ │ │
Viverridæ │ │ │ │ │
Canidæ │ │ │ 1│ │
Procyonidæ │ │ │ │ │
Ursidæ │ │ │ │ │ 1
│ │ │ │ │
Phocidæ │ │ │ │ │
│ │ │ │ │
Rodentia, Sciuridæ │ │ │ │ │
Muridæ │ │ │ 2│ │
Heteromyidæ │ │ │ 1│ │
│ │ │ │ │
Octodontidæ │ │ │ 1│ │
Hystricidæ │ │ │ │ │
Dasyproctidæ │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
Proboscidea │ │ │ │ │
Ungulata, Equidæ │ │ │ │ │
Bovidæ │ │ │ 1│ │
Cervidæ │ │ │ │ │
Camelidæ │ │ │ │ │
Suidæ │ │ │ │ │
Edentata, │ │ │ │ │
Dasypodidæ │ │ │ │ │
Marsupialia, │ │ │ │ │
Didelphyidæ │ │ │ │ │
Dasyuridæ │ │ │ │ │ 1
Peramelidæ │ │ │ │ │
Macropodidæ │ │ │ │ │
Passeres, Turdidæ │ │ │ │ │
Crateropodidæ│ │ │ │ │
Tanagridæ │ │ │ │ │
Fringillidæ │ │ │ │ │
Icteridæ │ │ │ │ │
Striges, Bubonidæ │ │ │ │ 1│
Psittaci, Loridæ │ │ │ │ │
Cacatuidæ │ │ │ │ │
Psittacidæ │ │ │ 7│ │ 1
│ │ │ │ │
Accipitres, │ │ │ 1│ │
Falconidæ │ │ │ │ │
Columbæ, Columbidæ │ │ │ 1│ │
Galli, Phasianidæ │ │ │ │ │
Fulicariæ, Rallidæ │ │ 1│ │ │
Anseres, Anatidæ │ │ │ 1│ │
Struthiones, Rheidæ│ │ │ │ │
───────────────────┼───────┼────────────┼───────┼─────────┼───────────
Total │ 1│ 2│ 16│ 1│ 3
───────────────────┴───────┴────────────┴───────┴─────────┴───────────
═══════════════════╤═══════╤═════════╤═══════════╤═════════════╤══════
Order Family │Adenoma│Carcinoma│ Chorion- │Hypernephroma│Mixed
│ │ │epithelioma│ │Tumors
│ │ │ │ │
───────────────────┼───────┼─────────┼───────────┼─────────────┼──────
„ „ │ „ │ „ │ „ │ „ │ „
│ │ │ │ │
───────────────────┼───────┼─────────┼───────────┼─────────────┼──────
Primates, │ 1│ │ │ │
Cercopithecidæ │ │ │ │ │
Cebidæ │ │ │ │ 1│
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
Lemures, Lemuridæ │ 1│ │ │ │
│ │ │ │ │
Carnivora, Felidæ │ 2│ 1│ │ │
│ │ │ │ │
Viverridæ │ │ 2│ │ │
Canidæ │ 3│ 1│ │ │ 1
Procyonidæ │ 1│ │ │ │
Ursidæ │ │ 2│ │ │
│ │ │ │ │
Phocidæ │ │ │ │ 1│
│ │ │ │ │
Rodentia, Sciuridæ │ 1│ │ │ 1│
Muridæ │ │ 3│ │ │
Heteromyidæ │ │ │ │ │
│ │ │ │ │
Octodontidæ │ │ │ │ │
Hystricidæ │ │ │ 1│ │
Dasyproctidæ │ │ 1│ │ │
│ │ │ │ │
│ │ │ │ │
Proboscidea │ │ │ │ │
Ungulata, Equidæ │ │ │ │ │
Bovidæ │ │ │ │ │
Cervidæ │ 1│ │ │ │
Camelidæ │ │ 1│ │ │
Suidæ │ │ 1│ │ │
Edentata, │ │ │ │ │
Dasypodidæ │ │ │ │ │
Marsupialia, │ 1│ 1│ │ │
Didelphyidæ │ │ │ │ │
Dasyuridæ │ │ 1│ │ │
Peramelidæ │ │ 1│ │ │
Macropodidæ │ │ 2│ │ │
Passeres, Turdidæ │ │ │ │ 1│
Crateropodidæ│ 1│ │ │ │
Tanagridæ │ │ │ │ │
Fringillidæ │ │ 2│ │ │
Icteridæ │ │ │ │ 1│
Striges, Bubonidæ │ │ │ │ │
Psittaci, Loridæ │ │ 1│ │ │
Cacatuidæ │ │ │ │ │
Psittacidæ │ 5│ 4│ │ 1│ 1
│ │ │ │ │
Accipitres, │ │ │ │ │
Falconidæ │ │ │ │ │
Columbæ, Columbidæ │ │ │ │ │
Galli, Phasianidæ │ │ 1│ │ │
Fulicariæ, Rallidæ │ │ │ │ │
Anseres, Anatidæ │ 1│ │ │ 1│
Struthiones, Rheidæ│ 1│ │ │ │
───────────────────┼───────┼─────────┼───────────┼─────────────┼──────
Total │ 19│ 25│ 1│ 7│ 2
───────────────────┴───────┴─────────┴───────────┴─────────────┴──────
═══════════════════╤═══════════════════════════════════════════
Order Family │ Organic Source of Tumor
│
│
───────────────────┼────┬──────┬───────┬──────┬──────┬─────────
„ „ │Lung│Muscle│Thyroid│Uterus│Kidney│Bone and
│ │ │ │ │ │Cartilage
───────────────────┼────┼──────┼───────┼──────┼──────┼─────────
Primates, │ │ │ │ │ │
Cercopithecidæ │ │ │ │ │ │
Cebidæ │ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
Lemures, Lemuridæ │ │ │ │ │ │
│ │ │ │ │ │
Carnivora, Felidæ │ │ │ │ 2│ │ 1
│ │ │ │ │ │
Viverridæ │ 1│ │ │ │ │
Canidæ │ │ │ 3│ │ │
Procyonidæ │ │ │ │ │ │
Ursidæ │ │ │ │ │ │
│ │ │ │ │ │
Phocidæ │ │ │ │ │ │
│ │ │ │ │ │
Rodentia, Sciuridæ │ │ │ │ │ 1│ 1
Muridæ │ │ 3│ │ │ │
Heteromyidæ │ │ │ │ │ │
│ │ │ │ │ │
Octodontidæ │ │ │ 1│ │ │
Hystricidæ │ │ │ │ 1│ │
Dasyproctidæ │ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
Proboscidea │ │ │ │ 1│ │
Ungulata, Equidæ │ │ │ │ │ │
Bovidæ │ │ │ │ 1│ │ 1
Cervidæ │ │ │ │ │ │
Camelidæ │ │ │ │ │ │
Suidæ │ │ │ │ 1│ │
Edentata, │ │ │ │ 1│ │
Dasypodidæ │ │ │ │ │ │
Marsupialia, │ │ │ │ │ 1│
Didelphyidæ │ │ │ │ │ │
Dasyuridæ │ │ │ │ │ │
Peramelidæ │ 1│ │ │ │ │
Macropodidæ │ 1│ │ │ │ │
Passeres, Turdidæ │ │ │ │ │ 1│
Crateropodidæ│ │ │ │ │ 1│
Tanagridæ │ │ │ │ │ │
Fringillidæ │ │ │ │ │ 2│
Icteridæ │ │ │ │ │ 1│
Striges, Bubonidæ │ │ │ │ │ │
Psittaci, Loridæ │ 1│ │ │ │ │
Cacatuidæ │ │ │ │ │ │
Psittacidæ │ │ 2│ 1│ 1│ 5│
│ │ │ │ │ │
Accipitres, │ │ │ │ │ │
Falconidæ │ │ │ │ │ │
Columbæ, Columbidæ │ │ │ │ │ 1│
Galli, Phasianidæ │ │ │ │ │ │
Fulicariæ, Rallidæ │ │ │ │ │ │ 1
Anseres, Anatidæ │ │ 1│ │ │ 1│ 1
Struthiones, Rheidæ│ │ │ │ │ │
───────────────────┼────┼──────┼───────┼──────┼──────┼─────────
Total │ 4│ 6│ 5│ 8│ 14│ 5
───────────────────┴────┴──────┴───────┴──────┴──────┴─────────
═══════════════════╤═══════════════════════════════════════════════
Order Family │ Organic Source of Tumor
│
│
───────────────────┼────────────────┬──────┬──────────┬──────┬─────
„ „ │Gastrointestinal│Liver,│Peritoneum│Lymph │Mamma
│ Tract │ &c. │ │Tissue│
───────────────────┼────────────────┼──────┼──────────┼──────┼─────
Primates, │ 1│ │ │ │
Cercopithecidæ │ │ │ │ │
Cebidæ │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
│ │ │ │ │
Lemures, Lemuridæ │ │ │ │ │
│ │ │ │ │
Carnivora, Felidæ │ │ 1│ │ 1│
│ │ │ │ │
Viverridæ │ 1│ │ │ │
Canidæ │ │ 2│ │ │
Procyonidæ │ │ │ │ │
Ursidæ │ │ │ │ │ 1
│ │ │ │ │
Phocidæ │ │ │ │ │
│ │ │ │ │
Rodentia, Sciuridæ │ │ 1│ │ │
Muridæ │ │ │ │ │ 2
Heteromyidæ │ │ │ │ │
│ │ │ │ │
Octodontidæ │ │ │ │ │
Hystricidæ │ │ │ │ │
Dasyproctidæ │ │ │ │ │
│ │ │ │ │
│ │ │ │ │
Proboscidea │ │ │ │ │
Ungulata, Equidæ │ │ │ 1│ │
Bovidæ │ │ │ │ 1│
Cervidæ │ │ 1│ │ │
Camelidæ │ │ 1│ │ │
Suidæ │ │ │ │ │
Edentata, │ │ │ │ │
Dasypodidæ │ │ │ │ │
Marsupialia, │ │ │ │ │ 1
Didelphyidæ │ │ │ │ │
Dasyuridæ │ 1│ │ │ │
Peramelidæ │ │ │ │ │
Macropodidæ │ 1│ │ │ │
Passeres, Turdidæ │ │ │ │ │
Crateropodidæ│ │ │ │ │
Tanagridæ │ │ │ │ │
Fringillidæ │ │ │ │ │
Icteridæ │ │ │ │ │
Striges, Bubonidæ │ 1│ │ │ │
Psittaci, Loridæ │ │ │ │ │
Cacatuidæ │ │ │ │ │
Psittacidæ │ 1│ 3│ │ │
│ │ │ │ │
Accipitres, │ │ │ 1│ │
Falconidæ │ │ │ │ │
Columbæ, Columbidæ │ │ │ │ │
Galli, Phasianidæ │ │ │ │ │
Fulicariæ, Rallidæ │ │ │ │ │
Anseres, Anatidæ │ │ │ │ │
Struthiones, Rheidæ│ 1│ │ │ │
───────────────────┼────────────────┼──────┼──────────┼──────┼─────
Total │ 6│ 9│ 2│ 2│ 4
───────────────────┴────────────────┴──────┴──────────┴──────┴─────
═══════════════════╤══════════════════════════════════════════╤════════════
Order Family │ │Notes Extra
│ │ cases not
│ │ tabulated.
───────────────────┼─────┬────────┬────┬──────┬───────┬───────┼────────────
„ „ │Ovary│Pancreas│Skin│Testes│Adrenal│Unknown│ „
│ │ │ │ │ │ │
───────────────────┼─────┼────────┼────┼──────┼───────┼───────┼────────────
Primates, │ │ │ │ │ │ │
Cercopithecidæ │ │ │ │ │ │ │
Cebidæ │ │ │ │ │ 1│ │Adenoma of
│ │ │ │ │ │ │ prostrate
│ │ │ │ │ │ │suggesting
│ │ │ │ │ │ │ cancer in
│ │ │ │ │ │ │ places.
Lemures, Lemuridæ │ │ │ │ │ │ │
│ │ │ │ │ │ │
Carnivora, Felidæ │ │ │ │ │ │ │Endothelioma
│ │ │ │ │ │ │ of pleura.
Viverridæ │ │ 1│ │ │ │ │
Canidæ │ │ 1│ │ │ │ │
Procyonidæ │ │ 1│ │ │ │ │
Ursidæ │ │ │ │ │ 1│ │Epithelioma
│ │ │ │ │ │ │ of tongue.
Phocidæ │ │ │ │ │ 1│ │
│ │ │ │ │ │ │
Rodentia, Sciuridæ │ │ │ │ │ │ │
Muridæ │ │ │ │ │ │ │
Heteromyidæ │ │ │ │ │ │ │Sarcoma of
│ │ │ │ │ │ │ bladder.
Octodontidæ │ │ │ │ │ │ │
Hystricidæ │ │ │ │ │ │ │
Dasyproctidæ │ │ │ │ │ │ │Squamous
│ │ │ │ │ │ │ carcinoma
│ │ │ │ │ │ │ of larynx.
Proboscidea │ │ │ │ │ │ │
Ungulata, Equidæ │ │ │ │ │ │ │
Bovidæ │ │ │ │ │ │ │
Cervidæ │ │ │ │ │ │ │
Camelidæ │ │ │ │ │ │ │
Suidæ │ │ │ │ │ │ │
Edentata, │ │ │ │ │ │ │
Dasypodidæ │ │ │ │ │ │ │
Marsupialia, │ │ │ │ │ │ │
Didelphyidæ │ │ │ │ │ │ │
Dasyuridæ │ │ │ 1│ │ │ │
Peramelidæ │ │ │ │ │ │ │
Macropodidæ │ │ │ │ │ │ │
Passeres, Turdidæ │ │ │ │ │ │ │
Crateropodidæ│ │ │ │ │ │ │
Tanagridæ │ │ │ │ │ │ 1│
Fringillidæ │ │ │ │ │ │ 1│
Icteridæ │ │ │ │ │ │ │
Striges, Bubonidæ │ │ │ │ │ │ │
Psittaci, Loridæ │ │ │ │ │ │ │
Cacatuidæ │ │ │ │ │ │ 2│
Psittacidæ │ 1│ │ │ 2│ 1│ 5│Glioma of
│ │ │ │ │ │ │ brain.
Accipitres, │ │ │ │ │ │ 1│
Falconidæ │ │ │ │ │ │ │
Columbæ, Columbidæ │ │ │ │ │ │ │
Galli, Phasianidæ │ 1│ │ │ │ │ │
Fulicariæ, Rallidæ │ │ │ │ │ │ │
Anseres, Anatidæ │ │ │ │ │ 1│ │
Struthiones, Rheidæ│ │ │ │ │ │ │
───────────────────┼─────┼────────┼────┼──────┼───────┼───────┼────────────
Total │ 2│ 3│ 1│ 2│ 5│ 10│
───────────────────┴─────┴────────┴────┴──────┴───────┴───────┴────────────
TABLE 22.
_Analytical Table Showing Data of Incidence, Sex, Breeding, Duration of
Captivity, Metastases and Embryological Origins and Distributions
According to Order._
════════════╤═══════╤═════╤════════╤═══════════════╤══════════╤═══════
Order │ Total │ Per │ Sex │ Breeding │ Range │Average
│animals│cent.│ │ │ known │ for
│ │ per │ │ │captivity │ tumor
│ │order│ │ │ │animals
────────────┼───────┼─────┼──┬──┬──┼────┬───────┬──┼──────────┼───────
„ │ „ │ „ │♂ │♀ │? │Wild│Captive│? │ „ │ „
────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼───────
Primates │ 2│ .4│ 2│ │ │ 2│ │ │3–4 yrs. │3½ yrs.
Lemures │ 1│ 1.1│ 1│ │ │ 1│ │ │4 yrs. │
Carnivora │ 17│ 3.5│ 8│ 9│ │ 14│ 3│ │1–18 yrs. │9 yrs.
Rodentia │ 12│ 6.│ 7│ 4│ 1│ 8│ 2│ 2│1 mo.–7 │2 yrs.
│ │ │ │ │ │ │ │ │yrs. │8 mo.
Insectivora │ 0│ │ │ │ │ │ │ │ │
Chiroptera │ 0│ │ │ │ │ │ │ │ │
Proboscidea │ 1│_33._│ │ 1│ │ 1│ │ │38 yrs. │
Hyracoidea │ 0│ │ │ │ │ │ │ │ │
Ungulata │ 7│ 1.9│ 2│ 5│ │ 5│ 1│ 1│2–16 yrs. │9 yrs.
Edentata │ 1│_6.2_│ │ 1│ │ 1│ │ │10 yrs. │
Marsupialia │ 7│ 4.│ 6│ 1│ │ 6│ 1│ │1 wk.–12 │5 yrs.
│ │ │ │ │ │ │ │ │yrs. │6 mo.
Monotremata │ 0│ │ │ │ │ │ │ │ │
────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼───────
Totals │ 48│ 2.58│26│21│ 1│ 38│ 7│ 3│ │
│ │ │ │ │ │ │ │ │ │
Passeres │ 7│ .51│ 4│ 2│ 1│ 6│ │ 1│1–14 yrs. │6 yrs.
Picariæ │ 0│ │ │ │ │ │ │ │ │
Striges │ 1│ .75│ │ 1│ │ 1│ │ │7 yrs. │
Psittaci │ 26│ 3.7│ 9│ 8│ 9│ 8?│ 16?│2?│5 mo.–9 │3 yrs.
│ │ │ │ │ │ │ │ │yrs. │
Accipitres │ 2│ 1.│ 2│ │ │ 2│ │ │(1)[93]–4 │
│ │ │ │ │ │ │ │ │yrs. │
Columbæ │ 1│ .63│ │ 1│ │ 1│ │ │4 yrs. │
Galli │ 1│ .33│ │ 1│ │ 1│ │ │? │
Hemipodii │ 0│ │ │ │ │ │ │ │ │
Fulicariæ │ 1│_2.8_│ 1│ │ │ 1│ │ │6 yrs. │
Alectorides │ 0│ │ │ │ │ │ │ │ │
Limicolæ │ 0│ │ │ │ │ │ │ │ │
Gaviæ │ 0│ │ │ │ │ │ │ │ │
Impennes │ 0│ │ │ │ │ │ │ │ │
Steganopodes│ 0│ │ │ │ │ │ │ │ │
Herodiones │ 0│ │ │ │ │ │ │ │ │
Odontoglossæ│ 0│ │ │ │ │ │ │ │ │
Palamedes │ 0│ │ │ │ │ │ │ │ │
Anseres │ 4│ 1.2│ │ 3│ 1│ 3?│ 1│ │(1)[93]-10│
│ │ │ │ │ │ │ │ │yrs. │
│ │ │ │ │ │ │ │ │(1)[93]-4 │
│ │ │ │ │ │ │ │ │yrs. │
Struthiones │ 1│_3.1_│ 1│ │ │ 1│ │ │(1)[93]-5 │
│ │ │ │ │ │ │ │ │yrs. │
Crypturi │ 0│ │ │ │ │ │ │ │ │
────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼───────
Totals │ 44│ 1.23│17│16│11│ 24│ 17│ 3│ │
────────────┼───────┼─────┼──┼──┼──┼────┼───────┼──┼──────────┼───────
Grand Totals│ 92│ 1.7│43│37│12│ 62│ 24│ 6│ │
────────────┴───────┴─────┴──┴──┴──┴────┴───────┴──┴──────────┴───────
════════════╤══════════════╤════════════════════════════════════
Order │Embryological │ Metastases
│ layer │
│ │
│ │
────────────┼────┬────┬────┼────┬─────┬──────┬───────────┬──────
„ │Ecto│Meso│Ento│Lung│Liver│Kidney│Lymphocytes│Spleen
────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼──────
Primates │ │ 1│ 1│ │ │ │ │
Lemures │ │ │ 1│ │ │ │ │
Carnivora │ 2│ 8│ 7│ 5│ 1│ │ 1│
Rodentia │ 2│ 7│ 3│ │ │ │ │
│ │ │ │ │ │ │ │
Insectivora │ │ │ │ │ │ │ │
Chiroptera │ │ │ │ │ │ │ │
Proboscidea │ │ 1│ │ │ │ │ │
Hyracoidea │ │ │ │ │ │ │ │
Ungulata │ │ 5│ 2│ │ 1│ 1│ 1│
Edentata │ │ 1│ │ │ │ │ │
Marsupialia │ 2│ 2│ 3│ 1│ 2│ 1│ 1│ 2
│ │ │ │ │ │ │ │
Monotremata │ │ │ │ │ │ │ │
────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼──────
Totals │ 6│ 25│ 17│ 6│ 4│ 2│ 3│ 2
│ │ │ │ │ │ │ │
Passeres │ │ 7│ │ 1│ 1│ │ │
Picariæ │ │ │ │ │ │ │ │
Striges │ │ │ 1│ │ │ │ │
Psittaci │ 1│ 17│ 8│ │ 2│ │ │ 1
│ │ │ │ │ │ │ │
Accipitres │ │ 2│ │ │ │ │ │
│ │ │ │ │ │ │ │
Columbæ │ │ 1│ │ │ │ │ │
Galli │ │ 1│ │ │ │ │ │
Hemipodii │ │ │ │ │ │ │ │
Fulicariæ │ │ 1│ │ │ │ │ │
Alectorides │ │ │ │ │ │ │ │
Limicolæ │ │ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │ │ │
Impennes │ │ │ │ │ │ │ │
Steganopodes│ │ │ │ │ │ │ │
Herodiones │ │ │ │ │ │ │ │
Odontoglossæ│ │ │ │ │ │ │ │
Palamedes │ │ │ │ │ │ │ │
Anseres │ │ 4│ │ │ │ │ │
│ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
│ │ │ │ │ │ │ │
Struthiones │ │ │ 1│ │ │ │ │
│ │ │ │ │ │ │ │
Crypturi │ │ │ │ │ │ │ │
────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼──────
Totals │ 1│ 33│ 10│ 1│ 3│ │ │ 1
────────────┼────┼────┼────┼────┼─────┼──────┼───────────┼──────
Grand Totals│ 7│ 58│ 27│ 7│ 7│ 2│ 3│ 3
────────────┴────┴────┴────┴────┴─────┴──────┴───────────┴──────
════════════╤═════════════════════╤══════════════
Order │ Metastases │Embryological
│ │ layer of
│ │ metastases
│ │
────────────┼─────────┬────┬──────┼────┬────┬────
„ │Intestine│Bone│Muscle│Ecto│Meso│Ento
────────────┼─────────┼────┼──────┼────┼────┼────
Primates │ │ │ │ │ │
Lemures │ │ │ │ │ │
Carnivora │ │ │ 1│ │ 5│ 5
Rodentia │ │ │ │ │ │
│ │ │ │ │ │
Insectivora │ │ │ │ │ │
Chiroptera │ │ │ │ │ │
Proboscidea │ │ │ │ │ │
Hyracoidea │ │ │ │ │ │
Ungulata │ │ │ │ │ 1│ 1
Edentata │ │ │ │ │ │
Marsupialia │ │ 1│ │ │ 2│ 3
│ │ │ │ │ │
Monotremata │ │ │ │ │ │
────────────┼─────────┼────┼──────┼────┼────┼────
Totals │ │ 1│ 1│ │ 8│ 9
│ │ │ │ │ │
Passeres │ 1│ │ │ │ 1│ 2
Picariæ │ │ │ │ │ │
Striges │ │ │ │ │ │
Psittaci │ 1│ │ │ │ 1│ 3
│ │ │ │ │ │
Accipitres │ │ │ │ │ │
│ │ │ │ │ │
Columbæ │ │ 1│ │ │ 1│
Galli │ │ │ │ │ │
Hemipodii │ │ │ │ │ │
Fulicariæ │ │ │ │ │ │
Alectorides │ │ │ │ │ │
Limicolæ │ │ │ │ │ │
Gaviæ │ │ │ │ │ │
Impennes │ │ │ │ │ │
Steganopodes│ │ │ │ │ │
Herodiones │ │ │ │ │ │
Odontoglossæ│ │ │ │ │ │
Palamedes │ │ │ │ │ │
Anseres │ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
│ │ │ │ │ │
Struthiones │ │ │ │ │ │
│ │ │ │ │ │
Crypturi │ │ │ │ │ │
────────────┼─────────┼────┼──────┼────┼────┼────
Totals │ 2│ 1│ │ │ 3│ 5
────────────┼─────────┼────┼──────┼────┼────┼────
Grand Totals│ 2│ 2│ 1│ │ 11│ 14
────────────┴─────────┴────┴──────┴────┴────┴────
For meaning of italics see foot note Table 1.
INCIDENCE OF TUMORS.
Examination of the table, (21) from the standpoint of differential
percentage reveals that mammals have 48 tumors giving an incidence of
2.58 per cent. whereas birds have 44 new growths equivalent to 1.23 per
cent. Were it not for the high figures for one single variety of bird
(Undulated Grass Parrakeet) this value for Aves would be still lower. At
all events our figures would indicate that the mammal is at least twice
as productive of neoplasms as is the bird. In our material the latter
class has had a better chance than Mammalia to show its susceptibility
since there have been nearly twice as many autopsies.
Within the classes the comparative figures have less value because of
the smaller and varying numbers. Such high percentages as are shown by
the elephants and armadillos cannot be taken as indicators for their
orders since too few specimens were examined. Judging by orders with
more than one hundred autopsies the rodents stand at the head of the
list followed by the marsupials and carnivores. It is interesting that
the animal nearest to man, the monkey, and with greatest number of
autopsies in its zoological class, has the lowest tumor incidence.
Psittaci lead the avian orders, followed by the Fulicariæ, but as there
are but thirty-five autopsies upon these, the second place rightly
belongs to the Anseres. All the principal orders are represented but the
only one of importance is the leader. The Psittaci are very prone to
have tumors in the renal area, sometimes of the kidney, at others of the
adrenal and occasionally of the sex glands. Some remarks have already
been given to this matter in the sections devoted to the kidney and
genitalia but it will be discussed again under tumor morphology.
Among these ninety-two animals, one bore multiple tumors, a Jaguar
(_Felis onca_) with adenomata of the liver and uterus and angiomata of
the mesentery. Careful study failed to reveal any parasitism as the
cause of the growths and since the first two were of slightly varying
structure it is not believed that one is a metastasis from the other.
The sex incidence stands in direct relation to the proportion of total
males and females posted or in other words it is the same for the two.
The figures might be somewhat affected were the gender of all the
parrakeets available but the tumors growing in the upper renal area
frequently destroy the sex gland.
Definite statements concerning the importance of breeding in the
causation of neoplasms cannot be made since we cannot quote figures for
the percentages of wild- and captive-born of our entire autopsy list.
The data are confused by scanty information concerning the twenty-six
parrots, the history of which is vague and I am perhaps too severe in
accrediting the birth of sixteen of them to captivity. This was done
because of a lack of exact information concerning these specimens and,
because their variety is known to breed when captive by the residents of
their habitat[94], the distribution into wild- and captive-born is based
upon what information we have. If the order Psittaci be subtracted
entirely, it leaves a total of 62 tumor-bearing animals of known
breeding, 49 of which were born in the wild, thirteen in captivity, a
fact which strengthens the thought that unnatural breeding increases the
chance of neoplasms.
The known length of captivity has also a direct bearing on this point.
The figures given in the columns “known captivity” and “average for
tumor bearers” were compared with figures obtained by averaging the
lives of fifty others (when possible) of the same order or of at least
three times as many as bore tumors. Animals dying from injury were
excluded. With one exception the average for “tumor bearers” exceeded
that for “non-tumor bearers”; the exception, the Ungulata, had the same
average for both groups. It seems then that tumors occur in animals in
captivity longer than the average for their order, or in specimens that
have the power to live under confined conditions until neoplasms
develop. In this respect I recall the statements made by Harlow
Brooks[95] that tumors will probably be found more commonly in animals
when they live in a manner comparable to that of urban man and that
racial degeneracy will favor their development. There is adduced here
perhaps the first definite evidence that long captivity allows tumor
tendency to express itself but it does not prove that confinement
increases tumors. Nor does the expectation of life, average or
potential, stand in any direct and definite relationship to the
frequency of neoplasms. The only clear case of long life and high tumor
incidence is to be found in Parrots; we feel however that some unknown
factor increases tumors of the renal-adrenal region in these birds and
that unqualified statements about age and tumor growth are not
permissible. Since tumors grow in many wild-born specimens, a high
percentage of which become known in the first few years of captivity, is
it not highly probable that tumors are reasonably common in the wild and
that we do not observe enough purely natural specimens to assume an
immunity on the part of free living beasts.
One of the undesirable features of captive breeding is consanguinity of
parents and there is good reason to believe that tumor susceptibility
can be bred into or out of a line of animals by mating tumor bearers and
non-tumor bearers, the tendency following the rules of Mendelian
inheritance (Slye). Is there any proof that inbreeding does not occur in
the wild and if it do, it is perfectly possible that tumor tendency may
be transmitted as a dominant character; the effect of artificial or
intentional inbreeding in captivity would only offer an opportunity for
a summation of these influences.
If injury and animal parasitism have any importance in neoplasmata then
this opportunity certainly occurs under natural conditions. Fibiger
observed gastric tumors in rats arising under the influence of nematodes
while Slye and Wells report facial neoplasms in mice apparently arising
at points of old injuries. It seems to me that we have no right to
assume an immunity of wild animals, in their native environment, to
tumors; the incidence is another matter but it may be considerable.
It was thought possible that there might be some light shed upon the
matter by an analysis of our sarcomatous and epitheliomatous tumors in
wild- and captive-born animals. In our second paper[96] upon this
subject I ventured the statement that sarcomatous growths occurred more
frequently in captive-born, epitheliomatous in wild-born specimens.
Greater data have not borne out this conclusion and information was
sought as to the embryonal derivation of tumor-bearing tissue. Analyzing
the cases in which all the factors could be obtained, it seems that
among seven tumors of captive-bred animals, five came from the entoderm,
two from the mesoderm, whereas in wild-bred animals, of the fifty-seven
tumors, five came from the ectoderm, thirty-two from the mesoderm and
fourteen from the entoderm. These figures do not include the parrots.
The sex values have no significance.
It is interesting and noteworthy, that, as in the human being, the
majority of the tumors came from tissues arising in the mesoderm and
that the entodermic derivatives received the largest number of
metastases; no ectodermic tissues were sites of secondary tumors. The
visceral seats of metastases are probably of little value for comparison
in so small a number; the lung and liver however occupy the prominent
places.
Interesting as the foregoing facts may be, they do not shed light upon
the question of breeding and degeneracy in the causation of neoplasms.
Attention is arrested however by the paucity of tumors in derivatives of
the ectoderm since in man new growths are common in the breast, at the
rectal and labial mucocutaneous junctions and on the skin. The immunity
of the ectodermic tissues to secondary growths is very distinct; this
holds true in man.
SPECIAL TUMORS.
The diagnosis of fibroma offers the same difficulty in the zoological
material as it does in man and even more care must be exercised for
solid tumors in certain localities. The bird often presents hard nodular
masses on the palmar and lateral aspects of the feet, sometimes
surmounted by callosities, to which the term fibroma or fibromatous
corns might be applied. Section of some of these will reveal areas of
granulation tissue about points of inflammation so that we have
considered them as infectious or the result of incorrect perches and
excluded them from the tumors. True fibromata have been encountered
thrice but in combination with muscle tissue as a fibromyoma thrice in
addition. The “fibroids” seen in the elephants and armadillo have
already been described.
The nodular growth sometimes accompanying degenerative disease of the
osseous system followed by attempts at repair as discussed under
osteitis deformans, leontiasis ossium and actinomycosis, are often
productive of masses to which it is easy to apply the term osteoma. If
one demand that an osteoma shall be a distinct neoplastic, localized
bony growth of unnatural or greatly exaggerated structure, then the
tumor is quite rare. We have seen one growing from the vertebræ and
clavicle of a gerbille and a fibro-osteoma on one jaw of an Isabelline
gazelle. The chondromata have been limited to one case, a unilateral
mass growing from the nasal cartilage of a caracal.
Lipomata are localized collections of fat consisting of cells with
greater fat capacity than normally, sometimes surrounded by an
indefinite capsule. Judging by the observations of Joest and Johne they
are reasonably common in horses and cows. We have not seen a single case
in mammals but eight cases appeared in the birds. These were with one
exception disposed under the skin mostly over the abdomen and chest and
once under the scalp. In a hawk the tumor grew as a pelvic mass
surrounding the cloaca and apparently caused decided obstruction to the
lumen. The lipomata of the Psittaci usually grow as pendulous masses on
the abdominal wall covered by thin, featherless, delicate skin, often
showing dilated veins. Upon section they are rather rich in blood
supply, “angiolipoma,” but fail to show any angiomatous or solid
cellular areas under the microscope. The frequency of the growths in one
variety (Roseate cockatoo—_Cacatua roseicapilla_) led to an attempt to
transplant the tumor. The plant seemed to thrive in the recipient for a
while but soon disappeared. Breeding experiments on the tumor bearers
are now under way.
Angiomata of lymph channels were observed in the omentum and mesentery
of a jaguar (_Felis onca_); this is the animal with three apparently
separate and distinct tumors. “The omentum is normally fatty and
slightly congested. In its meshes are myriads of tiny cysts containing
gray fluid. The main peritoneal area is negative but in the pelvic
region on anterior rectal wall, in the superior edge of the broad
ligament and in Douglas’ pouch, are cysts from a few millimetres to
several centimetres, with clear contents. The microscopic section of
omentum shows the multiple cysts as cavities of varying size, from that
of an arteriole to the diameter of a two-third lens field. They are
lined with flat, closely placed pavement cells with well stained but
vesicular nucleus. The septa are adult connective tissue. No contents or
granular eosin-staining material. No swollen cells like in adenomata. No
parasites seen.”
Two endotheliomata have been found, one of the flat variety with warty
excrescences common on serous surfaces, located in the pleura of a
leopard (_Felis nebulosa_), and one of the nodular variety, growing from
the clavicle of a Moorhen (_Gallinula chloropus_).
The sarcomata present their usual morphology grossly and minutely and
with the exception of the cases arising from the pectoral muscle and
from the genital area offer little of interest. Two instances in the
former location, observed in parrakeets, presented several puzzling
features. The component cells were spindle in shape, similar to a muscle
cell but were fitted with the round or elliptical nuclei of embryonal
cells. In a few places they were exceedingly large and had shadowy
outlines like a syncytium or they would be so arranged as to suggest a
glandular structure. The dominant type of cell was, however, everywhere
the spindle as it is seen in sarcoma. The sarcomata when they occur in
the genital area usually assume the alveolar arrangement and are of the
round or mixed cell variety. Only three of the sixteen sarcomata gave
metastases.
Papillomata of minor character appear occasionally on the skin of
animals as warts, but only one instance of any greater importance has
been found. The duodenal mucosa of an owl (_Bubo virginianus_) presented
a soft growth which partly obstructed the intestinal lumen. Papillary
adenomata, on the other hand, have been observed several times, but
since they have more importance as irregular hyperplasias of glandular
origin have been included in the next group. An interesting case was
seen in a baboon (_Papio hamadryas_) in which a large part of the
gastric wall was the seat of adenomata, presenting in addition several
distinct papillary outgrowths. A similar picture was found in the
duodenum of the rhea (_Rhea americana_).
The greatest interest in the adenomata centres around these growths in
the renal area in parrakeets, and as they have much in common with all
the glandular tumors of this region, a general discussion of this
subject may be introduced here. We have observed seven tumors
constructed on a glandular basis of renal or adrenal character. Grossly
these tumors develop as irregular masses usually of distinct brown
color, constructed on a lobular plan, delicate barely visible septa
dividing the growth. They seem devoid of large vessels, a gross
observation confirmed microscopically. There is no criterion to the
naked eye, which will distinguish the variety of epithelial hyperplasia
or permit separation of these neoplasms from some sarcomata; the latter
are usually gray but need not be so. Minutely studied, three of these
tumors proved to be adenomata, all papillary, one cystic as well. Three
had to be denominated carcinoma because of their distinct separate
crowded nests and incomplete acini. The cells comprising these growths
are comparable to the lining elements of the collecting tubules of the
renal lobule in that they have relatively large nuclei and a tendency to
basic staining protoplasm. The adenomatous picture is, however, more
comparable to the cortex than to the medulla. The remaining tumor was a
hypernephroma of the usual large cell, acinus-forming type and seemed to
originate in the adrenal. None of these tumors in the parrakeets sent
out metastases. Other hypernephromata have been diagnosed, to the number
of six. Upon review of their descriptions and sections, the
determinations are to be confirmed. However, it must be recorded here
that none of the three in mammals gave metastases, while two of the
three in birds did so. They are all of the usual type with large
vacuolated cells in glandular groups or strands.
Three rather interesting examples of epithelioma have been observed. The
first and most important was a basocellular growth of the tongue in a
black bear (_Ursus americanus_). The local damage—ulceration and
infiltration—and swelling sufficient to interfere with deglutition, were
quite considerable. The basal cell nests had penetrated deeply into the
muscle, but extension had taken place only to a single submaxillary
gland. A squamous epithelioma was found on the skin of the thigh of a
Tasmanian devil (_Sarcophilus ursinus_). The construction was somewhat
unusual in that it was cystic but lined with squamous and keratinized
plates. It could not be decided that it originated from glands like a
trichoepithelioma; it was not like a basal cell cancer. No metastases
had occurred. The third case was that of a tumor within the abdomen of
an Amazon (_Chrysotis leucocephala_). It consisted of an illy defined
basement membrane upon which were irregular stratified squamous
epithelial cells. Upon the surface were wavy bands of horny material,
very much like dried and cast-off epithelial scales, except more compact
and extensive. These latter seemed to form the bulk of the mass. Beneath
the membrane a few irregular accumulations of cells bearing a similarity
to those on the surface could be found, but they were probably large
plasma cells. The epithelial layer dipped down like in epithelioma. No
pearls or separate nests were found. While this mass was not localized,
it was doubtless an epithelioma, and should be included in this series.
Its possible origin in the small intestine has been considered.
The question of the occurrence of tumors in wild animals seems fairly
well settled when twenty-five examples of malignant epithelial neoplasms
can be discovered in fifty-three hundred autopsies. It is interesting to
note the incidence of these tumors in wild- and park-bred animals.
Exclusive of the parrakeets there are twenty-one cancers, seventeen in
known wild-bred, two in known park-bred specimens, and two with breeding
uncertain. The average known duration of captivity of the wild-bred
animals is about four years, while the two park-bred animals lived eight
and eighteen years. Thirteen of the twenty-one cases were males, eight
females. Adenocarcinoma was discovered twelve times, simplex nine times,
medullary and squamous each twice. Three tumors of the pancreas and
mammary gland were seen in which fibrotic or scirrhus areas were found,
but in no case was there detected that hard cicatrizing cancer so
commonly found in the human breast. All the interesting cases of
carcinoma have been recorded in the discussion of organs from which they
took origin. The only case of chorionepithelioma has been reported in
detail on page 308. The two cases of mixed tumors are as follows: Mixed
tumor of the thyroid and adenocarcinoma sarcomatodes in the liver; they
have been discussed in detail on pages 334 and 242 respectively.
[Illustration:
FIG. 49.—BASAL CELL CARCINOMA OF TONGUE. BLACK BEAR (URSUS
AMERICANUS). NOTE ULCERATION WHERE PIECE HAS BEEN EXCISED, AND ALSO
NODULAR THICKENING OF WHOLE BASE OF TONGUE.
]
[Illustration:
FIG. 50.—MICROSCOPICAL APPEARANCE OF TUMOR IN FIG. 49.
]
Analysis of the incidence of tumors according to organs is disturbed by
the large number of cases in Psittaci. Including this order the first
place is taken by the kidney, followed by the liver, uterus, muscle,
gastrointestinal tract, bone and cartilage, thyroid, adrenal and lung in
this order. Curiously enough, if these birds be subtracted the degree of
organ susceptibility to new growths is not greatly altered. The lead is
still held by the kidney, the uterus occupying the second place and then
in sequence the liver, gastrointestinal tract, muscle, thyroid and
adrenal. Examination of the figures for mammals shows the uterus to lead
in numbers, followed by the liver, thyroid, and mammary gland. For the
birds the kidney takes the undisputed head of the column with a total of
twelve tumors (27 per cent. of all avian tumors); the next figures are
shown by the liver, gastrointestinal tract and muscle.
ZOOLOGICAL AND PATHOLOGICAL LIST OF TUMORS
MAMMALIA
PRIMATES (2)
Cercopithecidæ—Hamadryas Baboon (_Papio hamadryas_)
Papillary adenoma of gastric mucosa
Cebidæ—Brown Cebus (_Cebus fatuellus_)
Hypernephroma of right adrenal
LEMURES (1)
Lemuridæ—Ring tailed Lemur (_Lemur catta_)
Papillary adenoma of prostate
CARNIVORA (17)
Felidæ—Clouded Leopard (_Felis nebulosa_)
Endothelioma of pleura
Caracal (_Felis caracal_)
Osteochondroma of nose
Lion (_Felis leo_)
Malignant adenoma of cervix uteri
Metastases to lung
Jaguar (_Felis onca_)
Fibroadenoma of uterus
Fibroadenoma of bile ducts
Lymphangioma of mesentery
Viverridæ—Indian Paradoxure (_Paradoxurus niger_)
Adenocarcinoma of pancreas
Malayan Civet (_Viverra tangalunga_)
Carcinoma of lung
Canidæ—Corsac Fox (_Canis corsac_)
Adenoma of pancreatic ducts
Red Fox (_Canis vulpes pennsylvanicus_)
Cystic adenoma of bile ducts
Raccoon-like Dog (_Canis procyonoides_)
Adenocarcinoma sarcomatodes of thyroid
Gray Fox (_Canis cinereo argenteus_)
Papillary cyst adenoma of bile ducts
Prairie Wolf (_Canis latrans_)
Sarcoma of thyroid region
Metastases to lungs
Prairie Wolf (_Canis latrans_)
Sarcoma of thyroid region
Procyonidæ—Common Raccoon (_Procyon lotor_)
Adenoma of pancreas
Ursidæ—Polar Bear (_Ursus maritimus_)
Adenocarcinoma of adrenals
Metastases to lungs, lymph nodes, diaphragm
Black Bear (_Ursus americanus_)
Medullary carcinoma of breast
Metastases to lungs
Black Bear (_Ursus americanus_)
Epithelioma of tongue
Phocidæ—California Hair Seal (_Zalophus californianus_)
Hypernephroma of adrenal
RODENTIA (12)
Sciuridæ—Beechy’s Spermophile (_Citellus grammurus beecheyi_)
Osteoma of sternum
Gray Squirrel (_Sciurus carolinensis pennsylvanicus_)
Hypernephroma of kidney
Woodchuck (_Arctomys monax_)
Adenoma simplex of liver
Muridæ—Waltzing Mouse (_Mus wagneri rotans_)
Adenocarcinoma of thigh muscles
White footed Mouse (_Peromyscus leucopus_)
Carcinoma simplex of mammary gland
White footed Mouse (_Peromyscus leucopus_)
Spindle celled sarcoma of leg
White footed Mouse (_Peromyscus leucopus_)
Carcinoma of mammary gland
Larger Egyptian Gerbille (_Gerbillus pyramidum_)
Fibrosarcoma of shoulder region
Heteromyidæ—Kangaroo Rat (_Perodipus richardsoni_)
Sarcoma of urinary bladder
Octodontidæ—Coypu Rat (_Myocastor coypus_)
Sarcoma of thyroid
Hystricidæ—Canada Porcupine (_Erethizon dorsatus_)
Chorionepithelioma uteri
Dasyproctidæ—Azara’s Agouti (_Dasyprocta azara_)
Squamous carcinoma of larynx
PROBOSCIDEA (1)
Indian Elephant (_Elephas indicus_)
Leiomyoma, uterine cornua and fimbria
UNGULATA (7)
Equidæ—Chapman’s Zebra (_Equus burchelli chapmani_)
Fibroma peritonei with sarcomatous and osseous
change and metastases to lung
Bovidæ—Isabelline Gazelle (_Gazella isabella_)
Osteofibroma of jaw with mucoid degeneration
Nylghaie (_Boselaphus tragocamelus_)
Fibroma uteri
Dorcas Goat (_Capra hircus_)
Lymphosarcoma of mediastinum with metastases
to liver, kidney and lymph nodes
Cervidæ—Common Deer (_Mazama virginiana_)
Fibroadenoma of bile ducts
Camelidæ—Alpaca (_Lama pacos_)
Carcinoma of liver or bile ducts with extension
to intestine
Suidæ—Wild Boar (_Sus scrofa_)
Carcinoma uteri
EDENTATA (1)
Dasypodidæ—Nine banded Armadillo (_Tatu novemcinctus_)
Fibroma uteri
MARSUPIALIA (7)
Didelphyidæ—Common Opossum (_Didelphys virginiana_)
Adenoma of kidney
Common Opossum (_Didelphys virginiana_)
Adenocarcinoma of mammary gland
Dasyuridæ—Spotted tailed Dasyure (_Dasyurus maculatus_)
Adenocarcinoma of intestines with metastases to
lymphatics, liver, spleen, lungs
Tasmanian Devil (_Sarcophilus ursinus_)
Cystic epithelioma of skin of thigh
Peramelidæ—Rabbit eared Bandicoot (_Thylacomys lagotis_)
Carcinoma of lung
Macropodidæ—Red Kangaroo (_Macropus rufus_)
Malignant papilloma of stomach
Metastases to liver, spleen, kidney
Red Kangaroo (_Macropus rufus_)
Carcinoma of lung
Metastases to spleen and gastric wall
AVES
PASSERES (7)
Turdidæ—American Robin (_Planesticus migratorius_)
Hypernephroma of kidney, metastases to intestine
Crateropodidæ—Jungle Babbler (_Crateropus canorus_)
Adenoma of kidney
Tanagridæ—Palm Tanager (_Tanagra palmarum_)
Lipoma of abdominal wall
Fringillidæ—Saffron Finch (_Sycalis flaveola_)
Adenocarcinoma of kidney
Chestnut-eared Finch (_Amadina castanotis_)
Adenocarcinoma of kidney with metastases to lung
Chestnut headed Bunting (_Emberiza luteola_)
Lipoma of scalp
Icteridæ—European Blackbird (_Merula merula_)
Hypernephroma of kidney region with metastases to liver
STRIGES (1)
Bubonidæ—Great Horned Owl (_Bubo virginianus_)
Papilloma of duodenum
PSITTACI (26)
Loriidæ—Musky Lorrikeet (_Glossopsittacus concinnus_)
Carcinoma of lung
Cacatuidæ—Roseate Cockatoo (_Cacatua roseicapilla_)
Lipoma of abdominal wall
Roseate Cockatoo (_Cacatus roseicapilla_)
Multiple lipomata of abdominal wall
Psittacidæ—Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Glioma of brain with metastases to liver
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Hypernephroma of adrenal
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Papillary adenoma of kidney
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Cystic papillary adenocarcinoma of kidney
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Adenocarcinoma sarcomatodes of liver
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Papillary cyst adenoma of kidney
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Adenoma of kidney
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Adenoma of kidney
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Adenocarcinoma of oviduct
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Carcinoma simplex of liver with metastases to
liver, spleen
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Carcinoma simplex of liver
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Multiple lipomata
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Multiple lipomata
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Sarcoma of pectoral muscle with metastases to liver
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Round cell sarcoma in region of liver, spleen, kidney
Undulated Grass Parrakeet (_Melopsittacus undulatus_)
Carcinoma simplex of thyroid
Blue fronted Amazon (_Chrysotis æstiva_)
Adenocarcinoma (?) of proventricle
White fronted Amazon (_Chrysotis leucocephala_)
Epithelioma in peritoneum (?)
