PART 4

ACUTE DISEASES RESEMBLING THE SPECIFIC INFECTIONS OF DOMESTIC ANIMALS

Specific communicable diseases are sometimes divided into those most often encountered as “herd diseases” and those which appear as single cases or in small groups. This would seem to imply that the first behave as easily disseminated epizoötics, their virus passing from animal to animal simply by proximity or by casual contact whereas the transfer of infective material is less readily accomplished by the second group, often demanding special assistance. Foot-and-mouth disease, pleural pneumonia, cattle plague, and influenza illustrate the epizoötics while tetanus, rabies, quarter-ill, malignant edema, and infectious vaginitis are examples of less easily transferred processes.

It is not intended that these remarks shall cover all possible means of transmission but instead they are intended to focus attention upon the sources of viruses whereby animals become infected. An original case must always be present in order for spread to occur. Where animals are being added to a herd a new comer may be diseased or the carrier of a virus; when animals are transported for sale or other reason, infection may be met in a new stall, conveyance or pasture; contaminated food may be offered. In menageries, with specimens, single or in small groups, and arrivals always quarantined before other animals are exposed, acute specific infections seldom appear. It is also improbable that a wild animal, infected at its source or in some dealer’s place, would survive the journey and arrive in an infective condition. Consultation with the reports of other gardens fails to discover records of any serious outbreaks of epizoötic disease except for fowl cholera and distemper, examples of infection with the bipolar organisms of the Pasteurella group, believed responsible for the hemorrhagic septicemias; instances of the occurrence of the group specified secondly—anthrax and the like— are also reported. This represents fairly well our own experience.

The bacteria variously named _Bac. avisepticus_, _ovisepticus_, _bovisepticus_, _canisepticus_, etc., grouped by Ligniere under the name Pasteurella, are doubtless of considerable importance and are probably quite widespread in natural surroundings. The viruses of the epizoötic conditions like cattle plague and influenza are apparently more definitely parasitic, requiring for their persistence ever renewed transfer from host to host. The former infections we have met in repeated single isolated cases and in small groups, whereas no cases of the specific epizoötics have been diagnosed.

Hemorrhagic septicemia, a denomination very descriptive of its pathological picture, has been encountered in many varieties, carnivores, ungulates, primates, rodents, and birds. The diagnosis depends upon the presence of hemorrhages with edema, degenerations of the parenchymatous organs, more or less respiratory catarrh to which may be added relatively mild gastrointestinal inflammation; the bacteria are found in the circulating blood and in exudates. A description of these organisms is not profitable, they being well known in veterinary pathology. What is more important, significant and supportive of the opinion expressed above concerning the widespread distribution of the virus, is the incidence of the infection. Exclusive of the condition known as fowl cholera, it has appeared among mammals and birds as single cases with one exception—that of two Barbary apes which had been in separate cages side by side. The total of cases with determined bacteriology is eleven, with undecided bacteriology but suggestive pathology nine additional. No pertinent history in common can be found in the records of the determined cases, except perhaps that they were all animals which had been in the collection at least three months, a period which would seem to exclude the probability of an imported infection. Because of the isolated character of the cases and impossibility of making a clinical diagnosis, no attempt at specific nomenclature as used in veterinary medicine has been made, hemorrhagic septicemia seeming to cover its identity and nature.

The disease known as fowl cholera is practically always associated with the bacteriological discovery of a member of the hemorrhagic septicemia group while its pathology corresponds with that of mammalian infection with these germs. Enteritis is a prominent feature. This disease has appeared thrice among our parrots carrying off from six to ten birds before hygienic measures became effective. In all three our cultures showed the bipolar organisms. Besides these specific outbreaks numerous isolated cases of acute general infection have occurred among small passerine and picarian birds which could not be determined as hemorrhagic septicemia by bacteriological methods although superficially resembling it in gross pathology; they yielded to the same hygienic measures. Perhaps we were dealing with fowl plague, a disease believed to be due to a filterable virus. That this is the case is strongly suggested by an outbreak of fowl typhoid in the parrots, from some fatal cases of which we were able to isolate _B. sanguinarium_, and by a group of deaths in small parrots from which no specific organism could be recovered.

The identification of these supposedly specific diseases—plague, typhoid, septicemia, leucemia—by pathological criteria is by no means simple even if we have at hand the complete description of Moore, of Hutyra and Marek, of Ellermann and of Ward and Gallagher. Bacteriology must decide and cultures should be made upon bodies recently dead. In addition to the above infections we have had two small outbreaks of psittacosis in parrots from which it was possible to isolate the specific organism. On both occasions there was more than one death before the specific nature of the disease was identified yet, noteworthily, no spread to the other birds in the same exhibition house occurred.

