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—