All Green Parrakeet (_Brotogerys tirica_)
Sarcoma of pectoral muscle
Red shouldered Parrakeet (_Palæornis eupatrius_)
Sarcoma of testes
Red shouldered Parrakeet (_Palæornis eupatrius_)
Sarcoma of testes
King Parrakeet (_Apromictus cyanopygius_)
Sarcoma of ovary
Crested Ground Parrakeet (_Calopsitta novæ-hollandiæ_)
Lipoma of muscle of abdomen and chest walls
ACCIPITRES (2)
Falconidæ—Red shouldered Buzzard (_Buteo lineatus_)
Retroperitoneal sarcoma
Sparrow Hawk (_Sparverius sparverius_)
Lipoma around cloaca
COLUMBÆ (1)
Columbidæ—Scaly Ground Dove (_Scardapella squamosa_)
Sarcoma (spindle) of kidney with metastases to tibia
GALLI (1)
Phasianidæ—Wild Turkey (_Meleagris gallopavo_)
Papillary adenocarcinoma of ovary
FULICARIÆ (1)
Rallidæ—Moorhen (_Gallinula chloropus_)
Endothelioma of clavicle
ANSERES (4)
Anatidæ—Red headed Duck (_Fuligula ferina americana_)
Papillary adenoma of kidney
Black Duck (_Anas obscura_)
Hypernephroma of adrenal
Lesser Snow Goose (_Chen h. hyperboreus_)
Fibroma on clavicle
Bean Goose (_Anser fabalis_)
Myxosarcoma of pectoral muscle
STRUTHIONES (1)
Rheidæ—Common Rhea (_Rhea americana_)
Cystic papillary adenoma of duodenum
SECTION XVII
THE COMMUNICABLE DISEASES—PART I
TUBERCULOSIS.
Nearly all infectious diseases have either a limited natural zoological
distribution or are encountered chiefly in one order or division. Thus
typhoid fever is peculiar to man, hog cholera to swine, foot-and-mouth
disease to cows. A second group, including for example anthrax, variola,
hemorrhagic septicemia and malignant edema, is somewhat less specific,
and may occur in several varieties. There is no more widespread,
important infection, zoologically, economically and hygienically, than
tuberculosis, and it would seem that all kinds of vertebrates are
subject to it. Its manifestations too, are sufficiently similar to
support the idea that there must have been originally a common ancestor
of the viruses which we now designate separately by a term to indicate
their immediate source (human, avian, etc.), and moreover it has been
shown that any of the artificially separated varieties or subspecies may
under certain circumstances infect all zoological families.
There is, however, a varying resistance to the tubercle bacillus,
certain zoological groups standing out preëminently as more or less
susceptible to it. There is also a tendency for each animal group to
present features more or less peculiar to itself, but nevertheless the
characteristics, both gross and minute, of the disease caused by the
_Bacillus tuberculosis_ are sufficiently similar to permit close analogy
and to establish a diagnosis when the bacteria are found.
The data collected at this Garden are well suited to elucidate the
susceptibility of wild animals under captive conditions and to
illustrate the nature of lesions in them. Perhaps they do not offer a
perfect cross section of zoological distribution of tuberculosis because
of the predominance in the display of birds, of monkeys and of
ungulates, but the figures will be found significant in certain
respects. Such records cannot be compared with those obtained for
domesticated animals in farms or breeding places, nor can our material
be used to show the incidence for individual species, such as cows, dogs
and the like, in a manner commonly used in veterinary literature. Those
who are interested in this phase of the problem can find in Lubarsch-
Ostertag’s _Ergebnisse_, 1917–18, No. 2, a summary by Eber of all recent
literature, covering nearly 1,700 references, which really amounts to a
review of all modern knowledge of tuberculosis in the lower animals. The
article does not, however, attempt to compare or contrast the incidence
per order or family in wild varieties since little information is
available on these points. There are no reliable data concerning the
existence of tuberculosis in the wild. It is noted in the report of the
British Tuberculosis Commission that monkeys were received with this
disease; Eber mentions that wild swine from a private preserve presented
undoubted evidence of tuberculosis and another similar experience with
pheasants, but these and other citations can give no proper estimate of
exact conditions nor allow a decision that the infection exists at all
under natural environment for in all cases the association with human
beings or domesticated animals cannot be excluded. Tuberculosis is
usually described as a disease of civilization and its incidence surely
varies directly with crowding.
THE TABLE.
Description of Table 23. The study of our autopsy records was begun by
the preparation of the accompanying table, which is based first upon the
zoological classification per order with subdivisions for families where
there are sufficient examples within important orders, and second, upon
percentage of total cases. For the analysis of the pathological types,
headings of probable origin, gross anatomical lesions and visceral
distribution were then made. The first vertical column shows the total
autopsies per order, and where families are given, for each of them. In
three instances Primates, Ungulata and Galli, not all families are
represented, so that the total for the order is greater than that for
the subdivisions quoted. It is noteworthy that we have had no
tuberculosis among nine families of ungulates; this will be discussed
later. The second column gives the total cases of tuberculosis for the
order and family, respectively, followed by a third line of percentages.
For the analysis of the pathology in these animals all the protocols
were reviewed. Forty-eight of them being found unsuitable, deductions
were made according to the natural group, thereby leaving the number
shown in the fifth column for separation according to origin and type.
Analyses in the succeeding columns are made upon number of cases and not
upon percentages, because of the confusion arising from small decimals.
The actual relationships will be pointed out in the notes. Percentage is
not so necessary because comparisons and contrasts are usually made with
classes or orders where the figures are comparable.
TABLE 23.
_Analytical Table Showing Incidence of Tuberculosis per Order and for
Some of the Principal Families, to Which are Added Columns Showing
Probable Origin of Infection, Pathological Type of the Disease and the
Visceral Distribution of the Morbid Process._
════════════════════╤═════════╤════════════╤══════════╤════════════
Order Family │ No. of │ Cases of │Percentage│ Cases not
│autopsies│Tuberculosis│ │sufficiently
│for order│ │ │ described
│or family│ │ │for analysis
────────────────────┼─────────┼────────────┼──────────┼────────────
„ „ │ „ │ „ │ „ │ „
│ │ │ │
│ │ │ │
│ │ │ │
────────────────────┼─────────┼────────────┼──────────┼────────────
Primates │ 498│ 192│ 38.5│ 8
Simiadæ │ 7│ 3│ 43.│ 0
Cercopithecidæ│ 353│ 171│ 48.4│ 8
Cebidæ │ 106│ 18│ 16.9│ 0
Lemures, Lemuridæ │ 86│ 23│ 26.7│ 3
Carnivora │ 481│ 17│ 3.5│ 4
Rodentia │ 199│ 5│ 2.5│ 0
Ungulata │ 365│ 35│ 9.6│ 2
Equidæ │ 11│ 1│ 9.│ 0
Bovidæ │ 123│ 12│ 9.7│ 1
Cervidæ │ 171│ 19│ 11.1│ 1
Camelidæ │ 25│ 3│ 12.│ 0
Proboscidea │ 3│ 2│ 66.│ 0
────────────────────┼─────────┼────────────┼──────────┼────────────
Totals for Mammalia │ [97]1860│ [97]274│ [97]14.7│ 17
Passeres │ 1355│ 18│ 1.3│ 6
Picariæ │ 87│ 11│ 13.│ 0
Psittaci │ 698│ 38│ 5.4│ 3
Loriidæ │ 24│ 3│ 12.5│ 0
Cacatuidæ │ 80│ 7│ 8.7│ 1
Psittacidæ │ 585│ 28│ 4.8│ 2
Striges │ 133│ 6│ 4.5│ 3
Accipitres │ 196│ 11│ 5.6│ 1
Columbæ, Columbidæ │ 157│ 50│ 32.│ 5
Galli │ 299│ 42│ 14.│ 5
Phasianidæ │ 252│ 22│ 8.3│ 3
Cracidæ │ 38│ 17│ 44.│ 1
Megapodidæ │ 5│ 3│ 60.│ 1
Fulicariæ │ 35│ 9│ _27._│ 0
Hemipodii │ 2│ 1│ _50._│ 0
Alectorides │ 37│ 10│ _27._│ 2
Odontoglossæ │ 6│ 2│ _33._│ 1
Anseres │ 317│ 16│ 5.│ 5
Struthiones │ 32│ 3│ _9.4_│ 0
Crypturi │ 5│ 2│ _40._│ 0
────────────────────┼─────────┼────────────┼──────────┼────────────
Totals for Aves │ [97]3505│ [97]219│ [97]6.2│ 31
────────────────────┼─────────┼────────────┼──────────┼────────────
Grand Totals │ [98]5365│ [98]493│ [98]9.1│ 48
────────────────────┴─────────┴────────────┴──────────┴────────────
════════════════════╤════════╤══════════════════════╤═══════════════
Order Family │Net no. │ Probable origin │Pathological Type
│of cases│ │
│ in │ │
│analysis│ │
────────────────────┼────────┼──────────┬───────────┼───────┬───────
„ „ │ „ │Pulmonary-│Intestinal-│ Acute │Massive
│ │aerogenic │ lymphatic │Miliary│caseous
│ │ │ │ │
│ │ │ │ │
────────────────────┼────────┼──────────┼───────────┼───────┼───────
Primates │ 184│ 86│ 98│ 3│ 52
Simiadæ │ 3│ 3│ │ │ 2
Cercopithecidæ│ 163│ 76│ 87│ 2│ 46
Cebidæ │ 18│ 7│ 11│ 1│ 3
Lemures, Lemuridæ │ 20│ 6│ 14│ │ 5
Carnivora │ 13│ 6│ 7│ │ 1
Rodentia │ 5│ 3│ 2│ │ 3
Ungulata │ 33│ 27│ 6│ │ 6
Equidæ │ 1│ │ 1│ │ 1
Bovidæ │ 11│ 10│ 1│ │ 1
Cervidæ │ 18│ 14│ 4│ │ 4
Camelidæ │ 3│ 3│ │ │
Proboscidea │ 2│ 2│ │ │
────────────────────┼────────┼──────────┼───────────┼───────┼───────
Totals for Mammalia │ 257│ 130│ 127│ 3│ 67
Passeres │ 12│ 9│ 3│ │ 5
Picariæ │ 11│ 1│ 10│ │ 2
Psittaci │ 35│ 13│ 22│ 1│ 9
Loriidæ │ 3│ 1│ 2│ │ 1
Cacatuidæ │ 6│ 4│ 2│ │ 1
Psittacidæ │ 26│ 8│ 18│ 1│ 7
Striges │ 3│ 3│ │ │ 1
Accipitres │ 10│ 5│ 5│ │ 2
Columbæ, Columbidæ │ 45│ 10│ 35│ │ 12
Galli │ 37│ 10│ 27│ │ 12
Phasianidæ │ 19│ 2│ 17│ │ 4
Cracidæ │ 16│ 7│ 9│ │ 7
Megapodidæ │ 2│ 1│ 1│ │ 1
Fulicariæ │ 9│ 1│ 8│ │ 1
Hemipodii │ 1│ 1│ │ │ 1
Alectorides │ 8│ │ 8│ │ 2
Odontoglossæ │ 1│ │ 1│ │
Anseres │ 11│ 2│ 9│ │ 4
Struthiones │ 3│ 3│ │ │
Crypturi │ 2│ │ 2│ │
────────────────────┼────────┼──────────┼───────────┼───────┼───────
Totals for Aves │ [99]188│ 58│ 130│ 1│ 51
────────────────────┼────────┼──────────┼───────────┼───────┼───────
Grand Totals │ [99]445│ 188│ 257│ 4│ 118
────────────────────┴────────┴──────────┴───────────┴───────┴───────
════════════════════╤════════════════════════╤════════════════════════
Order Family │ Pathological Type │ Visceral Distribution
│ │
│ │
│ │
────────────────────┼───────┬──────────┬─────┼─────┬─────┬──────┬─────
„ „ │Nodular│ Chronic │Pearl│Lungs│Liver│Spleen│Lymph
│caseous│ fibrous │type │ │ │ │nodes
│ │ and │ │ │ │ │
│ │ulcerative│ │ │ │ │
────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼─────
Primates │ 108│ 16│ 5│ 173│ 122│ 149│ 145
Simiadæ │ │ │ │ 3│ 2│ 3│ 3
Cercopithecidæ│ 96│ 16│ 3│ 156│ 111│ 136│ 128
Cebidæ │ 12│ │ 2│ 14│ 9│ 10│ 14
Lemures, Lemuridæ │ 15│ │ │ 17│ 14│ 17│ 12
Carnivora │ 8│ 4│ │ 11│ 4│ 2│ 6
Rodentia │ 2│ │ │ 4│ 2│ 2│ 4
Ungulata │ 1│ 24│ 2│ 28│ 7│ 3│ 25
Equidæ │ │ │ │ │ │ │ 1
Bovidæ │ 1│ 9│ │ 9│ 4│ 2│ 7
Cervidæ │ │ 13│ 1│ 17│ 2│ │ 14
Camelidæ │ │ 2│ 1│ 2│ 1│ 1│ 3
Proboscidea │ │ 2│ │ 2│ │ │
────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼─────
Totals for Mammalia │ 134│ 46│ 7│ 235│ 149│ 173│ 192
Passeres │ 7│ │ │ 9│ 5│ 5│
Picariæ │ 8│ │ 1│ 2│ 9│ 6│ 1
Psittaci │ 25│ │ │ 18│ 24│ 14│ 2
Loriidæ │ 2│ │ │ 3│ 3│ 1│
Cacatuidæ │ 5│ │ │ 5│ 5│ 2│
Psittacidæ │ 18│ │ │ 10│ 16│ 11│ 2
Striges │ 2│ │ │ 3│ 3│ 2│
Accipitres │ 7│ 1│ │ 8│ 6│ 8│ 1
Columbæ, Columbidæ │ 33│ │ │ 24│ 40│ 34│ 1
Galli │ 24│ 1│ │ 20│ 34│ 29│ 2
Phasianidæ │ 15│ │ │ 7│ 18│ 15│ 1
Cracidæ │ 8│ 1│ │ 12│ 15│ 13│
Megapodidæ │ 1│ │ │ 1│ 1│ 1│ 1
Fulicariæ │ 8│ │ │ 4│ 8│ 8│ 1
Hemipodii │ │ │ │ 1│ 1│ 1│
Alectorides │ 6│ │ │ 4│ 8│ 7│ 2
Odontoglossæ │ 1│ │ │ │ 1│ 1│
Anseres │ 5│ 2│ │ 4│ 7│ 8│ 1
Struthiones │ │ 3│ │ 3│ 2│ 3│ 2
Crypturi │ 2│ │ │ 1│ 2│ 2│
────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼─────
Totals for Aves │ 128│ 7│ 1│ 101│ 151│ 128│ 13
────────────────────┼───────┼──────────┼─────┼─────┼─────┼──────┼─────
Grand Totals │ 262│ 53│ 8│ 336│ 300│ 301│ 205
────────────────────┴───────┴──────────┴─────┴─────┴─────┴──────┴─────
════════════════════╤══════════════════════════════════════════════════════
Order Family │ Visceral Distribution
│
│
│
────────────────────┼─────────┬──────┬─────────┬──────┬─────┬─────┬────────
„ „ │Intestine│Kidney│ Serous │Bones │Brain│Heart│Pancreas
│ │ │membranes│ and │ │ │
│ │ │ │joints│ │ │
│ │ │ │ │ │ │
────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼────────
Primates │ 30│ 84│ 70│ 2│ 2│ 7│ 3
Simiadæ │ 2│ 1│ 1│ │ │ │
Cercopithecidæ│ 24│ 76│ 63│ 2│ 2│ 7│ 2
Cebidæ │ 4│ 7│ 6│ │ │ │ 1
Lemures, Lemuridæ │ 2│ 7│ 1│ │ │ │ 1
Carnivora │ 1│ 4│ 3│ 1│ │ │
Rodentia │ 1│ 2│ 2│ 1│ │ │
Ungulata │ 1│ 2│ 7│ │ │ │
Equidæ │ │ │ │ │ │ │
Bovidæ │ 1│ 1│ 1│ │ │ │
Cervidæ │ │ │ 5│ │ │ │
Camelidæ │ │ 1│ 1│ │ │ │
Proboscidea │ │ │ │ │ │ │
────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼────────
Totals for Mammalia │ 35│ 99│ 83│ 4│ 2│ 7│ 4
Passeres │ 4│ │ 4│ │ │ │
Picariæ │ 4│ 1│ 3│ 1│ │ │
Psittaci │ 12│ 6│ 6│ │ │ 1│
Loriidæ │ 1│ 1│ 1│ │ │ │
Cacatuidæ │ │ 1│ 1│ │ │ 1│
Psittacidæ │ 11│ 4│ 4│ │ │ │
Striges │ │ │ 3│ │ │ │
Accipitres │ 4│ 3│ 6│ │ │ 2│
Columbæ, Columbidæ │ 16│ 13│ 20│ │ │ 1│
Galli │ 20│ 7│ 15│ │ │ │ 1
Phasianidæ │ 10│ 2│ 6│ │ │ │ 1
Cracidæ │ 10│ 5│ 7│ │ │ │
Megapodidæ │ │ │ 2│ │ │ │
Fulicariæ │ 3│ 3│ 4│ │ │ │
Hemipodii │ 1│ 1│ 1│ │ │ │
Alectorides │ 3│ 3│ 7│ │ │ │
Odontoglossæ │ 1│ │ │ │ │ │
Anseres │ 3│ 4│ 4│ │ │ │
Struthiones │ │ 1│ 1│ │ │ │
Crypturi │ 2│ 1│ │ │ │ │
────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼────────
Totals for Aves │ 73│ 43│ 74│ 1│ 0│ 4│ 1
────────────────────┼─────────┼──────┼─────────┼──────┼─────┼─────┼────────
Grand Totals │ 108│ 142│ 157│ 5│ 2│ 11│ 4
────────────────────┴─────────┴──────┴─────────┴──────┴─────┴─────┴────────
See page 484, for description of tabulation.
For meaning of italics see foot note Table 1.
These and figures set opposite them are cases not percentages.
It is generally conceded that the principal and only significant routes
of origin for tuberculosis are via the respiratory and alimentary
tracts. The criteria upon which to decide the route that has been
followed are by no means definite and may not be for any given case
unexceptionable. In birds the alimentary tract is conceded to be the
important one, while in mammals an aerogenic route is believed to be the
rule. However, since feeding experiments have shown that tubercle
bacilli can gain the lungs by passing through the intestinal wall and
abdominal lymphatics without leaving gross traces, the decision that one
or the other route has been taken may be erroneous, and statistics
therefore can often be fallacious. It is usually the rule to assume that
the oldest or best developed lesions occur where the originally settled
organisms exerted their maximum effect. The questions of infection-path
and of original lesion not having been settled it is obvious that
decision as to the route must be in the nature of an estimate. With
these limitations in mind I have divided the cases into probable
respiratory and alimentary origins according to the following criteria.
Where the lesions were wholly respiratory or within the lymph glands of
the trachea and bronchi the decision was not so difficult. Predominance
of the pulmonary disease with recent lesions in other organs was taken
to indicate an aerogenic origin. The chronic ulcerative or fibrous
pulmonary lesions were also ascribed to those beginning in the lungs.
The alimentary tract was considered for this purpose as beginning in the
tonsillar area and ending at the anus. This is as I understand the
customary teaching. When the lymph nodes of the alimentary area were
advanced in the process, the intestinal method was held responsible. It
is of course not to be forgotten that organisms coughed up from the
lungs and swallowed may be responsible for lesions within the alimentary
system. However, a predominance of intestinal, splenic, hepatic and
lymphatic lesions caused me to place the case with those originating
from the alimentary tract. Granting the limitations of our knowledge, of
the criteria and of my own judgment, it is noteworthy that the results
of this division of the table are not contradictory to the usual
teaching, the most conspicuous being the predominance of the alimentary
infection of Aves and in the order Primates, whereas the pulmonary route
has the highest figures for the Ungulata.
The next subdivision of the table concerns the gross pathological type.
Beginning with the most acute form, the acute miliary, progression is
made in terms of chronicity—then following in order the massive caseous
form including caseous pneumonia, the caseous miliary or nodular form so
well represented by the monkey, then the fibroulcerative type such as
one encounters in human consumption, including also forms in which
fibrosis predominates, and lastly the rather uncommon pearl disease.
This classification has been relatively easy to follow and can be
readily imagined by the reader. There are of course intermediate cases
or transition forms and there have been instances partaking of more than
one character. The groupings present only gross appearances and, with
few exceptions, are not to be taken as direct indications of type
incidence in special groups.
Visceral distribution is shown in the last gross section of the table;
single cases or unusual locations are not tabulated but will be
separately discussed. The visceral distribution is made upon evident
gross lesions or their discovery in organs whose condition suggested the
need of microscopic study for confirmation. The figures in the table
will be reviewed first upon the incidence as a whole and then between
classes and orders. This will be succeeded by an analysis of the
particulars for each order and then for each of the pathological
headings.
TOTAL AND CLASS INCIDENCE.
The autopsies upon 5,365 animals have revealed the existence of
tuberculosis in 492, a percentage of 9.1. This means that lesions due to
the _Bacillus tuberculosis_ were present, but they were not always the
cause of death, since many specimens have been executed and others have
had sufficient pathology to kill, aside from the tuberculous changes.
Deaths due to the disease alone are difficult to estimate, but seem to
be about 325 or 6 per cent. These figures, while they represent the
total incidence, lose considerably in significance when the factors are
analyzed. Mammalian incidence is 14.7 per cent., Avian 6.2 per cent.,
but the former is based upon figures obtained from six of twelve orders
numbering 1,860 animals, whereas the latter represent the cases in
fourteen of twenty orders numbering 3,505 birds. The percentages are
considerably increased by high figures for a few orders, Primates,
Lemures, Columbæ for examples. There are missing from the list very few
orders of which we have any notable number of autopsies, Marsupialia and
Herodiones being the only important ones; it would seem that these
orders have a high resistance to the disease.
Investigation into the origin of the disease in mammals and birds shows
with definiteness the preponderance of the alimentary route influence in
the latter, but for the former the figures cannot be said to be
conclusive. The bird excretes large numbers of bacilli with the feces
thereby soiling the feed and the ground. This is due to the frequency of
intestinal open lesions and to the really enormous numbers of bacilli
which are in the morbid tissue. I think it can be said with safety that,
other things being equal, the bird excretes bacilli constantly and in
greater numbers than does the mammal, and that in physically comparable
lesions there are more bacilli in the avian than in the mammalian.
The inconclusive figures for the origin of the disease in the mammal can
be clarified very little by the subtraction from the tables of the
figures for the very susceptible Primates. By doing this it would seem
that the respiratory route dominates as 43 to 29, whereas if the
reasonably susceptible Lemures be also deducted the ratio becomes as 38
to 15. It would seem that the evidence favors the aerogenic route in the
mammal.
PATHOLOGICAL TYPES.
An inquiry into the gross pathological types reveals at once the
frequency with which the nodular and massive caseous forms appear. If
the number of cases be reduced to percentage it will be found that 59
per cent. of all specimens presented the nodular variety and 26.6 per
cent. the massive caseous form. These large figures (equaling when
combined 85 per cent.) coupled with the fact that only 12 per cent. of
the total were fibroulcerative and 1.8 per cent. of the pearl type,
would seem to indicate that the nodular and massive caseous processes
are the lesions to be expected in wild animals. Furthermore, if these
nodular and caseous forms speak for recent infection or acuteness of the
morbid process, it would seem that wild animals have a low tissue
resistance to tuberculosis. It is a widespread belief, in some degree
well supported, that a disease new to an animal species is highly fatal
and that the survival of the race depends upon an active self-
immunization or the survival of the pathologically least susceptible. If
tuberculosis be a disease of civilization, these figures would suggest
that it is absent in nature. As a further support of this idea it can be
said that with the exception of two cases in ungulates, no fibroid
tuberculosis, approaching the quiescent type as seen in man and rarely
in domestic animals, was encountered. Very rarely calcareous deposits
will be found in both simian and ungulate lesions but these need not
indicate a tendency to general healing although at that place the
process may be inactive. The bird uses considerable fibrous tissue in
the construction of its tuberculous mass but fibrosis never masters the
situation with the formation of scar tissue sufficient to wall off the
process. Pearl disease, a fibrocaseous condition, is not a healing
fibroid procedure and is, in our material, of no numerical significance.
VISCERAL DISTRIBUTION.
The distribution of the morbid lesions in the viscera presents some
interesting features. In the first place the data leave no doubt that
the most susceptible tissue in the wild animal body is, as in the case
of human and domestic animals, the lung. The susceptibility of this
organ in the two classes is however a different matter since in the
mammal 91.4 per cent. show pulmonary lesions while only 53.7 per cent.
of birds are so affected. Part of the reason for this appears in the
figures for the principal abdominal organs, of which the liver and
spleen occupy the prominent places. The mammalian livers show 58.2 per
cent., the avian 80.3 per cent.; 67.5 per cent. of mammalian spleens,
68.0 per cent. of avian spleens have tuberculous lesions. The figure for
the mammalian spleen is distorted because of the peculiar susceptibility
of this organ in the monkey, it being conspicuously free of lesions in
most mammalian orders. The intestines presented discernible lesions in
practically 40 per cent. of birds but only in 13.5 per cent. of mammals.
Renal involvement was found in 38.4 per cent. of mammals and 22.9 per
cent. of birds.
A study of the changes in the serous surfaces is complicated by the
difference of anatomy in the two classes. The mammal has separate closed
serous sacs well guarded against invasion from mucous surfaces whereas
in the bird the air sacs and serous cavities are closely related, the
latter being loosely applied to viscera they are intended to cover.
Moreover in Aves direct infection of the air sacs seems a definite
possibility. Notwithstanding the fact that the bird’s sacs and serous
surfaces appear so open to infection there is no great preponderance of
lesions within them—Aves 39.3 per cent. Mammalia 32 per cent. The lymph
nodes were tabulated as a tissue rather than according to location, the
latter method being found profitable for discussion in a few orders
only. As might be expected the abundant lymph nodes of the mammal were
affected out of all proportion to those in the bird. These matters will
be discussed later. The remaining figures on the table have no
comparative value.
ORDINATE CHARACTERISTICS.
The Primates as an order have shown low resistance to tuberculosis, a
fact well known to general observation. How much this is due to the
unsanitary surroundings to which these naturally free active beasts are
subjected, in catching, transporting and storing for sale, must at
present remain conjectural, but they are probably infected with ease as
our experience in this laboratory suggests. Desiring a tuberculous
monkey for certain tuberculin tests, I injected one hundredth of a
milligram of a human culture, known to produce definite lesions in
rabbits; the animal died in three months with advanced general
tuberculosis. The unexpected and interesting feature of our figures is
the susceptibility of different families within the order. The Old World
monkeys, Simiadæ and Cercopithecidæ have a combined incidence two and
one-half times as great as the New World Cebidæ, and the marmosets had
no tuberculosis at all in the thirty-two specimens. Possibly this is a
matter of transportation and handling, which reduces the resistance and
offers chance to infect apes and baboons. The New World capucin monkeys
have their exposure too since many of them are household pets before the
Garden receives them. Their usual life in captivity is however shorter
than that of Old World varieties, they therefore being exposed to
infection for a shorter time. It would seem however that American
Primates are more resistant to the disease than African and
Australasian.
The form of tuberculosis to which this order is liable is well described
in text-books, it being so characteristic that the term “monkey
tuberculosis” is used to distinguish it. The purpose of the term is to
compare the lesions with certain cases of generalized tuberculosis in
children. It is characterized by a nodular involvement of the liver and
of the spleen particularly, sometimes also of the lungs but in fatal
cases the last organ is commonly the seat of massive caseation or
caseous pneumonia. The prominence of the pulmonary lesions often makes a
decision of origin difficult since important changes may be found in the
liver and abdominal nodes. Blair at New York, and Rabinowitsch at Berlin
are of the impression that many cases of monkey tuberculosis start by
pharyngeal and tonsillar infection because they found cervical adenitis
so commonly. Our records and specimens would support this idea in only
fourteen instances and I am of the impression that the lower intestinal
route is more often responsible, even to a higher figure than is
recorded in the table. This view is based upon the frequent occurrence
of enlarged glands in the mesentery, retroperitoneum and posterior
mediastinum, in the latter location being quite as prominent if not more
so than in the bronchial and tracheal area. Occasionally deposits of
calcareous matter will be found in old caseous glands but in such
animals there has always been some other spot of activity of
tuberculosis. The frequency with which the liver and spleen are affected
gives opportunity for hematogenic spread, a method of no small
importance in the opinion of Eber. The chronic ulcerative form is quite
well displayed in monkeys, interestingly enough to cite an illustrative
case at the end of this division of the discussion. Five cases of
distinct chronic cavitation were encountered; several small recent
cavities were found in the massive caseous pneumonic cases. The two
acute miliary cases and one of the pearl type will be discussed briefly
on a later page.
Despite the prominence of the liver, spleen and lymph nodes, the lungs
stand ahead of all others by a safe margin of visceral incidence. The
spleen stands in the third place in this order and in the next, Lemures,
but in no other mammalian group does this organ occupy so prominent a
position. The susceptibility of lymphatic tissue in the monkey is
further illustrated by the large number of cases showing lesions in
lymph nodes. It is rather striking however that our material showed very
few active ulcerations in the lymphoid plaques of the intestinal wall
nor indeed do the intestines present a large numerical involvement.
Serous membrane tuberculosis is chiefly that of the pleura, upon which
early precaseous tubercles are frequently found, usually in conjunction
with pulmonary disease. Tuberculous peritonitis of the plastic and
nodular variety occurred only six times, though light adhesions to
nodules in the liver and spleen were quite common. Pericarditis was
found five times, in three of which there was myocardial disease; which
of the two was primary was not indicated in the notes but from present
reading it would seem that the heart muscle was involved first.
The next order, Lemures, has a susceptibility of about half that of the
monkeys judging by the percentage incidence. Analytically the members of
this group react quite like the preceding order in having the same types
of origin, pathology and organic distribution. Since they are so close
zoologically, present similar lesions and are tested in the same manner
as the monkeys, we group them together and shall proceed to discuss
special cases of interest in both orders.
Special Cases in Primates and Lemures. Acute general miliary
tuberculosis occurred thrice in Old World and once in New World monkeys.
The first case took its origin in a caseous gland in the bronchotracheal
area, the lung showing a minor degree of involvement with milia but no
older process. The second took its origin in the mesenteric area and the
organs of this section of the body were most affected. The only case in
the Cebidæ seemed to be of intestinal origin since an acute plastic
peritonitis with fluid exudate accompanied the generally miliary
disease.
Pearl disease of the bovine type has been encountered on four occasions
but it cannot be said to have developed to the state of perfection seen
in the cow. There is lacking the masses of nodules growing together in a
fungoid character usually seen on the pleura and peritoneum. The monkey
form is in isolated nodules of gray-yellow color which may show caseous
centres. The visceral lesions are in firm separate areas not tending to
soften or coalesce. Two of these monkeys died from recent pulmonary
exacerbations. From one of the cases a bovine bacillus, judging from
culture and rabbit virulence, was isolated.
As a good example of monkey tuberculosis, illustrating at the same time
a chronic ulcerative pneumonitis with cavitation, the following case is
cited:
Green Monkey (_Cercopithecus callitrichus_) ♀ . Was coughing and
drooping for two days before death. Chronic ulcerative tuberculosis of
lungs with cavity formation; early conglomerate tuberculosis of liver;
conglomerate caseous tuberculosis of spleen; early conglomerate
tuberculosis of ileum (Peyer’s patches); acute catarrhal enteritis;
miliary tuberculosis of right kidney. The animal is well preserved,
sleek, with a moderate amount of fat. The left pleura is largely
obliterated by adhesions in the lower portion. As lung is freed it is
torn, showing a cavity measuring 3 × 3 × 4 cm., which is filled with a
curdy gray material. Cavity has well defined walls. Rest of lower lobe
in which this cavity lies is solidified, red and edematous and
contains numerous conglomerate tubercles. Upper lobe practically free
of tubercles; shows compensatory emphysema. The right lung closely
resembles the left but lacks the cavity. The liver is enlarged, soft
and friable, of red color, spotted yellow. Serous and section surfaces
show closely packed early conglomerate tubercles. The spleen is of
normal size, soft, has red pulp with large conglomerate tubercles
which project slightly on the capsule. The kidneys are apparently
normal except for the presence of two or three subcapsular large,
solitary tubercles in the right organ. The duodenum has thickened
walls, mucosa bright, brilliant scarlet hue. In the ileum the walls
are thickened, mucosa bright red, agminated follicles hyperplastic
elevated and display several (4–12) miliary tubercles. These may be
seen shining through on the serous surface but there is no peritoneal
tuberculosis. No ulceration of Peyer’s patches. Contents of large
intestine is rather dry and here the mucosa shows exaggerated rugæ
which cannot be smoothed out. Walls are thickened, and ulceration,
while suggested, cannot surely be determined.
An interesting case of primary tuberculosis in the larynx detected at
postmortem after a tuberculin injection is as follows:
[Illustration:
FIG. 51.—BOVINE TUBERCULOSIS IN THE MONKEY. THIS SPECIMEN SHOWS THE
BOVINE PEARL DISEASE ON THE COSTAL PLEURA, AND SERVES AS WELL TO
ILLUSTRATE THE NODULAR TUBERCLES COMMONLY FOUND IN THE SPLEEN OF ALL
PRIMATE TUBERCULOSIS.
]
Black and White Lemur (_Lemur varius_) ♂ . Miliary tuberculosis of
larynx; perilaryngitis and retropharyngeal lymphadenitis. Killed
because of unsatisfactory chart after injection of tuberculin. The
only tuberculous lesion to be found in the body, which is in excellent
shape, is in and about the larynx. The lesions within are on the
epiglottis, false and true vocal cords and the main ventricle. On
either side of the root of the epiglottis, there are a few recent
tubercles. The lesion in the retropharyngeal lymphatics is recent and
diffuse. This is probably primary as it is not known that the
retropharyngeal glands drain to or from the larynx. About the lesions
on the laryngeal mucosa there is an area of congestion probably due to
the tuberculin injection.
Local lymphatic tuberculosis of comparative interest was encountered a
few times. Three cases of cervical adenitis, large enough to be visible,
were seen, of which one broke down about two weeks before death, and
discharged. The others did not ulcerate through the skin but, contrary
to the usual rule for the human being, remained as isolated glands only
lightly adherent to one another where they lay adjacent. There was also
seen an ulcerating tuberculous lymph node in the groin of one monkey,
the animal having rather pronounced abdominal and pelvic tuberculosis.
Two instances of tonsillar tuberculosis are recorded, in both of which
the lesion was of some duration and associated with caseation in the
lymph node lying immediately behind and below it. A Guinea Baboon
(_Papio sphinx_) had as an unusual part of his general tuberculosis, an
active caseopurulent collection in the antrum of Highmore, which
attacked the upper maxilla and immediately adjacent muscle; tubercle
bacilli could be demonstrated.
One of the cases of nodular or massive peritoneal tuberculosis is quite
like the tumor-forming variety of human adolescents; it is as follows:
Reddish Macaque (_Macacus rufescens_). Caseous tuberculosis of
mesentery and spleen; miliary tuberculosis of lungs, pleura and liver;
chronic myocarditis. The lymphatic glands of the posterior and
superior mediastinum and bronchi are slightly enlarged, soft and
anthracotic but do not show any tuberculous change. Both lungs are
riddled with small, firm, gray miliary tubercles, some surrounded by a
clear mantle of connective tissue. The intervening lung is practically
normal. Pleura over base of right lung on both surfaces shows small,
pale miliary tubercles. The liver contains various sized miliary
tubercles. There is a large caseous mass in posterior end of spleen
with adhesions to kidney, stomach and colon. Retroperitoneal glands
are much enlarged, firm, homogeneous—probably tuberculosis of a
different type. Lesser omentum contains one caseous gland. Few caseous
glands in great omentum. In the right iliac region there is a large
mass involving many coils of intestine. It is found to arise probably
from the ileocecal glands and can be traced along the mesentery to the
central lymphatic stalk. The mass involved the tissues of the
mesentery and surrounds many coils of intestine. Cecum and first part
of colon can be traced over its right side. Rectum is free except on
right side where it is lightly attached to the mass. Epicardium is
gray and irregularly thickened and the muscle just beneath serous
membrane is pale and streaked with red lines.
There have been three cases of tuberculosis of the internal male genital
area, one of which was suspected of having been the primary seat of the
disease; it was described on page 315. The other two could have been
secondary since other points of morbid change were as old or older. One
of these cases formed a tumor as large as a goose egg at the vesical
neck, obstructing the flow of urine and blocking up the seminal vesical,
in consequence of which paralytic distention occurred in the bladder
while the vesicles were tightly filled with inspissated semen. A case of
Fallopian salpingitis has also been cited. Two instances of cerebral
tuberculomata have already been described.
Carnivora. This order has the reputation of being quite resistant to the
tubercle bacillus, based upon the relative infrequency among cats and
dogs in contrast to cows and swine. Some veterinary statistics cite the
incidence up to 5 per cent., and occasional references may be found to
tuberculosis in circus lions and tigers. Our records would suggest that
in gardens the wild varieties of this order have about as much of the
infection as the domestic carnivores, 3.5 per cent. The group is made of
six Felidæ, one Viverridæ, three Canidæ, six Procyonidæ, and one Ursidæ.
The first family includes a lion, tiger, a jaguar and three smaller
cats. The Canidæ are all small foxes. The Procyonidæ are all coatis. The
features of this order are the occurrence of the fibroulcerative variety
with cavitation in the Felidæ and the caseous nodular abdominal and
glandular disease in the coatis. All these animals, even those of the
last named variety and pathological type, tend to show some tissue
resistance to the tuberculous disease. Connective tissue activity is
characteristic of the process, considerable distortion being produced by
the fibrosis. This feature is borne out where the tissues are studied
microscopically. Definite milia are sometimes found, but they consist of
epithelioid and round cells with imperfect caseation, giant cells being
often missing. About the miliary tubercles a diffuse and not essentially
specific tuberculous granulation tissue is found, mixed with which is
much connective tissue growth. The fibrotic adhesion-forming serous
membrane tuberculosis of carnivores seems worthy of emphasis by the
citing of a case in point. White nosed coati (_Nasua narica_), was
received in poor condition and died in a few days. Upon dissection a
slightly turbid yellowish fluid was found to occupy what remained of the
peritoneal cavity which was reduced in size by dense adhesions of the
intestines into an inflammatory mass. The omentum was a diffuse
thickened apron, also beset with fine tubercles, lying over the mass.
Fine young tubercles could also be found upon the intestines and liver
while the mesenteric lymph nodes were early in caseation; thoracic
organs not infected.
One of the most interesting cases concerned hypertrophic osteitis in a
chronically tuberculous lion; the feet are discussed on page 346. This
process was described by Marie for human beings many years ago, and was
reported in dogs by Cadiot[100] in 1912. This beast was one of five
large cats which have died from tuberculosis in its chronic ulcerative
form. Three of the cats, one fox and the bear showed definite
cavitations of a ragged loculated form. The cavities were usually of the
multiple variety and were found in the posterior, that is lower lobe.
Rodentia. The paucity of cases in this order permits little information
to be drawn from the form of tuberculosis. The total seems to have been
swollen by a group of three beavers, all of which came in one shipment.
The remainder were a Capybara and an Agouti. The general type is that of
much caseation with little or no surrounding fibrosis. One illustrative
case is cited:
American Beaver (_Castor canadensis_). General tuberculosis. The
animal presents generalized tuberculosis. The regional lymph nodes
show caseous nodules. The right hip joint shows caseous material about
the acetabulum with necrosis and pathological fractures in the os
innominatum immediately above the acetabulum and including its cavity.
Lungs show almost no normal respiratory tissue, the process being a
diffuse precaseous, partly gelatinous pneumonic phthisis. The superior
and posterior mediastina show caseous glands. There is miliary
tuberculosis of the liver. Nodular caseous tuberculosis of the spleen
with small tubercles and some cirrhosis of the intervening tissue.
There are caseous nodules in all perirenal glands and in the kidney
cortices. The psoas muscle glands are densely caseous. The pelvic
organs except about the right acetabulum escape involvement. Adrenals
not opened but probably not involved.
Ungulata. This order shows the most definite figures among those for the
order of mammals. Nearly one-tenth of the whole number of specimens have
had some form of tuberculosis and of a very definite character. It is
well at first to mention, however, that only four of thirteen families
are represented, from which four came 328 of the total 365 autopsies.
The remaining thirty-seven were such animals as tapirs, giraffes, swine,
and peccaries, in all of which tuberculosis has been reported from
elsewhere.
Pulmonary disease with less prominent lesions in other organs,
especially the intestines and their related glands, speaks in favor of
the aerogenic route being the common one. This of course has been a bone
of contention among veterinarians, and I do not presume to settle the
matter with these figures.
This order resists tuberculosis to a certain degree as attested by the
fibroulcerative character of the majority of the cases. Two instances,
one in a buffalo and one in a deer, showed very highly fibrotic
pulmonary lesions with a partial attempt to surround and wall off
numerous areas of caseation. So too in this order there is a greater
tendency to calcification, both in the intra- and extrapulmonary nodes.
It is to be emphasized that in our material the thoracic lymph nodes are
affected more than the abdominal and regional as 3 to 1. The apparent
immunity of the spleen of this order is well illustrated.
The paucity of serous surface involvements in the wild Bovidæ and their
prominence in the Cervidæ cannot be ignored in the figures, but it seems
misleading since pleural growths and adhesions are quite common in the
domestic Bovidæ. The case in the Equidæ was that of a Zebra with a large
tuberculous abscess in the retroperitoneal glands forming a tumor in the
left renal region. It was quite well surrounded by fibrosis, and the
infection had not extended; it seemed quite recent. Analysis of the
figures for the remaining three families of ungulates offers little for
contrast and much for comparison; it is the usual picture as seen in the
domestic cow. Some special cases are worthy of review.
An interesting specimen of softened glands chiefly on one side of the
neck was found in a Fallow deer (_Cervus dama_). It resembled the
juvenile human cases that require surgical attention. Although palpable
lymph nodes can be found in practically all cases of generalized
tuberculosis in the Ungulata, this is the only case in our records in
which they have presented a large tumefaction and broken down. Pulmonary
cavitation is recorded but thrice, one for each of the last three
families. Fibrocaseous tuberculosis of the testes was discovered in a
Nylghaie (_Boselaphus tragocamelus_), but there is no knowledge of
mating or offspring. An ischiorectal abscess was found in an American
Bison (_Bison bison_) showing nodular precaseous tubercles of the lung.
The former was the cause of death. No tubercle bacilli could be found in
the abscess contents, so that the tuberculous basis is inferred, not
proven. Tuberculous salpingitis in a Nylghaie was discussed on page 306.
Proboscidea. Eber mentions in the article already referred to that there
are three reports in the literature of tuberculosis in elephants. When
looking for an explanation of tuberculosis in this animal it must be
remembered that it is one of the most attractive objects in a zoological
garden and receives perhaps more attention, including feeding, from
visitors than any other specimen. The beast while possessing some tissue
resistance to tuberculosis, is by no means immune thereto, as has been
thought by some persons on account of its reputed longevity, and
therefore he is to be protected from infection just as much as other
animals. It would appear that he may present caseous pneumonia or
nodular caseous disseminated lesions. Our two cases, in animals at the
Garden twenty and thirty-eight years respectively, were both of the
fibrocaseous variety; the lesion was confined to the lungs. A brief
description of their lesions is as follows:
Indian Elephant (_Elephas indicus_) ♂ . Chronic polyarthritis. Chronic
myocarditis. Chronic hepatitis (cirrhosis). Parenchymatous nephritis.
Chronic tuberculosis of the lungs, partly encapsulated. Pigmentation
of the spleen. The pleuræ are very fat but the surfaces are smooth and
devoid of adhesions. The lymph nodes of the mediastinum are about
10 × 20 cm. for the largest while the smaller ones vary around 2 × 4
cm. They are firm, deep red-brown without clear divisions into medulla
and follicular cortex. There are several large, firm, pale rather
cheesy follicles in all the large ones and a few of the small. These
do not appear like tuberculosis. The lungs are flaccid and soft; gray
and red mottled. The bronchi are firm and stand open. Around one in
the upper lobe of the right lung, there is a large area of cheesy
degeneration around which a zone of connective tissue has formed. This
extends about the bronchus about halfway in a sheath-like manner.
There is also a separate nodule the size of a cherry with a cheesy
centre. The trachea appears normal. Tubercle bacilli could be
demonstrated in the cheesy material. Microscopic section of lung
around the cheesy area shows a low grade chronic granulation tissue in
some places enclosing cheesy masses with giant cells on the margin.
The neighboring septa are slightly thickened and in some places
broken, forming emphysematous cavities. Some of these cavities are
edematous.