Distemper, a disease variously held as due to cocci, to influenza-like organisms and to a filterable virus, may appear in sporadic or epizoötic form. The diagnosis during life is not so easy unless all the cardinal features are present, while after death the same thing holds good. I am inclined to think that from the standpoint of diagnostic accuracy, the term is used much too loosely, a ready excuse for such laxity however being that it stimulates to greater care in hygiene. Whether or not _B. bronchi-_ or _canisepticus_ be the cause of the disease, organisms corresponding to it can be found in stained smears from nearly every case in which the respiratory, cutaneous, nervous and internal signs suggest the disease. To make a diagnosis of distemper it is my practice to require at least three of the cardinal clinicopathological features, whereupon, if the bacterial findings be as described, the denomination is permitted. This was dictated because during the period, now happily well in the past, when the cats and dogs suffered frequently with enteritis, nasopharyngeal signs occasionally presented themselves or spasms were reported, but no skin eruptions appeared, yet seldom were all of these signs combined nor could we find the bipolar organisms. I note that in 1915 Doctor Blair of New York observed a toxic enteritis resembling but not identical with distemper. As with our cases he failed to find that the condition was communicable. We ascribed our cases to spoiled food—fowl heads or dirty horse meat (see page 179). Our acceptable examples of distemper number three, two ferrets and a lynx, but very suggestive cases were found in foxes, wolves and raccoons. Since writing the above notes, sixteen wolves, foxes and wild dogs died in an outbreak of distemper imported by a newly arrived specimen admitted to the colony by mistake. When we were aware that the disease had appeared antiserum was administered therapeutically to all that were sick and prophylactically to all the rest—large doses, 25–35 cc., were given for treatment, smaller quantities, 10–20 cc., being used as a preventive. Seven sick animals recovered and no animal (8) given serum prophylactically became sick. This experience encourages us to think that with antiserum and rigidly enforced quarantine rules, distemper will not be a serious matter to handle.

The hygiene of the foregoing conditions is of a general character— removal of the specimens when known to be sick, thorough cleansing of the cages, segregation of mates or of neighbors when this is practicable, burning of refuse, liming of the ground and such other measures as the local conditions may indicate.

DIPHTHERIA.

Although no cases of mammalian diphtheria have been observed, three and possibly four birds have suffered with this disease. The three acceptable cases were in cassowaries (_Casuarius occipitalis_) occupying adjoining cages and sickening within a few weeks of one another. Just how the infection was brought to them must remain a mystery since no additions had been made to the group for some time previously. All three birds were observed during life, and from the first case the _Bac. diphtheriæ avium_ was isolated; in smears from the other two similar bacteria were seen but isolation was unsuccessful. The two acutely fatal cases showed large pseudomembranous collections on the nasopharyngeal mucosa and beneath the tongue while the nares were occluded by the same material. Plaques of membrane were also found on the surface of the esophagus and proventricle. The exudate ran out of the mouth and formed dried crusts upon the cervical skin. Pseudomembranes of a continuous character were lacking in the third bird, their place being taken by small yellow or yellow pink nodular elevations, apparently just beneath the surface, here and there upon the reddened, slimy buccal, lingual and pharyngeal mucosæ. Crusts upon the skin of the neck also formed in this case.

These cases are of interest not only because of their appearance without satisfactory explanation but because one improved very much after injections of human diphtheria antitoxin, this remedy being used because we were then unaware of the existence of an avian diphtheria antitoxin. No claim can be made _post hoc ergo propter hoc_ that the human antitoxin helped the attack—it may have been mild—but the experience is worth recording. Dosage was as follows: December 3, 3,000 units; December 8, 1,500 units; December 21, 5,000 units; December 27, 5,000 units. Shortly after the inception of the treatment the bird was noticed to eat better and to be more lively; this was followed by a reduction in the mucous strings in the mouth and the crusts upon the skin. This improvement continued and the bird seemed well in about two months but, after the lapse of three months more, a mucous nasopharyngitis was again observed. Despite two injections of 5,000 units human diphtheria antitoxin the bird succumbed five days after the beginning of this attack. Autopsy revealed much the same condition as was found in the first birds and from the larynx the _Bac. avium_ was isolated. Another case suggestive of diphtheria was seen in a hornbill but antemortem observation being impracticable and postmortem decomposition being advanced when autopsy was performed, the diagnosis could not be confirmed.

An unusually well developed case of molluscum contagiosum was seen in the Wild Turkey (_Meleagris gallopavo_) recorded here by photograph and in the form of notes upon the histology made by Doctor Weidman.