Indian Elephant (_Elephas indicus_) ♀ . Miliary and conglomerate
caseous tuberculosis of lung. Edema of lungs. Endarteritis deformans
of lung. Cloudy swelling of liver. Chronic passive congestion of
liver. Hemosiderin pigmentation of liver. Acute parenchymatous
nephritis. Chronic passive congestion of spleen. Chronic hyaline
perisplenitis. Multiple calcified fibroid tumors of uterus. Leiomyoma
of uterine cornu. Senile atrophy of ovaries. Acute catarrhal
enteritis. There are some adhesions of the upper lobes of the lung to
the ribs. The lungs are large, increased in weight, color pink and
mottled red, air content diminished. There are several masses of
tubercles, each as large as a cocoanut, in both lobes. In one such the
tubercles are yellow and caseous; some are fibroid but none are
liquefied or calcified. The fibrous tissue of the lung parenchyma here
is much overgrown. In one instance the terminus of a bronchus is
solidly plugged by caseous material. Mucosa of bronchi is reddened,
markedly ulcerated, ulcers overlaid by mucopus.
INDIVIDUAL FEATURES OF AVIAN TUBERCULOSIS.
The avian form of tuberculosis is somewhat peculiar in its physical
appearance as well as in its distribution. The isolated nodular type is
far and away more common by more than 100 per cent. than all the other
types combined. These nodules are usually well circumscribed, and to the
naked eye suggest that they have a restraining fibroid wall. This is,
however, not the case, the impression being due to the dense but
actively growing fibrocellular cortical zone of the tubercle. The centre
of the nodule, instead of having the soft character like Camembert
cheese, resembles the firm but brittle American dairy cheese. Upon
opening such an area the central necrotic mass may split away from its
cortex and even shell out, leaving a cavity lined by a gray-yellow
membrane. These characters are best displayed in nodules of moderate
size, the small ones being like the yellow mammalian analogue, the large
being like indefinite cheesy masses. In the surrounding tissue evidences
of inflammatory processes seem decidedly greater in our material than I
am accustomed to see in human and veterinary pathology. This, it seems,
should be emphasized since secondary infection with pus cocci and other
pathogenic germs appears less often in birds than in mammals.
The difference speaks, therefore for a difference either in the tubercle
bacillus of birds or the avian physiology. Judging by the limited morbid
processes produced by injecting avian bacilli into rabbits and guinea-
pigs the reaction of the bird itself would not seem wholly responsible
for the difference. The local tissue reaction in all avian lesions is
mononuclear and fibrous, softening and pus being rare. It would seem
from this and similar operations that the bird expresses its resistance
to the bacteria by a fibrocellular reaction which goes on to fibrosis
without softening; perhaps this means also that their polynuclears are
not sufficiently active, but the pathogenic power of the bacillus itself
doubtless is individualistic.
The character of the cheesy degeneration is likewise different from the
mammalian. It seems like an abrupt hyaline necrosis of a large central
mass and not the slower cell death seen in the other types of tubercle.
At times the degenerated area, instead of having the yellowish color of
caseation, will present what we have designated “gelatinous
tuberculosis,” the whole infiltrated area resembling boiled sago or
tapioca. This seems to be a complete homogeneous coagulation or hyaline
necrosis of the whole mass out to the delicate fibrous mantle supplied
by the tissue in which the tubercle lies.
The organic distribution of tuberculous lesions has already received
some attention and is to be discussed with the orders. There are,
however, some localities affected conspicuously in the bird. The skin
lesions often attract attention during life. They occur around the eye,
at wing joints, on the cresta sterni and on the legs. Parrots and jays
have shown nodular or diffuse growths around the eye, originating both
in the lids and orbit, which on section have proved to be tuberculous.
These seldom ulcerate, but those upon the skin of the breast and wings
tend to have superficial erosions or deep ulcers. The latter lesions are
more common upon pigeons but have been seen in Psittaci and Galli.
Toucans and pigeons when pinioned, have on three occasions shown a
tuberculous mass on the stump.
[Illustration:
FIG. 52.—MASSIVE TUBERCULOSIS IN LIVER AND SEVERAL MURAL TUBERCLES OF
INTESTINE. COMMON PEA FOWL (PAVO CRISTATA).
]
[Illustration:
FIG. 53.—NODULAR HEPATIC LESIONS IN THE LIVER OF A DOVE.
]
Two parrots with hyperkeratosis of the beak and of the skin of the feet,
have also had tuberculosis. These have been mentioned in literature as
of tuberculous origin. One case well studied failed to show tubercle
bacilli in the corns. In the absence of tubercle bacilli, one is
inclined to think that this might be explained on the basis of a
circulating toxin such as is assumed to be responsible for hypertrophic
periosteitis. This latter condition has not been seen in birds.
Still another type of occasional occurrence deserves mention. While most
of the lesions in birds correspond to the description given in the
preceding pages, some lesions fail to degenerate in the centre,
retaining instead a solid homogeneous fleshy character of dull gray-
yellow color. Upon section these have been found wholly cellular in
construction. To distinguish them from the ordinary nodules they have
been designated tuberculomata. Lesions of this kind may occur along the
lymphatic paths, indeed seem more common in the lateral cervical and
thoracic chain, and upon bones and nerves. When they are numerous the
nodular caseous type is inconspicuous. They suggest the bovine infection
(Pearl disease), but one attempt to prove this failed. We are of the
opinion that this is the avian lymphatic form, as our examples
correspond to the literary descriptions of cervical tuberculous
lymphatics in birds. No especial variety of bird is more often affected
by this process.
Intestinal tuberculosis among the Aves may be said to assume three
forms. The best known, indeed the form usually spoken of as representing
the common picture, is that which produces varying sized nodules upon
the serosa, sometimes associated with adhesions to neighboring
intestines. Just how this type develops is not known. In some quarters
it is believed to originate by the penetration of the tuberculous
granulation tissue from the mucosa through the intestinal wall by
following lymphatic channels and that irregular contractions of the
musculature squeeze the exudate outward under the serosa. Other
observers think that the bacilli are carried _via_ the lymphatics to the
superitoneal tissue, there starting the tubercle. The truth of the
matter will probably be that both methods are operative although we have
seen more cases suggestive of the second than of the first explanation.
When these peritoneal nodules are numerous and prominent, mucosal ulcers
are uncommon and _vice versa_.
The second form is the ulcerative, flat ragged or crateriform defect
situated in a diffusely thickened wall. This was well illustrated in
cases of pulmonary infection in doves and guans, suggesting reinfection
of the gut tract from swallowed tubercle bacilli or a backward
development of the disease after the lungs were nearly solid.
The third form of tuberculous enteritis is quite interesting and
striking. It is best seen in the duodenal loop but may occur anywhere.
Diffuse thickening of the enteric wall is noted, and when palpation is
practiced a resilient but leathery sensation is obtained. Careful
inspection reveals the mucous surface to be velvety, a condition due to
a swelling, that is widening, of the villi which retain their erect
position and, when washed in flowing water, will be seen to move like a
field of grain in a breeze. The serosa may be, usually is, negative.
Studied microscopically the peculiarity of this form is in the
development of tubercles and diffuse cellular exudation in the villus
stalk, sometimes extending into the submucosa also. Round cell masses
like lymph follicles are sometimes prominent. This form is not
associated with any peculiar organic distribution so far as my studies
go.
[Illustration:
FIG. 54.—TUBERCULOUS MASSES OF INTESTINAL WALL SHOWING OUTWARD GROWTH.
SOMETIMES THESE MASSES OBSTRUCT THE LUMEN.
]
Passeres. The peculiarity of this order seems to be in the predominance
of the pulmonary route as origin of tuberculosis. Perhaps in no other
order has there been such extensive and advanced lesions as in these
little birds. Sometimes one whole lung will be solid while its fellow
will be half occupied by caseous material. The doves alone seem to
approximate the Passeres in ability to live with so much tuberculous
exudate.
Picariæ. Specimens from this order illustrate well the intestinal origin
and distribution of tuberculosis. There was, among these birds, one case
showing tuberculomata which was, because of its gross anatomy, listed as
the pearl type. Its description is as follows:
Lesson’s Motmot (_Momotus lessoni_). The region above and behind the
right clavicle in front of the brachial plexus on the internal surface
of the thorax, exterior to the first and second ribs, and on the
internal surface of the ribs at the junctions of ribs with the alæ of
the sternum, there are many small, irregular, smooth, firm, yellowish
white nodules varying in shape from spherical to sweet potato and in
size from 3 × 3 mm. to 3 × 7 mm. These are found quite homogeneous on
cross section. They do not resemble tubercle or mould infection but
make one think of neuromata. There are also a few present in the left
lateral air sacs, close to but not joining the intestine. The lungs
are apparently normal. Histological section of the masses described as
distributed along the nerves consist of sharply outlined but not well
encapsulated masses made up of irregularly disposed bunches of large
cells with vesicular nuclei in a stroma of loose connective tissue
very inconspicuous in amount. There is also quite a number of small
round cells and a few leucocytes. The large cells first described have
the nucleus eccentric for the most part. Many of them have two nuclei
and a few three and occasionally a giant cell is observed. Blood
vessels have a very delicate wall and are frequently encountered in
the centre of these masses. Atypical mitoses can be found. Here and
there a seal ring placement of the nucleus can be found. A few
eosinophiles are present not definitely placed. Necroses, with large
quantities of nuclear fragments, are scattered irregularly through the
mass. The diagnosis rests between an infectious granuloma, false
neuroma and sarcoma. Tubercle bacilli were found by stain in great
numbers both within and without the cells.
Psittaci. Tuberculosis occurs in this order somewhat more frequently in
the varieties whose habitat is the Eastern world, although South
American birds also suffer from it in the characteristic manner. There
seems to be no difference in the pathology of these two groups. Parrots
present very beautifully the separate solid or semisolid nodules of
avian tuberculosis, whether they be in the lungs, liver, or spleen. When
the lung becomes riddled with masses, coalescence occurs and the whole
mass turns into a cast of the hemithorax. Lesions in the liver are
mostly isolated, but the spleen often appears like one large pink
tuberculous nodule. The liver occupies as usual the first place in
organic incidence.
Striges. Owls (and Struthiones—see below) present the interesting
exception to the rule of intestinal origin of tuberculosis in birds.
Perhaps the platting is incorrect but the birds in the order under
discussion had older and much more advanced lesions in the lungs and
thoracic serosa than they did in the abdominal organs. That this was
true in all three examples is in itself noteworthy. Perhaps they possess
less pulmonary and more intestinal resistance. One of these birds showed
a small recent cavitation in the posteroinferior angle of one lung.
Accipitres. With one exception the cases of this order occurred among
the Falconidæ, that is in hawks, buzzards, and eagles. Their lesions are
usually generalized as indicated by the figures for visceral
distribution, but that half the number should have the oldest, most
prominent lesions in the lungs is curious. Their intestinal tuberculosis
seems mostly of the diffuse infiltrative type.
Columbæ. These birds are obviously the most susceptible of all the
varieties of which there are sufficient autopsies to make a comparison.
Generalized nodular lesions emanating from the intestinal tract comprise
their usual form, while most of the hepatic lesions are small miliary
and nodular; occasionally one sees caseous masses destroying large
sections of the organ. Their intestinal lesions may assume any of the
three forms described.
Galli. This is an order of something over the average percentage
incidence for the birds but containing families that seem very
susceptible to tuberculosis. The small number of Brush Turkeys
(_Catheturus lathami_) had 60 per cent. of the disease, while South
American Cracidæ had 44 per cent. These two groups raise the incidence
for the order. Galli as a group have generalized nodular tuberculosis
originating by the intestinal route. This is especially seen in the
Phasianidæ, while the very susceptible Cracidæ have much more prominent
lesions in the lungs, often of a massive caseous type. It is really
astonishing at times how much of the pulmonary tissue is occupied by
infiltrate before death has supervened.
Fulicariæ are represented by a special contingent of rails and
gallinules. Avian characters are well illustrated in the order. So too
the succeeding order, Alectorides, another variety of shore birds, run
true to the avian form. It is interesting to note that in the two cases
from each of these orders tuberculosis and aspergillosis have been
combined. The former has assumed the firm nodular type, while the
mycosis has been of the air sac variety. The following case is worth
citing as possibly illustrating infection _per cloacam_. There is,
however, no trace of this bird having been with a male with the disease.
Demoiselle Crane (_Anthropoides virgo_) ♀ . General tuberculosis
including the oviduct. All organs are thickly beset by caseous
tuberculous nodules except the lungs which have only a few scattered
ones. The oviduct is, for its lower two-thirds, much enlarged, firm,
tough, pale yellow, thickly beset with caseous nodules; upper parts
uninvolved. The kidneys are definitely enlarged, irregular, almost
mulberry-like, brownish yellow, firm and tough. On section the lobules
are irregular, connective tissue increased, urates in pelves.
Tubercles in intestines seem to be wholly peritoneal. This seems like
a tuberculosis of genital origin judging from condensation of
tubercles in the lower abdomen (mass around cloaca). The ovaries are
not involved. Lungs and thoracic air sacs relatively free. The
pericardium shows a whitish thickening of both layers due to the
presence of whitish granules like urates. Histological section of
kidney shows the capsule not greatly altered. Glomeruli largely
negative but a few show hyaline capsular thickening of vacuoles in
tufts or fibrosis in tufts or obliteration of whole structure. Tubules
largely degenerated, distended or distorted. Interstitial tissue
between the tubules definitely but irregularly increased. No real
attempt at regeneration. Few vessels show perivascular fibrous change.
One tubercle seen.
Anseres. These birds present no especial features so far as percentage
or organic incidence are concerned. The individuals are mostly geese and
swans, ducks being somewhat more often affected by mycosis than by
tuberculosis. However, both these diseases tend to assume the nodular
type in Anseres so that the diagnosis should be supported by
bacteriological discovery of the respective organisms.
Struthiones. The marked feature of this order is the prominence of the
isolated and confluent nodules in the lungs, of apparently greater age,
certainly of great size, than similar lesions in the abdominal viscera.
Caseation of the avian variety is well illustrated in these birds. The
thyroid body was involved in two of the three cases, the ovary in one.
The representatives of the Crypturi, two tinamous, came at the same time
and lived only a few months. Miliary tuberculosis of the small
precaseous variety was the form exhibited by both specimens.
HISTOLOGY OF THE TUBERCULOUS LESIONS.
The initial and characteristic unit of tuberculosis, the miliary
tubercle, seems to be constructed upon the same general principles in
all cases of the disease and in all members of the zoological groups in
our study and in a manner entirely comparable to that well known for man
and for the domestic animals. There are, however, certain minute
differences which are interesting and may at some time become important.
It is customary to speak of the bovine tubercle and of the human
variety, but there are also slight variations of the microanatomy of
each of these, while one may find on occasion a tubercle of the human
type in a cow and _vice versa_. Not all the domestic animals show the
bovine form, although in sheep and swine it is approximated very
closely. In the horse there is much greater tendency to a central
softening and fibrosis is not so common as in the bovine tubercle. I
have attempted to study the histological anatomy of each of the
zoological orders, but it has not resulted in any profitable discovery.
It is, however, possible to contrast the type commonly found in monkeys
with that characteristic for man and the ungulates and also to emphasize
the construction of the avian tubercle that it may be distinguished from
mammalian tuberculosis and from avian mycosis.
[Illustration:
FIG. 55. DIFFERENT VARIETIES OF THE MILIARY TUBERCLE.
A.—THE BOVINE FORM SHOWING THE NUMEROUS LANGHANS’ GIANT CELLS, THE
ABUNDANT SMALL EPITHELIOID CELLS. THE MODERATE NUMBER OF SMALL ROUND
CELLS, AND THE ACCOMPANYING CONNECTIVE TISSUE INCREASE. THERE IS
MODERATE CASEATION.
]
[Illustration:
FIG. 55. DIFFERENT VARIETIES OF THE MILIARY TUBERCLE.
B.—THE HUMAN TUBERCLE WITH CENTRAL COMPLETE NECROSIS. TYPICAL GIANT
CELLS, ABUNDANT EPITHELIOID CELLS AND THE RELATIVELY NARROW SMALL
ROUND CELL MANTLE.
]
[Illustration:
FIG. 55. DIFFERENT VARIETIES OF THE MILIARY TUBERCLE.
C.—THE TUBERCLE FREQUENTLY FOUND IN MONKEY TUBERCULOSIS. WITH RAPIDLY
ADVANCING CENTRAL NECROSIS ENCLOSING MUCH CHROMATIN DEBRIS. THE
ABSENCE OF LANGHANS’ GIANT CELLS. THE PRESENCE OF LARGE, PALELY
STAINING EPITHELIOID CELLS OF LANGHANS’ TYPE AND THE VERY SLIGHT
CIRCUMFERENTIAL REACTION.
]
[Illustration:
FIG. 55. DIFFERENT VARIETIES OF THE MILIARY TUBERCLE.
D.—AN AVIAN TUBERCLE WITH CENTRAL SHARPLY MARGINATED NECROSIS
CONTAINING MUCH CHROMATIN DEBRIS. THE IRREGULARLY ARRANGED
POLYNUCLEAR CELLS TYPICAL OF AVIAN TUBERCLES. THE SMALL NUMBER OF
REGULARLY ARRANGED EPITHELIOID CELLS. THE PAUCITY OF SMALL ROUND
CELLS AND THE PRONOUNCED CONNECTIVE TISSUE MANTLE.
]
The tubercle of the Primates is a loosely constructed affair lacking the
fibrous mixture of the bovine and the close cellular packing of the
human form. Studied from the periphery to the centre, there will be
found very little fibrocellular reaction in the immediately surrounding
organ, while the mantle of round cells, rather prominent in the human
tubercle, is often quite inconspicuous. The principal cellular component
of the miliary granuloma is the large pale endo- or epithelioid cell,
which is abundant, loosely arranged and without apparent purpose. In the
centre is an irregular necrosis usually retaining some chromatic matter,
probably the remains of recently destroyed nuclei, but this caseous
midpoint does not assume the dense acid staining common for many milia.
Giant cells of the Langhan’s or foreign body type are often entirely
missing, and when present are scanty. There may be large cells,
resembling the aforementioned epithelioid cells, with two or even three
large palely staining nuclei, but these latter are arranged irregularly
and not like the spokes of a wheel near the cell wall.
This picture suggests a rapidly growing inflammatory mass and indeed
this is the type that tuberculosis follows in monkeys. In a few cases
gross evidence of fibrosis in the serous surfaces and in the lungs has
been observed, but they are too rare to permit one to think that
connective tissue activity is an important part of the reaction of this
beast to the disease.
The avian tubercle as it rests in the tissue seems like a sharply
outlined almost encapsulated body. This is in part due to the
homogeneity of its structure and in part to the fibrocellular
condensation around the caseous part of the growths. Examined from
without inward, there is a round cell mantle, between the elements of
which course fine but easily perceptible fibrils; elastic tissue has
been seen among them. The small cells continue more deeply than the
fibres, to be succeeded in prominence by epithelioid cells of rather
dense character, the nuclei especially seeming quite rich in chromatin
and round. The rotundity of the nuclei remains not only in the single
separate cells forming the middle zone of the cellular cortex, but can
be found in the nuclei of the compound or giant cells which comprise the
internal layer lying upon the necrotic centre. These giant cells are
characteristic for the avian tubercle in assuming a form like syncytia
with nuclei arranged in irregular radiating columns. This internal large
cell area may completely surround the central necrosis or it may be
interrupted by the large single cells. Tubercle bacilli are more common
in and between single cells than multinuclear ones. Within the cellular
zone lies the necrotic centre, often, indeed usually, full of chromatic
debris. This centre is commonly quite amorphous but occasionally one
will see what is probably the remains of a coarse coagulum. Between the
necrosis and the cells one usually finds a split, a sort of separation
of the gangrenous from the living part. Old tubercles with denser
fibrous capsule retain this microanatomy in part, but the cellular zone
gradually becomes thinner and thinner until all that remains is a narrow
cortex of round cells and imperfectly retained multinuclear cells.
Tuberculous granulation tissue without definite milia consists entirely
of the round cells with small vacuoles and a fine but definite fibrosis.
Tuberculomata consist of cells of varying sizes with small round nuclei.
Interstitial fibrosis is delicate and barely visible unless especially
sought. Giant cells may be encountered but are not so large as in milia.
Necrosis occurs but not in an orderly manner in relation to cells as in
an isolated tubercle. Tubercle bacilli are very numerous.
[Illustration:
FIG. 56.—PHOTOGRAPH OF YOUNGEST AVIAN TUBERCLE AFTER COMPLETE
FORMATION.
]
[Illustration:
FIG. 57.—TUBERCULOMA, A SOLID TUMOR-LIKE MASS, CONSISTING OF CLOSELY
PACKED LARGE CELLS FITTED WITH RELATIVELY SMALL ROUND LOOSE NUCLEI.
THESE CELLS ARE CROWDED WITH BACILLI.
]
TYPES OF BACILLARY INFECTION.
According to experimental and statistical research, all the tubercle
bacilli of the higher vertebrate classes can be infective for any member
of these classes. Thus, for example, human bacilli have been found in
many orders of mammalia and in birds. The bovine form has been found in
swine. The lesson from this is that while the special predilection of a
variety of the tubercle bacillus may be for one kind of animal, it is
potentially a virus for other kinds. Hygienic principles have therefore
been laid down at the Garden which aim at the protection of all
specimens from every variety of tubercle bacillus. For this reason and
because the laboratory has not attempted extensive research on
bacteriology, few type determinations have been made and those at hand
offer nothing new or unusual; they are noted here as a matter of record.
Bovine bacilli have been judged by their slow growth and infectivity for
rabbits, human bacilli by the reverse of these characters. Avian
tubercle bacilli can be cultivated with reasonable ease directly from
lesions not bearing a mixed bacterial flora, and grow in a yellow,
moist, even, spreading colonization. In our two attempts at infection of
guinea-pigs, no success was had, although Rabinowitsch and others had no
difficulty in so doing; this strain may vary in virulence as do other
tubercle bacilli. No avian culture was obtained from a mammal, but a
bovine was found in a parrot and a human in a duck. Bovine bacilli were
isolated once from a monkey (see page 496) and in another case of
lymphatic type, bacilli of the short heavy blunt shape, supposed to be
characteristic of this variety of the germ, could be stained. Monkey
tuberculosis in our experience is usually due to the human tubercle
bacillus, judging by the staining characters and two successful
cultures.
DISCOVERY OF TUBERCULOSIS DURING LIFE.
Fully developed chronic tuberculosis may be recognized with reasonable
ease in the human being and some domestic animals. The diagnosis rests
largely upon the history and symptoms and partly upon the appearance of
the individual and upon signs elicited by physical examination. There is
good reason to believe that these latter methods are entirely applicable
to certain wild animals, notably those that can be caught and held
quiet, but because of their naturally great reserve many specimens offer
little reason for suspicion as to their tuberculous condition until near
death. Certain ungulates with chronic pulmonary disease get thin and
weak but remain on their feet with good appetite and satisfactory
discharges for many months. Primates, Carnivora, Rodentia and Aves not
uncommonly come to autopsy with very good coats and without great
emaciation and yet are heavily infected. It can be stated with fair
positiveness that no chain of historical data or gross observations are
certainly known to us as indicative of tuberculosis in the wild beast.
Coughing is not necessarily characteristic of chronic pulmonary
infection, although when continuous it rouses considerable suspicion,
especially in the Ungulata. It is to be interpreted with care in all
animals that have loose bedding as bits of straw or seeds get into the
throat causing irritation; the dust of hay may cause coughing in horses.
However much chronic or fatal tuberculosis may be interesting from the
standpoint of pathology or of zoological or visceral incidence, the most
important factors in our knowledge of the disease are its early
recognition and treatment, either for curative or hygienic purposes.
Since we have learned that advanced lesions may exist in an animal
without materially affecting its external appearance and behavior, it
naturally follows that early cases, possibly of an “open” or infectious
character are still less likely to give evidence of their existence.
This is well recognized by veterinarians as being true of cattle, but is
perhaps less well known, or possibly admitted, by those who handle the
very susceptible monkey.
Upon a visit to a foreign garden I was told that experience alone is
sufficient to enable an observer to detect tuberculosis, and that the
disturbance entailed in physical examination and tuberculin tests is
prejudicial to the well-being of all varieties, but especially the
delicate ones. I learned later that they had the disease in their
exhibition cages all the time but decided to put their method to the
test. Shortly after my return from abroad a splendid specimen of Grivet
Monkey (_Cercopithecus sabæus_) was condemned by the tuberculin test. He
was well studied by the superintendent and two very experienced keepers,
all of whom pronounced him one of the finest specimens they had ever
seen, and stated that he was behaving quite normally. Despite their
protests he was sacrificed, tuberculosis with early cavitation being
found in the upper lobe of the left lung. Incidentally vague physical
signs were found by auscultation, but as the monkey was unruly and had
long pectoral hairs little weight was placed on the observation.
However, it is frequently possible to make very thorough physical
examination of the lungs of the more tractable specimens, diagnoses of
pneumonia and bronchitis being frequently made in this and other parks,
so that treatment may be instituted.
IMPORTANCE OF TRANSMISSION AND KNOWN SUSCEPTIBILITY.
Some light upon possible reasons for the poor condition of an individual
animal is of course shed by a knowledge of the disease to which that
particular variety is most susceptible, to which may be added the data
obtained from previous deaths in the same group or enclosure. Thus, for
example, a sickly monkey would be suspected of having tuberculosis or
early osteomalacia, whereas no suspicion of these diseases would fall
upon the marsupials. The same position would be assumed if a dove and a
heron were out of condition.
In so far as enclosures are concerned, the matter is somewhat different.
Whenever a case of tuberculosis occurs in a cage, the remaining
specimens if any are removed and the place cleaned by soap and water and
disinfectant and paint. The naked flame from a blast lamp is used when
possible. Out-of-doors enclosures are vacated, spread with lime and
allowed to lie fallow for as long a time as practicable. These methods
have been in the main successful in clearing a cage of the disease, and
all our experience demonstrates the effect of cage hygiene and the
selection of non-infective replacements. A few places such as those
occupied by doves and guans have not been freed of infection, if one
judge by its appearance when new specimens are placed in them, but they
may of course be due to the infection from elsewhere. The history of
seven years in the new bird house where the hygienic conditions are
excellent, seems to indicate that a cage thoroughly cleaned is no longer
a source of danger, and that a repetition of tuberculosis in such an
enclosure is due to its importation with new exhibits.
The spread of the disease to nearby cages seems to depend upon two
factors. If the number of cases has been large and the infection
virulent, immediately adjoining cages are involved, but the tendency to
spread is directly proportional to the proximity of orders or families
that have a high susceptibility for tuberculosis. This second factor
seems to be the more important and is illustrated by our experience in
one corner of the new bird house. In this area are exhibited certain
doves and pheasants, among which are many cases, while the passerine
varieties nearby are little affected. So too in the flying cage the
disease has occurred in varieties with high general susceptibility.
There are at the present writing ten orders on exhibition in this large
enclosure and there have been more. An occasional case of the disease
occurs, but only in the orders which show it elsewhere. The Herodiones,
of which we have had nearly one hundred autopsies and many now are on
exhibition, are always well represented in this cage and yet show no
tuberculosis. In the ten orders mentioned above three show no cases of
the disease.
These observations illustrate the spread of tuberculosis, especially to
the most susceptible varieties, and how non-susceptibles under good
hygienic conditions fail to become infected even when infected animals
are near them. The freedom of activity in the large enclosure is
doubtless an important factor.
The history of the past three years with regard to the control of
tuberculosis in the small cages shows that twenty-nine were infected,
but by the measures employed nineteen have remained free of the disease
for one year; three of the remaining ten are known to have received
newly arrived and possibly infected specimens.
The accredited method of transmission in birds, the swallowing of
material soiled with the feces richly laden with germs, is the principal
reason why infected enclosures and their immediate environment are the
principal breeding places for tuberculosis. To be sure air currents may
blow the virus around, allowing it to light upon food in other cages but
this cannot be a great menace if for no other reason than that we have
had no epizoötic outbreak of the disease, when there were groups of
deaths in doves and guans.
Evidences with which to trace transmissions are much clearer in the
birds than in the mammals with the exception of monkeys and some
ungulates. Of course cases are perhaps too few in the carnivores and
rodents to permit correct deductions but it is very rare that more than
one case occurs in the same enclosure containing groups of these
varieties. Nor do animals in adjoining cages seem to “catch” the
infection. This observation does not suggest that any relaxation of
hygiene need be allowed but probably it implies that not many bacilli
are excreted by these animals; they cough very rarely. Groups of
ungulates (bison and deer) are often known to be infected but just how
it has arisen is seldom clear. Transmission from monkey to monkey has
been observed so frequently that it cannot be doubted, nor will anyone
wonder at it if reflection is given to the close personal contact of
these animals during their natural behavior. They huddle, pluck lice
from one another, take food from the mouth of another, bite and perform
many other actions greatly facilitating the transfer of any virus.
Bacilli may also be disseminated by coughing, drooling and with the
fecal discharges, for which latter there seems ample opportunity since a
notable percentage of cases have intestinal lesions. Monkeys do not seem
to raise sputum and expectorate it but they do eject saliva from their
lips.
Contraction of the disease from infected cages is believed to have
occurred at least once in our experience but the lesson of complete
sanitary cleaning of the enclosure learned from that happening, seems to
have enabled us to forestall its repetition.
THE TUBERCULIN TEST.
Tuberculosis presents the greatest single problem among the specific
infectious diseases which the director of a menagerie must attempt to
solve. Even though one may possess a knowledge of its zoological
distribution, clinical characters and pathological effects, these are
insufficient criteria for its detection at a stage when the animal might
be saved by treatment or, what is most important, removed from its
companions that they might be protected. To this end there remains but a
single procedure for the discovery of the existence of tuberculosis—the
use of tuberculin in one of its forms by one of its methods of
application. The use of this test in veterinary medicine needs no
commentary, having made its place in clinical and hygienic practice for
a quarter century or more. Armed with the knowledge of the satisfactory
use of the toxins of tubercle bacillus in cows, Dr. Penrose, Dr. C. Y.
White, Dr. A. E. Brown and Dr. Leonard Pearson began in 1901 a series of
experiments with old tuberculin of Koch which have led to the
development of a technique for its use in the detection of infected
monkeys. These interesting and instructive animals, being known as
highly susceptible since most of the collection died of the disease in
those days, and being handled with reasonable ease by experienced men,
were investigated as the most important specimens upon which to perfect
the method. Other varieties have been studied since and I shall refer to
them individually. The greatest amount of work and the most conspicuous
success attended the observations upon monkeys and the results of this
study are now in daily use in this Garden.
The work, conclusions and results, originated by Doctor Penrose, Doctor
White, and Doctor Brown can be described as one of the most completely
satisfactory series of observations in scientific medicine. Applying the
principle that a tuberculous animal reacts to the injection of
tuberculin by a temperature rise, the normal temperature curve of the
monkey was studied, that of the tuberculous monkey determined by killing
many specimens. This enabled them to state which animal was infected,
which was not and to place on exhibition only healthy specimens. Added
to this, strict hygienic principles in the housing and handling of the
animals have resulted in the elimination of the disease from our
exhibition house. Occasionally a case may develop, perhaps from feeding
by visitors, but the matter is no longer a problem. I know of no more
complete and satisfactory experiment and its practical application than
this work, which is condensed in the succeeding paragraphs.[101]
THE TEMPERATURE OF MONKEYS.
The success of the tuberculin test in the lower animals as in man
depends chiefly upon the alterations in temperature following the
injection of the toxin. It is generally admitted to-day that a healthy
animal’s temperature will not be affected by the introduction of this
material. There are in addition changes in the pulse and respiration
rate and in the physical signs but these are detected with difficulty
and are much less definite than thermometric records. The first
essential was therefore a thorough familiarity with the normal
temperature of the monkey, a requirement which met with considerable
difficulty from the beginning since the earliest observations revealed
puzzling irregularities. This necessitated the establishment of certain
regulations of technique which, after the preliminary tests, have been
found satisfactory enough to continue until the present day. All monkeys
are received in the quarantine rooms of the laboratory where they are
observed by the officials of the Garden and of the laboratory and there
they remain in separate cages until passed, as free from tuberculosis,
to the exhibition house.
The handling of monkeys for the purpose of taking temperatures is a
matter of no small importance since excitement will quite definitely
increase the registration. We have been fortunate enough to have in
charge of this work since its inception the same man, Keeper McCrosson,
who is thoroughly experienced in the care of these beasts and who can
catch and hold them with a minimum of disturbance. To him and to the
interested laboratory helpers much credit is due. Small specimens like
capucins and spider monkeys are caught with the gloved hand or with the
protection of a piece of heavy cloth. Larger specimens may be caught in
a net while strong monkeys are fitted with a collar and chain by which
they are pulled into the corner of the cage and held, while the door is
opened to permit a helper to catch the feet and arms. Two experienced
men can take the temperature of any monkey that can be handled at all
safely. The knowledge of how to do such work reduces the excitement of
the animal and renders more accurate the observation of its temperature.
During the period of temperature-taking food is given in small
quantities and only after the record is made.
Temperatures are taken in all animals by rectum,[102] the thermometer, a
separate instrument but always the same for each animal, well greased
with plain vaseline, being passed along the anterior rectal wall and
allowed to register for twice its indicated speed. During the
preliminary work, special instruments of officially standardized
accuracy were obtained by Doctor Brown but once the normals were
obtained, ordinary good thermometers registering from 94°F. to 108°F.
have been employed. If the record vary very much from the expected, such
as the figures obtained at the same time on the preceding day, or if the
rectum be crowded with feces, the instrument is shaken down and
reintroduced. In order to facilitate timing of exposures we use sand
glasses of three minute run.
After some experimentation by taking records at various times of day it
was found that monkeys as a group do not have a uniform temperature
during twenty-four hours but register a higher figure during daylight
than during darkness. This is probably due, as I shall discuss, to the
period of activity, not to the time of day. Figures obtained at various
hours indicated that the highest and lowest temperature would be
obtained if records were made at four-hour intervals at three, seven and
eleven o’clock AM. and PM. To give the normal temperature of a monkey,
the kind and the time of day are necessary adjuncts. Reference to forty-
eight hour charts which are used for the illustration of normal records,
and for contrast with tuberculin reactions later, will convey to the
reader a better idea of the normal daily rhythm of the simian heat
regulating system than would verbal description.
[Illustration:
CHART A. ORANG UTAN (Simia satyrus). Non-tuberculous at death.
]
NOTE.—In the temperature charts degrees indicated by circles and
connected by dashes are from records made after diagnostic tests by
injecting tuberculin.
The anthropoid apes (Curves A and B) have on the whole a mean
temperature nearer the human being than do the lower monkeys, but they
too present daily variables far greater than man. The high point of
their curve, at three PM., is in the neighborhood of 100°F. the lower
point around 97.5°F. From these charts and other records it can be said
that while the higher apes have a daily temperature curve with its high
point at three PM. and its low point at three AM., there is in them not
by any means the regularity of curve to be found in Cercopithecidæ and
Cebidæ. Our records of temperatures in the Hylobates (_Gibbons_) are not
extensive enough to quote but what we have approach those of the lower
monkeys.
[Illustration:
CHART B. CHIMPANZEE (Pan niger). Non-tuberculous at death.
]
Graphic curves of the normal temperatures of the various genera of
Cercopithecidæ and Cebidæ present striking similarities in the
regularity with which the daily rhythm is performed. In the seven genera
of which we have accurate records the normal high points fall between
102°–103°F. and the low points between 99°–100°F. while the curve of the
four-hourly steps is closely comparable. The curves D to J are
composites from charts of animals that have been tested with tuberculin,
which thereafter died or were killed and found free from tuberculosis.
Not every individual chart that may come to hand necessarily follows the
exact course detailed in these illustrative curves but these latter
offer a guide as to what is to be expected of the different varieties.
They show unequivocally the V-shaped curve of the temperature of the
monkey during twenty-four hours.
[Illustration:
CHART C. Composite chart of twenty-two non-tuberculous Lemures.
]
The Callitrichidæ or Hapalidæ have failed to show tuberculosis in our
Garden and little has been done upon them. As a matter of record there
is reproduced the only satisfactory chart at hand (K) taken very early
in the researches. It shows a similarity to those of the higher monkeys;
because of its very high afternoon record the animal was killed; no
tuberculosis was found.
[Illustration:
CHART D. Composite chart of eighteen non-tuberculous Cercopithecus.
]
The Lemures, being close to the Primates zoologically and presenting a
high incidence of tuberculosis, were included in this study.
Observations upon their normal temperature were hampered more than upon
that of monkeys and even to-day we cannot feel the same confidence in
the records. Irregularity is most marked and they seem easily disturbed
by handling. Chart C shows a composite temperature for forty-eight hours
of twenty-two proven non-tuberculous Lemures. The tendency for the
“night drop” is certainly existent but with much less definiteness than
in the Primates.
CONDITIONS WHICH MODIFY THE TEMPERATURE.
[Illustration:
CHART E. Composite chart of seventeen non-tuberculous Macacus.
]
Observations by A. E. Brown[103] and by Simpson and Galbraith[104] would
seem to indicate that the diurnal variation in monkeys is due to
periodicity of activity. Doctor Brown found that the temperature of a
night monkey is reversed, that it is higher during the dark than the
daylight hours. See chart of Potto (_Perodictus potto_) chart L. The
Scotch observers report that if the activity of day monkeys were
reversed, daytime being made artificially dark and activity forced
during the night, the temperature curves were likewise reversed.
[Illustration:
CHART F. Composite chart of eleven non-tuberculous Papio.
]
Perhaps the most important discoveries of these investigators concerned
the influence of excitement upon the temperature records. These
observers indicate definitely that the greater the physical activity and
nervous excitement the higher the thermometric record. We have noted
that the substitution of a strange keeper who may not be gentle and
tactful with the monkeys can serve to raise the temperature above the
records obtained by an experienced man with whose methods the animals
are familiar.
A knowledge of these facts dictates at least two important precautions
on our part—our specimens must be kept under identic conditions peculiar
to their kind, and surroundings must be established offering comfort
with a minimum of annoyance in transfer and handling. To this end all
specimens upon receipt are put into separate cages suitable to their
size and allowed to become accustomed to their surroundings for several
days before attempt at temperature-taking is made. Mention has already
been made of the experience and interest of the principal keeper; the
regularity of records is an attest to his work. Daily three o’clock
afternoon temperatures are taken first to accustom the animal to the
matter, before test records or tuberculin injections are made.
The existence of pathological states undoubtedly affects normal
temperature curves and tuberculin reactions. Gastroenteritis has the
effect of increasing the whole level and of making irregular the midday
and afternoon records. Respiratory tract disease cannot be said to have
a very definite effect; its most frequent influence seems to be to drive
the night records lower so that there is a long fall between seven and
eleven PM. and a long rise between seven and eleven AM.
THE TEST.
The preliminary rest of the new arrivals having passed daily three
o’clock afternoon temperatures are taken until an even level is
obtained; this requires usually four days but in very nervous specimens
it may be much longer. The afternoon temperature course provides not
only a means of teaching the monkey what is coming but supplies us with
a high point record for comparison. When a new variety is received, a
full normal twenty-four hour record is usually made. This preparatory
routine being fulfilled, the animal is injected under the skin of the
thigh or flank with freshly diluted mixed bovine and human tuberculin.
THE DOSAGE.
Early trials with this substance revealed the fact that a dosage based
upon the weight in comparison to man failed to elicit a definite
response whereas if based upon relative weight of cow was too large. The
finally determined quantity was arrived at, as was the case in early
human and bovine work, by experiment and trial and was as follows: A
monkey of five to ten pounds (2.3 to 4.5 kilos) received an initial dose
of 1. milligram and for each additional five pounds (2.3 kilos) 0.5 mg.;
this is 0.2 to 0.4 mg. per kilo. The amount given to man varies from 2.
to 5. mg.; if the body weigh 60 kilos this is 0.03 to 0.08 mg. per kilo.
Cows are given usually in this country 400 mg. or, for a cow of 250
kilos, 1.6 mg. per kilo. In the early work, doses comparable to the
figure for man failed, whereas at least two animals died very quickly
after 1.+ mg. per kilo; 5. mg. was the original high dose. While the
death of a monkey after a large dose was of no moment and was perhaps
desirable, it would only be the heavily diseased specimens and this
would give no criterion upon which to judge the appropriate dose for
all. Experience seems to warrant us in continuing with our present
figures since all tuberculous monkeys have reacted to it. Subsequent
cases for retest are increased from 50 to 100 per cent. depending upon
the size of the monkey, the very robust and vigorous ones receiving an
increase represented by the higher figure. One monkey injected eight
times has risen from 1. to 24. mg. with constantly a negative response
over a period of nine years.
Doses for Lemures are relatively higher, averaging 1.5 mg. or about 0.5
mg. per kilo; they are increased in the same manner as above.
THE TEMPERATURE TAKING.
Injections are usually made in the late forenoon, temperature records
being started at the usual three PM. hour and continued at four-hour
intervals for forty-eight hours, giving thirteen records over two days,
a time period presenting two complete cycles of diurnal variation. This
was found necessary because certain cases do not react during the first
day. Explanation of this was sought in the nature of the lesion but
could not be found further than that mild early lesions may give it but
it cannot be read as indicative of low activity since one case of
laryngeal tuberculosis had this “delayed reaction.” At times it has
seemed to occur when the injection fluid formed a blister under the
skin, a pocket in the areolar subcutaneous tissue, whence absorption
would be slow. Whatever the correct explanation, experience has
justified the recording of temperatures for full forty-eight hours.
[Illustration:
CHART G. Composite chart of five non-tuberculous Cynopithecus.
]
[Illustration:
CHART H. Composite chart of eleven non-tuberculous Ateles.
]
THE REACTION.
The experience gained with these monkeys supported definitely the
general opinion that tuberculin injected into healthy animals will not
disturb the temperature but will produce decided changes in that of
tuberculous animals. The reaction in the tuberculous animals may assume
several characters, of which usually two are combined in a chart. The
commonest and most convincing is a definite rise in the first twelve
hours, amounting to one degree or more; rarely it may be three degrees
(W). This is followed either by a maintenance of a high level or an
attempt to perform the night drop. It may be said that in general there
is an abortive attempt in nearly all tuberculin reactions to simulate
the V of the normal cycle; this can be seen in charts M, N, O and P.
Another rise may be attempted during a similar period of the second
twenty-four hours or the whole course may at that time approximate the
normal. A modification of this type of reaction is the performance of
the whole daily rhythm on a high level, set, as it were, by the initial
three PM. record. This form is confusing at times and has been
responsible for at least one of our mistakes. Combined with this high
level of curve is a tendency for the second twenty-four hours to be
higher than the first day (See Variegated Cebus Q and Sooty Mangabey R
and Chacma Baboon W). The second type of reaction, illustrated by chart
S, fails to resemble the normal daily cycle of the monkey temperature
but has sudden rises and falls as its characteristic feature. We have
learned to look with suspicion on all charts with sudden marked changes
of record even if they follow in the main a rhythmic course. The sudden
fall exhibited by a very sick monkey illustrated by Grivet Monkey (T)
and Campbell’s Monkey (U) is a bad sign. It has been met more often in
advanced caseous pulmonary tuberculosis than in any other tuberculous
lesion. On two occasions it has been seen in the absence of tuberculosis
so that retest is indicated if the specimen be valuable; such animals
however rarely survive the disturbance incident to the test as they are
usually suffering with some serious disease. Illustrative charts of
several positive reactions serve to elucidate their character better
than description. If comparison and contrast of the normal and post-
injectional temperature be made, the conclusions are definite.
[Illustration:
CHART I. Composite chart of eight non-tuberculous Cercocebus.
]
[Illustration:
CHART J. Composite chart of twenty non-tuberculous Cebus.
]
It cannot be said that any type of reaction indicates a particular form
of disease although the last type, the falling of the temperature beyond
the thermometric registration point, usually means advanced lesions
especially of the caseous pneumonic form. A very small lesion may give a
definite reaction as in Cebus (V).
[Illustration:
CHART K. GEOFFROY’S MARMOSET (Leontocebus geoffroyi). Non-tuberculous.
]
The examples given are those of a definite character but there are many
charts that vary from the normal upon which a decision is extremely
difficult to make. Such animals are held in quarantine to be retested
after the lapse of three months. Early in the work a suspected specimen
was reinjected after two weeks, failed to give a reaction but died in
about two months of tuberculosis. The nullification of the test by
previous injections of tuberculin is well known. Three months’ interval
permits a disappearance of the non-sensitivity and allows any latent
tuberculosis, possibly stimulated by the toxin, to develop. Repetition
upon the same monkey has occurred as high as ten times without apparent
harm.
[Illustration:
CHART L. POTTO (Perodicticus potto). Healthy.
]
There are sometimes in human beings local reactions at the point of
injections. These have been entirely lacking from our monkey specimens.
Nor have we ever seen secondary tuberculous lesions appear at the point
of the needle-stick. Aseptic syringes and generally cleanly technique
have also protected against local abscesses. When an animal is injected
he may scratch or pick at the spot for a minute or two but thereafter
seems to ignore it entirely.
[Illustration:
CHART M. MONGOOSE LEMUR (Lemur mongoz). Tuberculous.
]
[Illustration:
CHART N. BLACK HANDED SPIDER MONKEY (Ateles geoffroyi). Tuberculous.
]
RESULTS.
The value of the test can best be estimated by a recital of the
mortality of monkeys, from tuberculosis, since its inception. Before the
test was started practically every monkey in the collection for
sufficient length of time to be exposed died from the disease. The
average duration of exhibition life of all specimens up to 1903 did not
exceed eleven months. The time has risen almost uninterruptedly until
now it is thirty-five months. There are, at time of writing, sixty-eight
specimens in the cages which have been on view from one to one hundred
and eighty-five months with an average of fifty-four months. These
figures speak for themselves as evidence of the reduction of infection.
The average mortality from enteritis and degenerative bone disease has
remained about the same through all these years. Percentage figures such
as are recorded in our yearly report are misleading because all monkeys
written into the property record of the Garden are listed and since some
of these specimens remain in quarantine, they do not properly belong to
the exhibition collection. Up to 1906 when the test technique was
perfected nearly all deaths were due to tuberculosis, the figure for
1906 (including experimental animals) being 78 per cent. However from
February 1906 to October 1907 and from then until May 1910 no case of
tuberculosis occurred in the exhibition cages and both deaths at these
given times seem like infection from visitors. During the next three
years thirteen monkeys died of the disease in the exhibition and many
more in quarantine. By 1913 the outbreak was stamped out. Its
explanation is not so very far to seek. In the fall of 1910 we obtained
some suspected monkeys which were kept in one of the quarantine rooms.
After repeated testing two were passed. From them five cases are known
to have originated and it was not until in 1912 when the whole
exhibition house was cleaned of specimens, thoroughly disinfected and
fumigated and until every specimen was retested, that the infection
passed. In 1914 no cases occurred, while in 1915 a case either slipped
through undetected or was a visitor infection; 1916 two cases, 1917 one
case, 1918 one case (see orangutan charts), 1919 and 1920 none and 1921
one case, 1922 no cases. Since 1912 the whole monkey collection has been
tested every two years, a method which enabled us to catch a small group
in 1916 and has protected the collection since then. Three of the six
monkeys specified above were never placed free in the general cages of
the exhibition house, they being segregated in smaller cages. One, the
orang, was with its mate in an isolated cage. The other two were in
larger cages and their history suggests visitor infections.
[Illustration:
CHART O. RHESUS MACAQUE (Macacus rhesus). Tuberculous.
]
[Illustration:
CHART P. ORANG UTAN (Simia satyrus). Tuberculous.
]
We have never underestimated the possibility that an occasional very
early case might evade detection by this test but we believe the history
just outlined warrants us in depending upon it for the protection of the
exhibition. By the tuberculin test we have detected the existence of the
disease in twenty-three per cent. of specimens. Every condemned
specimen, forty-one, showing tuberculosis, gave a positive test. Fifteen
monkeys condemned on their temperature charts failed to show the
disease. Eight per cent. of the tests resulted in suspicious charts, and
the animals finally died of the disease in quarantine. Fifty-six
tuberculous monkeys died on exhibition, of which thirty-one were
original there and twenty-five their contacts. Twelve of the thirty-one
were in the early stages of the work, thirteen due to our misadventure
of 1910 and the remainder, six, scattered over nine years.
[Illustration:
CHART Q. VARIEGATED CEBUS (Cebus variegatus). Tuberculous.
]
[Illustration:
CHART R. SOOTY MANGABEY (Cercocebus fuliginosus). Tuberculous.
]
Another interesting experience concerns the exhibition of a group of
Rhesus Macaques in an open “band stand” cage. The idea arose in an
attempt to find a separate exhibition space for some good specimens that
gave unsatisfactory charts, with the purpose of applying at the same
time the “open air” treatment if tuberculosis existed. The experiment
has been entirely successful since in the eleven years during which this
enclosure has been used there has been but a single case of tuberculosis
among twenty-six monkeys. Curiously enough this exception gave a good
chart and we suspect it was a visitor infection; no secondary case arose
from it. The animals housed in this cage keep in excellent condition,
their coats responding to our severe winter by increasing in thickness
and glossiness. Frozen toes, fingers and tails are sometimes seen but
these monkeys seem just as happy as the others. Breeding is active and
the young are lusty and husky. Practically the only deaths are due to
accident, or to abuse of old and less vigorous members of the colony. We
are unable to give comparative exhibition periods and death rates for
monkeys in the large house and this open cage because some specimens
have been changed from one to the other but it is certain that the
appearance of the “band stand” monkeys is better than those in the house
and there are four of eleven animals in the former which have been there
eleven years and only four among the seventy in the exhibition house for
that length of time.
[Illustration:
CHART S. VERVET MONKEY (Cercopithecus lalandii). Tuberculous.
]
[Illustration:
CHART T. GRIVET MONKEY (Cercopithecus sabæus). Tuberculous.
]
The results of the foregoing work seem to demonstrate that the
tuberculin test permits the separation of tuberculous and non-
tuberculous monkeys and that its employment serves the purpose of
maintaining a healthy exhibition by excluding infected specimens. These
experiences form further corroboration of the facts that tuberculosis
begets tuberculosis, that a healthy individual is not a source of
infection. It follows that an obviously tuberculous animal should not,
need not, be a source of danger; the hidden or unrecognized case is the
menace. There is little or no problem when an unequivocally good or bad
temperature record is obtained; it is when there are slight variations
from the standard for the group that decision as to the disposition of
the specimen must be made. Nearly always such specimens are retested
until the records are definite. If they be constantly irregular the
animal is either sacrificed or exhibited in a separate cage far from
other monkeys. It is by the sacrificing of infected specimens or the
segregation of suspected ones that our collection is kept clear of
disease.
[Illustration:
CHART U. CAMPBELL’S MONKEY (Cercopithecus campbelli). Non-tuberculous.
(See page 533).
]
Hygiene of a general character must be maintained also. Our quarantine
rooms are disinfected by formaldehyde and mechanical cleansing after
every case detected as tuberculosis, and painted every two years.
Monkeys associated with infected ones, are retested and then given a
bath of carbolized water before being put on exhibition. The exhibition
house is mechanically and chemically disinfected at the injection time
each two years. All keepers are examined for tuberculosis upon beginning
their employment and those handling monkeys, periodically thereafter.
When a case of tuberculosis dies, all animals in the same and adjoining
cages are removed for retest and the enclosure scrubbed and disinfected.
[Illustration:
CHART V. WEEPER CEBUS (Cebus capucinus). Tuberculous.
]
There is a source of tuberculosis upon the importance of which we can
only speculate—the visitor. There were two isolated cases in animals
which had passed the test with unexceptionable charts, three and four
months on exhibition; curiously enough no other cases occurred in their
cages. These we have laid to visitor infection since no previous
exposure can be traced for the specimens and no secondary cases
occurred.
I can conclude this discussion of the tuberculin test and of the control
of tuberculosis by its use, by mentioning the possibilities for the
solution of the problem in man. While the eradication of the disease
cannot be accomplished as easily as if a potential source could be
eliminated by sacrifice, it will come in direct relation to the
earliness of detection of infection and isolation of the sources of
danger. Not so much the cough-racked consumptive but the unrecognized
early lesion whose bearer hawks and spits in public places or at home,
unaware of his malign power!
[Illustration:
CHART W. CHACMA BABOON (Papio porcarius). Tuberculous.
]
THE SKIN AND EYE TESTS WITH TUBERCULIN.
The first of these can be dismissed briefly, for in a few cases it was
absolutely of no value. A known tuberculous monkey was injected _into_
the skin of the chest with 0.5 mg. of old tuberculin. The small bleb
disappeared in a few hours and was followed by no reaction whatsoever.
Other attempts likewise failed, some of them I believe due to the
technical difficulty of injecting into the skin. This tissue is very
thin, delicate and loose at the less hairy places where a reaction might
be read—arm, chest, abdomen. The hairless parts of the rump might be
used, but are so often scratched and soiled with dirt that readings
might be misleading. The Von Pirquet test was done on the first
mentioned specimen and was likewise negative. His tuberculin test was
afterward positive.
[Illustration:
CHART X. BLACK APE (Cynopithecus niger). Tuberculous.
]
The ophthalmic reaction is highly spoken of in the New York Zoological
Park and has been used elsewhere. It was tried by me at the time Doctor
Blair first discussed it, but with variable results. One set of two
monkeys was treated with Calmette’s purified tuberculin into the
conjunctival sac and given a subcutaneous dose of old tuberculin.
Another set received 1 per cent. old tuberculin into the conjunctivæ and
the usual subcutaneous dose. Although all these monkeys gave a
temperature reaction only one gave a conjunctival reaction. Fearing that
the two tests simultaneously might be an unfair trial, another poor
specimen was given an eye test which resulted negatively; a later
subcutaneous test and autopsy revealed the disease. Because of these
experiences and the fear that any reacting conjunctivæ might become
secondarily infected from the uncertain personal hygiene of the beast,
we decided to omit this method and rely upon the temperature test.
PATHOLOGICAL EFFECTS OF THE INJECTION OF TUBERCULIN.
It is generally believed that tuberculin injected into tuberculous
animals, in doses large enough to produce a marked reaction at the site
of disease, may stimulate the process to growth and spread and that
certain parenchymatous organs in such bodies undergo degenerative
changes. We can give little information concerning the first point
because known infected animals have not been sacrificed during the test
and we are not informed of the degree of morbid lesion in those dying,
since we had no previous knowledge of its existence.
[Illustration:
FIG. 58.—EFFECT OF TUBERCULIN ON THE KIDNEY. AN UNUSUALLY SEVERE
REACTION IN THE RENAL TUBULES AND INTERSTITIAL TISSUE FOLLOWING A
TEST DOSE OF TUBERCULIN. SUCH A MARKED CHANGE SUGGESTS THAT IN THIS
CASE PRE-EXISTING RENAL DAMAGE WAS AGGRAVATED. THE ANIMAL WAS
TUBERCULOUS BUT HAD NO LESIONS IN THE KIDNEY.
]
An interesting and practically useful observation has, however, been
made upon the kidneys of several monkeys dying shortly after tuberculin
injection. It consists in a marked cloudy swelling of the renal
epithelium and a congestion or even thrombosis of the glomerular
capillaries, accompanied sometimes by increase of nuclei in the tuft and
by amorphous material in the space of Bowman. Grossly such kidneys are
but little changed, albeit the cortical zone may be dull and opaque and
swell out slightly on section; very occasionally bloody streaks may
separate the cortical and medullary striæ. In a few kidneys there have
been suggestions of preëxisting nephritis but usually the findings are
confined to those given above. At all events true glomerulonephritis is
not often found. Monkeys which have this condition may or may not
exhibit a behavior suggesting its existence. Sometimes it will be noted
that the animal is dull and eats little, at other times the keeper will
report that the cage is seldom wetted and we know of cases in which only
an ounce or two of urine has been passed in a day. Two monkeys were
distinctly ataxic and incoördinate and one of these had a convulsion.
From one a specimen of urine showed albumen but no casts.
These signs of renal affection are not always alone nor are the kidneys
necessarily the only part diseased since postmortem records show a
variety of accompanying lesions, bronchitis and enteritis, for example.
There are, however, several cases dying in a few days after tuberculin
injection, both with and without tuberculosis, in which the renal
changes were quite prominent; two examples, without tuberculosis,
exhibited the damage to the kidneys very well and with no other evident
visceral pathology. The relation of cause and effect may not be
unequivocal, but these findings suggest that the condition of the
kidneys deserves attention when tuberculin is to be injected. My
associate, Dr. Corson-White, is firmly convinced that the substance
whips up a preëxistent parenchymatous disease and wants to see a
urinalysis from every monkey that is in any way abnormal.
THE TUBERCULIN TEST IN OTHER ANIMALS.
Two cases of tuberculosis occurred in White nosed Coatis (_Nasua
narica_) so that it was decided to test their neighbors in the next
cage. There is reproduced a composite (Y) of the temperature record of
three of these animals after receiving 2 mg. of tuberculin under the
skin. No tuberculosis was found in them at death, all dying within two
years. The similarity to the primate type of temperature curve is
striking.
Chart Z shows the course of temperature before and after tuberculin
injection in a Bactrian Camel (_Camelus bactrianus_) ♀ which lived for
some months and showed no infection at autopsy.
Charts AA and BB show the temperature ranges of respectively a healthy
and a tuberculous Bison (_Bison bison_.)
Chart CC is that of a Malayan Sambur Deer (_Cervus equinus_) which died
a week after injection, showing fibrocaseous tuberculosis. The failure
to make an initial rise is noteworthy, but the fall in temperature may
be explained by the severity of the lesions and the approaching death.
Chart DD represents daily and post-injection records of a Virginia Deer
(_Cervus virginianus_) which at death was found free of the disease.
Chart EE is that of a healthy American Elk (_Cervus canadensis_).
[Illustration:
CHART Y. Composite chart of three non-tuberculous coatis.
]
[Illustration:
CHART Z. BACTRIAN CAMEL (Camelus bactrianus). Non-tuberculous.
]
[Illustration:
CHART AA. AMERICAN BISON (Bison bison). Non-tuberculous.
]
[Illustration:
CHART BB. AMERICAN BISON (Bison bison). Tuberculous.
]
[Illustration:
CHART CC. SAMBUR DEER (Cervus equinus). Tuberculous.
]
[Illustration:
CHART DD. VIRGINIA DEER (Mazama virginiana). Non-tuberculous.
]
[Illustration:
CHART EE. AMERICAN ELK (Cervus canadensis). Non-tuberculous.
]
SECTION XVII—PART 2
MYCOSIS
This is a general term applied to the infections with Hyphomycetes, but
in the zoological material discussed here it refers chiefly to the
growth of aspergillus in the air sacs and viscera of birds. A few cases
of cutaneous mould growth have been seen in mammals but are of trifling
importance; brief mention will be made of them on a later page.
Under the names of Aspergillosis and brooder pneumonia, the infection
with _Aspergillus fumigatus_, _A. glaucus_ and others is well known to
breeders of chickens, ducks and ostriches. Literary references to its
occurrence in zoological collections are numerous, but there seems to be
no record indicative of its frequency in the various orders nor
discussion of the pathological types best exhibited by different birds.
There has indeed been some discussion of the actual entity, mould
disease, the picture found at autopsy being referred to secondary
contamination with fungi in the presence of bacterial infection.
Experiments by DeLong and others have been indifferently successful in
the production of the disease by inhalation of mould spores. The
appearance of groups of cases in breeding places, apparently all
exhibiting the same organism, in the absence of other varieties of avian
epizoötics seems to warrant the conclusion that the hyphomycetes can at
least be associated with a fatal morbid lesion of quite uniform
character whether or not they be the original invaders.
Judging by our experience it would seem probable that the aspergillus
can, under conditions not fully explained, cause inflammation of the
avian air sac and tubercles in viscera, in the absence of other evident
causes of illness and death. Over three-fourths of our cases have no
other diagnosis than “mould disease”; this may be in part due to
overlooking other things, but to a much greater extent to the very
extensive mould growth which obscures all other changes. That
unexplained preparatory conditions may exist is indicated by general
observation and some experimental work. Whereas in breeding
establishments this disease occurs in epizoötics, or in groups of cases,
with us it is enzoötic, constantly present, never, however, bursting
forth in virulent form with high mortality. Nor is the condition highly
contagious.
In an attempt to explain its source I examined over forty varieties of
feed and found therein several strains of aspergillus and of mucor; the
latter occurs occasionally in the avian air sac. The infective material
is therefore constantly present, and it would seem that if it were
capable of initiating a fatal disease many more cases should come to our
attention. Perhaps these moulds do gain access to the avian air sac and
are killed off, or only assume a pathogenic rôle when they are in large
numbers or a preëxisting disease assists them. Since our records do not
support the idea that a preceding condition must exist for a growth of
mould to be successful, and yet pathological and experimental
observations suggest that something helps its colonization in the air
sac, what are such conditions? Moulds grow on feed and litter in which
birds pick; from this it is quite possible for a piece of grain or even
inorganic matter laden with spores to be inhaled and lodged in a
secondary alveolus near the air sac whence extension into the air spaces
could occur. In addition I think it quite conceivable that a whole
colony of mould might be inspired with the same result, the mechanical
obstruction being sufficient physical damage to incite inflammation. The
continuous moist surfaces of the bronchial passages and air sacs afford
conditions favorable to the growth of mould and as inflammation is not
vigorous, little resistance is presented to its spread.
The mode of operation of these hyphomycetes has usually been assumed to
be a mechanical one, local colonization replacing healthy tissue or
spreading along surfaces so that function is physically impossible. A
support of this idea is to be found in the fact that inflammation, as
produced by schizomyces, is trifling or absent; the necrosis that occurs
is due to choking off of tissue by the intricately tangled masses of
mycelia and blocking off of air or blood supply. The existence of an
infiltrating and necrotizing form in some parrots and gallinaceous
birds, suggested to me that a toxin might be responsible for some part
of mould action. Proof for this speculation was sought by injecting into
the pectoral muscles of pigeons an emulsion of a dead mould and a
filtered broth culture. Necroses occurred but only to an extent which I
interpreted as due to the physical destruction of muscle by the injected
material; they were larger with the dead mould than with broth filtrate.
I concluded therefore that aspergillus perhaps has no toxin as usually
described for bacteria.
TYPES OF MYCOSIS.
Avian mycosis occurs in three different forms, two of which are probably
of similar nature and two are frequently combined. The first variety,
most often seen in gallinaceous and anserine birds, consists of
thickening and opacity of the air sac walls, upon the surface of which
either a curd-like pseudocoagulum or a velvety or fluffy mould growth
appears. This variety usually begins about the anteroinferior pulmonary
stoma on the right side extending thence to the related sac, upward
toward the wing and downward to the abdominal spaces. Occasionally the
middle thoracocervical space is involved, probably _via_ the opening in
the syrinx. Extension takes place by the way of normal passages, but
when the growth is dense it also seems to occur by continuity through
tissue. This variety may or may not be associated with the second, an
infiltrative type of lesion best seen in the lung. Under what seems to
be a true picture of mycotic pneumonia, dirty gray consolidated areas
will be found around the bronchial space, infiltrating in all directions
and without definite boundaries. A similar lesion has been seen also in
the liver on rare occasions, but the lung is its usual seat. Judging
from microscopic appearances this is a process complicated by the
addition of bacteria.
[Illustration:
FIG. 59.—NODULAR OR TUBERCULAR MYCOSIS IN THE LUNGS OF A DUCK. ONE-
HALF OF THE LUNG IS CUT AWAY AND LAID ON THE INTESTINES TO CONTRAST
THE PLEURAL AND SECTION SURFACES.
]
The third variety is nodular or tubercular mycosis, a process of
probably more chronic nature since around the isolated lesions
connective tissue is perceptible, it being absent or inconspicuous in
the other types. The formation of gray or yellow-white nodules from a
few millimetres to a centimetre in cross section, is the characteristic
production in this variety. Lungs, liver, spleen, intestines and air
sacs are involved in about this order. Attempts at explanation of this
peculiarity of growth were made in the direction of identification of
the species of mould, kind of bird and probably degree of resistance. No
conclusions could be drawn since the same variety of mould was found in
this as in other types; no bird showed a special susceptibility or
resistance to it. It is quite difficult to obtain a culture from nodular
mycosis, it being necessary to crush or grind the solid masses before
making cultural implants. This variety should always be differentiated
from tuberculosis by staining for the organisms.
Histologically studied these three types are not as easily separated as
the gross appearances would warrant one to expect. The original mould
nodule begins in essentially the same manner in all, a small
colonization of mycelia and spores which grow centrifugally, but ever
becoming more intricately wound in their first location. As the tissue
is invaded, total necrosis takes place, no recognizable cellular
architecture being left. When fully formed the mycotic tubercle consists
from the centre outward of a necrotic mass, in which spores and mycelia
stain indifferently well, surrounded by a dense zone of fully formed
mould beyond which mononuclear cells and a few loose fibrils may be
found. The circumferential tissue of the viscus supplies a mild
congestion and perhaps a moderate connective tissue capsule. Giant
cells, as known for tuberculosis, do not appear.
Where the process involves loose tissue like the lung, especially when
growing rapidly, the sporulating heads of the mycelia stretch out in
advance of the main mass and resemble rays. So too in a rapidly growing
nodule radiating mycelia are sometimes seen but never with the
regularity of arrangement typical for actinomycosis. Diffuse and
irregular mycelial spread is characteristic of the second or
infiltrative type of lesion and between the mould stalks one may
discover well preserved tissue cells and at times bacterial forms like
cocci or bacilli. This picture, suggesting as it does bacterial
admixture and more active inflammation, leads one to the conclusion that
the morbid process in which it is found does not represent mould disease
_per se_, but a mixed infection. Whether or not the bacterial disease
exists first and paves the way for the mould I am unprepared to say; I
am inclined to the view that mycosis can start by itself.
INCIDENCE IN AVIAN ORDERS.
Mycosis may be said to occur in all birds although the appended list
fails to show cases in a few of the orders included in this study; the
sum total of autopsies from missing orders is only 45, so that they may
be ignored.
═══════════╤═══════════
│ per cent.
Passeres │ 3.7
Picariæ │ _1.2_
Psittaci │ 3.9
Striges │ 6.7
Accipitres │ 5.1
Columbæ │ .6
Galli │ 2.7
Fulicariæ │ _8.6_
Alectorides│ _2.7_
Gaviæ │ _10._
Impennes │ _40._
Herodiones │ _2._
Anseres │ 6.
Struthiones│ _9.4_
───────────┴───────────
For meaning of italics
see foot note Table 1.
[Illustration:
FIG. 60.—MICROSCOPIC APPEARANCE OF ONE OF THE NODULES. NOTE THE
CENTRAL NECROSIS AND THE CLOSE FIBROCELLULAR PACKING IN THE
RESTRAINING CAPSULE.
]
[Illustration:
FIG. 61.—MYCELIAL GROWTH IN AN ALVEOLUS IN THE RAPIDLY SPREADING
VARIETY OF PULMONARY MYCOSIS. SEVERAL FRUIT-HEADS ARE VISIBLE.
]
These figures hardly permit conclusions as to relative vulnerability
unless the large percentage of cases for the small number of Impennes,
Gaviæ and Struthiones be permitted to stand. Judging from orders upon
which there are at least one hundred autopsies, owls, ducks and eagles
are most likely to suffer with mycosis. The percentages are, however,
not very convincing, and it would seem better with these data to
conclude for the present that any variety of bird is susceptible to
mould. Ostriches have long had the reputation of succumbing to this
affection, so that their outstanding position in the list is more easily
credited.
It was to be hoped that the various susceptibilities would assist in an
explanation of the genesis of mould disease, but the result of the
analysis is suggestive only in one direction which can be stated quite
briefly. Ostriches, owls, shore and swimming birds have large stomata
between the lungs and the lateral air sacs and show a high mould disease
incidence. The natural thought is that access of mycelia and spores to
the air sacs is facilitated. More comparative data is being assembled
upon this point. Water birds are more susceptible to mould than land
birds; the percentages based upon cases and totals for orders is 5.4 to
3.7.
The hygiene of mycosis is that of scrupulous cleanliness. Being hampered
by incomplete knowledge as to its genesis one can only apply common
sense measures. The germs having been found upon all the vegetable
feeds, it naturally follows that they cannot be eradicated, but their
colonization in large numbers can be prevented by repeated cleansing or
sterilization of bins and pans so that no mouldy or musty material is
given to the animals. At times of serious outbreaks sterilization by
burning all old feed, starting fresh with good material in bins painted
or saturated with disinfectant and then deodorized, is the only
salvation. Where the blast lamp can be applied, it is the safest
procedure. Autoclave sterilization should be thorough if practiced. By
constant vigilance we believe that our large exhibition house is
protected, but the sanitation of the pond, where many ducks have the
disease, can never be so satisfactory.
Mycosis among mammals as an organic pathological entity is certainly a
rare condition, indeed almost always to be considered an accidental or
secondary one. In so far as human pulmonary disease is concerned it is
among the pathological curiosities deserving of individual report.
Moulds of several varieties have been found in intestinal ulcers, in
cranial sinuses and in the ear, while generalized mycosis from thrush
and favus are reported (cases of thrush in kites with fatal outcome has
been described on page 168). Cutaneous infestation with mould is quite
another matter for ring worms and similar conditions are now believed to
be due solely to the penetration by spores and mycelia into the
superficial dermis and into hair follicles. Numerous small lesions have
been detected on dogs and cats that correspond to the ring worms
described for them; to these we have devoted little study, because when
discovered the animal is removed, treated or killed to protect others.
Doctor Weidman has discovered several varieties of hyphomycetes which he
will report upon at a later time. No case of generalized mould disease
has been found in mammals, but Doctor Weidman has discovered a hitherto
undescribed mould in ulcers and cutaneous abscesses of seals; no
extension beyond subcutaneous areolar tissue occurred in these cases.
Botryomycosis, while not strictly belonging to the foregoing group, may
be mentioned here because of its nodular tumor-forming superficial
growths. The case to be cited certainly belongs to this illy defined
group of diseases even if the organism was not isolated. It cannot be
accepted as wholly demonstrated that the disease described under this
name is always the same or that it has a single cause.
California Hair Seal (_Zalophus californianus_) ♀ . Had sore spots on
side for several months. Ate well up to three days before death but
ate something to time of death.
DIAGNOSIS.—Chronic enteritis with acute hemorrhagic exacerbation. Low
grade chronic diffuse nephritis. Botryomycosis. General condition
poor, subcutaneous fat practically absent. On the left side of the
thorax there is a warty and nodular thickening of the skin overlying
diffuse and flat thickening of subcutaneous tissues. There are warty,
pustular, fistulous communications in four places between surface and
deep mass. They are covered over with light crust. On dissection mass
is found to be in subcutaneous tissue well outlined and encapsulated
and consisting on section of dense, white, firm trabeculæ forming a
mesh around yellow, soft areas which can be squeezed out. An adjoining
lymph node is much enlarged, dense, tough, resilient, on section
showing great connective tissue increase and solid brown medulla. The
thyroids are solid, brown, 3. x 2. x .6 cm. and 3.7 × 1.8 x .6 cm.
Trachea and bronchi contain pink froth but mucosa is negative.
Anterior edges of lungs are distinctly emphysematous. Remainder of
lung is uniformly congested and lobules are quite prominent. No
consolidations. Bronchial lymph nodes are slightly large, anthracotic
and wet. The heart is dilated, filled with mixed clot, muscle firm and
deep brown color. The liver surface is smooth, edges sharp, size
normal, color dull brown with greenish cast, consistency firm and
tough. Section surface is glistening, smooth, moist, lobules
indistinct but probably normal. The gall-bladder is full of fluid
yellow bile. The common duct is patulous. The spleen is of normal size
and shape, capsule opaque gray. The trabeculæ are prominent, the pulp
stippled rusty brown. The kidney is of normal size, capsule is smooth,
strips easily leaving a smooth purple surface. The organ is firm. The
lobules and lobular markings are distinct. The adrenal has a narrow
regular brown cortex and gray homogeneous medulla. The stomach
contains whole fish. The mucosa shows digestion, congestion and mucus
formation. Beginning at the pylorus and extending to the colon the
mucosa is swollen and edematous, yellow brown. In the lower part it is
quite firm and opaque. In the upper part it is more translucent except
where there are diffuse hemorrhagic mottlings of the submucosa. Here
and there are shallow erosions but no ulcers. The lymphatics of the
mesentery are definitely enlarged, white, pale and very firm. Smear
from the surface of the growth in side fails to show any definite
yeasts or moulds by Loeffler’s or Gram’s stains. It is largely made up
of polynuclear cells with many large mononuclears, many of which are
phagocyting polynuclears and nondescript bodies. Cultures failed to
grow. Microscopic section of liver shows marked congestion with slight
hydropic degeneration of the epithelium. The kidney capsule is not
thickened. Interstitial tissue not grossly exaggerated but connective
tissue nuclei fairly numerous. Some tufts have decidedly more
elongated nuclei than others and connective tissue around the stalk
vessels seems hyaline. Capsule for most part not thickened but space
contains cells and detritus in many instances. Epithelium of the
tubules for the most part swollen, loosened and without nuclei. Some
imperfectly formed casts. The intestine shows distinct congestion of
the whole mucosa with here and there definite small hemorrhages well
out in the villi. Slight round cell increase but no definite fibrosis.
In submucosa around vessels connective tissue is hyaline in many
places. The tumor on side consists of dense strands of connective
tissue forming alveoli of varying size containing an exudate of fibrin
and cells, about three-fourths of the latter being mononuclears.
Neither connective tissue nor cells are arranged in a characteristic
or peculiar manner so the observer is forced to conclude that this is
one of the conditions of the group called Botryomycosis.
SECTION XVII—PART 3
THE STREPTOTHRICOSES
The organisms belonging to the genera Streptothrix, Actinomyces,
Discomyces and Nocardia as named by various authors have in common the
power to produce local chronic inflammation of gradually spreading
character and chronic course. Their most conspicuous representative, the
ray fungus, is best known as the producer of lumpy jaw in cattle and as
an occasional pathogen in man. Other members of the group cause certain
lymph-channel disease in domestic animals and pulmonary disease in man.
Pathogenic power, it is believed, lies in the ability of these organisms
to colonize and irritate, thus producing continuously enlarging
tumefactions, no evidence being at hand that any of them produce a toxin
either in their surroundings or within their own bodies. Because of
their constant irritation, bacterial mixed infection often ensues so
that purulent degeneration may occur at the original site of disease and
thence may spread via the blood vessels, or by continuity of tissues or,
if the mucous membrane of the pharynx be diseased, by the air passages.
The study of the genesis of actinomycosis is by no means a closed one.
While it is believed that pastures and fodder carry the organism and
that it gains access to the tissues by passing into small wounds that
are made by sharp sticks or grain beards, the exact origin of the
disease is not understood. The original lesion is certainly trifling and
the fully developed one may not be discoverable until it is well under
way and causes external deformity. Even when sloughing has occurred, the
disease is not very communicable. The method of contraction of lymphatic
streptothricosis in cattle is believed to be from other cases _via_ skin
wounds or if abrasions be soiled by infective dirt. Just how human
beings contract these infections, in the absence of infected cattle is
unknown, but for the pulmonary form the route usually followed in
tuberculosis is probably taken.
The material of our zoological collection permits few observations of
value upon “lumpy jaw” but we have encountered a streptothricosis of
kangaroos which may throw some light upon the whole subject and to these
cases I shall devote considerable space since no description of it
occurs in the literature.
ACTINOMYCOSIS.
This disease has been diagnosed with certainty in two American Tapirs
and with reasonable satisfaction in three deer. Two Malayan Tapirs have
also had lumpy jaw clinically but the organisms were not found. It is
interesting and noteworthy that other zoological collections have
observed the disease in this same animal, a fact which suggests the high
susceptibility of the tapir to actinomycosis. There are recorded in the
protocols a few times sluggish ulcers on the tongue in other ungulates
but I am not prepared to label them as actinomycotic since on one
occasion smears and sections were studied with great care and nothing
found to justify such a diagnosis; nor were there maxillary or pulmonary
lesions. Before passing to a discussion of the diagnosis and morbid
characters it seems worthy of emphasis that our cases of this disease
should appear in one family of Perissodactyla and in one family of
Artiodactyla, in the latter not affecting Bovidæ, the family to which
domestic cattle belong.
The diagnosis of lumpy jaw depends upon the growth of tumors in the neck
and maxillary regions which tend to break down and discharge a thick pus
containing “sulphur granules,” little masses of necrotic matter
surrounding colonies of the ray fungus. When these conditions are
fulfilled, the matter is easily enough settled. This was possible with
the tapirs but in the deer the conclusion was not so easily reached and
the diagnosis had to be made partly by exclusion. Anatomically the gross
and microscopic appearances of lumpy jaw in the tapirs follows the text-
book descriptions but our cases in the deer deserve separate comment.
Whether or not these differences mean a peculiarity of resistance on the
part of the animal or a new variety of streptothrix only further study
can settle.
The beginning of the lesion in the deer was in the jaw bone as
circumscribed or fusiform swellings appearing on the under surface.
Growth usually progressed into the pharyngeal cavity and backward under
the ear, but a large tumor stretching down the neck was only observed
once. Suppuration and ulceration occurred twice but only once were
bacteriological observations possible before death, and then they were
negative. The fatal outcome seemed to be due to inanition, possibly
because the animal could not eat, for respiratory tract involvement was
only present once and then to a trifling degree. At autopsy, actinomyces
in ray form were found in one animal only, the diagnosis resting upon
histology in the other two. Nor did the degenerated centre of the
swelling contain the sulphur granules in any case.
The microscopic characters of the tumors resembled those of giant cell
sarcoma and chronic rarefying osteoperiosteitis with areas of round cell
infiltration but no granulomata as are occasionally seen in lumpy jaw. I
have always felt that a “giant cell sarcoma” with inflammation when
seated in the jaw of a lower animal should be looked upon with grave
suspicion and be searched diligently for fungi. The organisms could not
be found in sections of any of these cases, although present in the pus
from a pocket in one. Reference has been made in discussing tumors of
the bones in gazelles and opossums to their resemblances to osteofibroma
and actinomycosis. The diagnoses were made after long study of the notes
and sections. Actinomycosis is usually unilateral while leontiasis
ossium is commonly bilateral; the tumors have not broken down nor spread
into the neck. In one macerated jaw bone the osteoporosis and
hypertrophic periosteitis were comparable to those of the bovine form
but the masses were not so extensive as is common for domestic cattle.
Treatment of this disease was attempted in the tapirs but not in the
deer; the latter are too nervous to be handled repeatedly with safety to
themselves. Following the usual method, potassium iodide was
administered in saturated solution on bread, beginning at twenty grains
thrice daily and rising in two cases to sixty grains thrice daily. It
cannot be stated that any material improvement followed this heavy
dosage although in one case the disease was very protracted—some six
months, so that it may have modified the progress of the lesion.
However, other things were done for the beast so that the effect of any
one kind of treatment is difficult to evaluate. It was noted that iodide
served to keep the stools quite loose and that its withdrawal was
followed by constipation; upon resumption of the drug normal bowel
movements appeared. Every soft spot was opened surgically to allow the
pus to drain away. A vaccine of _Act. bovis_ was prepared and injected
under the hide beginning at 0.5 mg. and rising to 2.5 mg. in five doses
after which the animal became so unruly that the injections had to be
discontinued. On the whole we are not impressed with the probability of
success in the treatment of actinomycosis in tapirs. In the future we
propose to try operation and the use of Dakins solution or Dichloramin
T.
STREPTOTHRICOSIS OR NOCARDIOSIS OF KANGAROOS.
A fatal disease of Australian marsupials characterized by swellings and
ulcerations about the lips, teeth, tongue and cervical tissues is known
apparently all over the world by observers of these animals in
collections. From commercial shippers of animals, from zoologists and
naturalists we have reports that wherever kangaroos and wallabies are
exhibited this disease makes its appearance and carries off a
considerable percentage of the collection. A fully developed case bears
a noteworthy resemblance to lumpy jaw, being called “jaw disease” by
non-medical observers. However, it is highly probable that, while the
most conspicuous morbid changes occur around the jaw, the agent
provocative of the disease is capable of causing different pathological
effects and that certain cases of septicemia and gastroenteritis are due
to it; Doctor Blair of New York concurs in this opinion. Our study of
the problem would inculpate a variety of Nocardia, possibly assisted by
certain schizomyces. I have seen in the literature, but unfortunately
cannot locate, a reference to an article by a Russian who observed the
disease and was convinced that its cause is to be found in a
streptothrix[105] obtainable from the necroses in the soft tissues of
the jaw, a view entirely in accord with our findings.
The disease is not very communicable because its appearance in a pen
need not be followed by secondaries in the mates of the sick beast. It
appears chiefly in newly acquired specimens but may develop sporadically
in those exhibited a long time and apparently not associated with recent
acquisitions. This suggests two or three possibilities. It may be
imported by new arrivals, or newcomers may meet a germ to which they are
unaccustomed and therefore less resistant, the strange surroundings
reducing their opposition to it. Old specimens may have enough
resistance to withstand infection entirely or only succumb to large
doses. Lastly one comes to the explanation commonly employed for
actinomycosis, the presence of the organisms in fodder or pasture,
perhaps all the time, but gaining entrance to the animal’s body _via_
wounds made by sharp sticks or the beards of grain.
While circumstantial evidence offers some support to this general idea,
it cannot be accepted as proven. I have not made studies of the feed for
the purpose of isolation of the streptothrix but cultures from the lips
and gingival margin of healthy and infected animals were made for its
cultivation. These attempts were fruitless, and without wonder since the
germ when isolated from a fully developed case is quite finical in its
manner of growth; there are so many kinds of bacterial life that they
may easily overgrow the one in quest. So, too, cultures made directly
from subcutaneous necrotic areas may not always give a positive growth
although smears from the same material may reveal numerous threads under
the microscope.
The idea that sharp grasses are responsible for the origin of Kangaroo
disease finds a protagonist in Dr. A. S. LeSouef, Director of the
Zoological Garden at Sidney, Australia, a gentleman whose judgment
carries weight. He writes: “We have found that it is entirely due to
getting spear or barley grass in their food; owing to the formation of
the mouth, this grass gets wedged in between the teeth and the cheeks,
penetrates the flesh and allows the bacteria to get a footing, this in
time heaps up on the inside and forms an abscess that bursts exteriorly.
Formerly all the Australian Zoos lost animals through this cause, but
now, through being very careful not to give any rough spined grasses, we
never have the trouble.” Since receiving this letter we have removed
straw bedding, and feed only soft alfalfa which is carefully inspected
for foreign substances. During this time we have had two cases but the
period of observation is too short for final judgment as to the value of
feeding grasses without sharp beards and spines. The appearances of
cases sporadically without reference to the arrival of new specimens,
the low communicability of the disease, its beginning in the jaw in most
cases and the prominence of pulmonary and gastric lesions, all seem to
support the thought that the virus is received with the fodder or drink.
The anatomy of the kangaroo’s buccal cavity favors the collection of
material between the gums and cheeks and between the root of the tongue
and the molars, while the “hare lip” also affords a crevice in which
food particles or foreign bodies may accumulate. These three places seem
to be the starting points of most of the cases.
THE COURSE OF THE ATTACK.
Despite careful watching of the exhibition specimens it is often
difficult to detect the beginning stages of the disease. Since our last
outbreak it has been the practice to examine all kangaroos thrice yearly
by catching them, inspecting the buccal membranes, teeth, tongue and
nose and by palpating the jugular and sublingual regions. This procedure
succeeded in catching one very early case from which the original
changes can be described.
The animal appeared in generally good condition but close inspection
revealed a “running nose,” a purplish mottling along the gingival margin
of one lower jaw below which was a doughy swelling; no internal
ulceration had appeared nor was there a visible change in the external
contour of the jaw. Within a few days a small fusiform lump appeared
along the body of the lower maxilla which spread gradually backward, the
nearby soft parts becoming involved very shortly. This particular animal
died without ulceration but with evidences of septicemia. Usually at the
time that the lump is noticeable the animal loses appetite, becomes
inactive and seems depressed; no especial change in the coat need be
perceptible although it may be lusterless or at times ruffled. In the
cases with great involvement of the cervical tissues, dyspnœa is an
early sign but I lay this more to pulmonary disease than to mechanical
obstruction of the upper air passages. The loss of appetite is in large
part due no doubt to the discomfort of chewing and swallowing in the
presence of an inflammatory mass in the neck. The eyes usually remain
normal until quite late. No change in the character of the droppings is
recorded.
A slightly different course is followed by the cases that have the
primary lesion in the “hare lip” and nose; from these the masses along
the jaw may be entirely missing. After an initial stage of “running
nose” with or without swelling of the upper lips and alæ of the nose,
the animal rapidly goes down hill, with dyspnœa, loss of flesh, perhaps
loose stools, lusterless eyes and a “dead” coat, a series of signs
indicative of a septicemic state not pronounced in the first variety;
any form of this infection may however present course and pathology of a
septicemic character. If the beast live long enough ulceration may
appear on the upper lips or a large area of necrosis between them may be
discovered.
There have been in our series two cases, believed to be due to the same
virus, which gave a picture of septicemia with pulmonary localization;
they will be discussed in detail later but are of interest here because
they were not known to be sick until the day before their death. A
similar failure to evince signs of sickness is found in the
gastrointestinal cases, those with ulcerations in the stomach and
perhaps an accompanying catarrhal intestinal inflammation. At most the
report will be that the specimen was “off its feed.”
[Illustration:
FIG. 62.—KANGAROO STREPTOTHRICOSIS. ULCERATIVE AND NECROTIZING PROCESS
IN “HARE LIP” AND IN MUCOSA AND BONE OF ANTERIOR PORTION OF HARD
PALATE; TEETH HAVE FALLEN OUT ON LEFT SIDE.
]
The signs of Kangaroo disease with exception of those applying directly
to the nose and jaw are therefore very vague and one is limited to
observation of the contour of the head and of the discharge from the
nostrils. Because of the indefinite nature of the earliest changes, the
duration of the disease cannot be stated with accuracy but from the time
that the swellings are perceptible it is not very protracted if no
treatment be given. Some cases die in four or five days while others may
last up to three weeks and we believe that two of our cases may have
been existent longer than that. It is impossible to estimate the
duration of the septicemic and gastric forms although the latter,
judging by the appearance of the ulcers, are believed to be chronic. We
believe that frequent inspection and the precautions as to the character
of fodder are the only special hygienic measures indicated.
THE INCIDENCE OF THE DISEASE.
Not the least puzzling character of the disease is the variability of
its appearance. There have been groups of cases in our records; for
example the following periods showed several while the intervening years
lacked them entirely—1905, 1907–8, 1911–2, and 1920–1. The second and
fourth outbreaks were definitely related to a new arrival but the
records do not show that such was the case for the other two. Mr. Joseph
who supplied us with many specimens, tells us that he has had an
experience of fifty-four cases in 200 kangaroos and then failed to
encounter the disease for years. Perhaps this irregularity of appearance
has something to do with the character of food supplied to the animals.
Among seventy deaths of Macropodidæ we have had thirty-three cases of
the varieties which I have included in this infection, made up of the
following forms: cases limited to the jaws, pharynx and neck, six; cases
of this sort with extension to lungs and stomach, ten; cases of this
sort with general spread suggesting septicemia, five; gastrointestinal
and hepatic, eight; nasal and sinus infection without necrosis in the
jaw and with general spread including the lungs, four. The total
incidence in Kangaroos is therefore 47 per cent., the necrotizing forms
being 30 per cent., the gastrointestinal 11.4 per cent.
THE PATHOLOGY.
The essential features of the necrotizing variety of this disease are
similar to those of actinomycosis—an inflammation giving rise to much
fibrous tissue overgrowth enclosing pockets of softening, the whole
process causing a deforming tumefaction. While primarily developing in
the soft parts, this streptothricosis behaves like the ray fungus in
that it spreads not only along clefts of tissue but directly through
muscles and organs and even bones. Rarefying osteitis with irregular
attempt at repair in the form of productive periostitis may be found in
both infections. There is however a greater tendency to ulceration and
general disease in the marsupial form, variations which seem referable
to secondary invaders. When however the massive tumorous, necrotic and
ulcerative characters of this streptothrix disease are insignificant or
absent, the pathology is modified to the extent of obvious bacterial
mixed infection, there then being catarrhal and fibrinous inflammations
with degenerations of the viscera.
BACTERIOLOGY.
Since the pathology varies with the bacteriology as seen at this
laboratory, it is well to pause at this time in a discussion of the
former subject to introduce a brief statement of our findings in the
latter, leaving however a full description thereof for later paragraphs.
It is relatively easy to find in smears from necrotic masses threads of
streptothrix, straight or curved with heavy blunt, but not bulbous, ends
and never branched. Similar forms may be found in the necrotic tissue,
both free in the softened area and near the margin of the healthy
tissue, as irregular colonies growing in a tangled mass from the edge of
which radiating threads may be seen. It has not been possible to find a
“ray” growth with anything like the regularity so characteristic of the
actinomyces nor do the ends present the bulb distinctive of that
organism. Branching has been found once only, it being very uncommon in
tissues although beautifully developed in cultures. While not especially
sought, cocci and bacilli have not been seen, by Gram stains, within or
immediately around the streptothrix colonies. Surrounding the mycelial
groups is a necrotic zone about which is a loose connective tissue full
of mononuclears and a few polynuclears. The centre of the colony is made
up of tangled mycelial threads and necrotic debris. From uncontaminated
necrotizing masses we have obtained cultures three times out of very
many attempts.
[Illustration:
FIG. 63.—KANGAROO STREPTOTHRICOSIS. ANTEROPOSTERIOR SECTION OF HEAD,
SHOWING MASSIVE TUMEFYING PROCESS IN LOWER JAW BONE.
]
When ulceration or suppurative softening has taken place mixed infection
with lower bacterial forms naturally occurs and the whole picture
changes. Pulmonary complications, with or without evident ulceration in
the pharynx, also admit other bacteria. Streptothrical forms are often
easy to detect in stained smears and in cultures but the very extensive
bacterial flora soon overgrows them and attempts at isolation are
fruitless. Under the best of conditions their colonial development is
slow and tiny until they are well accustomed to saprophytic life. The
complicating bacteria that have been identified are _Streptococcus
pyogenes_, pneumococcus, pyocyaneus and colon bacilli to which may be
added moulds of the Aspergillus group but these all have been variable
in numbers and appearance; the most frequent and therefore probably most
important secondary invader is an organism we have not been able to
identify.
This germ, a tiny, Gram-negative, non-motile rod with a tendency to
bipolar staining, will appear in smears from an ulcerated necrotic mass,
from the nasopharyngeal exudate and from pulmonary lesions and may
develop upon agar or blood media for the first generation but refuses to
grow after that despite our best efforts. At present we hope to have it
by growing material a long time in blood broth. Microscopical
examination has not revealed it in the tumor-forming variety but on one
occasion it was found in the lung; its Gram-negative characters make its
detection in tissue very difficult. For obvious reasons the importance
of this germ cannot be estimated but it seems from the frequency with
which it is encountered that in some manner the streptothrix may be
aided by this unidentified bacillus especially in the ulcerative and
septicemic varieties of Kangaroo disease.
In so far as the diagnosis of this infection in the uncomplicated form,
like lumpy jaw, is concerned the finding of streptothrix by stain seems
adequate and its presence in the gastric ulcers and hepatic necroses
identifies this variety. The most difficult question to decide is the
identity of the cases without one or the other of these distinctive
features but with mucocatarrhal or purulent nasosinusitis followed by
pneumonia or septicemia, and of cases of primary pulmonary involvement.
These instances have been diagnosed as belonging to the same category
because of the presence of streptothrix in the exudate at the site of
the important lesions and because the type of lesion is similar to that
which complicates accepted characteristic cases. Inability to reproduce
experimentally any of these infections limits our criteria for judgment
in the matter. I am inclined to view these septicemic cases therefore as
initiated by the streptothrix, growing in the nose and sinuses or
inhaled into the lungs, aided by lower bacteria, an unidentified Gram-
negative bacillus being the most important.
Having reviewed briefly the bacteriology of Kangaroo disease, its strict
pathology may be discussed more definitely in terms of the type of
infection. Reference has already been made to the method of pathogenesis
employed by the streptothrix and its congeners. Whether or not a toxin
is elaborated by these organisms is an unsettled question, especially
for the marsupial variety because as yet it cannot be made to produce
lesions in other animals. It is highly probable that all these organisms
find colonization easy in the animal’s body once they get well settled,
and that they act mechanically, producing necroses by their growth and
by attracting leucocytes in such large numbers that digestion of
devitalized tissue occurs, to an extent that resembles pus. The
inflammatory tissue is not distinctive, except in so far that fibrosis
enclosing pus pockets is peculiar to it. In softer tissue, like the
liver, fibrosis is not so prominent, whereas diffuse and irregular
spread is more pronounced. At the margin with the healthy tissue,
reactive, that is resistant, inflammation is no more in evidence than
within the tumor growth itself and as a matter of fact the tissues do
not seem to put up a good fight against the spread of the inflammation.