The bird’s head was affected universally from beak to ears by horny nodules up to the size of a pea. They were so large and numerous around the eyes as to completely close them. There were no lesions elsewhere on the body, none of the other turkeys were similarly affected and though watched, none have since developed a similar condition. Histological examination shows a keratosis, many of the cells showing characteristic “molluscum bodies” which appear the same and behave the same tinctorially as the human examples. This turkey case differs from the human, however, in that there are none of the pocket-like epithelial extensions deep down into the corium and this turkey case may be very useful in the further study which is contemplated to show that such things as molluscum bodies are not sufficient of themselves to stamp a dermatosis as a pathological entity, but that they are general pathological processes which may occur in a number of different diseases. The disease has been reported in sparrows, pigeons, but never so far as I can find, in turkeys.

A few isolated cases of infectious disease are included here as a matter of record although they may not be especially significant or important. Rabies was found in a pair of deer which had been bitten by a stray dog. The period of excitement was relatively long, while the paralytic stage was only a few hours. Negri bodies were found. Tetanus killed a Persian Wild Ass (_Equus onager_) the infection wound seeming to be a bruised and abraded area on the rump. From the contused muscle tetanus bacilli were isolated. A gas-bacillus infection, emanating from the vagina which was protuberant and lacerated because of injury by mates, was seen in a pregnant llama (_Llama lama._) On two occasions nodular masses have been found under the skin of seals, not unlike the one studied by Doctor Wiedman and thought by him to be due to moulds. These two have, however, failed to show mycelia or yeast-like bodies, and one thinks only of placing them in the group of botryomycosis. I have never seen a case of this disease, so that I am forced to rely upon literature, a method that inspires no especial confidence in the diagnosis. The bacteria usually held responsible for botryomycosis could not be isolated. Just what can be done for the condition is difficult to state, since seals are scarcely tractable animals.

[Illustration:

FIG. 70.—MOLLUSCUM CONTAGIOSUM. WILD TURKEY (MELEAGRIS GALLOPAVO). ]

The following case has some features like paralytic hemoglobinuric fever and is reported as a matter of record. The long standing gastroenteritis may have been the basis for the intoxication which led to the paralysis and muscular degeneration. This laboratory has now under way studies upon the laming of ungulates, accompanied by weakness of the hind quarters, but no conclusions have been reached. It is interesting to note that Hutyra and Marek quote Johne as having seen a case of hemoglobinuric paralysis in a zebra in 1879.

Burchell’s Zebra (_Equus burchelli burchelli_). The only symptom observed in this animal was gradually increasing lassitude which was first noticed about three months ago; toward the end he habitually stood with tucked tail and nose to the ground as if asleep. He ate well and digestion appeared good, but he became very weak as shown by his inability to rise when he got down on the third and second day before he died, although on both occasions he was able to stand when lifted. Injury, hemorrhage in thigh muscles, chronic gastritis, sciatic neuritis. Œstrus larva in stomach, ascaris in intestine. Both lungs are widely distended and the caudal half of both is the seat of passive congestion. Upper lobes are slightly edematous. No consolidations. Heart normal. Abdomen contains about two quarts of clear straw colored fluid. Liver is of normal size, smooth surface, sharp edges, firm, friable. On section it is very bloody, veins distended, some with clot. Architecture normal. Spleen is of normal size, soft, tough, capsule rough. Section surface is homogeneous, pulp purple, trabeculæ normal, follicles not visible. The kidney capsule is smooth, strips easily leaving a smooth brown surface, firm. Striæ normal, rather wide, glomeruli not visible. Stomach is filled but not distended with partly digested straw. Mucosa of cardia dry, roughly irregular, some irregular mammillations. Two flat papillary growths. Œstrus larva attached to a smaller elevation. The mucous membrane of the fundus is soft, moist, irregular, in some places, translucent, in others opaque; near pylorus mucous membrane is swollen edematous, pink, slightly eroded at pyloric valve. Small intestine has smooth, flat, pale yellow translucent mucosa. Lumen filled with mucopurulent matter like mixed egg. Ileum slightly congested but mucosa firm and translucent. Pancreas is soft, slightly uniformly congested. All mesenteric lymph glands are slightly enlarged and edematous but with normal architecture. In the posterior thigh muscles beside the sciatic nerve, most marked on the right side, is a large hemorrhagic infiltration. There is edema of muscles and intermuscular septa all about this area extending upward as well as to pelvis and psoas muscle. This latter within the abdomen shows slight blood stained edema. No other muscle shows this hemorrhage. Microscopic section of liver and kidney are negative aside from congestion. The stomach shows very irregular epithelial covering, in some places wholly desquamated. Where this is most marked there is a dense round cell infiltration in the villi with some increase in the connective tissue cells. This chronic inflammatory reaction is present in all fields, most marked, of course, in upper layers of mucosa. Glands are distorted and upper epithelium of them is polychromatophilic. The intestine shows similar changes in less intense manner.