[Illustration:
FIG. 64.—KANGAROO STREPTOTHRICOSIS. STOMACH, SHOWING TWO ULCERATIONS
AND DEEP INFILTRATIONS OF THE WALLS.
]
Histologically, aside from the finding of the streptothrix colonies,
there is nothing distinctive, the peculiar expressions of the disease
being most manifest in their gross characters. For the purpose of
describing the pathological features, the cases have been divided into
the necrotizing form around the jaw, a similar process in the stomach
and liver, necrotic cervical cases followed by lung involvement, the
nasal variety upon which pneumonia succeeds and a septicemic form
arising from any locality. Illustrative cases will be cited for each of
these forms, a method of presenting the pathology thought to be superior
to a general discussion.
The first illustrative case is one localized in the tongue and
pharyngeal wall; it is quoted because of its strict localization.
Great Gray Kangaroo (_Macropus giganteus_). Sick four days, tongue
swollen so he could not eat.
DIAGNOSIS.—Necrotizing process of floor of mouth and pharyngeal wall,
dilatation of heart, passive congestion of liver, acute diffuse
nephritis, inflammatory edema of lungs. General condition good. Jaws
and teeth negative. Floor of mouth firm in places, boggy in others,
but generally infiltrated. Anterior two-thirds of tongue purple and
green as if gangrenous. Root of tongue and adjacent floor of mouth
yellowish, wet as if from recent coagulation necrosis. In the muscle
of the tongue a line of demarkation is shown at end of hemorrhagic
zone behind which muscle is fairly good. Sides of pharynx, palate,
tonsillar region show superficial pseudomembranous inflammation and
yellowish gray, wet infiltration of muscles. Epiglottis purple and
swollen to twice normal size. Laryngeal mucosa deeply injected,
swollen and covered with tenacious gray mucus. Trachea and bronchi
deeply injected and slimy. The lungs are uniformly deeply injected and
along course of bronchi in lower lobe, lung tissue is distinctly more
boggy than elsewhere. On section this area is slightly paler and more
granular than the rest of the lung. Lung is everywhere slightly
edematous. The bronchial lymphatics are swollen, pale pink and
edematous. The heart is dilated acutely judging from the left
ventricle wall which is nowhere over 1 cm. The liver is slightly
enlarged, surface smooth, edges sharp, color deep purple, section
surface very bloody. The spleen is soft, capsule smooth, pulp
homogeneous purple, follicles not visible, trabeculæ normal. The
kidney is slightly large, capsule smooth, strips easily leaving purple
surface. The cut surface swells out, has irregular striæ, congested
lines between, glomeruli visible and large. Smear from centre of
tongue muscle shows staphylococci in some places in colonies, and
long, slender rods.
The following case is one of gastric, intestinal and hepatic
involvement, apparently primary, the last possibly arising by a
hematogenic or lymphogenic route. Judging by the slides of the gastric
wall the process started deeply and broke through the mucosa. This
cannot be asserted definitely since kangaroos are susceptible to
gastritis so that the streptothrix may have been implanted upon a
preëxisting inflammation.
Black Wallaby (_Macropus ualabatus_). Congestion and edema of lungs,
abscess of stomach and liver (streptothrix), ulcerative enteritis,
necroses of spleen and lymph nodes, congestion of kidney. The animal
is thin, hair loose. The mouth and nose seem to be absolutely healthy.
The weight of the lungs is increased by congestion, they are solid,
homogeneously red, with no air in any lobe except at edges. A piece
cut from centre of lung sinks quickly in water. The trachea contains
frothy blood. The heart muscle is soft, flabby and lustreless,
chambers dilated, valves normal. The liver is of normal size, firm,
smooth surface, sharp edges, red-brown color. The small sublobe of the
liver which lies between the gall-bladder and the pyloric end of the
stomach shows a large abscess 4 × 3 cm., apparently starting in the
substance of the liver _via_ the bile ducts. This is certainly not
extension from the stomach abscess as the liver lying against the
stomach is nearly normal. The abscess is sharply circumscribed with a
zone of congestion about it. Aside from congestion the rest of the
liver is normal. The common bile duct is large and freely patulous.
The capsule of the spleen is thick, consistency firm, pulp deep red,
irregularly mottled by pale areas of necrosis. The kidney capsule is
smooth, strips easily leaving a smooth, brown surface. The organ is
firm. The section surface is glistening, the cortex wide and
congested, the medulla normal. The adrenal medulla is deep purple with
congested line between it and the pale cortex. Most of the gastric
mucosa seems good. At about the middle of the lesser curvature is an
ulcer about 4 cm. across. The shelving edges are covered with
apparently normal mucosa. The centre contains bloody pus and nodular
masses of the submucosa extending in finger-like projections through
the pus. At one point on the greater curvature there is a small pocket
of pus on the serous side which has not ulcerated through to the
mucosa nor broken into the peritoneum. The large intestine is deep red
and the follicles appear from the serosa as darker areas. On the mucus
side the follicles have ulcerated, having a necrotic centre and
shelving edges. The rest of the mucosa in the neighborhood is swollen
and deep red. The colon mucosa is dry and the contents are hard, dry
“baked” feces. The main pancreatic duct and the common bile duct form
a thick, firm, cord-like mass running through the pancreas and
enlarging the papilla of Vater into the duodenum. All abdominal lymph
nodes are large, firm and on section mottled with red areas. Culture
from the liver abscess failed to grow. Histological section of lung
shows moderate congestion, collapse of alveoli or their filling by
edema, epithelial and small round cells. There seems to be no fibrin.
This could be an early stage of pneumonia. Bronchi are for the most
part negative, little peribronchial round cell infiltration. No
streptothrix in two areas of round cell infiltration or in bronchi.
Liver section shows a part of the liver destroyed by hemorrhage,
degeneration and necrosis. The abscess consists of necrotic matter
surrounded by a zone of about equal numbers of mono- and polynuclears
and around this a loose fibrocellular zone. Streptothrix abundant in
the abscess. Lymph nodes show chronic inflammation and coagulation
necrosis without abscess formation. No streptothrix in areas of
necrosis. Kidney is very much congested with little or no damage to
secreting parts. Spleen shows enormous congestion, moderate amount of
pigmentation, connective tissue both trabeculæ and through pulp
increased, no areas of necrosis. In the stomach the mucous membrane
shows slight cellular activity and some degeneration—this amounts to a
true catarrhal gastritis especially in view of the submucous cellular
infiltration and the granulation tissue which has separated the
muscularis and involved most of the connective tissue. The edge of the
necrotic part begins abruptly, the mass of necrosis lying on an active
fibrocellular submucous and muscular layer. Streptothrix can be seen
at edge and in necrosis.
Pneumonia originating either by inhalation or _via_ the blood stream, is
illustrated in two stages by the succeeding cases. The first history
illustrates the pulmonary involvement as secondary to necrotic
streptothricosis around the jaw and tongue while the second animal’s
disease began in the nose and related sinuses. These two protocols
provide material for a discussion of two phases of the subject.
The character of the early bronchopneumonia in the first is
peribronchial, and there is distinct indication of a generalized process
suggesting a hematogenic origin, whereas there is but one area of
bronchopneumonia in the second—a necrotizing lesion beginning in the
bronchus. Streptothrices are rare in the first case but reasonably easy
to find in the second. This latter is one of the cases which seem to
support the idea that nasosinusitis may have a streptothrix as its basis
in the absence of the usual picture of necrotizing “lumpy jaw.” These
cases also indicate that pneumonia may originate either by inhalation or
by the blood stream, and that perhaps the hepatic lesion may have the
latter origin. There have been two instances of necrotizing
periarthritis, in one of which the threads could be found. This also
suggests that spread through the blood stream can occur, possibly in
this respect to places where previous injury prepares for the reception
of the organisms.
[Illustration:
FIG. 65.—KANGAROO STREPTOTHRICOSIS. ULCERATION IN GASTRIC WALL AND
MASSIVE NECROSES IN LIVER.
]
[Illustration:
FIG. 66.—KANGAROO STREPTOTHRICOSIS. SECTION OF LUNG SHOWING EARLY
ABSCESSES AND NECROSES, ONE WITHIN A BRONCHUS, ONE IN
SEMICONSOLIDATED PULMONARY TISSUE. NOCARDIAL STRANDS COULD BE FOUND
IN BOTH AREAS.
]
Thigh striped Wallaby (_Macropus thetidis_). Streptothricosis of soft
tissues of jaw. Early bronchopneumonia. Acute fermentative gastritis.
Acute general infiltrative enteritis. Cloudy swelling of myocardium.
The general condition of coat and of nutrition is good. The jaws are
wide and the maxillocervical region full, both due to an indurative
inflammation of the gums, tongue, floor of mouth and upper cervical
tissues. At either side of the tongue and running around body of
maxilla both sides, the inflammatory tissue becomes softer and there
is an area about one inch long where it is soft, gray and contains
yellow gray bodies in a grumous matrix. The teeth seem sound as do the
external buccal tissues. The nasopharynx is free from induration. The
bone on the left side shows a periosteitis with involvement of the
superficial layers of bone, while on the right side the periosteum is
swollen and opaque but the bone is free. The thyroid is imbedded in
the edematous infiltration of the lower cervical tissues. The pleuræ
are free of fluid and adhesions. Lungs are collapsed, uniformly pink
somewhat emphysematous at places but give the impression of being
lumpy. On palpation numerous nodular areas are detected. These prove
to be peribronchial areas of gray-red solidity which swell out on
section. The bronchus contains a gray and bloody thick mucoid matter.
There is distention of the mesenteric vessels especially near the
enteric insertion. The liver surface is smooth, edges very sharp,
consistency firm, tough, resilient, color deep red, the section
surface is glistening, moist, opaque, architecture probably normal.
The gall-bladder is distended with viscid green bile; the common duct
is patulous. The spleen has a rough, thin capsule, consistency tough
and resilient, the section surface is mottled red with purple points;
on section two small, pale objects seem to be squeezed out. The kidney
capsule is smooth, strips easily leaving a smooth, deep red surface,
the consistency is soft, the cortex is deep red, then a purple line
between it and the red medulla, striæ invisible. The stomach contains
frothy grayish mush. The mucosa is finely mammillated, deep pink until
the last third when it becomes deep red, deeply injected and somewhat
thickened. The pylorus is closed. Externally the gut is congested, in
places translucent but for most part seems thickened by reddish
swelling of both external layers and mucosa. The mucosa is granular or
pebbly with here and there a small bloody suffusion. The histological
section of lung shows alveoli open, septa relatively thin but somewhat
congested, bronchi mostly open and connective tissue not increased.
Some few bronchi, especially the larger, show a slight catarrhal
bronchitis but mostly an infiltrative peribronchitis. The nearby veins
and arteries show the most striking change, there being in nearly all
of them a distinct thrombosis without circumferential pneumonia. In
one place a distinct peribronchial pneumonitis was found. The kidney
shows very marked congestion of all parts, causing compression,
cloudiness and granularity of the epithelium. Glomeruli and connective
tissue about normal. The intestinal serosa is negative save for
congestion. Submucosa is densely infiltrated with mononuclears, some
in definite groups. Section does not show areas mentioned in notes but
these could be accumulations of cells with congestion. No streptothrix
forms. Section from the infectious focus of face consists of active
granulation tissue, densely injected and filled with mononuclears of
two types, one the lymphoid cell, the other of the young connective
tissue type. Areas of grouping like abscesses are seen and some
necroses. Streptothrix in small numbers in the cellular collections.
Nail tailed Wallaby (_Macropus unguifer_). Kangaroo disease of nasal
region. Necrotizing bronchopneumonia (Aspergillus fumigatus and
Micrococcus albus). Acute diffuse splenitis. Congestion of liver and
kidney. The general condition of coat and nutrition is good. The face
is wide just below the eyes. About the “hare lip” and the nose the
soft tissues are soft, gray, necrotic. All the internal nasal tissues
seem swollen, gray-red. There is subcutaneous edema, bloody in places,
around the right face, eye and jugular angle. Tissues of nasopharynx
swollen, deeply injected and covered by a thick mucus. Pharyngeal and
buccal cavities negative. Tonsillar areas pink and flat. Larynx and
trachea slightly swollen but pale on mucosa. Salivary glands and
cervical glands normal in size and pale pink. Pleuræ pale and empty.
Lungs swollen out uniformly, quite cottony except at lower right base
where there is a nodule about 3 × 5 cm. firm and doughy. On section it
is found to be a peribronchial consolidation of pale reddish gray
color and indefinite outline. The bronchus itself is deeply congested
and contains a grumous mass. The peribronchial lymph nodes are small,
soft, pink, homogeneous. The heart is negative. The liver is large,
surface smooth, edges sharp, color deep purple, consistency soft.
Section surface is glistening, smooth, moist, very dark purple with
obscure markings. The gall-bladder contains fluid brown bile; common
duct is patulous. The spleen is soft, tough, capsule pebbly, section
surface is mottled, light and deep pink, follicles and trabeculæ not
distinguished. The kidney capsule is smooth, strips easily leaving a
smooth purple surface, section surface is glistening, deeply
congested, striæ obscure but seem normal, glomeruli not visible, organ
is soft. The gums and teeth are not involved in the mycosis. The
stomach contains mushy digesting food. The mucosa is mottled pink,
soft, digesting, at lower half submucosa is deep pink, a few small
ecchymoses. From pylorus to ileum, serosa is deeply injected,
edematous, mucosa swollen and edematous, deep pink, loosened in
places, but translucent. Below this the mucous membrane becomes
smooth, flat, pink-yellow. Lower ileum and colon contain rather firm
fecal balls. Follicles nowhere prominent. The pancreas is small, soft,
yellow pink. The follicles of the mesentery are small, pink gray and
homogeneous. Smears from the bronchopneumonia show a threadlike Gram-
positive form and a few Gram-negative rods. Cultures from lung show
_Aspergillus fumigatus_ and _Micrococcus albus_. Nose too foul for
culture. Histological section of lung shows the alveoli mostly open
but the septa widened by congestion. Blood vessels are open and
contain recent clots; one vessel near lesion below is thrombotic. The
two large bronchi in section show catarrhal bronchitis and
infiltrative peribronchitis of which the latter is more severe and
advanced. Beside the larger is a necrotizing pneumonitis from which
nearly all the architecture has disappeared. The exudate is chiefly
mononuclear around the edges; centre no cellular identity. Another
mononuclear process not connected with bronchus in section is found
with an early necrosis. Streptothrix strands may be found in the
bronchial exudate and near the margin of the necrotic patch. They do
not grow in colonies however. The spleen shows general congestion
without pigmentation. Follicles large, solidly lymphoid. Connective
tissue about normal. The kidneys show marked congestion everywhere.
Capsule and intrarenal fibrous tissues about normal. Very severe
congestion which seems to have caused compression and granularity of
the epithelium.
The last case, judging by stained smears, is one of pure nasosinusitis
from streptococci and streptothrices. Cultures were not tried because of
the enormous bacterial flora.
[Illustration:
FIG. 67.—KANGAROO STREPTOTHRICOSIS. LOW POWER PHOTOMICROGRAPH OF A
NOCARDIA COLONY WITH NECROSIS WITHIN AND AROUND IT. THIS WAS FOUND
IN A SECTION FROM THE LIP OF THE SPECIMEN SHOWN IN FIG. 62. THE
BLACK BORDER CONSISTS OF PARALLEL THREADS SO CLOSELY PLACED THAT
THEIR SEPARATION UNDER THE CAMERA IS PRACTICALLY IMPOSSIBLE. THIS
TYPE OF COLONY RESEMBLES THE “RAY” COLONY OF ACTINOMYCES.
]
Robust Kangaroo (_Macropus robustus_). Acute purulent ethmoiditis.
General acute purulent anterior cranial sinusitis. Acute necrotizing
glossitis and pharyngitis. Cloudy swelling of kidney. The face seems a
little full and the subcutaneous tissues slightly edematous. The
nasopharynx contains a thick tenacious mucopus. Ethmoid and frontal
sinuses and turbinate spaces contain a thick purulent matter, the
mucosa being densely injected, swollen and velvety. Pharyngeal wall
and right half of posterior half of tongue are involved in a dull
brown and necrotizing process, quite sharply outlined by zone of
congestion. This process is comparable to the necrotizing gingivitis
seen in front of jaw in kangaroos. Larynx, trachea and lungs seem
uninvolved save for slight generalized congestion. Cervical lymph
nodes especially those about the larynx are definitely enlarged, soft,
moist and brown. Mediastinal nodes slightly enlarged, soft and pink.
The heart is negative. Liver normal. Spleen is soft, homogeneous dull
red. The capsule of the kidney is smooth, strips easily leaving a
purple surface. The glistening section surface swells slightly, vasa
recta are congested, striæ wide and pale, glomeruli not visible;
consistency is resilient. The mouth and teeth are not involved in the
process mentioned above. There is a small quantity of properly
digesting food in the stomach. Stomach and intestines negative. Brain
not involved. No extension from anterior cranial sinusitis. Smears
from the mucopus confirm the gross appearance and contain short chains
of streptococci and large diplococci. Smear from cut surface of tongue
shows innumerable small bacilli and diplococci but especially mycelia
with rather heavy clubbed ends but without true branching. One group
was found arranged like ray fungus. It is noteworthy that there is no
aspiration pneumonia and very slight evidences of septicemia.
BIOLOGY OF N. MACROPODIDARUM.
The original discovery of the streptothrical forms was made in stained
smears from necrotizing lesions. They were considered as secondary
invaders until repeated observations of a similar character aroused the
suspicion that they stood in some important relationship to the lesion.
Early attempts at their cultivation were made under anaerobic
precautions, a method now known to be almost certainly doomed to failure
because a strain long under cultivation requires two to three weeks to
make an appreciable growth in the absence of air. Finally in 1911 a
successful cultivation occurred by searing the surface of an unopened
mass in a freshly dead animal and planting bits of the interior upon
aerobic blood serum plates. Colonies grew after three or four days and
from them the first strain was started. It grew for several generations,
long enough for the preparation of a vaccine, which will be described
later, when by mischance it was lost. In 1920 another successful
cultivation occurred, this time by incising a mass in the soft
sublingual tissue and plating in the same manner; upon this culture the
biology is described. Smear preparations offer no more than has already
been mentioned.
Colonies develop upon blood serum plates as opaque, pale yellow,
circular, discrete masses with a slightly depressed uneven centre, but
without umbilication. They remain smooth and slightly glistening for
several days, then become slightly wrinkled and twisted with a more
definitely raised edge and a tendency to an uneven sinking in of the
centre. Transfers to agar slants show wrinkled continuous opaque, dull
yellow, sharply outlined growths which soon wrinkle, fold, and twist
like certain tubercle bacillus cultures. Spreading occurs, but is slow
after forty-eight hours. As medium becomes drier it is possible to see a
thin, colorless, wrinkled film stretching out from the main growth. If
the medium be dry or old or if only a small portion of seed material be
used and this scattered over the surface of the slant, discrete colonies
arise. These are circular, seldom exceeding 3 mm., dirty yellow-white,
distinctly umbilicated and without clear film of spreading around them.
In nearly all quite old cultures, a white chalky efflorescence appears
over the surface.
The morphology of the young agar culture is chiefly mycelial or
filamentous, whereas from a culture on dried media and those showing
efflorescence, the organisms are short, heavy, deeply granular and of
the mycobacterial type.
Glycerine agar.—Corresponds to agar.
Blood agar.—Similar to agar but much less luxuriant.
Blood serum.—Limited dirty yellow, raised, dull, wrinkled and
granular, tightly adherent to the medium.
Potato.—Spreading, dirty yellow, much wrinkled, friable, tightly
adherent.
Gelatine.—Limited growth as a wrinkled, tough scum only on surface.
[Illustration:
FIG. 68.—KANGAROO STREPTOTHRICOSIS. HIGHER MAGNIFICATION OF EDGE OF
STREPTOTHRIX COLONY, FIG. 67. IT SHOWS THE DEEPLY STAINING MYCELIA
SEPARATING MUSCLE FIBRES WHICH ARE DEGENERATING.
]
Litmus milk.—No change for six days, then beginning slight alkalinity
which increases very little, shows digestion of the caseinogen,
slight, thin filmy growth on surface.
On media such as litmus lactose agar and old Endo it grows slowly on
surface and assumes the color of the medium.
Broth.—Only surface growth appearing during early generations, after
3–6 days as a wrinkled, pale yellow scum very much like the tubercle
bacillus growth; later generations grow perceptibly in one to three
days. Medium perfectly clear. If a large mass be seeded into neutral
broth there is a perceptible increase in the growth after ten days.
The medium thereafter tends to a faint turbidity. Titration of broth
growth after twelve days shows alkalinity requiring 0.3 cc. decinormal
acid, while the control tube incubated same length of time showed an
acidity requiring 0.57 cc. of decinormal NaOH.
On the following sugars there is a slight surface growth without
change in the color, Andrade indicator—dextrose, lactose, saccharose,
maltose, mannite, dextrin, galactose, salicin.
Cultures observed on two per cent. neutral agar.
A.—Stained by Loeffler’s stain.
Twenty-four hours.—Shows threads growing out from a central amorphous
mass, but the whole does not retain the regularity or parallelism of
actinomyces. Threads are poorly stained and rather disconnected but
not jointed. Small number of metachromatic bodies apparently in older
individuals, certainly in the better formed ones. No intercalary
spores, unless the metachromatic bodies be so considered. Individual
threads measure from one-third to one micron in width. Metachromatic
bodies measure on the average one micron.
The threads in the forty-eight hour preparation seem distinctly wider,
up to one micron and possibly become heavier toward the end, but do
not have a distinct bulbous extremity.
In three days the threads are much longer, show distinct branching and
a tendency to transverse segmentation. More than one metachromatic
body may be present in one segment.
Four days.—Still coarser, short segments have appeared separately.
Metachromatic body is coarser and blacker; some of the masses have
gone to pieces and show only a diffusely staining smudge of
metachromatic bodies. The short segments show a tendency to grow out
into threads.
Fifth day.—Condition is much the same plus many young, delicate,
poorly staining threads.
Sixth day.—The same but all seem to be somewhat wider and diffusely
staining.
Seventh day.—More diffuse staining and decidedly fewer metachromatic
bodies.
A.—Stained by Gram’s stain.
Twenty-four hours.—All forms are light purplish. The threads stain
much more clearly than by Loeffler’s and show distinct transverse
segmentation of rather uniformly long bacilliform shape. Metachromatic
bodies not so distinct but seem larger where found. Coarser threads
have swellings in some of the areas which are not segmented and this
type seems to have more branching and metachromatic bodies; in other
words it would seem that this is a form that reproduces by budding or
intercalary spore formation.
Forty-eight hours.—Much the same, more long threads with transverse
division, somewhat more delicate, generally fewer coarse threads with
swellings and spores. Still pale purple and not distinctly Gram-
positive.
Three days.—Condition much the same.
Four days.—Two forms present—definitely Gram-negative delicate slender
threads, nearly Gram-positive, and heavier, curved and twisted long
bacillary forms, some streptococcoid threads and a few bulbous short
threads. Very few metachromatic bodies.
Five days.—Condition much the same except that the delicate threads
are inconspicuous and the darker purple bacilli have increased.
Metachromatic bodies increased as have swellings in coarser threads.
Six days.—Much the same but for the appearance of young, delicate
definitely Gram-negative threads. There are fewer metachromatic bodies
and internal spores.
Seven days.—The same.
B.—Grown on Loeffler’s blood serum.—Loeffler’s stain.
Twenty-four hours.—Delicate, poorly stained short threads, few tiny
metachromatic bodies.
Two days.—Not well stained, relatively short threads show numerous
metachromatic bodies varying from exceedingly tiny dots to coarse
granules wider than the thread. These may be numerous in the same
segment and form a row from six to ten. Many short bacillary forms.
Three days.—Poorly stained, metachromatic bodies apparently more
numerous but much smaller.
Four days.—Almost entirely short, heavy bacillary forms, some of which
are very like diphtheria bacillus in the irregularity of width; many
metachromatic bodies, distinct branching, some of the small heavy ones
have fusiform swellings; practically no long, heavy threads.
Five days.—Essentially the same, individual elements slightly larger,
fewer but coarser metachromatic bodies, more numerous round forms
suggesting large pale cocci.
Six days.—Much the same but elements shorter, smaller and some more
segmented.
Seven days.—More long forms of uniform staining but still a majority
of coccoid or short bacillary forms with irregular staining and
metachromatic bodies; no long threads.
B.—Gram’s stain.
Twenty-four hours.—Pale purple, almost Gram-negative, long, slender
but well outlined threads, a few coccoid forms, practically no
granules.
[Illustration:
FIG. 69.—KANGAROO STREPTOTHRICOSIS. PHOTOMICROGRAPH SHOWING THE
SEPARATE THREADS OF NOCARDIA IN A SOFT NECROTIC LESION.
]
Two days.—Very pale, almost Gram-negative threads, very many coccoid
forms and short rods, considerable segmentation of the longer threads.
Three days.—Increase in short, heavy bacillary forms with bulbous
ends, deeply stained ones and the granules being lightly Gram-
positive; long, slender threads are disappearing.
Four days.—Almost exclusively short, heavy forms with bulbous ends
with coccoid forms, heavier forms almost definitely Gram-positive,
granules Gram-positive.
Five days.—Much the same but more segmentation in the bacillary forms,
coccoid forms become more numerous.
Six days.—Individuals are somewhat longer but there are many rods with
fusiform swellings containing granules; coccoid forms present in
chains sometimes.
Seven days.—More long rods or short threads, pure coccoid and
bacillary forms.
The morphology upon bouillon depends somewhat on age and upon the
location. Upon the surface the long branching mycelial type appears
early and persists until the whole surface is covered whereupon the
segments divide into coccoid elements with metachromatic bodies. If
heaping-up develop the coarse grains on the mass consist of granular
or coccoid rods. When growing in the depth the coccoid form is the
predominant one, only a few delicate mycelia, usually Gram-negative,
being found.
The Gram character of the organism should be emphasized. The young,
delicate mycelia are negative or take a very feeble blue stain. The
heavy bacillary forms are Gram-positive. Like the ray fungus the heavy
ends are sharply Gram-positive, but unlike it, there has never been
seen a Gram-negative bulbous capsule around this end.
The determination of this organism was undertaken from the
classifications of Petruschky (Kolle-Wassermann), of Castellani in
Castellani and Chalmers’ _Tropical Medicine_, and of the Society of
American Bacteriologists. In the first classification it corresponds in
some ways with _Streptothrix hominis_, and in some ways with
_Streptothrix capræ_. As for the second authority it falls into the
Nocardiaceæ, section parasitica, subsection I, in that a distinct earthy
odor is absent and that there is no liquefaction of coagulated protein.
It resembles several of the species given in this subsection, but does
not correspond exactly with any of them. Consultation of the
classification of the American Bacteriologists would place it among
Mycobacteriaceæ. The facts that it is strongly aerobic, produces whitish
efflorescence which may possibly be aerial hyphæ and breaks up into
short segments, place it in the genus Nocardia. It seems, however, to
belong to a division of Nocardia which is close to the Mycobacterium
since the short elements are swollen, cuneate and usually heavy, which
is unusual in the more typical Nocardia. It is not, however, acid fast
and therefore cannot be classified among the Mycobacteria. This culture
seems to be a variety not heretofore described, and since its
association with the disease is so definite, whether or not it be the
cause, the name NOCARDIA MACROPODIDARUM is proposed, because the
kangaroos belong to the order Marsupialia, family Macropodidæ.
The discovery of these organisms within tissues is by no means easy even
though the larger colonies may be located by staining. If Loeffler’s
method be used the central mass stains quite diffusely and the spreading
mycelia around the edge stain faintly. For study purposes this stain is
preferable to Gram-Weigert, since despite the positivity of the
cultures, the blue dye can be removed very easily from sections and only
with great care will enough remain to permit tracing of the separate
threads; with Gram stain no detail can be made out in the centre of the
colony, it being a diffuse blue. Careful search near the edge of these
necroses will usually succeed in the discovery of a few mycelia
stretching in between the mono- and polynuclears of the low grade
inflammation. This is best seen in the margin of gastric ulcers, but may
also be found in the cervical masses. When searching in the pulmonary
tissues the organisms are to be found in the bronchial exudate or at the
edge of pneumonias. In one nasal mucosa the mycelia were dispersed, not
growing in colonies as in localized inflammations.
EXPERIMENTS AT THE REPRODUCTION OF THE DISEASE.
When the first culture was isolated it was injected into guinea-pigs;
its loss stopped further work because it could not be regained from the
animals. The present culture had been injected into guinea-pigs,
rabbits, opossums—all with negative results; such an experience is not
unknown for actinomyces. Intraperitoneal, intravenous methods having
failed, inoculation was made into the gums of rabbits and of opossums
with no result, even after traumatizing the mucous membrane. The
injection of about 5. mg. of a twenty-four-hour agar culture was made
directly into the masseter muscle of an opossum without producing even a
lump at the site. Atomizing a culture into the nose and throat of an
opossum seemed also without effect. Injection of cultures into the nose,
gums and labial tissues of a wallaby have been negative; nor has any
perceptible effect followed the atomizing of a heavy nocardial
suspension in broth into the trachea of this animal.
The results of these experiments are in accord with those of many
similar attempts to reproduce actinomycosis. Perhaps in Kangaroo disease
the small Gram-negative bacillus is a necessary factor.
SPECIFIC PREVENTION AND TREATMENT.
Encouragement that we were upon the right track was, however, found in
another direction. Improvement in human and bovine actinomycosis having
followed the use of vaccines, it occurred to me to try this method as
treatment and prophylaxis. The first culture to be isolated was just at
hand, so that it could be used at once. Five injections were given under
the skin of the thigh to a recently developed case of the ulcerative
gingival variety, a noticeable improvement occurring almost at once, and
at death there was an apparent cure of the local lesion. However, the
accompanying protocol made at the time tells the whole story, no
adequate explanation being at hand.
Red Kangaroo (_Macropus rufus_). Disease of the mouth first noticed
March 31, 1912, died September 13, 1912. Necrotizing osteitis,
arthritis and periarthritis of left ankle, subacute fibrinous right
pleuritis, hemorrhagic bronchitis with atelectasis in right middle
lobe, abscess of right middle lobe; passive congestion of lungs,
liver, kidney, chronic splenitis, chronic general lymphadenitis. The
animal is in general good condition except for a fusiform swelling
about the left heel with evidence of fracture. The necrotic process in
the hare lip, nose and palate has entirely disappeared. One front
incisor has gone and the other is loose. There is a scar on the under
part of the soft palate in a small healed channel between palate and
floor of nose. There is no evidence of pyorrhœa. Cervical and axillary
lymph nodes are much enlarged, pale yellow, firm and of the appearance
like early stages of Hodgkin’s disease. Fascias of cavities congested.
The lungs are mottled purple, air content decreased, section surface
purple, exuding frothy blood. The whole right lung is covered with a
thick fibrinous exudate, most intense over middle lobe at site of
atelectasis. There are light scattered adhesions. The anterior margin
of the lung is adherent to the pericardium which is covered in the
front by exudate. Upper and lower lobes show hypostatic congestion.
Middle lobe has separate bronchus filled with necrotizing blood clot
extending into a smaller bronchus with complete occlusion. The alveoli
supplied by the last show atelectasis like hemorrhagic infarct. There
is a small subpleural abscess near the margin of this atelectatic
area. The bronchial lymph nodes are slightly enlarged, mottled yellow
and pink, firm with large, diffuse follicles. The pericardium contains
2–3 cc. clear fluid. The heart muscle is pale, purple and soft. All
the vessels are full of currant jelly clot. On the posterior surface
of the aorta internally about an inch above the valves there is a
patch of roughening with a suggestion of thickening and opacity. It is
comparable to the early stages of syphilitic aortitis. The liver is
normal in size, surface smooth, edges sharp, consistency firm and
friable, color purple. The section surface is glistening, smooth,
moist, and shows passive congestion. The gall-bladder contains fluid
brown bile and the common duct is patulous. The spleen is slightly
enlarged, firm and tough, capsule wrinkled. Section surface is mottled
red and purple with irregular gray trabeculæ and faint scattered
follicles with diffuse margins. The kidney capsule is smooth, strips
easily leaving a smooth brown surface. Organ is firm. The section
surface is glistening with a line of passive congestion with distended
vessels between the cortex and medulla which are of normal widths.
Intestines seem normal throughout. The pancreas is firm, pale pink,
slightly edematous. The mesenteric lymph glands are moderately
enlarged, yellow, firm, homogeneous with congested centres. About the
left ankle joint there is a necrotizing infection which has involved
the bone causing a pathological fracture of the lower end of the
tibia. Smears from the periarthritis, pleuritis and blood clot in the
bronchus show streptothrix, a short colon-like rod and a coccus in
fours—a picture precisely like that obtained from the jaw bone cases.
In addition to the above there is a very distinct encapsulated
pneumococcus form in smears from the blood clot in the bronchus. This
is the animal which was vaccinated with a culture made from the depths
of a necrotic mass, upon which treatment she rapidly improved and as
seen from the above notes recovered from the palate condition. Why she
should have a second infection apparently with the same organism is
difficult to determine. Possibly the second batch of vaccine was not
sterile, it not having been controlled because the first batch of
vaccine was sterile after one hour at 60° C. Possibly the animal was
sensitized and a few bacteria settled in the leg. It was along this
leg that the inoculations were made.
We permit ourselves the facetious observation that that vaccine
prevented the labial and cervical variety for five years, because during
that period it stood in the icebox, and there was no case of that
particular form to which to give it, although a few of the nasal and
gastric varieties occurred. It was recontrolled and did not show living
organisms. That it should have cured the disease in the jaw and
apparently later permitted a lighting up of a septicemic and pulmonary
form with necroses in the leg is difficult to explain.
Just recently we have used a vaccine from the current culture upon
another case beginning in the gums and jaw bones. This case was detected
early and was treated with ascending doses beginning at 0.3 mg. and
running up to 10. mg. At first there was some improvement, but the
animal finally died from pulmonary complications. The course of the
disease, however, instead of being three weeks, as is the customary
duration, lasted two months, an extension of the course which has made
us hopeful. These two experiments, indefinite though they be, have
offered encouragement and seem to supply a little additional support to
the idea that the organisms stand in etiological relationship to the
disease.
The employment of the vaccine has been extended to its use as a
prophylactic in animals exposed to the disease or specimens that have
slight reddenings or erosions on the buccal mucosæ suggesting possible
early stages of streptothricosis. Five animals have now had a course of
vaccine injections, ranging in number from 5 to 10 and in quantity from
0.3 to 2.4 mg. over a period of a month. Fourteen months have elapsed at
the time of writing and only one case has developed, but this of course
cannot settle the efficacy of the method; perhaps it would be safer to
demand that no case should ever appear in a treated animal, while the
disease did appear in the untreated.
The preparation of the vaccine is by no means a simple matter, since the
surface growth upon solid media is so tenacious. Methods such as are
employed for the tubercle bacillus have to be used. The first two
vaccines were made by scraping off surface colonies from agar and
grinding with glass balls. One successful batch was made recently by
simply triturating the colony directly on the agar slant, but the latest
method seems to offer the simplest and most generally satisfactory way.
Neutral broth is placed in flasks containing glass beads and sterilized
in the incubator. This is seeded with the Nocardia, incubated at 37° C.
until the surface is covered, heated to 60° C. in a steam sterilizer and
tested for sterility. If growth occur it is reheated until dead,
whereupon the broth is syphoned off, the growth emulsified by whirling
the flask, thus grinding the bacterial mass by the glass beads.
Sufficient saline is added to make a workable emulsion, and the fluid
then poured into bottles. Control by reculturing is again done, and if
the fluid be found sterile, 0.5 per cent. trikresol is added to keep it
so. These organisms cannot be counted accurately because of the
variation in length, their budding and coccoid forms. Standardization is
done by weight. A definite equal quantity of the suspension and of the
saline used to make it are evaporated to dryness in weighed vessels and
the whole then weighed. The difference is the weight of the organisms
suspended in the saline. Such a fluid can be diluted so that a given
bulk will contain a convenient weight of germs. The one now in use
contains 8. mg. per cubic centimetre. Dosage as indicated above usually
begins at 0.5 mg., a quantity which does not produce any local
inflammation at the site of injection. It is perhaps well to adopt a
quantity of 0.1 mg. per kilo as the initial quantity.
The Garden has encountered no case of the remaining important chronic
infections, glanders, lymphangitis, and infectious abortion.
SECTION XVII—PART 4
ACUTE DISEASES RESEMBLING THE SPECIFIC INFECTIONS OF DOMESTIC ANIMALS
Specific communicable diseases are sometimes divided into those most
often encountered as “herd diseases” and those which appear as single
cases or in small groups. This would seem to imply that the first behave
as easily disseminated epizoötics, their virus passing from animal to
animal simply by proximity or by casual contact whereas the transfer of
infective material is less readily accomplished by the second group,
often demanding special assistance. Foot-and-mouth disease, pleural
pneumonia, cattle plague, and influenza illustrate the epizoötics while
tetanus, rabies, quarter-ill, malignant edema, and infectious vaginitis
are examples of less easily transferred processes.
It is not intended that these remarks shall cover all possible means of
transmission but instead they are intended to focus attention upon the
sources of viruses whereby animals become infected. An original case
must always be present in order for spread to occur. Where animals are
being added to a herd a new comer may be diseased or the carrier of a
virus; when animals are transported for sale or other reason, infection
may be met in a new stall, conveyance or pasture; contaminated food may
be offered. In menageries, with specimens, single or in small groups,
and arrivals always quarantined before other animals are exposed, acute
specific infections seldom appear. It is also improbable that a wild
animal, infected at its source or in some dealer’s place, would survive
the journey and arrive in an infective condition. Consultation with the
reports of other gardens fails to discover records of any serious
outbreaks of epizoötic disease except for fowl cholera and distemper,
examples of infection with the bipolar organisms of the Pasteurella
group, believed responsible for the hemorrhagic septicemias; instances
of the occurrence of the group specified secondly—anthrax and the like—
are also reported. This represents fairly well our own experience.
The bacteria variously named _Bac. avisepticus_, _ovisepticus_,
_bovisepticus_, _canisepticus_, etc., grouped by Ligniere under the name
Pasteurella, are doubtless of considerable importance and are probably
quite widespread in natural surroundings. The viruses of the epizoötic
conditions like cattle plague and influenza are apparently more
definitely parasitic, requiring for their persistence ever renewed
transfer from host to host. The former infections we have met in
repeated single isolated cases and in small groups, whereas no cases of
the specific epizoötics have been diagnosed.
Hemorrhagic septicemia, a denomination very descriptive of its
pathological picture, has been encountered in many varieties,
carnivores, ungulates, primates, rodents, and birds. The diagnosis
depends upon the presence of hemorrhages with edema, degenerations of
the parenchymatous organs, more or less respiratory catarrh to which may
be added relatively mild gastrointestinal inflammation; the bacteria are
found in the circulating blood and in exudates. A description of these
organisms is not profitable, they being well known in veterinary
pathology. What is more important, significant and supportive of the
opinion expressed above concerning the widespread distribution of the
virus, is the incidence of the infection. Exclusive of the condition
known as fowl cholera, it has appeared among mammals and birds as single
cases with one exception—that of two Barbary apes which had been in
separate cages side by side. The total of cases with determined
bacteriology is eleven, with undecided bacteriology but suggestive
pathology nine additional. No pertinent history in common can be found
in the records of the determined cases, except perhaps that they were
all animals which had been in the collection at least three months, a
period which would seem to exclude the probability of an imported
infection. Because of the isolated character of the cases and
impossibility of making a clinical diagnosis, no attempt at specific
nomenclature as used in veterinary medicine has been made, hemorrhagic
septicemia seeming to cover its identity and nature.
The disease known as fowl cholera is practically always associated with
the bacteriological discovery of a member of the hemorrhagic septicemia
group while its pathology corresponds with that of mammalian infection
with these germs. Enteritis is a prominent feature. This disease has
appeared thrice among our parrots carrying off from six to ten birds
before hygienic measures became effective. In all three our cultures
showed the bipolar organisms. Besides these specific outbreaks numerous
isolated cases of acute general infection have occurred among small
passerine and picarian birds which could not be determined as
hemorrhagic septicemia by bacteriological methods although superficially
resembling it in gross pathology; they yielded to the same hygienic
measures. Perhaps we were dealing with fowl plague, a disease believed
to be due to a filterable virus. That this is the case is strongly
suggested by an outbreak of fowl typhoid in the parrots, from some fatal
cases of which we were able to isolate _B. sanguinarium_, and by a group
of deaths in small parrots from which no specific organism could be
recovered.
The identification of these supposedly specific diseases—plague,
typhoid, septicemia, leucemia—by pathological criteria is by no means
simple even if we have at hand the complete description of Moore, of
Hutyra and Marek, of Ellermann and of Ward and Gallagher. Bacteriology
must decide and cultures should be made upon bodies recently dead. In
addition to the above infections we have had two small outbreaks of
psittacosis in parrots from which it was possible to isolate the
specific organism. On both occasions there was more than one death
before the specific nature of the disease was identified yet,
noteworthily, no spread to the other birds in the same exhibition house
occurred.
Distemper, a disease variously held as due to cocci, to influenza-like
organisms and to a filterable virus, may appear in sporadic or epizoötic
form. The diagnosis during life is not so easy unless all the cardinal
features are present, while after death the same thing holds good. I am
inclined to think that from the standpoint of diagnostic accuracy, the
term is used much too loosely, a ready excuse for such laxity however
being that it stimulates to greater care in hygiene. Whether or not _B.
bronchi-_ or _canisepticus_ be the cause of the disease, organisms
corresponding to it can be found in stained smears from nearly every
case in which the respiratory, cutaneous, nervous and internal signs
suggest the disease. To make a diagnosis of distemper it is my practice
to require at least three of the cardinal clinicopathological features,
whereupon, if the bacterial findings be as described, the denomination
is permitted. This was dictated because during the period, now happily
well in the past, when the cats and dogs suffered frequently with
enteritis, nasopharyngeal signs occasionally presented themselves or
spasms were reported, but no skin eruptions appeared, yet seldom were
all of these signs combined nor could we find the bipolar organisms. I
note that in 1915 Doctor Blair of New York observed a toxic enteritis
resembling but not identical with distemper. As with our cases he failed
to find that the condition was communicable. We ascribed our cases to
spoiled food—fowl heads or dirty horse meat (see page 179). Our
acceptable examples of distemper number three, two ferrets and a lynx,
but very suggestive cases were found in foxes, wolves and raccoons.
Since writing the above notes, sixteen wolves, foxes and wild dogs died
in an outbreak of distemper imported by a newly arrived specimen
admitted to the colony by mistake. When we were aware that the disease
had appeared antiserum was administered therapeutically to all that were
sick and prophylactically to all the rest—large doses, 25–35 cc., were
given for treatment, smaller quantities, 10–20 cc., being used as a
preventive. Seven sick animals recovered and no animal (8) given serum
prophylactically became sick. This experience encourages us to think
that with antiserum and rigidly enforced quarantine rules, distemper
will not be a serious matter to handle.
The hygiene of the foregoing conditions is of a general character—
removal of the specimens when known to be sick, thorough cleansing of
the cages, segregation of mates or of neighbors when this is
practicable, burning of refuse, liming of the ground and such other
measures as the local conditions may indicate.
DIPHTHERIA.
Although no cases of mammalian diphtheria have been observed, three and
possibly four birds have suffered with this disease. The three
acceptable cases were in cassowaries (_Casuarius occipitalis_) occupying
adjoining cages and sickening within a few weeks of one another. Just
how the infection was brought to them must remain a mystery since no
additions had been made to the group for some time previously. All three
birds were observed during life, and from the first case the _Bac.
diphtheriæ avium_ was isolated; in smears from the other two similar
bacteria were seen but isolation was unsuccessful. The two acutely fatal
cases showed large pseudomembranous collections on the nasopharyngeal
mucosa and beneath the tongue while the nares were occluded by the same
material. Plaques of membrane were also found on the surface of the
esophagus and proventricle. The exudate ran out of the mouth and formed
dried crusts upon the cervical skin. Pseudomembranes of a continuous
character were lacking in the third bird, their place being taken by
small yellow or yellow pink nodular elevations, apparently just beneath
the surface, here and there upon the reddened, slimy buccal, lingual and
pharyngeal mucosæ. Crusts upon the skin of the neck also formed in this
case.
These cases are of interest not only because of their appearance without
satisfactory explanation but because one improved very much after
injections of human diphtheria antitoxin, this remedy being used because
we were then unaware of the existence of an avian diphtheria antitoxin.
No claim can be made _post hoc ergo propter hoc_ that the human
antitoxin helped the attack—it may have been mild—but the experience is
worth recording. Dosage was as follows: December 3, 3,000 units;
December 8, 1,500 units; December 21, 5,000 units; December 27, 5,000
units. Shortly after the inception of the treatment the bird was noticed
to eat better and to be more lively; this was followed by a reduction in
the mucous strings in the mouth and the crusts upon the skin. This
improvement continued and the bird seemed well in about two months but,
after the lapse of three months more, a mucous nasopharyngitis was again
observed. Despite two injections of 5,000 units human diphtheria
antitoxin the bird succumbed five days after the beginning of this
attack. Autopsy revealed much the same condition as was found in the
first birds and from the larynx the _Bac. avium_ was isolated. Another
case suggestive of diphtheria was seen in a hornbill but antemortem
observation being impracticable and postmortem decomposition being
advanced when autopsy was performed, the diagnosis could not be
confirmed.
An unusually well developed case of molluscum contagiosum was seen in
the Wild Turkey (_Meleagris gallopavo_) recorded here by photograph and
in the form of notes upon the histology made by Doctor Weidman.
The bird’s head was affected universally from beak to ears by horny
nodules up to the size of a pea. They were so large and numerous around
the eyes as to completely close them. There were no lesions elsewhere on
the body, none of the other turkeys were similarly affected and though
watched, none have since developed a similar condition. Histological
examination shows a keratosis, many of the cells showing characteristic
“molluscum bodies” which appear the same and behave the same
tinctorially as the human examples. This turkey case differs from the
human, however, in that there are none of the pocket-like epithelial
extensions deep down into the corium and this turkey case may be very
useful in the further study which is contemplated to show that such
things as molluscum bodies are not sufficient of themselves to stamp a
dermatosis as a pathological entity, but that they are general
pathological processes which may occur in a number of different
diseases. The disease has been reported in sparrows, pigeons, but never
so far as I can find, in turkeys.
A few isolated cases of infectious disease are included here as a matter
of record although they may not be especially significant or important.
Rabies was found in a pair of deer which had been bitten by a stray dog.
The period of excitement was relatively long, while the paralytic stage
was only a few hours. Negri bodies were found. Tetanus killed a Persian
Wild Ass (_Equus onager_) the infection wound seeming to be a bruised
and abraded area on the rump. From the contused muscle tetanus bacilli
were isolated. A gas-bacillus infection, emanating from the vagina which
was protuberant and lacerated because of injury by mates, was seen in a
pregnant llama (_Llama lama._) On two occasions nodular masses have been
found under the skin of seals, not unlike the one studied by Doctor
Wiedman and thought by him to be due to moulds. These two have, however,
failed to show mycelia or yeast-like bodies, and one thinks only of
placing them in the group of botryomycosis. I have never seen a case of
this disease, so that I am forced to rely upon literature, a method that
inspires no especial confidence in the diagnosis. The bacteria usually
held responsible for botryomycosis could not be isolated. Just what can
be done for the condition is difficult to state, since seals are
scarcely tractable animals.
[Illustration:
FIG. 70.—MOLLUSCUM CONTAGIOSUM. WILD TURKEY (MELEAGRIS GALLOPAVO).
]
The following case has some features like paralytic hemoglobinuric fever
and is reported as a matter of record. The long standing gastroenteritis
may have been the basis for the intoxication which led to the paralysis
and muscular degeneration. This laboratory has now under way studies
upon the laming of ungulates, accompanied by weakness of the hind
quarters, but no conclusions have been reached. It is interesting to
note that Hutyra and Marek quote Johne as having seen a case of
hemoglobinuric paralysis in a zebra in 1879.
Burchell’s Zebra (_Equus burchelli burchelli_). The only symptom
observed in this animal was gradually increasing lassitude which was
first noticed about three months ago; toward the end he habitually
stood with tucked tail and nose to the ground as if asleep. He ate
well and digestion appeared good, but he became very weak as shown by
his inability to rise when he got down on the third and second day
before he died, although on both occasions he was able to stand when
lifted. Injury, hemorrhage in thigh muscles, chronic gastritis,
sciatic neuritis. Œstrus larva in stomach, ascaris in intestine. Both
lungs are widely distended and the caudal half of both is the seat of
passive congestion. Upper lobes are slightly edematous. No
consolidations. Heart normal. Abdomen contains about two quarts of
clear straw colored fluid. Liver is of normal size, smooth surface,
sharp edges, firm, friable. On section it is very bloody, veins
distended, some with clot. Architecture normal. Spleen is of normal
size, soft, tough, capsule rough. Section surface is homogeneous, pulp
purple, trabeculæ normal, follicles not visible. The kidney capsule is
smooth, strips easily leaving a smooth brown surface, firm. Striæ
normal, rather wide, glomeruli not visible. Stomach is filled but not
distended with partly digested straw. Mucosa of cardia dry, roughly
irregular, some irregular mammillations. Two flat papillary growths.
Œstrus larva attached to a smaller elevation. The mucous membrane of
the fundus is soft, moist, irregular, in some places, translucent, in
others opaque; near pylorus mucous membrane is swollen edematous,
pink, slightly eroded at pyloric valve. Small intestine has smooth,
flat, pale yellow translucent mucosa. Lumen filled with mucopurulent
matter like mixed egg. Ileum slightly congested but mucosa firm and
translucent. Pancreas is soft, slightly uniformly congested. All
mesenteric lymph glands are slightly enlarged and edematous but with
normal architecture. In the posterior thigh muscles beside the sciatic
nerve, most marked on the right side, is a large hemorrhagic
infiltration. There is edema of muscles and intermuscular septa all
about this area extending upward as well as to pelvis and psoas
muscle. This latter within the abdomen shows slight blood stained
edema. No other muscle shows this hemorrhage. Microscopic section of
liver and kidney are negative aside from congestion. The stomach shows
very irregular epithelial covering, in some places wholly desquamated.
Where this is most marked there is a dense round cell infiltration in
the villi with some increase in the connective tissue cells. This
chronic inflammatory reaction is present in all fields, most marked,
of course, in upper layers of mucosa. Glands are distorted and upper
epithelium of them is polychromatophilic. The intestine shows similar
changes in less intense manner.
Waterfowl Epizoötic. There is reproduced here an account of an
unexplained epizoötic among ducks and geese from the _Annual Report of
the Zoological Society_ for 1916. Nothing additional has been learned
and no repetition has occurred since the drainage and cleaning of the
lake.
There began on August 27 a series of deaths among the waterfowl and in
one month there were lost forty-one specimens including both ducks and
geese. Four additional cases were scattered through the next four
months, the last case dying January 11, 1916. All of these came from
the lake, none being from the adjacent stream for rare waterfowl or
from the more distant stream into which the lake drains. The symptoms
were most marked and striking. In the early stages the wings drooped,
then the legs became weak followed by inability to raise the head. In
the latest cases the voice (ducks) lost its normal character and
became hissing. The mind appeared clear for the eyes were bright,
feathers unruffled and the bird attempted to escape when approached.
Diarrhœa was present, dejecta thin, watery white, no admixture of
mucus. Autopsy findings were not frank. At most some swelling of the
spleen and a little pale thickening of the intestinal wall constituted
the picture. Smears from intestine and nasal mucosa showed no
protozoa. The blood taken from the living sick ducks showed no
parasites or anemic changes in either raw or variously stained
preparations. From the spinal cords of three ducks a 50 per cent.
glycerine emulsion was prepared and was injected into the cerebral
substance and abdomen of domestic ducks with negative results. A
variety of different bacterial cultures was obtained from the liver,
spleen, blood and congested nasal mucosa of several birds dead with
the disease and injected into domestic ducks with negative results.
Histological sections were cut from the important organs of thirteen
birds. The kidneys, lungs and pancreas showed no abnormalities. The
heart muscle in some cases and also some of the skeletal muscles
showed Zenker’s hyaline degeneration together with minor hemorrhages
and edema. Several of the proventricles showed low grade inflammatory
signs toward the gizzard. The intestines regularly showed lymphatic
infiltrations of the villi most marked toward the tips but without
congestion. The lumen showed no parasites, bacteria or protozoa. Liver
showed in almost every case pigmentation by hemosiderin at times as
heavy as that seen in pernicious anemia. The finer bile ducts here
showed peripheral round cell infiltrate, which was not continued into
the major ducts as determined by serial sections. Parenchymal cells
were cloudy and swollen. Spleen showed in early cases
polymorphonuclear infiltrate of the follicles, in later cases atrophy
of follicular splenocytes and more or less pigment occurred in both
stages. The spinal cord and various peripheral nerves showed no
inflammation or degeneration as determined by the appropriate special
nerve stains. The above clinical, histological, protozoological, and
bacteriological examinations having failed to detect the cause and the
epizoötic now being over, its nature becomes a matter of deduction.
The only constant features of any importance were the paralysis, the
intestinal round cell infiltrate and thickening, the pigmentation of
the liver and degeneration of skeletal muscles. Of the various
possibilities, beriberi was early considered. This is not possible
because the food of the birds was a varied one and furthermore none of
the nerve degenerations of beriberi were noted. Second, acute
bacterial or protozoal infections are unlikely because no constant
primary lesions were discovered at autopsy, the numerous cultures
failed to produce the disease and other birds living on the stream
draining the lake were not similarly affected. Third, a food
poisoning. This is possible first because paralytic symptoms were
present such as are seen in vetch and mussel-poisoning and secondly
because the epizoötic ceased when the birds were taken from the lake
and placed upon the grass. If this be the case the toxic material
produced the paralysis by direct action upon the muscle fibres just as
that of typhoid fever does and must have caused hemolysis as shown by
the hepatic pigmentation. The source of this food poisoning is
conjectural. Perhaps a dead fish decomposed in the water or there were
some algæ with poisonous properties present. The outbreak has a
resemblance, but only a superficial one, to infection with one of the
group of botulism bacilli. The cause of the trouble must be considered
as undetermined.
Enterohepatic Disease. Since the normal drainage from the intestinal
tract passes so largely through the liver, there is little to wonder at
in morbid lesions of the latter organ consequent upon disease in the
former. Not only does this succeed upon bacterial infection of the
digestive tube but also upon infestation with animal parasites, under
the latter condition forming changes of much more considerable extent,
at least in gross bulk, than in the former. Changes in the liver
secondary to enteric disease from bacterial infection take the form of
cholangitis, thrombosis, degenerations and probably cirrhosis while
abscesses and necroses succeed upon protozoal or metazoal parasitic
involvement. The latter is exemplified by amebic abscess in man and
other mammals and by “blackhead” and “quail disease” in birds; it is to
the latter conditions that attention is now directed. The chapter upon
the cause of these diseases has yet to be completed, although many reams
have been written about it, while the transmission is fairly well
understood and the pathology well described. My purpose here is to
discuss our experience with the two above mentioned diseases which,
while far from conclusive, may assist somewhat in explaining their
etiology. There is also reproduced our original report upon quail
disease from the Society’s Report of 1915, giving data and figures.
Blackhead has been found in five wild turkeys. An unusual case in a
Berwick’s Swan is recorded since it bears a striking resemblance to the
disease.
The points at issue in the determination of the etiology of blackhead
are the importance of _Heterakis papillosa_ in the ceca and the
frequency and activity of ameba or histomonas. In three of the five
cases of the disease in turkeys the nematode was found macroscopically
in the ceca, in two it was not; in one its absence was confirmed
microscopically. In two of the turkey cases, forms corresponding to the
ameba or histomonas were discovered while the descriptions of the
hepatic lesions in two birds use the term coccidia which, from a
revision of the slides, is probably incorrect although some of the
parasites seem to be possessed of a doubly contoured refractile margin.
The larger, more diffuse and ameba-like forms in the intestinal wall
suggest that the hepatic inclusions belong to the same group. In only
one case was exhaustive search made for coccidia, and without success;
the material was not preserved. In two turkeys entirely free of lesions
distinctive of blackhead, cecal nematodes (one heterakis, one unknown)
are recorded, and in the intestinal wall of another, also free from the
disease, forms indistinguishable from ameba could be discovered.[106]
The protocol of the Berwick’s Swan is interesting because the full
fledged disease is not known in this bird. While this case is not by any
means typical, the chronic cecitis and ameba-bearing necroses in the
liver stamp it as of a kind with the true infection of turkeys. Perhaps
the resistance offered by the swan effected a modification of the
disease, preventing the usual necrotizing enteritis and turning it into
a chronic interstitial variety.
Berwick’s Swan (_Cygnus berwicki_). About a month before death passed
several large clots of blood. Acute catarrhal enteritis, mural
endocarditis, chronic colitis, chronic nephritis, passive congestion
and necroses in liver, acute follicular splenitis, edema of lungs,
chronic pericarditis, chronic salpingitis, hydrothorax,
hydropericardium, hydroperitoneum. Tissues generally are slightly
yellow. In serous cavities of thorax is about three ounces of clear
fluid. Lungs are distended, subcrepitant, pale red and gray, highly
edematous. The pericardium contains about one-half ounce of clear
watery fluid. Epicardium is glistening, congested, irregularly
thickened especially near the blood vessels. The heart is contracted,
slightly large, pale brown-red muscle. On the posterior surface of the
right ventricle extending from the auricular opening to the pulmonary
valve is an irregularly curved line of grouped, recent red vegetative
granulations. Valves negative, they and chambers competent. Aorta
negative except heavily blood stained. Liver is slightly large. What
of the liver remains undamaged is homogeneous deep purple. Major
portion of right lobe badly contused; this seems to have been partly
antemortem because there is blood staining and mottling under capsule.
In view of colon finding and history of possible injury it is probably
the result of degenerations in the liver plus slight trauma. There are
several small, pale gray, well outlined, homogeneous areas probably
necroses in the liver. The spleen is slightly large, soft, egg-shape,
capsule smooth. Section surface shows bright red homogeneous pulp with
clearly cut, large follicles. The kidney capsule is smooth, surface
smooth brown, consistency firm and tough. The section surface gives a
dull gray-brown appearance, seemingly from connective tissue. Markings
indistinct. Oviduct is negative except over a distance of an inch near
the cloacal opening. Here there is a compound curve with constriction
to almost obliteration of lumen. This does not seem to be connected
with the colonic trouble. The stomach is negative containing only a
few small pebbles. Beginning at the pylorus and extending through the
whole of the small gut is a recent, moderately severe catarrhal
enteritis with so much exudate as to form almost a cast of the tube.
Colon and cloaca show an infiltration of submucosa with areas of
hemorrhage. Mucosa swollen as if by edema, glistening and covered by
bloody mucus. Ceca negative except that they seem to have been closed
as their contents are scanty and firm. Histological section of cloaca
shows it to be the seat of a chronic inflammation which has
constricted and distorted the tubules into simple masses of nuclei.
Marked polynuclear and round cell infiltration of mucosa and
submucosa. This is apparently due to ameba-like bodies—a large vacuole
with a delicate limiting membrane and a piece of diffuse chromatin in
the centre—a few of which may be found deep in the mucosa. Liver shows
marked passive congestion, here and there areas of necrosis with some
fatty infiltration. Small groups of ameba-like bodies can be found
apparently lying in sinusoids of liver and in neighborhood of
necroses.
Quail disease, since the careful work of Morse in 1907, has been thought
by most observers to be due to an organism of the colon group, but I am
informed recently by the Pennsylvania State Board of Animal Industry
that coccidia have been found often enough in the droppings and in the
morbid lesions to warrant a suspicion of their etiological importance.
Although they were not especially sought in the work about to be
reported, their presence probably would not have escaped detection
during that investigation. I have recently had occasion to examine three
birds with lesions identical with those accepted as characteristic of
quail disease, one of which was subjected to the proverbial “fine tooth
comb” methods; no coccidia were found in the liver or intestinal
lesions.
The idea that quail disease, with its ulcerative typhlitis and
necrotizing hepatitis, is identical with blackhead or at least that if
the latter be due to protozoa, the former is also, requires no special
stretch of imagination to one familiar with the morbid lesions. A
decision is the more difficult because of one’s inability to reproduce
quail disease at will and the none too great certainty of the
intentional production of blackhead. At all events the transmission is
potentially the same, ground or food soiled with droppings, indicating
that hygienic measures should take the form of segregation and
disinfection. Here follows the report of our original observation:
“An epizoötic disease has decimated three newly imported lots of quail,
Scaled quail (_Callipepla squamata_), Gambel’s quail (_Lophortyx
gambeli_) and Texas bobwhite (_Colinus texasus virginianus_). On January
5, 1915, the first lot of twenty-four quail arrived from northern New
Mexico _via_ Kansas City; on January 11th a second lot of twelve
bobwhite arrived from Brownsville, Texas, _via_ Kansas City; the first
of this lot died the day after arrival with lesions of this infection.
From this lot of birds the first lot was probably infected, the first
death occurring on January 20th, no other deaths having occurred in the
first lot since arrival. On January 21st the third lot of twelve quail
arrived direct from Mexico. The first of this lot died of the disease on
January 24th. Some birds were also sent at the time of the arrival of
the third consignment, to Doctor Kalbfus of the State Game Commission.
It is to be emphasized that to date no cases of infectious enteritis
have occurred in the lot sent to Doctor Kalbfus. The first case appeared
at this Garden on January 12th, more than a week before the third lot
arrived. It would seem that the disease was brought to the Garden by the
second lot of birds, and that they picked it up on the way from Texas to
Kansas City to Philadelphia. The birds made a stop at Kansas City. The
birds died at long intervals for the first two weeks, but late in
January and early in February several died each day. The last death with
characteristic lesions occurred February 11th. After the epidemic
reached its height it subsided very quickly.
“During the illness the birds exhibited very few symptoms, indeed some
of them were not known to be sick. A few sat huddled in a corner with
ruffled feathers and drooping head; the stools were little if any
altered as far as could be determined among so many in the enclosure. At
death the birds were in good condition, feathers fairly smooth, skin
clear, body plump and fat in good amount—not abundant, nor were the
animals emaciated. The principal lesions were enteritis, degenerative
necroses and abscesses in the liver, congestion of all the viscera and
plastic peritonitis in a few. A small number showed congestion of the
lungs and two had patches of pneumonia. Many but not all of the birds
had Heterakis in the ceca. The process seemed to start as a focal
necrotizing lesion in the mucosa or submucosa of the ileum just above
the ceca and colon; many had lesions in the ceca and as far down in the
colon as the cloacal dilatation. Among the animals dying late in the
epidemic several showed lesions involving the whole small intestine, a
few indeed with greater involvement of the duodenum than of the lower
parts.
“Judging from the gross and microscopical appearances it seems that the
virus causes at first a cellular infiltrate in the mucosa or submucosa
upon which necrosis shortly supervenes. The overlying mucosa soon
degenerates, and the surface is covered with an indefinite slough. In
other cases, especially early in the epidemic, the process extended
outward and appeared as muscular or subperitoneal necrotic areas before
the mucosa was much involved. At all events necrosis was an early change
in every case. The blood vessels were usually thrombotic. In the cases
that spread toward the peritoneum a plastic peritonitis of varying
severity was present. The focal liver lesions were not present in every
case. They took the form of focal necroses or abscesses. Some fatty or
parenchymatous degeneration was always present. The liver lesions
probably started as inflammations of the veins from which necrotizing or
infiltrative lesions spread. The splenic lesions were those of lymphoid
hyperplasia, only distinctive in the enormous number of large lymph
cells. Typical microscopical changes are as follows, quoted from one of
the autopsy protocols: The lung showed moderate congestion with here and
there a little epithelial swelling and a mild bronchitis and
peribronchitis. The type of bronchitis is infiltrative rather than
catarrhal. The heart muscle showed granular degeneration of the fibres
with breaking up or irregularity of the striæ. Some increase in
interfibrillar nuclei and especially those of the capillaries. There is
moderate congestion. Epi- and endocardia are slightly raised as if by
edema. Here and there slight fragmentation of fibres. The liver cells
are granular and some show fat droplets. There is moderate congestion
and more than the normal number of round nuclei between the columns.
Here and there are focal necroses of varying sizes without
circumferential reaction. Here and there are also some small collections
of round cells near to which the liver nuclei are large and show
attempts at regeneration. In these collections but not in the necroses,
bacillary forms may be found. There is no reaction on the part of the
bile ducts. The larger vessels are thrombotic, and in one section a
thromboangiitis was found. One stretch of early plastic perihepatitis
was found. The kidney showed slight granularity with slight cloudy
swelling of the epithelium. The nuclei of the glomeruli are prominent.
There is moderate congestion. The spleen showed distinct large lymph
cell hyperplasia with relative inconspicuousness of small round cells.
The follicles are very diffuse, their centres filled with large lymph
cells. The cords are hyperplastic and the sinuses compressed. Moderate
congestion; no unusual blood destruction; one area of hyaline necroses
found. The proventricle and gizzard are negative with the probable
exception of active desquamation on the surface of the former. The outer
coats of the duodenum are negative except for slight richness in nuclei.
The deep mucosa is very rich in nuclei and red blood cells. The outer
parts of the villi are either swollen with a cellular infiltrate or by
an area of granular necrosis, or have disappeared. It would seem that
the surface of the mucosa rapidly degenerates and desquamates. Bacteria
are very numerous. The adjacent pancreas is negative. The ileum showed
round cell infiltration of the deep mucosa, swelling of the villi and a
desquamation of the surface. One ulcer was found having its base on the
swollen muscularis and being covered with necrotic slough. Adjacent
peritoneum is slightly infiltrated, but chiefly congested and edematous.
This ileum lesion seems to be the characteristic one of the disease.
Bacteriological observations were made upon cultures obtained from the
intestinal mural lesions, the peritoneal exudate, the liver necroses,
and the heart’s blood in eleven cases. In seven cases I was able to
isolate a motile rod like the _B. coli communis_ and in four cases a
non-motile rod of the _Bact. aerogenes_ type. The former is quite
similar to the _B. scoticus_ (Migula) reported in Grouse disease.
“We obtained from Doctor Kalbfus of the Pennsylvania State Game
Commission, four perfectly healthy birds for experimentation. A culture
of the isolated germ was injected into two of them and mixed with the
food of the remaining two. It does not seem profitable to cite the
details of the work as the results were entirely negative, no lesions
resulting that bore the slightest resemblance to the spontaneous
disease. The birds either lived indefinitely or succumbed to wholly
foreign conditions. This negative experiment is of course no proof that
the organism is not the cause of quail disease, for the methods employed
might not be the correct ones to propagate the virus or the germ may
have lost its virulence during the laboratory culture work. However, as
some observers have not reported this bacillus in the disease this germ
loses something in importance by the negative inoculation experiment.
“Judging from reports and based upon the observations of Morse upon
Grouse disease it would seem that the incubation period of the disease
is about eight to ten days. However, one of the third lot of our birds
died within three days of its arrival at this Garden, and therefore
within three days of its exposure to the second arrivals; if it be
correct that this second lot brought the disease and the third lot did
not have it, it would seem that the incubation period can be as short as
three days; how long it may be is only suggested by the fact that some
of the third lot did not die for three weeks after arrival and exposure.
All the Gambel’s and scaled quail succumbed to the disease, but two of
the twelve bobwhite survived. It would seem that although these last
birds probably introduced the disease, they still possessed more
resistance than the others, for the second death among them occurred
seventeen days after the first death. The epidemic as we have seen it
here seems to be the same as Grouse disease of Scotland and as the
Grouse disease in this country as reported by Morse (Bureau of Animal
Industry Report 109, May 18, 1907).
“The means of transmission of the disease is not exactly known, but is
in all probability by a pollution of the food, the water supply or the
ground. Since the lesions are so marked in the lower ileum, cecum and
colon, a possible transmission by cohabitation must not be entirely
overlooked. There does not seem to be any means of limiting the epidemic
in a flock by segregation or sacrifice of the infected birds, because
symptoms are few and do not appear until shortly before death. Each bird
would have to be put into a separate cage until proved infected.
Scrupulous cleansing of the enclosure is desirable, but its efficiency
is difficult to estimate.”
SECTION XVIII
THE ANIMAL PARASITES, THEIR INCIDENCE AND SIGNIFICANCE
FRED D. WEIDMAN, M. D.
It is quite to be expected that animal parasites would be found in the
animals of zoological gardens, garnered as these beasts are from all
parts of the world, tropical and otherwise. It inevitably follows that
many of the forms should be strange and new, enticing one to the
fascinating determination of their identity, life history and hygienic
importance; and, developing from all this, one can easily imagine how
limitless the opportunities are for scientific work in parasitology in a
laboratory like ours.
As in other biological fields, the taxonomic range of parasites here is
wide. It extends from the lowly protozoa to the insecta, and, dropping
to the smaller subdivisions, includes not only most of the genera
familiar to human parasitology but many known only among the lower
animals. From the standpoint of the host, the biologic state of
parasitism extends from the lowest protozoa to homo.
The above will suffice to indicate the wide range of parasitism in
animals, but the extent of work actually done thus far in wild animal
material is a different story. Collated, consistent studies, so far as I
am aware, have been undertaken only at the London Garden, here at
Philadelphia, and at Washington, D. C., by Dr. Charles W. Stiles and
Albert Hassal. The data, collected by the last mentioned workers are
incidental to the Index Catalogue of Veterinary and Medical Zoology, and
embrace only the (index) phase indicated by the title, but it is so
valuable, and withal so altruistic, that it must be credited. What other
work there is is scattered where—not in literature—general biological,
medical and veterinary. That at London has been conspicuous through the
observations of Plimmer and of Beddard on filariæ and cestodes
respectively, while the work of Nicoll must not fail of mention.
That the reader may the better appraise the sections of our own work
which are to follow I wish at once to indicate their material basis.
Ordinarily only the larger parasites are looked for at the autopsy table
and there must be special indications to demand search for the finer
ones. Those of microscopic size, or so minute as to be overlooked in the
guise of seeds, vegetable fibres, etc., have not, both here and
elsewhere, been routinely studied as have macroscopic ones.[107] From
our autopsies there have accumulated records of nearly 900 parasites—
some determined generically, others but as to order. The parasites have
in greatest part been preserved and are available for further study; in
the past, special groups have been culled out from time to time and
examined. Where conditions have been pressing, as in certain epizoötics,
investigations have amounted to more than observations and descriptions,
and received detailed laboratory examinations with more or less animal
experimentation as the occasion demanded.
The foregoing may suffice to apprise the reader that the subject of wild
animal parasites has been but broached so that data are especially
incomplete on life histories—a phase most important in relation to
hygiene; but in spite of this and although the statistics are only
approximate, as is the case in most parasitological work, these data
have attained to sufficient proportions to justify at least a beginning
in the matter of collating and generalization. At any rate the time has
arrived to establish at least a nucleus for the accretion of data, which
can be later subjected to confirmation or correction. We draw just a
grain of comfort from the knowledge that the more fully worked field of
human parasitology is also vulnerable to criticism of very much the same
order.
THE VALUE OF PARASITOLOGICAL STUDIES IN ZOOLOGICAL GARDENS.
The foregoing chapters have made clear two fields of practical
usefulness of any study in such gardens. These—hygiene in relation to
the animals and comparison in relation to human beings—need therefore
only to be mentioned at present since it is obvious that both benefit by
our parasitological work. But there is yet a third—a scientific phase of
parasitology which may be considered purely academic. It consists in
morphological and other studies necessary for the identification of the
parasite, the determination of its life history, etc. These last studies
may still in a restricted sense include a modicum of the practical in so
far as they have a bearing on the disease with which they are
associated. But on the whole they are a source of danger for us since
such things as studies on the finer structures of worms, taxonomic
arrangements, descriptions of new species of commensals, etc., being
alluring, are likely to lead one so far afield that eventually an
attitude of stubborn resistance will have to be assumed in order to
conserve that precious, volatile laboratory asset—time—for the more
crying, practical problems ever reaching out to us.
However, in parasitological investigations as in other scientific work,
immediate abstract information may at some time prove to be of greatest
practical value. Thus for example if we can discover the exact facts
concerning one phase of the life history of a certain parasite, it may
be possible by hygienic measures, to break the cycle of development of
the parasite at one point thereby preventing its completion. This
information is perhaps obtained most readily in experimentation upon the
rôle of lower animal forms in the pathogenesis of disease but where
reliable evidence is lacking, help may be had by comparison with others
in the same taxonomic group. Undoubtedly systematic classification will
go far to help solve many of these riddles.
PATHOGENICITY OF ANIMAL PARASITES IN GENERAL.
The first question which arises in this connection concerns the actual
ability of animal parasites to produce disease in wild animals. At once
it will be seen that this must be a relative matter, for no one on one
side would contend that every symbiont in an animal is harmful—parasites
_sensu stricto_—nor on the other that none could possibly be, _i.e._,
that all are always commensals. It is evident that the issue boils down
to questions as to the extent to which they are harmful. Before
attempting the answer let us consider the means by which the parasites
may conceivably produce disease.
MODES OF DISEASE PRODUCTION (PATHOGENESIS).
The medical reader is familiar enough with the pathogenic powers of some
animal parasites, but may be sufficiently interested to glance over
specific wild animal instances illustrating them while they are being
listed for those less familiar with this subject.
1. MECHANICAL OBSTRUCTION.
I refer here particularly to simple blockage of normal body passages as
the result of bulk or mass. This occurs more commonly in the intestines
than elsewhere on account of the greater frequency, greater numbers and
larger size, in general, of parasites inhabiting this tract. Thus, we
have recorded a liothrix (_Liothrix luteus_)[108] where the combination
of a small host and consequently narrow gut and comparatively large
parasite induced obstruction. Plimmer[109] records microfilaria clogging
the brain capillaries. Shipley[110] mentions two specimens of _Ascaris
lumbricoides_ obstructing the nares of a chimpanzee (_Pan niger_).
Blockage may also be produced secondarily to the presence of the
parasite, even in the absence of notable numbers of them, and quite
apart from the element of verminous bulk. This occurs through
inflammatory swellings which the worms excite. We saw many serious
grades of this in our spiroptera epizoötic, the lumen of the
proventricle being narrowed by swelling of the mucosa and more or less
occluded by exudate and necrotic mucous membrane.
Yet another direction wherein a mechanical rationale pure and simple
obtains is by the production of diverticula. Worms encysted in the gut
wall may, by weight alone or by excitation of peristalsis, cause the
wall to bulge outwards (or inwards even) like a pocket. Such a
diverticulum has been noted in the gut of a Pale Cebus (_Cebus
flavescens_)[111] parasitized by acanthocephalus, but in this case there
were adhesions to the nearby stomach, and it is possible that in this
individual case the diverticulum was a traction one, _i.e._, pulled out
by the anchorage of adhesions externally.
[Illustration:
FIG. 71.—ACANTHOCEPHALUS (THREE SPECIMENS) PROJECTING FROM THE INCISED
INTESTINES OF A PIGMY MARMOSET. COMPARE THE SIZE OF THE PARASITES,
WHICH MAY BE DISTINGUISHED BY THEIR ANNULATIONS, WITH THAT OF THE
INTESTINES.
]
[Illustration:
FIG. 72.—BLOOD-RED NEMATODES PROTRUDING FROM FRONTAL SINUSES OF COMMON
OPOSSUM (DIDELPHYS VIRGINIANA). THE SKULLCAP HAS BEEN LIFTED OFF AND
THE POSTERIOR WALLS OF THE SINUSES BROKEN.
]
2. MECHANICAL IRRITATION.—In those instances where inflammation is the
manifestation which reflects the simple mechanical effects of parasites
it will be difficult indeed to prove, in the present state of our
knowledge, that it is not rather the effect of associated toxic
substances or excreta elaborated by the parasite. But instances of a
purely mechanical irritation there must be, although one can scarcely
put the finger upon them and say that this or that individual inflamed
mucosa did not become so from a toxic cause. Omitting these then, the
more certain, purer, more unequivocal examples will be those where
physiological processes become exalted as the result of the parasitic
irritation. An example in point is a case of volvulus in a Screech Owl
(_Otus asio asio_).[112] Here it is probable that the parasites excited
the gut to undue peristaltic action, and that during this process it
became twisted. Worms in such passages as the nose and nasal sinuses (I
have seen blood-red filariæ in the frontal sinuses of an opossum)
undoubtedly produce nervous effects by their presence and movements.
Those in the subcutaneous tissue (filariæ of wild cats) probably also do
so. It is difficult to judge those cases where doubtfully sensitive
parts are the ones affected. Probably the intestinal and intraperitoneal
worms, and less certainly the generally-migrating ones analogous to
_Filaria loa_, produce no nervous effects mechanically.
3. PRODUCTION OF HEMORRHAGES.—Hemorrhages large enough to kill suddenly
are theoretically possible, since worms occasionally produce aneurysms
which may rupture; we have seen such an accident in a Paradoxure
(_Paradoxurus leucomystax_). But certainly it is the long continued,
wasteful small hemorrhages that are important, inducing an anemia often
of severe and fatal grade. The hookworms are the shining offenders here,
yet we have seen very much the same effect from Acanthostoma in the
intestine of monkeys. Œsophagostomum has also been incriminated at the
London Garden in young Rhesus Macaques (_Macacus rhesus_)[113] where the
young forms of the parasite did the damage as they burrowed into the
wall of the gut.
4. OPENING UP AVENUES OF INFECTION.—This may be accomplished either by
passage of parasites from one position normally containing bacteria to
another which is susceptible to infection, or by devitalizing a tissue
which is ordinarily resistant to infection; _i.e._, creating a _locus
resistentiæ minoris_. The intestinal tract is the most common organ
concerned, but the illustrations to follow will give variety. Thus, the
mature examples of œsophagostoma in young rhesuses just referred to
above burrowed into the gut wall and led to both local and general
peritonitis. In one of our “spiroptera” parrots the worm had passed
through the proventricular wall and a chronic fibrosis resulted around
it. At the autopsy on a Rhesus Macaque Doctor Fox found a localized
abscess adjacent to the gut wall, and in it a whipworm was imbedded.
Passing from these examples of intestinal worms, I can mention the loss
of a valuable Philippine Spotted Deer (_Cervus alfredi_) as the result
of secondary infection of a cysticercus cyst of the lesser omentum which
led to a nearby peritonitis. Lung infections are not uncommon.
Murray[114] records that forty-four out of eighty-five young rhesus
monkeys dying from pneumonia showed an acarian, and he ascribed the
pulmonary irritation to certain crystals in the excreta of the mite. I
have studied a case of bronchopneumonia in a prairie dog where great
numbers of an arachnid were present. The reports of the London
Zoological Society are replete with notes of round worm pneumonias of
reptiles. These pulmonary cases must result from decreasing of tissue
resistance by the presence of the worms, and are easy to understand,
much more so than the intestinal infections when one recalls how
sensitive lung tissue is to foreign bodies, and that there seems to be
no indication that this tissue becomes accustomed to infestation such as
may be argued for the gut. All these citations must convince us that
parasites are most important predisposing agents to infection, and that
this is one of the most sinister phases of animal parasitism.
5. DESTRUCTION OF TISSUE.—This heading does not refer to the
comparatively trivial effects that accompany the more acute
inflammations secondary to parasites, albeit certainly the absorption of
their disintegrative tissue products has some effect on the economy; but
our ideas of such are so vague as to justify their being disregarded
here. What I refer to is the more massive destruction such as may occur
in the blood, for instance, from the action of protozoa. There is also
loss of mucosa in those chronic infestments of the stomach where we find
excessive fibrous tissue overgrowth. The most striking example of tissue
destruction we have seen was in the cirrhotic livers of prairie dogs
affected by _Hepaticola hepatica_, where in extreme cases, the amount of
functionating liver substance was reduced to a very small fraction of
its normal bulk.[115]
6. TOXINS.—We have no direct evidence to offer that noxious products of
parasites are concerned in producing disease in wild animals. The local
effects of such toxins are not distinctive enough—individual enough to
toxins or to the animal body—to separate them from the effects of such
accompanying factors as bacterial inflammations; nor can we separate the
general effects of these toxins from what might have been, for instance,
the effects of an accompanying anemia of hemorrhagic or other origin.
From a knowledge of what happens in human prototypes though, there is
scant doubt that some one of the multitudinous species must be capable
of producing toxins, but just which varieties are concerned cannot be
listed by anyone. By analogy we can at most only suspect the hookworms
and the dibothriocephalidæ. Under this same category of the toxins come
the worm-products which are reputed to have a destructive effect upon
the digestive enzymes in the gastrointestinal tract of the host, and
which would thereby interfere with the proper assimilation of pabulum,
resulting in malnutrition. For the same reasons as above indicated for
the toxins one is unable to speak for or against these “anti-enzymes.”
7. PRECLUSION OF NUTRITION.—This must be a very unimportant phase of the
activity of intestinal parasites, when one compares the bulk of food
which passes through the bowel and the average number of worms present;
and the same holds good for some interstitial parasites like the adult
filariæ. Even in amazingly heavy infestments of the intestines one will
be constrained to dismiss this idea when he compares the bulk of
parasites with that of the host, and recalls what the physiologist terms
the “factor of safety” inherent in this tract as elsewhere. But in the
case of blood parasites the matter may be different. Here we are
concerned with the withdrawal of refined foodstuffs—those which have
been worked over and over by subtle internal metabolic processes; and we
are not so sure, especially on recalling the enormous numbers of
parasites usual to blood infestments, that there is the capacity on the
part of these internal processes to meet increased demands that we count
upon for the intestinal functions. It is much more serious to be
deprived of the finished product than of the crude because it means the
undoing of “digestive” work all along the line, from gut to tissue cell.
Furthermore, a blood infestment guarantees that the parasite has been
feeding upon and depriving the animal of the precise foodstuffs the
cells require, and not by any chance upon, even in part, intestinal
substances that were wastes or residues. If we except the blood
parasites, then, it seems safe to conclude on the whole that the amount
of pabulum used by parasites is unimportant to the animal.
Having reviewed the manner in which parasites may conceivably be
harmful, it is time to return to the question of the actual exercise of
these powers.
The older appraisal of parasites in animals, namely that they were
rather innocent of disease production, was suggested by and borrowed
from the veterinarian, probably being engendered in him by their
frequency in what appeared to be normal domestic specimens. Yet it is
only proper to add that one of our former pathologists, and sometime
professor of veterinary pathology, Dr. C. Y. White, is a medical man and
is of much the same opinion. Older writers regarded worms even as
“guardian angels” of children. Very recently Schwartz[116] reviews some
work in this connection showing that, _in vitro_, some cestode extracts
were inhibitory to certain bacteria (_B. anthracis_, _B. pyocyaneus_ and
_B. dysenteriæ Shiga_). This relationship is so different from natural
conditions as to need no further comment.
At the London Garden the view appears to be different. In the 1910
report they charge five deaths against perforation by worms of the
stomach and intestines; in the 1911 report they record giant toads dead
from lung infestment; in 1912 “eighteen cases of enteritis were due to
worms”; and in 1917 they mention pneumonia in a toad and perforation of
the stomach of a puma. These reports represented evidently the more
striking, unequivocal examples of death from parasites which had
outspoken anatomical expressions, and omitted those in which the more
subtle agencies of parasitic pathogenesis were concerned. Their
experience has apparently been much the same as ours.
The ideal approach to a decision in reference to the importance of
parasites would appear to be a mathematical one, something as follows:
First, to determine what species infest animals and how commonly, then
to decide which ones are pathogenic and thirdly to estimate the severity
of the disease induced; so that finally, by an analysis and comparison
of the three results—a comparison and analysis judicial in the broadest
sense—we might hope to come to an opinion. Let us consider the three
avenues in order. At the first glance it must be evident that a list of
all possible parasitic varieties does not exist and may never be
compiled. The most that can be done is to tabulate the findings in
scattered laboratories, data usually recorded in terms of the individual
observer’s studies and often inadequate to give the compiler all the
facts desired. The same remarks apply to the percentage incidence of
parasitism. Not to prolong the academic discussion, suffice it to say
that very much the same obstacles present in the second avenue—that of
pathogenicity of the individual species. Our own data referring to this
second heading will be presented later, but after the failure of the
first avenue, the second and third lose greatly in value. At best,
statistics can be only suggestive. Unless critically and suspiciously
interpreted, and with a full appreciation of their limitations from a
foreknowledge of the way in which they were compiled, they would only
delude the reader and offend science, and so we abandon this line of
reasoning.
At present the best results of the study of pathogenesis by animal
parasites will probably be reached by a combination of methods, as
follows:
1. Direct. How commonly do we see clinical symptoms and morbid
anatomical changes that are incontrovertibly due to the parasite? We
restrict ourselves here to a narrow group of infestments indeed, and
think of such diseases as trichosomiasis in prairie dogs and
spiroteriasis in parrots.
2. By comparison with analogous infestments of domestic animals and man—
more thoroughly studied and therefore more accurately appraised, in
general, as to pathogenicity; a comparison from the standpoint of
disease production rather than natural habits of the parasite. Example,
coccidiosis and hookworm disease in foxes and dogs.
3. By inference through deduction. This is the most unsatisfactory
consideration of all, and should be well checked up and discounted. Here
we would evaluate the known propensities of the parasite first, such as
its size, motility, anatomic position in the host and the general
pathological traits of the genus and family to which it belongs, etc.,
and then compare these verminous properties with those of the host—its
size, temperament, physical stamina, etc. This third consideration must
necessarily overlap with or be supplementary to the first two. For
example, this consideration would have to be resorted to in many cases
of ascaris infestment where anatomical changes are generally not
demonstrable.
Acting on these three considerations, and after twelve years of
observation on parasites here in the Garden, a fresh review of our
records, and a recent review of the accessible relevant parasitological
literature I have come to the conclusion that, considering wild animal
collections the world over, there is no justification for an
unqualified, definite answer to the question of pathogenic parasitism
that will meet all conditions. We lack data on too many species that are
not sufficiently represented in collections or indeed not represented at
all. It is the liability to infestment of each order or family of beasts
that will have to be determined, and, depending on the assortment each
garden has on exhibition, will the importance of parasites to the garden
as a whole vary.
Speaking for the Philadelphia Garden, I have come to the conclusion that
on the whole parasitism does play an important part of our annual
losses. The financial loss which could be charged against spiroptera
alone is in the four figures, to say nothing of the difficulty of
replacement of rare species. And while touching the financial phase let
it be added that scientific work done now, it must be remembered, is not
restricted to the present time or place, but is to be measured in
dollars and cents with the yard stick applied to the future, and in
other places than that where the initial work is done. Even if we cannot
answer the question of the matter of importance the world over we can
guarantee that it is sufficiently so in the Philadelphia and London
Gardens to warrant a rigid supervision for parasitism; and since the
other larger collections are probably made up of similar animals, albeit
in different proportions, we surmise at least that it is likewise so
with them.
IMPORTANCE OF PARASITES IN OTHER FIELDS.—In addition to their importance
to exhibitions, animal parasites of wild animals are important first to
man. The animal hosts may serve as porters of infestation, and interfere
with attempts at eradication of the disease. The experience of the
European with African sleeping sickness attests to this. Not to go
farther than immediate examples I wish to note in this connection the
occurrence in this Garden of scabies in an orang which was transmitted
to a keeper, and of amebic dysentery in monkeys. Leiper[117] has called
attention to a guinea-worm in a leopard.
Parasites are important to certain wild animal industries. The ones that
have come to my attention are the fur seal (_Otoes alaskanus_) industry
of the Pribiloff Islands and fox-farming in Newfoundland. In both of
these instances the hookworm was concerned and entailed losses of
thousands of dollars. Lucas, who conducted a United States Government
commission to the seal grounds and after whom Stiles named the parasite,
has left very full notes of the former disease. I have identified the
same infestment in a young California hair seal (_Zalophus
californianus_) which was born and died in this Garden. This indicates
that the parasite might perhaps be found farther down the Pacific coast
than hitherto suspected.
To hunters parasitism of animals must be important, but to an unknown
and undoubtedly unimagined extent. The grouse plague of Scotland[118] is
an example to point. Who knows but that the disappearance of some of our
game animals, particularly birds, was not due more to disease than to
the ravages of man? There is at least food for thought here.
OCCURRENCE OF ANIMAL PARASITES IN THE WILD.—It would be unbelievable
that parasitism did not exist in the wild. It seems proper, however, to
record some evidence. Diesing’s _Systema Helminthum_ is replete with
references to Natterer’s Brazilian expedition. Nicoll speaks of a German
expedition to Spitzbergen in 1898, and a Swedish one to Egypt in 1901,
in both of which large numbers of parasitic forms were collected.
Nicoll[119] found _Trichosoma hepaticum_ in a hare shot in the wild, and
liver-flukes[120] in a kestrel shot on the coast of Scotland.
Leiper[121] found nine species of worms in hippopotami during an
expedition to Uganda, and[122] states that thirty-seven species of
helminths were collected on an Antarctic voyage by Surgeon Atkinson. In
an investigation of Grouse disease in Scotland, Fantham found many
different blood and intestinal parasites. Dr. Charles B. Penrose tells
me that all of the white-tailed deer he shot in the valley of the Swan
River, Montana, were infested with liver-flukes, so much so that the
liver was literally riddled by the disease, and yet the deer were fat.
The black-tail deer of the same valley were not thus parasitized and
were not as fat. In our own Garden we have found many tapeworms in wild
cats[123] which had been too recently captured for the worms to have
developed in captivity. Such instances might be still further
multiplied.
A more important consideration is the fate of the parasites thence
introduced into our Garden. Do they disappear of themselves? Naturally
we can never make sweeping predictions, for future events will depend
upon the life history of the individual parasite concerned. But by and
large, once introduced it is better to assume the attitude of pessimism,
and resign oneself against spontaneous disappearance and, what is worse,
realize that the parasitism is likely to become indigenous. We have
several pieces of evidence, however, that the infestment may
occasionally quite disappear. Thus, I have seen _Coccidium bigeminum_
spontaneously disappear from a Swift Fox (_Canis velox_) and _Spiroptera
incerta_ from a Macaw as proven at autopsy. Nicoll[124] remarks that
certain trematode infestations were heavier in newly arrived animals
than in ones long resident in the Garden. This is conceivable on the
basis of individual worms dying out, _i.e._, fulfilling their life spans
without the host becoming reinfested with fresh parasites. Precise
information on the subject is supplied by Ackert[125] who found that
cestodes disappeared from chickens in six to eight months when the birds
were confined, _i.e._, protected from reinfestment. Moreover, it is
known that worms can escape during acute infections, the infectious
state of the economy producing conditions obnoxious to the parasite. We
hear of many instances of their expulsion in human feces and vomitus
during malaria and the exanthemata of childhood and know of similar
discharge from animals during the death agony. I cite these data largely
because they explain the scarcity or absence of parasites at autopsy in
animals which were known to have been clinically infested.
FREQUENCY OF PARASITISM IN WILD ANIMALS
There can be little doubt that wild animals are more frequently infested
than man, and furthermore with a larger number of parasites. I have no
statistical basis for these opinions—they rest on personal observations
of human and animal autopsies, and reports of findings in the tropics
and elsewhere. They have therefore but the value of an individual
opinion. I should estimate rather cautiously that wild animals are
infested at least two or three times as frequently as man and much more
heavily.
The first step in the discussion of the incidence of parasites must be
that respecting the (host) classes and smaller taxonomic divisions—of
course as they have been studied in this Garden. Certain statistical
limitations were experienced and can be summarized as follows:
Data are not available on a sufficiently large number of animals to
justify conclusions as far down as genera and species, except for such
commonly and generously exhibited forms as monkeys and parrots. I have
therefore in tabulating and reviewing our records, distributed the
animals only as far as families—not into genera and species. The table
(24) to follow will be found not to contain every family because to do
so would needlessly enlarge it. Accordingly I have followed the policy
of only indicating those genera and species showing either frequent or
important infestment. I shall refer to those groups later as
“susceptible” groups. If no family is recorded in the table it means
that we have had no important numbers of infestments in it. The
“remarks” column shows the individual parasite that has been
particularly frequent or otherwise important. If there are no remarks it
means that the species of parasites found have been scattering.
RESULTS OF REVIEW AND TABULATIONS.
We now pass to an analysis and discussion of the findings brought out in
the previously mentioned review of our records and in Table 24. Viewed
broadly we find that there is a wide variation in the susceptibility of
different families to infestment. Those that are susceptible may be
located by consulting the table, and each will therefore not be
separately culled out and subjected to needless repetition. A few points
are however worthy of separate mention. While there is a familial or
generic susceptibility within certain orders it is unwise to generalize
too broadly. Thus for example the Corvidæ have a high percentage in
incidence for tropidocerca, syngamus and periproventricular worms, many
families of Ungulata harbor echinococcus, and Carnivora are prone to
show ascarids. On the other hand, among the copious exceptions to this
may be cited the irregular liability to infestment exhibited by the
Galli. Four varieties of these birds are represented but there are
missing such important kinds as curassows, guans, guinea fowl and
peafowl.
TABLE 24.
_Incidence of Parasites in Animal Groups._
══════════════════════╤═══════════════════════════════╤════════════════════
Animal │ MAMMALIA │ Remarks
──────────────────────┼───────────┬────────┬──────────┼────────────────────
„ │ Number of │ Number │Percentage│ „
│Autospecies│Infested│ │
──────────────────────┼───────────┼────────┼──────────┼────────────────────
Primates │ [126]538│ 51│ 9.4│
Cercopithecidæ │ │ │ │
Sooty Mangabey │ 34│ 4│ 11.8│
Cercocebus │ │ │ │
fuliginosus │ │ │ │
Rhesus Macaque │ 60│ 6│ 10.│
Macacus rhesus │ │ │ │
Callitrichidæ │ │ │ │
Marmosets │ 43│ 7│ 16.3│
Cebidæ │ │ │ │
Squirrel Monkeys │ 8│ 3│ 37.5│
Other Cebus │ 87│ 10│ 11.5│Eight had Filaria
Monkeys │ │ │ │ gracilis.
Lemures │ 86│ 6│ 7.│
Carnivora │ 498│ 84│ 16.9│
Felidæ │ │ │ │
American Wild Cat │ 28│ 11│ 40.│Stomach and
│ │ │ │ intestines, 22;
Felis ruffus │ │ │ │Bronchi, 4; Muscles,
│ │ │ │ 7.
Spotted Wild Cat │ 5│ 4│ 80.│
Felis ruffus │ │ │ │
texensis │ │ │ │
Canada Lynx │ 10│ 4│ 40.│Ascarids only.
Felis canadensis│ │ │ │
Lions │ 10│ 3│ 30.│Ascarids in stomach
│ │ │ │ and
Felis leo │ │ │ │intestines.
Ocelot │ 15│ 5│ 33.│Uncinaria.
Felis pardalis │ │ │ │
Canidæ │ │ │ │
Gray Fox │ 28│ 1│ 4.│Cestodes.
Canis cinereo │ │ │ │
argenteus │ │ │ │
Red Fox │ 17│ 2│ 12.│Uncinaria.
Canis vulpes │ │ │ │
pennsylvanicus│ │ │ │
Swift Fox │ 5│ 2│ 40.│Uncinaria.
Canis velox │ │ │ │
Gray Wolf │ 18│ 2│ 11.│Ascarids.
Canis mexicanus │ │ │ │
Mustelidæ │ │ │ │
American Badger │ 17│ 7│ 41.│Physaloptera.
Taxidea taxus │ │ │ │
Procyonidæ │ │ │ │
Raccoon │ 42│ 2│ 5.│
Procyon lotor │ │ │ │
Ursidæ │ │ │ │
Bears │ 37│ 6│ 16.│Ascarids.
Otariidæ │ │ │ │
Hair Seal │ 20│ 1│ 5.│Uncinaria.
Zalophus │ │ │ │
californianus │ │ │ │
Rodentia │ 198│ 32│ 16.│
Sciuridæ │ 44│ 4│ 9.│Scattered through
│ │ │ │ four
Castoridæ │ │ │ │different genera.
American Beaver │ 17│ 4│ 23.│In three cases
│ │ │ │ oxyuris
Castor │ │ │ │and flukes in cecum.
canadensis │ │ │ │
Hystricidæ │ │ │ │
Canada Porcupine │ 47│ 17│ 36.│Cestodes 8, filaria
│ │ │ │ 11, oxyuris 9,
Erythizon │ │ │ │in peritoneal cavity
dorsatus │ │ │ │ also intestine.
dorsatus │ │ │ │
Hyraces │ 7│ 2│ 28.│Cestodes in bile
│ │ │ │ ducts.
Cape Hyrax │ │ │ │
Procavia capensis │ │ │ │
Ungulata │ 365│ 44│ 12.│
Equidæ │ │ │ │
Zebras │ 7│ 7│ 100.│Nematodes,
│ │ │ │ intestine.
Cervidæ │ │ │ │
Axis Deer │ 6│ 1│ 17.│C. tenuicollis.
Cervus axis │ │ │ │
Barasingha Deer │ 8│ 0│ │
Cervus duvanceli│ │ │ │
Eld’s Deer │ 6│ 0│ │
Cervus eldi │ │ │ │
Fallow Deer │ 20│ 1│ 5.│Echinococcus cysts.
Cervus dama │ │ │ │
Hog Deer │ 21│ 0│ │
Cervus porcinus │ │ │ │
Japanese Sika Deer│ 14│ 0│ │
Cervus sika │ │ │ │
typicus │ │ │ │
Red Deer │ 14│ 0│ │
Cervus elaphus │ │ │ │
Elk │ 29│ 2│ 7.│Trichocephalus.
Cervus │ │ │ │
canadensis │ │ │ │
White tailed Deer │ 33│ 2│ 6.│Echinococcus in lung
│ │ │ │ (2).
Mazama │ │ │ │
virginiana │ │ │ │
Mule Deer │ 8│ 5│ 62.│Four Cyst.
│ │ │ │ tenuicollis.
Mazama hemionus │ │ │ │
Camelidæ │ │ │ │
Llama │ 14│ 2│ 14.│
Lama glama │ │ │ │
Camels │ 9│ 4│ 44.│Hydatid cysts.
Suidæ │ 19│ 2│ 10.│
Edentata │ 16│ 2│ 12.5│
Armadillos │ 10│ 2│ 20.│
Marsupialia │ 175│ 45│ 26.│
Didelphyidæ │ │ │ │
Common Opossum │ 84│ 40│ 48.│Physaloptera, 38;
│ │ │ │ oxyuris, 5;
│ │ │ │ cestodes, 5;
│ │ │ │ nematodes in
│ │ │ │ lungs, 3; cysts in
│ │ │ │ peritoneal areolar
│ │ │ │ tissue, 2;
│ │ │ │ trematodes in
│ │ │ │ ileum, 1.
Didelphys │ │ │ │
virginiana │ │ │ │
Macropodidæ │ │ │ │
Kangaroos and │ 70│ 0│ 0.│
wallabies │ │ │ │
──────────────────────┼───────────┴────────┴──────────┼────────────────────
│ AVES │
Passeres │ │ │ │
Corvidæ │ │ │ │
Common Crow │ 16│ 7│ 44. }│Tropidocerca and
│ │ │ │ occasional
│ │ │ │ intestinal
│ │ │ │ cestodes. Syngamus
│ │ │ │ in crows. Few
│ │ │ │ filaria.
Corvus │ │ │ }│
brachyrhynchos│ │ │ │
brachyrhynchos │ │ │ }│
Magpies │ 28│ 18│ 64. }│
Jays │ 41│ 22│ 55.│Periproventricular
│ │ │ │ filaria,
│ │ │ │ strongylus.
Pies, choughs, │ 35│ 12│ 33.│There is a striking
etc. │ │ │ │ consistency of
│ │ │ │ infestment in the
│ │ │ │ different members
│ │ │ │ of Corvidæ both as
│ │ │ │ regards degree of
│ │ │ │ infestment and
│ │ │ │ species of
│ │ │ │ parasite present.
Sturnidæ │ │ │ │
Starlings │ 63│ 19│ 30.│Periproventricular
│ │ │ │ filaria largely.
Turdidæ │ 25│ 8│ 33.│Periproventricular
│ │ │ │ filaria largely.
│ │ │ │Thrushes and Robins.
│ │ │ │ None in American
│ │ │ │ thrushes, one in a
│ │ │ │ robin.
│ │ │ │Finches. Not
│ │ │ │ examined closely
│ │ │ │ at autopsy, but
│ │ │ │ there is a
│ │ │ │ scattering of
│ │ │ │ periproventricular
│ │ │ │ filaria and
│ │ │ │ intestinal
│ │ │ │ cestodes through
│ │ │ │ most of the
│ │ │ │ species.
Canaries │ 24│ │ │Were free from
│ │ │ │ parasites.
Picariæ │ │ │ │
Picidæ │ │ │ │
Woodpeckers │ 4│ 2│ 50.│
Rhamphastidæ │ │ │ │
Toucans │ 30│ 9│ 30.│Spiroptera largely.
Striges │ 142│ 2│ 7.│Remarkably free of
│ │ │ │ parasites.
Psittaci │ [127]774│ 124│ 16.│
Loriidæ │ │ │ │
Lorys │ 24│ 5│ 20.│3 spiroptera, 1
│ │ │ │ hemoproteus, 1
│ │ │ │ intestinal worm.
Cacatuidæ │ │ │ │
Cockatoos │ 4│ 2│ 6.│2 spiroptera.
Crested Ground │ 45│ 4│ 9.│4 spiroptera.
Parrakeet │ │ │ │
Calopsitta novæ- │ │ │ │
hollandiæ │ │ │ │
Psittacidæ │ │ │ │
Old World (Totals)│ 453│ 65│ 14.3│
Undulated Grass │ 121│ 2│ 1.6│1 spiroptera, 1
Parrakeet │ │ │ │ coccidium.
Melopsittacus │ │ │ │
undulatus │ │ │ │
Pennant’s │ 21│ 6│ 29.│6 spiroptera.
Parrakeet │ │ │ │
Platycercus │ │ │ │
elegans │ │ │ │
Rosehill Parrakeet│ 48│ 21│ 44.│20 spiroptera, 1
│ │ │ │ cestode.
Platycercus │ │ │ │
eximius │ │ │ │
Other old world │ 86│ 12│ 14.│12 spiroptera.
parrakeets │ │ │ │
Old world parrots,│ │ │ │
lovebirds, │ 74│ 13│ 18.│13 spiroptera.
eclectus. │ │ │ │
New World (Totals) │ 321│ 69│ 21.5│
Macaws │ 26│ 9│ 34.│9 spiroptera.
Conures │ 62│ 16│ 26.│15 spiroptera, 1
│ │ │ │ hemoproteus, 1
│ │ │ │ blood larva.
Amazons │ 164│ 27│ 16.5│24 spiroptera, 3
│ │ │ │ nematodes.
Other new world │ 69│ 17│ 10.│7 spiroptera.
parrots │ │ │ │
Accipitres │ [127]201│ 13│ 6.7│
Falconidæ │ │ │ │
Buzzards │ 55│ 4│ 7.3│
Eagles │ 44│ 1│ 2.3│
Serpentaridæ │ │ │ │
Vultures │ 29│ 1│ 3.4│
Miscellaneous │ 73│ 7│ 9.6│4 were blood
│ │ │ │ protozoa.
Galli │ 299│ 42│ 14.│
Phasianidæ │ │ │ │
Pheasants │ 95│ 20│ 21.│Heterakis in ceca.
Partridges │ 14│ 3│ 21.│
Quail │ 70│ 10│ 14.│Heterakis.
Megapodidæ │ │ │ │
Wild Turkeys │ 39│ 7│ 18.│Intestinal cestodes.
│ │ │ │ Coccidia twice.
Columbæ │ [128]163│ 14│ 9.│Mostly intestinal
│ │ │ │ cestodes, but
│ │ │ │ several
│ │ │ │ spiroptera.
Fulicariæ │ [128]38│ 7│ 18.│
Alectorides │ [128]41│ 10│ 25.│
Gaviæ │ [128]21│ 3│ 14.│
Steganopodes │ [128]22│ 1│ 5.│
Herodiones │ [128]105│ 21│ 20.│
Anseres │ [128]319│ 28│ 8.8│
Swans │ 48│ 7│ 14.│No significant
│ │ │ │ groupings.
│ │ │ │ Parasites
│ │ │ │ scattering. Few
│ │ │ │ intestinal
│ │ │ │ cestodes.
Geese │ 83│ 13│ 15.6│
Ducks │ 188│ 8│ 4.│
Struthiones │ 36│ 1│ 2.8│
──────────────────────┴───────────┴────────┴──────────┴────────────────────
Nor do all members of a genus necessarily show the same susceptibility,
and the heterakis infestment in the pheasants illustrates this matter
very well. It was limited almost entirely to two species—Amherst’s and
Golden, whereas several frequently exhibited species showed none. The
following table brings this out in more detail:
TABLE 25.
_Heterakis in Pheasants._
════════════════════════════════════════════╤════════╤════════╤════════
Species │ Total │Infested│ Per
│ │ │ cent.
│ │ │infested
────────────────────────────────────────────┼────────┼────────┼────────
Golden Pheasant (Chrysolaphus amherstiæ) │ 18│ 12│ 67
Amherst’s Pheasant (Chrysolaphus pictus) │ 16│ 5│ 31
Silver Pheasant (Gennæus nycthemerus) │ 19│ 1│ 5
Reeves’ Pheasant (Phasianus reevesi) │ 16│ 1│ 6
Ringnecked Pheasant (Phasianus torquatus) │ 12│ 0│ 0
Swinhoe’s Pheasant (Gennæus swinhoii) │ 10│ 0│ 0
────────────────────────────────────────────┴────────┴────────┴────────
Enzoötics and environment played no part in the above figures. We have
had no real heterakis enzoötics, for in but two instances did three
heterakis deaths occur in a year, and two deaths per year have occurred
in but four instances in the past twenty years. During this time there
have been sufficient animals on exhibition and subjected to autopsy to
indicate definitely that the two species named—Amherst’s and Golden,
must be considered as more susceptible than the other varieties. Nearly
all of the heterakis in quail likewise occurred in one species—seven of
the ten cases occurred in a total of twenty-three Scaled Quail—but in
these birds the infestment appeared in enzoötic form and cannot be
viewed as indicating a preference for a species.
Psittaci are on the whole, not susceptible to worms. It is true that we
suffered a serious outbreak of spiropteriasis a few years ago, but if we
consider this a closed chapter we can accept the above generality as
stated. Among 774 parrots autopsied we have encountered but one cestode
and three intestinal round worms.
The deer, likewise, are singularly free from intestinal parasites. I
gave the detailed records of these animals in Table 24 to emphasize the
scarcity of parasites even when fairly numerous specimens had been
available for examination.
Other interesting features in the table are the outstanding infestments
of squirrel monkeys and marmosets among the monkeys, of gastric and
intestinal worms in the wild cats, and intestinal worms in the zebras.
The foregoing has had to do with parasitism from the standpoint of the
host. The next phase, that of the individual parasite itself, interests
more the strict parasitologist than the general zoologist; however, both
will see how it may have a very practical value.
TABLE 26.
_Distribution of Parasitic Cases According to Parasitic Groups._
═════════════════════════════════════╤════════════════╤════════════════
Nematodes │ 183[129]│
Spiroptera │ 145│
Filaridæ │ 138│
Ascaris │ 30│
Physaloptera │ 28│
Uncinaria │ 25│
Tropidocerca │ 23│
Heterakis │ 22│
Trichocephalus │ 11│
Syngamus │ 9│
Trichina │ 2│
Hepaticola │ 2│
Other Miscellaneous │ 4│
Total Nematodes │ │ 622
Cestodes │ 165[129]│
Echinococcus │ 9│
Cysticercus │ 7│
Tænia │ 4│
Miscellaneous │ 3│
Total Cestodes │ │ 188
Trematodes │ │ 22
Acanthocephalus │ │ 4
Protozoa │ │ 14
Arthropods │ │ 6
Unclassified │ │ 34
─────────────────────────────────────┼────────────────┼────────────────
Grand Total │ │ 890
─────────────────────────────────────┴────────────────┴────────────────
INCIDENCE ACCORDING TO PARASITIC GROUPS.
Inasmuch as it has been physically impossible to determine specifically
and classify efficiently the accumulations of verminous material from
our autopsies I will not be able to tabulate parasitic groups even as
closely as I did in the “animal host” table. Nevertheless sufficient has
been done to illuminate in part certain phases of parasitism and to
prevent a summary dismissal of the subject. Reviewing our cross index I
have distributed the data into the following Table 26, the parasites
being listed in the order of their frequency. It may serve only as a
panorama of the situation, inasmuch as determinative study of a group
amounts to a research in itself, and the multiplicity of them precludes
a consistent study of every one. The data are based upon “cases of
parasitism.” That is, each and every worm species occurrence has been
counted, regardless of whether it was the same species that has been
concerned over and over again, or in different anatomical positions (of
different individual hosts, of course) or whether it was in association
with other parasites.
ANALYSIS OF TABLE 26.
There is a grand total of 890 cases of animal parasitism embraced in the
above table, which is a sufficiently large number to give representative
value to some phases of the analysis.
In the first place nematode worms occur about three times as frequently
as all other forms of parasites. In gardens where spiroptera has not
figured so largely the proportion might be reduced to about two to one.
Cestodes rank a poor second, trematodes a worse third, and
acanthocephali a very bad last. This order agrees with our figures of
1913[130] and with the small series of Nicoll.[131] The latter worker
found that the order was not changed when pains were taken to include
also such smaller worms as could only be obtained from the host by using
sieves, etc. Cestodes were not likely to be overlooked, but very small
trematodes and nematodes were easily passed over.
VISCERAL DISTRIBUTION.
As to the individual organs which are most commonly parasitized our
records show that with Aves as well as Mammalia the intestines are the
parts most commonly affected. The stomach ranks second for both—the
proventricle rather than the gizzard of birds corresponding,
parasitologically speaking, to the stomach of mammals. We have found but
one parasitic species in the gizzard of birds, _i.e._, immature forms of
_Spiroptera incerta_ lying under the chitinous lining of the gizzard and
only discoverable after the lining has been peeled off. The peritoneum
comes third (air sacs of birds) due to the presence of filaridæ, and the
blood fourth for the same reason. It is to be emphasized that, in our
data, identical organs of mammals and birds should be about equally
liable to infestment with the possible exception of the lungs. But in
view of the small number of cases available there is no justification
for speculating about the reason for this last difference, albeit the
radical difference in the anatomy of the two classes is very inviting.
Now that our spiroptera enzoötic has subsided, the order above given
will be changed, and in view of like disturbing factors other gardens
should not expect the same order to hold invariably for their
collection, since their enzoötics will depend somewhat on the
preponderance of animals of one or another family which are likely to
compose their exhibits. A single such enzoötic may suffice to disarrange
the whole fabric, and if two or three are taken into account the order
of organ involvement can be quite disrupted. To attempt to construct
statistically an “order of frequency involved” which would stand for
every garden would only lead to interminable adjustments on the basis of
animals exhibited and of parasitic enzoötics, so that I have finally
been reduced to a combination of our Garden statistics and the
bloodparasitic ones of the London Garden. Doing this I have arranged in
Table 27 the frequency of organ involvement as follows and estimated the
percentage of animals infested. These figures are computed upon a
different basis from that of Table 24. They naturally cover all animals
and not the “susceptible” ones as in Table 24.
[Illustration:
FIG. 73.—HUGELY DISTENDED PROVENTRICLE OF PARROT DYING WITH
SPIROPTERIASIS. COMPARE ITS SIZE WITH THAT OF THE HEART WHICH IS
ABOVE AND TO THE LEFT, AND THAT OF THE GIZZARD BELOW AND TO THE
LEFT.
]
TABLE 27.
═══════════════════════════════════╤═══════════════════════════════════
Mammalia │ Aves
───────────────────────┬───────────┼───────────────────────┬───────────
│ per cent. │ │ per cent.
Intestines │ 9.0│Blood │ 6.5
Stomach │ 3.7│Intestines │ 3.5
Peritoneum │ 2.3│Proventricle │ 1.7
Blood │ 1.5│Air sacs │ 1.3
Lungs │ 1.0│Liver │ 0.3
Muscles │ 1.0│Gizzard │ 0.3
Liver │ 0.5│Scattering │ 0.4
───────────────────────┼───────────┼───────────────────────┼───────────
Total │ 20.0│Total │ 14.0
───────────────────────┴───────────┴───────────────────────┴───────────
The effect of this is at first sight startling in that it places the
blood parasites of birds so far in the fore, but it must be at once
recalled that the inquiries upon the blood parasites were much more
searching—microscopic, than in the case of the other organs. If similar
methods were applied to the others their percentage of parasitism might
be notably raised—particularly that of the intestines.
SPECIAL PARASITOLOGIC CONSIDERATIONS.
At this point the statistical considerations of parasitism will give way
to descriptions of certain specific infestments that have given us more
or less concern.
The occurrence of single parasitic varieties or of well known species in
an isolated host may occasionally be of practical importance, but
usually they amount to little more than an academic study, whereas the
repeated discovery of single parasitic kinds, or infestment of similar
hosts, especially when grouped, raises the matter to a very practical
level demanding attention. Such findings being not infrequent in our
experience, it has been possible to study our material in a manner
designed to show the frequency of various parasites in a certain host,
the susceptibility of certain animals to parasites in general and the
infestment of dissimilar hosts by the same parasite. The more important
of these now follow.
AVIAN SPIROPTERIASIS.
This disease concerned parrots particularly but toucans, pigeons, and
such widely separated species of birds as the starling, quail, thicknee
and barbet have been occasionally affected. To the naked eye the
parasite resembles the human hookworm, but differs in location, being a
resident of the proventricle where it produces a swelling of the mucosa
which interferes with the passage of food. Up to a hundred worms may be
present in the one bird, and immature forms are occasionally found under
the chitinous lining of the gizzard. The parasite burrows into the
mucous membranes, occasionally penetrates quite through the wall into
the air sacs, and on one occasion induced an adenomatous hyperplasia of
the mucous membrane, and an adjacent “peritonitis.” Mucus is sometimes
present in the droppings. Death may occur either acutely, or with
emaciation. Spiroptera incerta Smith[132] is the common parasitic
species of parrots, but I have found at least one other as yet
unidentified species in the toucan, and there are probably more. In the
eight year period 1906–1913 from 25 to 50 per cent. of our dead parrots
showed this parasite every year, the total loss being 113 birds for this
period—a most important infestment.
[Illustration:
FIG. 74.—HISTOLOGIC SECTION THROUGH PROVENTRICULAR WALL OF PARROT,
SHOWING SECTIONS OF SPIROPTERA IN THE LUMEN AND MUCOSA. THERE IS
SOME GLANDULAR HYPERPLASIA (ADENOMATOID) AND NECROSIS OF THE LUMINAL
PORTIONS OF THE MUCOSA.
]
[Illustration:
FIG. 75.—INFLAMMATORY ROUND CELL INFILTRATION AROUND NERVE TRUNK IN
WALL OF PROVENTRICLE. PARROT DEAD WITH SPIROPTERIASIS.
]
We approached the problem by diagnosing and isolating the infested birds
through a microscopic examination of droppings, finding that by boiling
the droppings in 5 per cent. NaOH solution we clarified them and made
examination easier and more certain without at the same time destroying
the parasitic ova. The result of the examination of all our parrots was
the isolation of 14 per cent. of the parrot population; and as these
died off the diagnosis of infestment was found confirmed at autopsy in
every case. The parrot house was thoroughly renovated and no newly
arrived parrots were admitted until after quarantining and examining
droppings for ova. The toucans and other species, being housed
elsewhere, were not quarantined. Following this, we were gratified to
experience no more spiroptera deaths in parrots for seven years. Then,
in 1920 and 1921, a new outbreak occurred in four toucans and several
other scattering species, including two parrots; but none of these came
from the main parrot house and probably represented a fresh importation.
We attempted to cure the isolated verminous birds by medication but were
unsuccessful. Likewise attempts at determining the life cycle of the
parasite brought us no farther than that the ova developed larvæ in
moist sand in six days. Feeding of ova, freshly passed and larvated did
not produce infestment in parrots or pigeons. On the whole we can quote
our experience with spiroptera as a most satisfactory example of the
value of hygiene and as a result which could never have been
accomplished by medication.
HEPATICOLA (TRICHOSOMA) HEPATICA IN PRAIRIE DOGS.
Bancroft[133] and Hall[134] have given us details concerning this
parasite and the disease it causes. It is threadlike, several inches
long, and permeates the livers of the gray rat, white rat and wild
hare.[135] We first saw it in the more or less cirrhotic livers of
several prairie dogs; later we observed it in a beaver and the gray rats
of the Garden. In the prairie dogs and beaver the liver resembled that
of fatty cirrhosis and was so considered on naked eye examination at our
first autopsy. We were only set right when we came to the histological
examination. It was remarkable how well conditioned some of the prairie
dogs were in in the face of very extensive liver destruction; but on the
other hand some were emaciated and a few of the spontaneously diseased
showed at autopsy an enormous ascites. The outstanding features at
autopsy were the large size of the liver and its pallor and hardness;
and fine yellow lines could sometimes be made out twisting over the
surface.
The disease affects wild rats differently from prairie dogs. In both the
spontaneous and experimental disease the infestment was insignificant,
amounting to perhaps three or four foci the size of a split pea near the
anterior margins of the liver. Diagnosis may be easily confirmed by
crushing the yellow infested portions of the liver between glass slides
and examining microscopically for ova.
We have seen such a small number of cases of this disease because so few
prairie dogs reach the autopsy table, yet there must be some important
mortal factor in our prairie dog enclosure, for the Superintendent
states that the population there does not increase in spite of the
frequent births and additions from dealers. The animals almost
invariably die under ground and their bodies are not recovered.
In order to test out the origin of the infestment we trapped two of our
exhibition specimens, and the liver of both was found infested on
surgical examination whereas six newly purchased ones had normal livers.
The latter were secured fresh from their native habitat in the West, and
their livers were examined through long surgical incisions and found
free of infestment. Later we fed the ova (embryophores) from rat livers
to these prairie dogs and on destroying them found them infested. We
were also successful in transmitting the disease in the opposite
direction, _i.e._, from prairie dog liver to white rat. From all this we
feel sure that the prairie dog disease in our Garden was transmitted
from the rat and that here is another reason for rat extermination in a
zoological garden.
[Illustration:
FIG. 76.—OVA OF HEPATICOLA HEPATICA IN LIVER OF PRAIRIE DOG. THEY HAVE
BIPOLAR OPENINGS. THERE IS DESTRUCTION OF LIVER TISSUE AND A LITTLE
INFLAMMATORY REACTION OF CELLULAR CHARACTER, BUT NO IMPORTANT
FIBROSIS.
]
[Illustration:
FIG. 77.—UNCINARIA SMITHI COILED IN INTRAHEPATIC BILE DUCTS OF
GIRAFFE. NOTE MARKED PERIDUCTAL FIBROSIS IN THE NEIGHBORHOOD OF THE
PARASITES.
]
The adult _Hepaticola hepatica_ of prairie dogs I have not seen in
sufficient entirety to compare with the rat species and therefore cannot
affirm that the two are identical species. It is presumably like that of
the rat, being threadlike and most difficult to separate from the liver
substance through which it ramifies. At maturity it dies and
disintegrates, leaving the ova distributed more or less in tracts
through the liver substance, so that we are limited to a certain period
wherein to obtain the mature form. The ova are not passed into the
intestine, but remain _in situ_, just as in the case of hydatid disease,
and therefore diagnosis cannot be achieved by examination of feces. For
the disease to be transmitted the host must die and its carcass be eaten
or otherwise so disintegrated that the ova are distributed abroad.
Another interesting observation is the long incubation period of the
ova. Confirming Bancroft, we found that the ova only became larvated
after they had lain in water at least three months.
HOOKWORMS.
These important parasites have been taken from several foxes: Gray Fox
(_Canis cinero argenteus_), Arctic Fox (_Canis lagopus_), Swift Fox
(_Canis velox_), Red Fox (_Canis vulpes pennsylvanicus_), a Gray Wolf
(_Canis mexicanus_), divers members of the Felidæ-Eyra (_Felis eyra_),
Jaguarundi (_Felis jaguarundi_), American Wild Cat (_Felis ruffus_),
Spotted Wild Cat (_Felis ruffus texensis_), Ocelot (_Felis pardalis_),
from two Giraffes (_Giraffa Camelopardalis_, _Giraffa capensis_), a
Malayan Tapir (_Tapirus indicus_), and a young California Hair Seal
(_Zalophus californianus_). It has been a most serious infestment in
American wild cats (_Felis ruffus_ and _Felis ruffus texensis_)—animals
which generally also harbor other species of worms. In view of the
petechial hemorrhages of the intestines and analogous circumstances in
dogs and human beings, it must be conceded that this worm is pathogenic.
At this point it is fitting to note the infestment as it affects hair
seals. The parasite concerned, _Uncinaria lucasi_, has long been a
scourge among the fur seals (_Otoes alaskanus_) of the Pribiloff
Islands. Its punctures are bloodless, being signalized instead by small
edematous plaques in the intestinal mucosa, The animal we autopsied was
a young California Hair Seal born in the Garden, and is singularly the
only hair seal in which we have seen it. The natural habitat of the hair
seal is the coast of California which means that the range of _U.
lucasi_ may extend farther southward than at first suspected. We have
none of the northern variety.
I point out two giraffe cases only because they are unique as to the
organ (liver) affected. So far as I know, mature hookworms have never
been reported from other organs than the intestines.
From the prophylactic standpoint it will be advisable to have as little
moist earth as possible, particularly sandy ground, in and around the
enclosures for the above mentioned susceptible animals because it is in
such soil that the earlier stages of the life cycle of the parasite are
passed.
We have never found any of the human hookworm species in our animals,
but it must be recognized that transmission is possible to a certain
degree. _Anchylostoma ceylanicum_ Lane[136] was found in man, cats,
dogs, and a lion; Leiper[137] reports _A. duodenale_ in a dog, and von
Linstow[138] states that the latter parasite also occurs in the
chimpanzee.
AMEBIC DYSENTERY IN MONKEYS.—We recently lost six monkeys in a small
outbreak of this disease—four black spider monkeys (_Ateles ater_), a
Pinche marmoset (_Leontocebus edipus_), and a woolly monkey (_Lagothrix
lagotricha_). Except for non-characteristic looseness of stools, there
were no symptoms until the usual terminal lethargy set in. Living amebæ
were found in feces. At autopsy only the colon was found to be
anatomically affected. It was hugely distended, fully an inch in
diameter, and there were numerous confluent ulcers of the mucosa covered
by a thick slough. The liver showed no abscesses. In the histological
sections amebæ were found in the interstices of vital gut tissue just as
they are in corresponding human lesions. I have not diagnosed the
species yet, but can vouch that it is not _Endameba histolytica_ or
_coli_.
[Illustration:
FIG. 78.—MICROSCOPIC SECTION OF LIVER OF GIRAFFE, SHOWING SECTIONS OF
UNCINARIA SMITHI IN BILE DUCT AND MARKED FIBROSIS AROUND THE DUCT.
]
[Illustration:
FIG. 79.—COLON OF MONKEY DYING WITH AMŒBIC COLITIS. HIGHLY ELEVATED
SLOUGHS COVER THE ULCERS.
]
According to Leidy’s recommendation, grated nutmeg was administered and
was followed by an improvement in symptoms. The animals became brighter
and the stools firmer, but the amebæ were not eradicated. Emetin
hypodermically and by mouth had no obvious effects on the disease or the
amebæ. One monkey thus treated with nutmeg recovered, but died the next
year of another affection and disclosed the scars of the old ulcers in
the colon. Our experience with this disease, however, is not unique. At
Washington, D. C.,[139] eight spider monkeys were affected, and sporadic
cases come to light from the West Coast[140], Manila, Khartoum and
Ceylon. Prowazek’s report concerned a young orang[141]. Liver abscesses
in addition to the intestinal lesions were found by three different
observers.
As to the transmissibility of monkey amebiasis to man, reporters are
divided. Both sides are probably right, in as much as _Endameba
histolytica_ was concerned in some cases and non-human species in
others. It is an infestment to be feared, and calls for examination of
stools from such newly arrived animals as are known to be susceptible
(spider and woolly monkeys, orangs).
PARASITES OF MARMOSETS AND SQUIRREL MONKEYS.—I give a special place to
this subject because Table 24 shows that these monkeys are so commonly
infested and because they are so commonly used as household pets. In
this connection the questions arising are, first, whether the infestment
is a menace to life, and second, whether it is existent outside the
Garden or only acquired here. The following lists set forth the
parasitic status as shown at autopsy. The figures indicate how long the
animal lived in the Garden:
═════════════════════════════════════════╤═══════════════════════════
Marmosets │ Squirrel Monkeys
─────────────┬───────────────────────────┼─────────────┬─────────────
Infested │ Not infested │ Infested │Not infested
─────────────┼───────────────────────────┼─────────────┼─────────────
1 day│ 6–15 days ( 4 animals)│ 2 days│ 3 months
1 day│ │ │
2 months│ 1 month ( 6 animals)│ 14 days│ 3 months
6 months│ 3–5 months ( 9 animals)│ 26 months│ 5 months
12 months│ 6 months ( 2 animals)│ │ 14 months
12 months│ 7 months ( 2 animals)│ │ 15 months
12 months│ 8 months ( 1 animal)│ │
13 months│ 9 months ( 2 animals)│ │
│ 10 months ( 1 animal)│ │
│ 12 months ( 1 animal)│ │
│ 14 months ( 1 animal)│ │
│ 15 months ( 1 animal)│ │
│ 17 months ( 1 animal)│ │
│ 18 months ( 2 animals)│ │
│ 20 months ( 1 animal)│ │
│ 21 months ( 1 animal)│ │
─────────────┼───────────────────────────┼─────────────┼─────────────
Totals 8 │ 35 animals│ 3 animals│ 5 animals
animals │ │ │
─────────────┴───────────────────────────┴─────────────┴─────────────
Reverting to the questions above raised, the data show that some of the
animals were certainly infested on arrival here, and that others
probably were; but since these animals were not examined for parasites
on arrival in the Garden the duration of infestment remains unknown, and
accordingly we are not justified in going farther in our conclusions. In
the case of the marmosets, though, if we confine ourselves to the non-
parasitized animals, it would appear that the “acclimatization” period
is within the first six months. I have attempted to arrive at a
conclusion on this basis, but the average lifetime of the four
parasitized marmosets which survived this period is the same as that of
the sixteen non-parasitized survivors, and we do not know at what time
the parasitized ones contracted the disease.
[Illustration:
FIG. 80.—ARACHNID (PNEUMONYSSUS FOXI) IN LUNG OF ADULT MONKEY (MACACUS
RHESUS). IT OCCUPIES THE CENTRE OF A CYST WHICH IMMEDIATELY
UNDERLIES THE PLEURA SEEN AT UPPERMOST PART OF THE ILLUSTRATION.
]
CYSTICERCUS TENUICOLLIS.—We have noted this bladder worm in the Aoudad
(_Ovis tragelaphus_), Red River Hog (_Potamochœrus porcus_),
domesticated Angora Goats and several deer (_Cervus alfredi_, _Capreolus
capreolus_, _Mazama mexicana_, _M. hemionus_) located with one exception
in the peritoneal cavity or membrane. One of the mule deer (_Mazama
hemionus_) exhibited the parasite also in the lung and liver. This
parasite is discussed because the very valuable Philippine spotted deer
(_Cervus alfredi_) died from a peritonitis secondary to an infected cyst
in the lesser omentum, and because the parasitism (_Tænia marginatum_)
is contractible from canidæ which are also on exhibition in the Garden.
It happens that the spotted deer did not become infested from the dogs,
but it is quite probable that the goats did, since they passed many
times daily in front of the wolf cages, drawing the children’s carriages
over the walks, and were stabled nearby. We have not discovered any of
the other tapeworm cysts in deer which might be transmitted to them from
the canidæ. Camels which are parked directly opposite them have only
exhibited echinococcus cysts, yet we have never found its adult form
(_Tænia echinococcus_) or its ova in the canine feces. The danger of
fatal disease from _C. tenuicollis_, even though the infestment be
present, is remote; but we feel that it is better, if possible, not to
exhibit the canidæ adjacent to susceptible animals.
PULMONARY ACARIASIS IN MONKEYS.—We have seen but two instances of this
affection in the Philadelphia Garden. The offending parasite in our
animals was a new species, _Pneumonyssus foxi_ Weidman[142]. It occurred
sparingly in small cysts under the pleura and was certainly benign in
our cases. The importance of the infestment consists in part in that
these lesions may be mistaken for tubercles.
At the London Gardens[143] acariasis was found in forty-four young
rhesuses dying of pneumonia, and the observers ascribed the inflammation
to irritation of certain doubly refractile crystals which occurred in
the excreta of the mite. There are four other recorded instances of such
disease in monkeys, all caused by different species of parasites.
As to pathogenesis of these arachnids, the London experience is most
illuminating in that it was young rhesuses that were affected. Our
specimens were mature, and nothing was stated to the contrary in the
other reported cases from various parts of the world. The parasites are
perhaps inhaled from the straw used as bedding, since such vegetable
material is a common habitat for mites. If the resultant acute pneumonia
is weathered the relics might remain only in the form of the subpleural
and parabronchial cysts such as we have seen at the Philadelphia Garden.
I am the more willing to accept the possibility that the simian
arachnids can induce an acute pneumonia after studying a very definite
case of bronchopneumonia in a prairie dog, which was induced by
_Cytoleichus penrosei_ Weidman 1916.[144]
PERIPROVENTRICULAR FILARIDÆ OF BIRDS.—Every year we report a number of
cases (up to twenty-three) of these worms, probably several species,
coiled under the serosa of the air sacs and most commonly around the
proventricle. Tentatively we have recognized two forms, a shorter (an
inch or so long) and a longer (three to four inches). The latter is most
inextricably coiled, but the former may be teased out. Microfilaria
occur in the blood of the latter cases, but not in that of the former.
The adults have been observed to penetrate from their position in the
air sac serosa into the lumen of the proventricle (goose), to have
caused rupture of the inferior cava (bulbul), to be associated with
subserous cysts of the intestine (weaver) and with profound anemia
(liothrix). The birds affected are mostly small, inexpensive ones, but
the infestment is important because of its frequency and deserves study
of the means of transmission.
[Illustration:
FIG. 81.—ARACHNID (CYTOLEICHUS PENROSEI) IN A BRONCHOPNEUMONIC FOCUS
IN THE LUNG OF A PRAIRIE DOG (CYNOMYS LUDOVICIANUS).
]
[Illustration:
FIG. 82.—FILARIAL WORM COILED NEAR PROVENTRICLE OF A FINCH.
]
PHYSALOPTERA IN OPOSSUMS AND BADGERS.—These worms were frequent findings
for a period of years and were particularly impressive on account of the
large number of parasites present. The stomach often contained scores,
more or less securely attached to the mucosa by the head. The worms
average an inch or two in length and perhaps an eighth of an inch in
thickness. _P. turgida_ is the only species we have identified (three
examinations). As to pathogenicity we have not observed that definitely
constant lesions are induced by the parasites. In several instances the
gastric mucosa has shown the mosaic appearance indicative of chronic
gastritis, a condition not necessarily incited by, but certainly
aggravated by, these worms; at least significant is the habit of the
worm to imbed its head in the gastric mucosa. In one instance the
microscope has revealed a most severe fibrosis of the submucosa. The
fibrosis was not so much diffuse as it was local or nodular, and in
favorable places the ova of physaloptera could be discovered in the
centres of the nodules, and thus betrayed the previous presence of the
adult worm there. In this individual animal the case against the
physaloptera is clinched by direct evidence. In other cases we have
circumstantial evidence. Whereas it is not a deeply burrowing parasite,
it is still a penetrative one, and this is sufficient to compromise the
all important “integrity of the mucosa.” It should therefore be
considered pathogenic in all cases, because open to suspicion in several
directions—abstraction of tissue juices, irritation by its products or
movements and by opening up an avenue for bacterial infection.
TROPIDOCERCA IN BIRDS.—This is a blood-red nematode of the size of a
mustard seed to that of a peppercorn which inhabits the depths of the
proventricular mucosa. At first sight its spheroidal form suggests that
of a fluke, but under the microscope it is found to be a nematode hugely
ballooned out by ova, and coiled up into a ball. In spite of its
dangerous appearance—being red—it is most likely quite innocuous, for
microscopic sections show no sign of inflammation around the worm.
Moreover, we know that a Concave Casqued Hornbill (_Dichoceros
bicornis_) now on exhibition has harbored the worms, as indicated by ova
in the droppings, for eight years and yet seems perfectly well. I have
made wax reconstructions of three of the worms and find that the coils
are not very intricate and that they assume no regular or constant
arrangement.
SYNGAMUS TRACHEALIS.—Our worst experience with this picturesque parasite
was in common crows (_Corvus b. brachyrhynchos_). In 1914 and 1915 alone
we lost five such birds. Some geese, swans and a pheasant complete the
short list of birds affected in addition to the crows. In no case was it
a young bird that was affected. Shipley[145] reports this parasite in
two grouse at the London Gardens, and Plimmer’s tables show that three
deaths were directly charged against them in one year[146].
EXTRA-INTESTINAL TAPEWORMS.—This discovery is worthy of record because
it is rare for cestodes to appear anywhere save in the intestines. We
have observed three instances where they had backed up into the bile
duct—twice in the Cape Hyrax (_Procaria capensis_) and once in a
Livingston’s Eland (_Taurotragus oryx livingstonii_). At the London
Gardens they were mentioned in the gall-bladder of a wallaby and in Cape
Hyraces. Beddard[147] carefully describes four new species of these
cestodes from the hyrax.
[Illustration:
FIG. 83.—PHYSALOPTERA IN STOMACH OF COMMON OPOSSUM (DIDELPHYS
VIRGINIANA). THIS IS NOT AN EXCEPTIONAL DEGREE OF INVOLVEMENT.
]
[Illustration:
FIG. 84.—ONE OF THE FIBROUS NODULES IN THE GASTRIC SUBMUCOSA OF AN
OPOSSUM. AN OVUM OF PHYSALOPTERA IS SEEN PRECISELY IN THE MIDDLE OF
THIS ILLUSTRATION.
]
TABLE 28.
_Occurrence of Blood Parasites._
(Adapted from Plimmer, nine year period)
_Animals examined—12,241 Mammalia—2,924 Aves—6,619 Reptilia—2,698._
══════════════════════════════════╤══════════════════╤════════╤════════
Parasite. │ Host │ No. │ %
│ │Infested│Infested
──────────────────────────────────┼──────────────────┼────────┼────────
1. Hemogregarines │Reptilia │ 316│ 11.8
2. Microfilaria │Mammalia │ 33│ 1.1
│Aves │ 191│ 3.
│Reptilia │ 24│ 1.
3. Hemoproteus │Aves │ 140│ 2.1
4. Trypanosomes │Mammalia │ 1│ 0.003
│Aves │ 28│ 0.4
│Reptilia │ 4│
│Amphibia │ 3│
5. Plasmodia │Mammalia │ 2│
│Aves │ 39│ 0.6
│Reptilia │ 5│
6. Leucocytozoa │Aves │ 16│ 0.2
7. Intestinal organisms[148] │Reptilia │ 16│ 0.5
8. Toxiplasma │Mammalia │ 1│
│Aves │ 1│
│Reptilia │ 1│
9. Spirochæta │Mammalia │ 1│
10. Babesia │Mammalia │ 1│
11. Hæmocystidium │Reptilia │ 1│
──────────────────────────────────┼──────────────────┼────────┼────────
Grand Total │ │ 824│
──────────────────────────────────┴──────────────────┴────────┴────────
SUMMARY OF TABLE 28.
═══════════════════════════════════╤═══════════╤═══════════╤═══════════
│Parasitized│ Animals │ %
│ │ examined │Parasitized
───────────────────────────────────┼───────────┼───────────┼───────────
Mammalia │ 39│ 2,924│ 1.5
Aves │ 415│ 6,619│ 6.5
Reptilia │ 367│ 2,698│ 14.0
───────────────────────────────────┼───────────┼───────────┼───────────
Total │ 821│ 12,241│ 6.7
───────────────────────────────────┴───────────┴───────────┴───────────
FILARIASIS IN WILD CATS (_Felis ruffus_).—This parasite was named
_Filaria fasciata_ because it coils in the fascia between the muscles—
generally those of the thigh and abdomen. The worms are easily detected
on skinning the animal and separating thigh and other muscles.
Microfilaria were always present in the blood. The grade of
pathogenicity is only conjectural.
PERITONEAL FILARIA IN MONKEYS.—Thread worms have been encountered eleven
times, largely in Cebidæ. In several instances _F. gracilis_ has been
the species identified, always inhabiting the peritoneal cavity, and in
one instance also the lung. Microfilaria were always present in the
blood. We have never seen lymphangitis or elephantiasis in our filarial
cases.
BLOOD PARASITES.—I justify this paragraph on the basis of the usefulness
it might have in the clinical direction, for while the taking of blood
specimens is not as easy as with man it can still be done with some
animals. From time to time we have encountered blood parasites in this
Garden, but the large numbers occurring in the experience of special
searchers in the London Garden and Plimmer’s particular interest in this
direction make their data much the more valuable. In one report of 6,430
animals examined he found 7 per cent. infested with blood parasites of
one sort or another. I have constructed the foregoing table (28) from
his various reports to show which animal classes were affected by the
several blood parasites.
This table (28) brings out that considering them as a whole and without
respect to host, just as the animals come day in and day out to the
autopsy table, blood parasites will be met in 6.7 per cent. of all
cases. They are seen most commonly in the form of hemogregarines of
reptiles (2.5 per cent. of all animals and 12 per cent. of all reptiles)
while microfilaria run a close second, being found in 2 per cent. of all
animals but much more commonly in birds. Hemoproteus of birds while
ranking third, should be emphasized on account of its acknowledged
blood-destructive properties. The remaining infestations were too
infrequent to be useful statistically.
Turning to individual groups of blood parasites, microfilariæ of birds
deserve special comment. They occurred four times more often in birds
than in other animals, or, put in another way, one out of every twenty-
two birds was affected, and only one out of every ninety other animals.
The high figure for birds is significant in relation to what we have
already said about periproventricular filaridæ in our Garden, indicating
that the same infestment probably also exists in London.
[Illustration:
FIG. 85.—ADAPTATION FROM RECONSTRUCTION OF TROPIDOCERCA CONTORTA. THE
WORM LAY IN THE WALL OF THE PROVENTRICLE OF A LOUISIANA HERON (ARDEA
TRICOLOR RUFICOLLIS).
]
[Illustration:
FIG. 86.—CESTODES (THREE) PROJECTING FROM THE SEVERED END OF THE BILE
DUCT OF A CAPE HYRAX (PROCARIA CAPENSIS).
]
A point brought out by Plimmer is to the effect that, of the several
blood parasites, the microfilariæ were the least harmful, and that of
these the adult forms were the only ones to produce symptoms; yet in one
place[149] he records microfilaria as plugging the cerebral capillaries
of birds. This is a very important lesion if permanent, and especially
so when affecting cerebral capillaries as do the organisms and pigment
of malaria. The adult forms were found in one-fourth of the cases where
microfilaria were demonstrated.
As to the pathogenicity of these blood parasites in general, it will be
unsafe to arrive at a definite conclusion, recalling the pitfalls that I
have already outlined in discussing pathogenicity of parasites in
general. Keeping in mind the wonderful adaptability on occasion of
animals to unfavorable circumstances we must hesitate to declare
unqualifiedly the importance of even blood parasites as morbid agents.
Where the parasite is known to destroy the blood cells of birds and
mammals it is otherwise, but even here experimental work would be
necessary to settle the question. The element of “racial” immunity and
of phylogeny is the fly in the ointment of our deductions.
TRANSMISSION OF ANIMAL PARASITISM FROM WILD ANIMALS TO MAN.
Examples of direct transmission will be only occasional, due to the
relatively infrequent contacts between the two hosts. Pets threaten the
most. Several such examples have been touched upon in the preceding
pages and it but remains to gather them into one place. There is one
concrete instance in the form of clear cut simian scabies being
transmitted to a keeper in this Garden[150] and a similar lot fell to
the keeper of a wombat at the Paris Garden[151] as well as to the
taxidermist who preserved its skin. We know that the skin and feathers
of our parrots and pigeons harbor mites[152] (plumicoles of Megnin) and,
recalling the occasional cases of poultrymen’s itch, a transient
affection might be conceded from pet parrots and other birds. Pediculi
are not as numerous on monkeys as popularly supposed—we see very few at
the autopsy table. We have seen _Trichinella spiralis_ in the polar bear
(_Ursus maritimus_)—an animal whose flesh is edible. The hydatid cysts
in the camel appear unimportant, but in the livers of deer it is
otherwise. Neither of these infestments is dangerous if the meat is
sufficiently cooked before eating.
Hookworm disease points thus far only to _Anchylostoma duodenale_ in the
chimpanzee and _Uncinaria ceylanicum_ in the lion and tiger. Both serve
as reservoirs of the disease, the ova being discharged by way of the
feces. Similarly the _Strongyloides intestinalis_ infestment which we
have seen in the orang might be transferred to man. Indirectly,
Europeans traveling in Africa have made the crucial test that certain
ungulates and other wild animals of Africa are the reservoirs of
_Trypanosoma gambiense_, the parasite of the well known African sleeping
sickness; for this example the blood stream of the beast is the
reservoir and a biting insect the means of transmission.
The above examples are cited to emphasize the possibility that parasites
of wild animals may have a pathogenic significance for man. They do not
exhaust the subject. Many more instances might be cited but the
foregoing bring out the important ones which have come to our attention.
TREATMENT.
The recognition of the existence of parasites during the life of an
animal, especially those of the skin and intestinal tract whose
discovery is easiest, suggests that some means of combating them should
be employed. But we are by now quite satisfied that medicinal and
disinfective therapeutic procedures, while they have their field of
usefulness, are much less to be depended upon for the protection of
exhibits than are preventive measures of general hygienic nature. Under
the latter heading come the prompt removal of excreta, frequent changes
of drinking water, routine examinations of feces of certain varieties,
autopsy examinations and incineration of autopsy remains—all of which
are part of the requirements of common cleanliness and general disease
prevention. I wish to amplify the matter of disposal of feces and
general cage-police. Our ideas as to what constitutes thoroughness in
this work have changed considerably since Fulleborn’s recent
demonstration that ascarid ova[153] could live in formaldehyde for four
or five years, and the older one of Galli-Valerio[154] that those of
_Hepaticola hepatica_ lived one month in 2 per cent. formaldehyde
solution. Evidently the same substances which disinfect do not
invariably disinfest; and if the occasion should arise for the most
exacting control in this respect, a special investigation of the
susceptibility of the individual ova in question would have to be
undertaken.
In addition to these general measures we have put up certain special
safeguards against parasites. Thus, each specimen of the large Carnivora
(lions, tigers, leopards, etc.), has received routinely a dose of
santonin every month over a period of several years. We have no figures
on which to base comparison with previous periods, but an examination of
feces of all the inmates of the Carnivora house in 1916[155] showed that
less than one-third of the animals were infested, and of these all save
the jaguars showed either small numbers of ova in the feces or
relatively non-pathogenic forms. The jaguars had been badly infested for
many years with dibothriocephalus. Prior to this examination we had been
under the impression that nearly every one of the felidæ ordinarily was
infested and if this impression was well founded, due credit must be
given, in company with general hygienic precautions, to the routine
santonin dosages. It goes without saying that where animals are detected
at autopsy with unequivocal transmissible and dangerous parasites
(coccidia, amebæ, etc.), the contacts are isolated, examined and if
necessary treated for the affection or even sacrificed.
To continue the preventive measures, it would be most desirable to
examine at least the blood and feces of all newly arrived animals, but
at present this is not practicable on account of the labor involved in
the laboratory and in collecting the material, and because all animals
do not stand the restraint involved when blood specimens are being
taken. At present we are limiting special examinations to the droppings
of newly arrived parrots and toucans for _Spiroptera incerta_ and to the
feces of certain monkeys for amebæ.
Further preventive measures will depend on the nature of individual
infestments as they crop up. Food inspection, screening, sulphur dips,
etc., are but a few examples of what might be found necessary
hygienically after investigating or establishing the life cycle of our
numerous parasitic groups. However we cannot forbear to emphasize again
the value of the blast lamp and of paint in the hygiene of animal
enclosures—means we believe to be much more potent and quite as
practicable as chemical disinfectants.
[Illustration:
FIG. 87.—TRICHINELLA SPIRALIS IN MUSCLES OF POLAR BEAR (URSUS
MARITIMUS). THIS WAS AN OLD INFESTMENT, AS INDICATED BY THE THICK
AND HYALOID CHARACTER OF THE CAPSULE.
]
Turning now to the active curative side of the subject, what medical
means we have against parasites appertain for the most part to the
intestinal ones. The treatment of tapeworms is very hazy and
unsatisfactory—areca nut is perhaps more useful in animals than any one
other drug. For round worms santonin is most to be depended on although
turpentine is useful against the round worm of the Equidæ. The dosage of
santonin per month has been—for large bears, ten grains; for lions,
tigers, large pumas, six grains; for jaguars, leopards, hyenas, four
grains; for wild cats, etc., two grains. The dose of areca nut
recommended for Carnivora is two grains per pound of body weight. Since
ungulates do not stand areca nut well, iron sulphate may be used. For
animals the size of a horse the dosage is two drams, and to this one or
two grains of arsenic trioxide may be added. On the basis of very
carefully controlled experiments on dogs, Hall recommends carbon
tetrachloride for hookworms in these animals—0.3 mils per kilo of body
weight, without purging. Its efficacy has been confirmed lately but we
have not had the occasion to test it.
From time to time we have broached other lines of medication against
worms which may be worth while relating if for nothing more than to
illustrate the uncertain ways of our vermifuges when applied to wild
animals.
I can speak first of thymol as employed on parrots parasitized by
_Spiroptera incerta_. The first thing that impressed us was the large
dosage which birds could endure. The lethal dose for pigeons was four
grains, suspended in mucilage of acacia. After we had established that
certain parrots withstood fourteen grains in mucilage, we administered
on one occasion twelve grains and on another sixteen grains, suspended
in glycerin. The drug is reputed to be absorbed when exhibited in the
latter vehicle and we hoped to get a certain anthelmintic effect on the
parasites from the blood side as well as from the lumen of the gut. The
bird itself, a very heavily infested cockatoo, showed no ill effects and
passed two dead female spiroptera and enormous numbers of ova. But
thereafter it passed even greater numbers of ova than before (we
estimated 182,000 per day for this bird over a five day period and
288,000 on a single subsequent day), and was obviously unimproved by the
treatment. The explanation of failure was clear, for the worms can
retire into the protecting mucus or mucous membrane lining the
proventricle until the thymol has passed by, and even though paralysed
may not be flushed out. In a later test on a toucan which died twenty
minutes after thymol administration we found at the autopsy that worms
deeply imbedded in the proventricle were translucent and motionless from
the effects of the thymol-glycerin mixture, _i.e._, saturated with the
medicament and apparently dead. Twenty minutes later they were placed in
normal salt solution in the incubator, and next morning were found
actively motile. Thymol evidently does not kill—it only stupefies, and
in the absence of means for flushing the parasites out, as we do in
human hookworm cases, this class of vermifuge will have to be abandoned
in work against this parasite.
Not with any serious hope of success, but feeling that arsenic was the
most promising drug available for parenteral use, we tried atoxyl
hypodermically and arsphenamine intravenously but without success. The
only positive results were to emphasize the tolerance of some lower
animals to arsenic. Thus in preliminary work pigeons received sixty
drops of Fowler’s solution by mouth without embarrassment, but five
minims killed a pigeon when administered hypodermically. The organic
arsenical, arsphenamine, was withstood intravenously by pigeons in six
times the proportional human dosage.
One of our drug trials was instructive in that it worked quite a
different effect from that in man, besides being most amusing. In
earlier diagnostic work on spiroptera we tested the practicability of
examining the vomitus for the worms, hoping thereby to get a greater
concentration of ova, which would facilitate the microscopic
examination. Hypodermic injections of apomorphine (0.1 grain) into an
amazon did not induce vomiting from the gizzard as hoped—only a
regurgitation from the crop, but it did cause some dizziness and most
ludicrous talking and laughter.
To illustrate further the difficulties of animal medication I quote our
experience with four red howling monkeys (_Alonatta seniculus_). One of
these died of intestinal obstruction from large ascarids—the case which
has been already cited. Ova were found in the stools of the remaining
three, and one of the monkeys was treated twice with santonin. It died
in thirty hours after the second dose—not of santonin poisoning, for
none of the clinical symptoms were present, but most likely from
absorption of toxic substances originating in the decomposing ascarids
which crowded the gut. It profits not to destroy these parasites, then,
unless we feel assured that they may thereafter be removed immediately.
If, for the sake of brevity, I were asked to state in a single sentence
the practical status of animal parasitic disease in this Zoological
Garden I would put it thus: Since there are various animal parasitic
diseases continuously present here of which we know, and since fresh
ones are from time to time cropping out, and since these are on the
whole of economic importance, it behooves us to continue and extend our
efforts against an issue extant—somewhat through therapeutic means, but
far more through clinical laboratory examinations, careful autopsy
searches, and by rigid general hygienic measures such as cage-police,
new quarters, isolation, or if necessary, destruction of the exhibit.
INDEX
Abortion, 305
Abscess of liver, 231
of lung, 155
Acariasis, lungs, 647
of monkeys, 647
Actinomycosis, 138, 568
in deer, 368, 568
tapirs, 568
treatment, 570
Adenoma, 474
Adrenal body, 336
Alimentary tract, 166
Amblyopia, 403
Amœbæ, 606, 644
dysentery from, 644
Amyloid, liver, 227
spleen, 128
Anatomy of labor, 290
Anchylostomum, see hookworms
Anemia, 87
primary, 98
secondary, 88
Aneurysms, 65, 80
Animal Parasitism, hygiene, 656
prevention, 656
treatment, 655
Animal Parasites, 614
disappearance of, 627
frequency, 628
of groups, 633
in blood, 652
incidence, 628–636
modes of action, 617
occurrence in wild, 627
transmission animals to man, 653
visceral distribution, 637
Angina pectoris, 49
Aorta, 72
fatty deposits in, 71
Arteries, 66
Arteriosclerosis, 71
Arteritis, 70
Arthritis, 347
gouty, 347, 411
Ascending nephritis, 276
Aspergillosis, 558
Aspergillus, varieties, 558
Ataxia, 375
Atrophy, acute of liver, 228
Autopsy list, 47
Avian spiropteriasis, 172, 640
Bacterial flora, 418
Basal cell carcinoma, 475
Beriberi, 439
Biliary tract, 225
calculi, 238
Birth canal, 287, 296
comparative anatomy, 287 et seq
obstructions to, 306
Blackhead, 206
Bladder, gall, 224, 238, 239
urinary, 286
Blood, diseases of, 83
Blood formation in birds, 98
Blood vessels, 66
Bone marrow, 83, 109, 111
Bones, diseases of, 343
effects of trauma, 343
tumors of, 368
Botryomycosis, 564, 602
Botulism, 604
Brain, 385
tuberculosis of, 378
tumors of, 384
weight of, 385
references to, 387
Breast, 312
Bronchi, 141
Bronchiectasis, 144
Cage palsy, 349
Calculi, biliary, 238
renal, 282
Carcinoma, 476
basal cell, 475
Cataract, 403
Cecum, 211
Cestodes, 637
Cholangitis, 239, 256
Cholecystitis, 239
Choledochitis, 239
Cholelithiasis, 238
Chondroma, 472
Cloaca, 211
Coccidiosis, 606
Cirrhosis of liver, 232
Comparative anatomy of uterus, 287
of pelvis, 297–303
Conjunctivitis, 402
Constipation, 209
Constitutional diseases, 410
Convulsions, 373
Cornea, 403
Coronary arteries, 49
Cowper’s gland, 313
Cretinism, 320, 331
Cysticercus tenuicollis, 647
Cystitis, 286
Cytoleichus penrosei, 647
Deficiency diseases, 438–443
Degenerations of kidney, 269
of liver, 228
Diabetes, 412
Diet, carnivorous, 452
herbivorous, 452
grain, 455
seed, 454
soft, 453
omnivorous, 402
relation to disease, 415
alimentary tract, 417
Dilatation of heart, 54
Diphtheria, 600
Dislocations, 345
Distemper, 599
Diverticula of intestine, 219
Diverticulitis, 219
Dysentery, amœbic in monkeys, 644
Dystocia, 292
Ear, 409
Echinococcus, 647
Emphysema, 161
Encephalomyelitis, 380
Endocarditis, 52
Endometritis, 305
Endothelioma, 165, 474
Enteritis, 177
in Aves, 202, 205
Mammalia, 185
Enterohepatitis, 605
Epithelioma, 475
Esophagus, 169
Exophthalmic goitre, 320, 323, 329
Eye, 402
tuberculosis of, 402
Fallopian tubes, 305
Fat infiltrations of kidney, 268
liver, 226
metabolism, 445
Fibroma, 472
Filaria, fasciata, 651
gracilis in monkeys, 651
in blood, 652
fascia, 651
muscles, 651
wildcats, 651
periproventricular, 648
peritoneum, 651
Food, 415
definition, 415
in relation to alimentary tract, 417
Food, disease, 422
poisoning, 457
Fowl cholera, 598
plague, 598
typhoid, 598
Fractures, 344
Gall stones, 238
Gas-bacillus infection, 602
Gastritis, 204
Gastroenterocolitis in Ungulata, 194
in Marsupialia, 198
Gangrene of lung, 155
Giraffe, hookworm in, 644
Gout, 53, 410
Heart, dilatation of, 54
hypertrophy of, 54
diseases of, 48
effects of, 55
effect of strain, 55–59
weight of, 63
relative vulnerability of, 61
Hemorrhagic septicemia, 598
Hemoglobinuric fever, 603
Hemorrhoids, 218
Hepaticola hepatica, 641
Hepatitis, 228
Hernia, 216
Heterakis in avian ceca, 606
Hookworms, 643, 654
in giraffe, 644
Hypernephroma, 339, 341, 342, 475
Hypertrophic periosteitis, 346
Hyperthyroidism, 320
Hypertrophy of heart, 54
in Aves, 60
Hypothyroidism, 320
Ileus, 213, 261
Infantilism, 433
Infiltrations of kidney, 268
liver, 226
Inorganic salts in diet, 427
Intestinal obstruction, 212
tract, 177
inflammation of, 181
mechanical obstruction of, 212, 617
relation to food, 422
Intestines, diverticula, 219
tumors of, 220
Iridocyclitis, 402
Kangaroo disease, 570
bacteriology, 576, 586
course of attack, 573
pathology, 575
prevention, 572
treatment, 591
Kidney, 263
abscess, 268, 278
calculi, 282
degenerations of, 269
hemorrhages, 271
hypertrophy of, 267
infiltrations of, 268
tumors, 284
weight of, 265
Labor from a comparative standpoint, 290
obstructions to, 306
Laryngitis, 139
Larynx, 138
Leontiasis ossium, 359, 472
Leucemia, 104
in birds, 108
lymphatic, 105
myeloid, 109
Leucocytes, 84–86
Limberneck of ducks, 604
Lipoma, 472
Liver, 222
abscess, 231
acute atrophy, 228
amyloid, 227
cirrhosis, 232
degenerations, 228
fatty changes, 226
infiltration, 226
inflammation, 228
chronic, 232
necrosis in, 230
tumors, 240
Lungs, 146
abscess, 155
congestion, 148
gangrene, 155
infarct, 160
tumors of, 162
Lymphadenitis, 117
Lymphatic leucemia, 105
tissue, 114
hyperplasia of, 115
in pharyngeal wall, 115, 138
Lymph nodes, 114
tuberculosis of, 121
tumors of, 122
Lymphomatosis, 118
Malnutrition, 424
Mammary gland, 312
Marmosets, parasites of, 645
Marrow of bone, 83, 109, 111
Meningitis, 376
Metabolism, carbohydrate, 443
fat, 445
inorganic, 427
protein, 447
Miliary tubercle, avian, 512
bovine, 510
human, 511
monkey, 511
Miscarriage, 305
Molluscum contagiosum, 601
Mönckeberg sclerosis, 74, 76
Monkey’s temperature, 520–528
Moon blindness, 405
Muscles, 370
Mycosis, 137, 558
of esophagus, 168
histology of, 561
hygiene, 563
incidence, 562
of lung, 562
method of action, 560
pharynx, 168, 564
types of, 560
Myelitis, 350, 381
Myeloma, 111
Myocarditis, 52
Myocardium, 49, 50, 65
Myxœdema, 320, 331
Necrosis, liver, 230
spleen, 130
Nematodes, 636
Neoplasms, 462
incidence of, 463, 468
embryonic origin, 471
in captivity, 469
in the wild, 462, 476
metastasis, 471
visceral origin, 477
Nephritis, 271
ascending, 276
effects of, 280
histology of, 279
toxic, 275
Nervous system, 372
Nocardia macropodidarum, 585
Nocardiosis, 570
Obesity, 446
Ophthalmia, periodic, 405
Osteitis, 346
Osteitis deformans, 359, 431
Osteoma, 368
Osteomalacia, 349
Ovary, cysts, 307
Pachymeningitis, externa, 331, 377
Paget’s disease, 359, 431
Pancreas, 244
degenerations, 250
tumors, 259
Pancreatitis, 250
Parasites, see animal parasites, 614
Parovarian cyst, 307
Pasteurelloses, 597
Pearl disease, 491, 501, 505
Pellagra, 441
Pelvis, comparative anatomy, 297–303
Penis, 313
Pericarditis, 53
Pericardium, position of effusion in, 54
Periosteitis, hypertrophic, 346
Periproventricular worms, 648
Perisplenitis, 131
Peritoneum, 260
tumors, 262
Peritonitis, 260
Pharyngitis, 168
Pharynx, 168
Phimosis, 313
Physaloptera turgida, 649
in opossums, 649
Plants, poisonous, 459
Pleura, 163
Pleuritis, 164
Pneumonia, 149
broncho, 152
fibrinous, 151, 153
in Aves, 153
origins of, 154
lobar, 151
Pneumonokoniosis, 159
Pneumonyssus foxi, 647
Poisonous plants, 459
Poliomyelitis, 380
Prostate gland, 313
enlargements of, 314
tuberculosis of, 315
tumors of, 314
Proventricle, 171
worms in, 172, 640
Psittacosis, 208, 597
Pyelonephritis, 277
Quail disease, 608
Rabies, 602
Rachitis, 349, 429
Rectum, prolapse of, 218
Reproductive organs, female, 287
male, 317
Respiratory tract, 134
Rhinitis, 135
Rickets, 349, 429
Renal calculi, 282
Salpingitis fallopii, 305
Santonin, 657
Sarcoma, 471, 474
Scurvy, 440
Seminal vesicles, 315
Sinusitis, 135
Skeleton, 343
Spinal cord, 373
Spiroptera incerta, 638, 640
detection, 640
eradication, 640
in parrots, 172, 208, 640
Spiropteriasis, 172, 640
Spleen, 114, 122
amyloid, 128
congestions, 125
enlargements, 124
hemorrhage, 125
inflammation, 126
in anemia, 130
in hepatic cirrhosis, 130
necrosis, 130
size, 124
tuberculosis of, 132
Squirrel monkeys, parasites of, 645
Starvation, 425
Stomach, 174
tumors of, 176
ulcers of, 175
Streptothricosis, 567
Suprarenal body, 336
Syngamus trachealis, 140, 650
Tænia echinococcus, 647
Tape worms, 637
in liver, 650
Temperature of monkeys, 520–528
Testes, 313
tumors of, 313
Tetanus, 602
Thrombosis, 69
Thymol, 657
Thymus, 120, 336
Thyroid body, 316
atrophy of, 330
hyperplasia of, 325
size of, 318
tumors of, 333
Tonsils, 115, 138
Trachea, 140
Tropidocerca contorta, 649
Tubercle bacillus, types of, 513
Tuberculin test on monkeys, 518
other animals, 549
dose, 529
effect on kidneys, 548
eye, 546
reaction, 530
skin, 546
Tuberculoma, 505
Tuberculosis of brain, 378
avian characters, 503, 512
Carnivora, 498
control, 514–548
diagnosis of, 514
discovery during life, 514
distribution in birds, 504
Tuberculosis of eye, 402
gelatinous, 504
histology, 510
hygiene, 516
in Aves, 503
in Mammalia, 492
in Primates, 492
in various avian orders 506–510
incidence, 489
intestinal in birds, 505
Lemures, 495
lymph nodes, 121, 494
nonsusceptible animals, 490
ordinate characters, 492
frequency, 489
pathological type, 490
Proboscidea, 502
Rodentia, 499
routes of infection, 485
Tuberculosis, sanitation of cages, 516
susceptible animals, 490, 515–517
Ungulata, 500
visceral distribution, 491
Tumors, see neoplasms
Ulcer, gastric, 175
Uncinaria, 643
Uremia, 281
Urethra, 315
Uterus, comparative anatomy, 287
inflammation, 305
tumors of, 308
Vitamins, 438
Waterfowl epizootic, 604
Zoological list, 43
A LIST OF THE PUBLICATIONS FROM THE LABORATORY OF COMPARATIVE PATHOLOGY
OF THE PHILADELPHIA ZOOLOGICAL SOCIETY 1909–1923
1. Results of Tuberculin Tests in Monkeys at the Philadelphia
Zoological Garden, by C. Y. White, M.D. and Herbert Fox, M.D.
_The Archives of Internal Medicine_, December, 1909, Vol. 4, pp.
517–527, Chicago, Illinois.
2. Note on the Occurrence of a Ciliate (_Opalinopsis nucleolobata,
n.s._) in the Liver of a Mammal (_Canis latrans_), by Allen J.
Smith, M.D. and Herbert Fox, M.D. _University of Pennsylvania
Medical Bulletin_, February, 1909, Philadelphia, Pennsylvania.
3. The Tuberculin Test in Monkeys: with Notes on the Temperature of
Mammals, by Arthur Erwin Brown, D.Sc., C.M.Z.S., Sec. Zool.
Soc., Phila. _Proceedings of the Zoological Society of London_,
1909, pp. 81–90.
4. Observations on the Occurrence of Neoplasms in Wild Animals, by C.
Y. White, M.D. and Herbert Fox, M.D. _Proceedings of the
Pathological Society of Philadelphia_, February, 1910.
5. Observations on the Comparative Anatomy of the Female Genitalia,
by Edward A. Schumann, M.D. _American Journal of Obstetrics and
Diseases of Women and Children_, Vol. LXIV, No. 4, 1911, New
York.
6. Observations Upon Neoplasms in Wild Animals in the Philadelphia
Zoological Garden, by Herbert Fox, M.D. _The Journal of
Pathology and Bacteriology_, Vol. XVII. (1912), pp. 217–231.
England.
7. A Study of Metazoan Parasites Found in the Philadelphia Zoological
Garden, by Fred D. Weidman, M.D. _Proceedings of the Academy of
Natural Sciences of Philadelphia_, March, 1913, pp. 126 to 151,
Philadelphia, Penna.
8. The Pathology of the Thyroid Gland in Wild Animals, by Herbert
Fox, M.D. _Journal of Comparative Pathology and Therapeutics_,
Vol. 27, p. 23. Edinburgh, Scotland.
9. The Mechanism of Labor From the Standpoint of Comparative Anatomy,
With a Report of Cases of Dystocia in Wild Animals, by Edward A.
Schumann, M.D. _American Journal of Obstetrics and Diseases of
Women and Children_, Vol. LXIX, No. 3, 1914, New York.
10. Cirrhosis of the Liver in Wild Animals, by Herbert Fox, M.D. _New
York Medical Journal_, December 19, 1914.
11. The Dynamics of the Female Pelvis; Its Evolution and Architecture
with Respect to Function, by Edward A. Schumann, M.D. _American
Journal of Obstetrics and Diseases of Women and Children_, Vol.
LXXI, No. 1, 1915, New York.
12. _Pneumonyssus foxi, Nov. Sp_. An Arachnid Parasitic in the Lung of
a Monkey (_Macacus rhesus_), by Fred D. Weidman, M.D. _Journal
of Parasitology_, September, 1915, Vol. II, pp. 27–45, Urbana,
Illinois.
13. _Cytoleichus penrosei_, A New Arachnid Parasite Found in the
Diseased Lungs of a Prairie Dog, (_Cynomys ludovicianus_).
_Journal of Parasitology_, December, 1916, Vol. III, pp. 82–89,
Urbana, Illinois. Fred D. Weidman, M.D.
14. A Method of Obtaining Duplicate Reconstructions from the One
Series of Wax Plates, by Fred D. Weidman, M.D. _New York Medical
Journal_, March 3, 1917, New York.
15. Papers: Read at the Meeting of the Pathological Society at the
Philadelphia Zoological Garden.
Pancreatitis in Wild Animals, by Herbert Fox, M.D.
Report of an Enzootic of Parasitic Proventricular Worms
(_Spiroptera incerta_, Smith) of Parrots, with Control of Same,
by Fred D. Weidman, M.D.
_Coccidium bigeminum_, Stiles, in Swift Foxes (habitat Western U.
S.), by Fred D. Weidman, M.D.
Distribution of Uncinaria Among the Lower Animals, by Fred D.
Weidman, M.D.
An Arachnoid (_Pneumotuber macaci_, Landois and Hœpke?) Parasitic
in the Lungs of a Monkey (_Macacus rhesus_), by Fred D. Weidman,
M.D.
A Note Upon the Lesions of the Female Genitalia in Wild Animals,
by Edward A. Shumann, M.D.
Amblyopia in a Young Monkey (_Macacus nemestrinus_), by H. M.
Langdon, M.D. and W. B. Cadawalder, M.D.
Remarks on Examinations of a Series of Brains, by W. B.
Cadawalder, M.D.
_Journal of Comparative Pathology and Therapeutics_, December,
1915, Vol. XXVIII, Part 4, pp. 298–336, Edinburgh, Scotland.
16. Reversionary Pseudobile Canaliculi Formation in the Cirrhotic
Liver of a Vulpine Phalanger, by Fred D. Weidman, M.D. _New York
Medical Journal_, March 9, 1918, New York.
17. A Contribution to the Anatomy and Embryology of _Cladorchis_
(_Stichorchis_) _Subtriquestrus_, Rudolphi, 1814 (Fischoeder,
1901), by Fred D. Weidman, M.D. _Parasitology_, Vol. X, No. 2,
January 22, 1918, Cambridge University Press, London, England.
18. Nutritive and Blood Changes in Rats on Cancer-Inhibiting and
Cancer-Stimulating Diets, by E. P. Corson-White, M.D.
_Pennsylvania Medical Journal_, March, 1919, Vol. XXII, p. 348,
Athens, Penna.
19. Pemphigus in an Orang Utan Infested with Strongyloides
(intestinalis?) and Dying from Advanced Tuberculosis, by Fred D.
Weidman, M.D. _Journal of Cutaneous Diseases_, March, 1919, Vol.
XXXVII, pp. 169–173, Chicago, Ill.
20. Arteriosclerosis in Wild Animals, by Herbert Fox, M.D. _American
Journal of Medical Sciences_, June, 1920, No. 6, Vol. CLIX, p.
821, Philadelphia, Penna.
21. Osteomalacia in Wild Animals, by E. P. Corson-White, M.D.
_Archives of Internal Medicine_, November, 1922, Vol. 30, pp.
620–628, Chicago, Illinois.
22. Osteitis Deformans in Monkeys, by E. P. Corson-White, M.D.
_Archives of Internal Medicine_, December, 1922, Vol. 30, pp.
790–796, Chicago, Illinois.
23. Certain Dermatoses of Monkeys and an Ape, by Fred D. Weidman, M.D.
_Archives of Dermatology and Syphilology_, March, 1923, Vol. 7,
pp. 289–302, Chicago, Illinois.
24. Acute Papular and Desquamative Exanthem in an Orang Utan, by
Herbert Fox, M.D., and Fred D. Weidman, M.D. _Archives of
Dermatology and Syphilology_, April, 1923, Vol. 7, pp. 462–464,
Chicago, Illinois.
-----
Footnote 1:
Those who are interested in the subject of disease in its effect on
evolution are referred to Morley Roberts, _Proceedings, Zoological
Society, London_, 1918, p. 247.
Footnote 2:
_Proceedings, Zoological Society, London_, 1911.
Footnote 3:
_Proceedings, Zoological Society, London_, 1911, p. 425.
Footnote 4:
_Proceedings, Zoological Society, London_, 1911, p. 620.
Footnote 5:
_Br. Med. Jour._, 1910, 2, 1161.
Footnote 6:
_Proc. London Zool. Soc._, 1907.
Footnote 7:
Total is the number of individual animals showing lesions, not the sum
of the listed changes.
Footnote 8:
_Comptes Rendus Soc. Biol._, T, 62–206.
Footnote 9:
This is done by determining the percentages of hypertrophy and
dilatation for the total number of each class examined at autopsy.
Footnote 10:
_Arch. für. Ges. Physiologie_, 1908, 125, 507
Footnote 11:
dal Piaz: Papers from the Department of Anatomy, University of
California, 1912. Bergmann: _Dissertation_, Munich, 1884. Loer: _Arch.
f. die gesamte Physiologie_, 1911, V. 140–293. Grober: _Arch. f. die
gesamte Physiologie_, 1908, V. 125–507. Grober: _Deutsch Archiv f.
Klin. Med._, 1907, V. 91, 502. Welcher and Brandt: _Arch. für
Anthropologie_, 1903, V. 28. Vierordt: _Tabellen_, 1906. Parrot:
_Zoologischer Jahresbericht_, 1893. Hasenfeld and Romberg: _Arch. f.
Exp. Path. und Pharmacol._, 1897, V. 39–333. Joseph: _Jour. Exp.
Med._, 1908, V. 10–521.
Footnote 12:
These values are obtained in part from the literature, in part from
our own specimens. At this laboratory the hearts of animals killed or
dying from a short illness, organs showing no pathological change,
were removed by cutting at the base of the vessels, washed free of
blood and weighed. The weight of the whole animal was obtained after
death.
Footnote 13:
These figures are obtained by determining mathematically the
percentage of each feature in each class and then reducing the numbers
to their lowest value.
Footnote 14:
_Verh. deutsch Path. Gesel._, 1906, X, 149.
Footnote 15:
With Coronary sclerosis only.
Footnote 16:
With Coronary sclerosis only.
Footnote 17:
_Proc. London Zool. Soc._, 1916.
Footnote 18:
_The Leucoses of Fowls_, London, 1922.
Footnote 19:
Lubarsch-Ostertag, _Ergeb. aus der Allg. Path._, 1908.
Footnote 20:
Vide Sisson’s _Veterinary Anatomy_ and Owen’s _Anatomy of the
Vertebrates_.
Footnote 21:
Ball, _Jour. Vet._, 1907.
Footnote 22:
See Magnan, _Compt. Rendus d. l’ Acad. de Science_, 1910 and 1911,
Vol. 150, 151, 152.
Footnote 23:
_C. R. Soc. de Biologie_, Paris, T. 73–526. _Bull. Mus. Hist. Nat.,
Paris Ann._, 1911, 492 et seq.
Footnote 24:
See Woodland, _Proc. London Zool. Soc._, 1906, and MacLeod, _Chemical
and Physiological Medicine_, Chicago, 1923.
Footnote 25:
_Proc. Zool. Soc. London_, 1905.
Footnote 26:
_Bull. Soc. Anat._, 1898, 73, 491
Footnote 27:
_Amer. Med._, 1903, 996
Footnote 28:
_Surg. Gyn. and Obst._, 1919, 28, p. 529.
Footnote 29:
_Jour. A.M.A._, 1921, 77, 194.
Footnote 30:
_Ibid._, 197.
Footnote 31:
Garrod, _Schorstein Lect._, 1920.
Footnote 32:
_Anatomical Record_, 1917, 13, p. 305, On the morphology of the renal
tubule in the vertebrates.
Footnote 33:
Policard, _C. R. Assoc. Anat._, 1910, 12, 57.
Footnote 34:
Huber, _Anat. Record_, 1916, 10, 201.
Footnote 35:
_Bull. Mus. Hist. Nat._, 1911, 493 and 1912, 527, and C. R. Acad. Sc.,
155, 182.
Footnote 36:
_C. R. Soc. Biol._, 1898, 5, 188.
Footnote 37:
_Monatsh._, 1893.
Footnote 38:
_Inaug. Diss. Giessen_, 1911.
Footnote 39:
_Arch. f. Tierheilk._, V. 38–99.
Footnote 40:
Comparative Anatomy of the Female Genitalia, _Am. Jour. of Obstet._,
Vol. LXIV, No. 4, 1914. Mechanism of Labor from a Comparative
Standpoint, _Ibid._, Vol. LXIX, No. 4, 1914. Dynamics of the Female
Pelvis, its Evolution, etc., _Ibid._, Vol. LXXI, No. 1, 1915.
Footnote 41:
_Proc. L. Z. Soc._, 1919, p. 16.
Footnote 42:
_Journ. Phys._, Vol. 34, 295.
Footnote 43:
_Am. Jour. Phys._, Vol. 30, 129.
Footnote 44:
Carlson, Rooks and McKie, _Loc. cit._
Footnote 45:
Vincent and Jolly, _Loc. cit._
Footnote 46:
See Blair and Brooks, Osteomalacia of Primates in Captivity, _Ninth
Annual Report, New York Zoological Society_, 1904, p. 135.
Footnote 47:
Campbell and Cleland, _Jour. Comp. Path. and Ther._, Vol. 32, p. 95.
Footnote 48:
_Med. Chir. Trans._, Vol. 60, 37, 1877.
Footnote 49:
_These de Lyon_, 1901.
Footnote 50:
_Verein Freibürger Aerzte_, May, 1902.
Footnote 51:
_Arch. f. Wiss. u. Prak. Tierhk._, Vol. 36, 652, 1910, and Vol. 39,
164, 1913.
Footnote 52:
_Vet. Med. Inaug. Diss. Giessen_, 1913.
Footnote 53:
_Traite d’ Anatomie Path._, 1883.
Footnote 54:
_Jour. Med. Res._, Vol. 24, 43, 1911.
Footnote 55:
_Publ. Jefferson Med. College_, Vol. 6, 1, 1915.
Footnote 56:
We have observed later, however, one case with very definite
degenerative arterial disease; it will be discussed under the
affections of the eye since the most definite and indeed only lasting
sign of trouble was amblyopia, the attack being ushered in by a
nondescript fit.
Footnote 57:
_Chemistry of the Proteins_, Mann.
Footnote 58:
_Ann. Inst. Past._, 1899, XIII, 558, and _Skandinavisches Arch. f.
Physiol._, 1904, XVI, 249.
Footnote 59:
_Skandinavisches Arch. für Physiologie_, Vol. 17, p. 211, 1905.
Footnote 60:
_Jour. Physiologie et Path._, Vol. 14, 108, 1912.
Footnote 61:
_Carnegie Institute Publication_, No. 203, p. 247, 1915.
Footnote 62:
_Jour. Biol. Chem._, Vol. 14, p. 59, 1913.
Footnote 63:
_Publication of the Jefferson Medical College and Hospital_, Vol. 6,
p. 1, 1915.
Footnote 64:
_These de Lyon_, 1901.
Footnote 65:
_Verein Freiburger Aerzte_, May 30, 1902.
Footnote 66:
_Vet. Med. Inaug. Diss. Giessen_, 1913.
Footnote 67:
_Chemistry of Food and Nutrition_, Macmillan, 1918.
Footnote 68:
Ohio Agricultural Experiment Station Bull., 295.
Footnote 69:
_Skandinavisches Archiv. f. Physiologie_, Vol. 17, p. 211, 1905.
Footnote 70:
_Bull._, 185, Experiment Station, U. S. Dept. Agriculture, 1907.
Footnote 71:
_Physiological and Pathological Chemistry_, Blakiston, 1902.
Footnote 72:
_Journ. Physiol._, 1912, XLIV, 425.
Footnote 73:
Die Vitamine und ihre Bedeutung für die Physiologie und Pathologie mit
besonderer Berücksichtigung der Avitaminoses, Wiesbaden, 1914.
Footnote 74:
_Newer Knowledge of Nutrition_, Macmillan, 1919.
Footnote 75:
_Bull._, 34, Bureau of Amer. Ethnology.
Footnote 76:
_Jahrhuch. Kinderheilk._, 1904, LIX, 175.
Footnote 77:
_Journ. Am. Med. Assoc._, 1917, LXVIII, 1516.
Footnote 78:
_Arch. Path. Anat._, 1897, CXLVIII, 523.
Footnote 79:
_Lancet_, London, March 12, 1910, 733.
Footnote 80:
_Lancet_, London, 1911, II, 1266.
Footnote 81:
_Bull._, Dept. of Agriculture, Dec. 13, 1915.
Footnote 82:
Bureau of Animal Industry, 1895–96, 172.
Footnote 83:
_Z. Hyg. u. Infektionskrankh._, 1913, LXXV, 334.
Footnote 84:
_Jour. Biol. Chem._, 1917, XXXI, 229.
Footnote 85:
_Jour. Infect. Dis._, 1916, XIX, 478.
Footnote 86:
_Jour. A.M.A._, 1922, 79, 2132.
Footnote 87:
_Pflüger’s Arch._, 1909 (129), 63.
Footnote 88:
_Chemical Pathology_, Philadelphia, 1918.
Footnote 89:
These botanical names are taken from Chestnut’s _Poisonous Plants of
America._
Footnote 90:
_Textbook of Histology_, 1920.
Footnote 91:
_Zeitch. für Krebsforsch_, Vol. 15, p. 1.
Footnote 92:
_Proceed. Phila. Path. Soc._, 1910, and _Journal of Pathology and
Bacteriology_, Vol. XVII, 1912.
Footnote 93:
Figures in parentheses are numbers of animals with captivity known.
Footnote 94:
See Gould’s _Birds_, Vol. II, p. 83.
Footnote 95:
_Am. Jour. Med. Soc._, 1907, 133–769.
Footnote 96:
_Jour. Path. and Bact._, Vol. XVII, 1912.
Footnote 97:
Totals and percentages for class, including all members.
Footnote 98:
Grand Totals, all autopsies.
Footnote 99:
Totals used for analysis after deduction of cases insufficiently
described.
Footnote 100:
_Rev. de Med. Vet._ T. 89, p. 221.
Footnote 101:
White and Fox, _Archives of Internal Medicine_, 1909, Vol. IV, p. 517.
Footnote 102:
The temperature in the axilla is often .5°F. higher than by rectum,
but the difficulties of the axillary method render it impracticable.
Footnote 103:
A. E. Brown, _Proc. London Zool. Soc._, June, 1909, p. 81.
Footnote 104:
Simpson and Galbraith, _Trans. Royal Soc._, Edinburgh, XIV, p. 1, 65,
1906.
Footnote 105:
This term will be used in the following pages to mention the organism
since by many persons it is better known than Nocardia and moreover
describes the form better. I believe genus Nocardia is the correct
nomenclature for reasons given on a subsequent page.
Footnote 106:
Those interested in the investigation of the cause of Blackhead are
referred to the recent literature by Tyzzer and by Smith, in the
_Jour. of Exp. Med._ and _Jour. of Med. Research_, 1918–1922.
Footnote 107:
There are certain exceptions to this, as with Nicoll’s (_Proc. Zool.
Soc. London_, 1912, p. 858) careful search for trematodes with sieves,
but this means a separate research, and is incompatible with the all-
round, general policies of present routine laboratory organization.
Footnote 108:
_Phila. Zool. Soc. Rep._, 1920, p. 28.
Footnote 109:
_Proc. Zool. Soc. London_, 1910, p. 134.
Footnote 110:
_Proc. Zool. Soc. London_, 1905, p. 252.
Footnote 111:
_Phila. Zool. Soc. Rep._, 1920, p. 29.
Footnote 112:
_Phila. Zool. Soc. Rep._, 1921, p. 31.
Footnote 113:
_Proc. Zool. Soc. London_, 1919, p. 15.
Footnote 114:
_Proc. Zool. Soc. London_, 1919, p. 15.
Footnote 115:
_Phila. Zool. Soc. Rep._, 1916–1921.
Footnote 116:
_Journal of Parasit._, June, 1921, p. 194.
Footnote 117:
_Proc. Zool. Soc. London_, 1910, p. 147.
Footnote 118:
Fantham, _Proc. Zool. Soc. London_, 1910, p. 672.
Footnote 119:
_Loc. cit._, 1911, p. 674.
Footnote 120:
_Loc. cit._, 1915, p. 87.
Footnote 121:
_Loc. cit._, 1910, p. 233.
Footnote 122:
_Loc. cit._, 1914, p. 222.
Footnote 123:
_Phila. Zool. Soc. Rep._, 1912, p. 40.
Footnote 124:
_Proc. Zool. Soc. London_, 1914, p. 140.
Footnote 125:
_Jour. Parasit._, June, 1921, Vol. VII, p. 198.
Footnote 126:
This figure and a number of others in the tables do not correspond
with those in other sections of this book because certain injured,
decomposed and newly arrived animals were available and accepted for
my purposes, but were objectionable for the general medical statistics
and therefore excluded.
Footnote 127:
For foot note see page 630.
Footnote 128:
For foot note see page 630.
Footnote 129:
Not generically diagnosed.
Footnote 130:
_Proc. Acad. Nat. Sci. Phila._, March, 1913, p. 127.
Footnote 131:
_Proc. Zool. Soc. London_, 1912, p. 858.
Footnote 132:
_Proc. Acad. Nat. Sci. Phila._, 1913, p. 133.
Footnote 133:
_Proc. Roy. Soc. N. So. Wales_, Sydney, Vol. 27, pp. 86–90, 1893.
Footnote 134:
_Proc. U. S. Nat. Mus._, Wash., D. C., Vol. 50, 1916, p. 31.
Footnote 135:
_Proc. Zool. Soc. London_, 1911, p. 674.
Footnote 136:
_Indian Med. Gaz._, June, 1913, p. 217.
Footnote 137:
_Jour. Trop. Med. Etc., London_, 1913, XVI, p. 334.
Footnote 138:
_Am. Med. Phila._, V. 6 (16), 1903, p. 611.
Footnote 139:
Eichhorn and Gallagher, _Jour. Inf. Dis._, XIX, No. 3, Sept., 1916, p.
395.
Footnote 140:
Macfie, _Ann. Trop. Med. and Parasit._, 1915, 9, p. 507.
Footnote 141:
_Arch. f. Protistenk_, Jena, V. 26 (2), 22, July, p. 241.
Footnote 142:
_Jour. Parasit._, Sept., 1915, V. 2, pp. 37–45.
Footnote 143:
_Proc. Zool. Soc. London_, 1919, p. 14.
Footnote 144:
_Jour. Parasit._, Dec., 1916, V. 3, pp. 82–89.
Footnote 145:
_Proc. Zool. Soc. London_, 1909, p. 335.
Footnote 146:
_Loc. cit._, 1912, p. 236.
Footnote 147:
_Loc. cit._, 1912, p. 576.
Footnote 148:
The exact taxonomic position could not be stated,-probably an ameba.
Footnote 149:
_Proc. Zool. Soc. London_, 1910, p. 134.
Footnote 150:
Weidman (F. D.), “Dermatoses of Monkeys,” _Arch. Derm. and Syph._,
Chicago, March, 1923, p. 289.
Footnote 151:
Railliet Traite de Zool. Med. et Agric. Paris—Asselin et Houzeau,
1895, p. 659.
Footnote 152:
Megnin, Les Parasites Articules, 1895, Masson et Cie, Paris.
Footnote 153:
Quoted by Jensen (V.), _Hospitalstidende_, Copenhagen, 1922, 65, No.
28, p. 457.
Footnote 154:
Centr. f. Bakt. u. Parasitk., (etc.), Jena 1—Abt. V. 35 (1), 5, 1903,
orig. p. 89.
Footnote 155:
_Phila. Zool. Soc. Rep._, 1917, p. 36.
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TRANSCRIBER’S NOTES
● Typos fixed; non-standard spelling and dialect retained.
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Disease in captive wild mammals and birds : $b incidence, description, comparison
Fox, Herbert
Chimera55
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