Waterfowl Epizoötic. There is reproduced here an account of an unexplained epizoötic among ducks and geese from the _Annual Report of the Zoological Society_ for 1916. Nothing additional has been learned and no repetition has occurred since the drainage and cleaning of the lake.

There began on August 27 a series of deaths among the waterfowl and in one month there were lost forty-one specimens including both ducks and geese. Four additional cases were scattered through the next four months, the last case dying January 11, 1916. All of these came from the lake, none being from the adjacent stream for rare waterfowl or from the more distant stream into which the lake drains. The symptoms were most marked and striking. In the early stages the wings drooped, then the legs became weak followed by inability to raise the head. In the latest cases the voice (ducks) lost its normal character and became hissing. The mind appeared clear for the eyes were bright, feathers unruffled and the bird attempted to escape when approached. Diarrhœa was present, dejecta thin, watery white, no admixture of mucus. Autopsy findings were not frank. At most some swelling of the spleen and a little pale thickening of the intestinal wall constituted the picture. Smears from intestine and nasal mucosa showed no protozoa. The blood taken from the living sick ducks showed no parasites or anemic changes in either raw or variously stained preparations. From the spinal cords of three ducks a 50 per cent. glycerine emulsion was prepared and was injected into the cerebral substance and abdomen of domestic ducks with negative results. A variety of different bacterial cultures was obtained from the liver, spleen, blood and congested nasal mucosa of several birds dead with the disease and injected into domestic ducks with negative results. Histological sections were cut from the important organs of thirteen birds. The kidneys, lungs and pancreas showed no abnormalities. The heart muscle in some cases and also some of the skeletal muscles showed Zenker’s hyaline degeneration together with minor hemorrhages and edema. Several of the proventricles showed low grade inflammatory signs toward the gizzard. The intestines regularly showed lymphatic infiltrations of the villi most marked toward the tips but without congestion. The lumen showed no parasites, bacteria or protozoa. Liver showed in almost every case pigmentation by hemosiderin at times as heavy as that seen in pernicious anemia. The finer bile ducts here showed peripheral round cell infiltrate, which was not continued into the major ducts as determined by serial sections. Parenchymal cells were cloudy and swollen. Spleen showed in early cases polymorphonuclear infiltrate of the follicles, in later cases atrophy of follicular splenocytes and more or less pigment occurred in both stages. The spinal cord and various peripheral nerves showed no inflammation or degeneration as determined by the appropriate special nerve stains. The above clinical, histological, protozoological, and bacteriological examinations having failed to detect the cause and the epizoötic now being over, its nature becomes a matter of deduction. The only constant features of any importance were the paralysis, the intestinal round cell infiltrate and thickening, the pigmentation of the liver and degeneration of skeletal muscles. Of the various possibilities, beriberi was early considered. This is not possible because the food of the birds was a varied one and furthermore none of the nerve degenerations of beriberi were noted. Second, acute bacterial or protozoal infections are unlikely because no constant primary lesions were discovered at autopsy, the numerous cultures failed to produce the disease and other birds living on the stream draining the lake were not similarly affected. Third, a food poisoning. This is possible first because paralytic symptoms were present such as are seen in vetch and mussel-poisoning and secondly because the epizoötic ceased when the birds were taken from the lake and placed upon the grass. If this be the case the toxic material produced the paralysis by direct action upon the muscle fibres just as that of typhoid fever does and must have caused hemolysis as shown by the hepatic pigmentation. The source of this food poisoning is conjectural. Perhaps a dead fish decomposed in the water or there were some algæ with poisonous properties present. The outbreak has a resemblance, but only a superficial one, to infection with one of the group of botulism bacilli. The cause of the trouble must be considered as undetermined.

Enterohepatic Disease. Since the normal drainage from the intestinal tract passes so largely through the liver, there is little to wonder at in morbid lesions of the latter organ consequent upon disease in the former. Not only does this succeed upon bacterial infection of the digestive tube but also upon infestation with animal parasites, under the latter condition forming changes of much more considerable extent, at least in gross bulk, than in the former. Changes in the liver secondary to enteric disease from bacterial infection take the form of cholangitis, thrombosis, degenerations and probably cirrhosis while abscesses and necroses succeed upon protozoal or metazoal parasitic involvement. The latter is exemplified by amebic abscess in man and other mammals and by “blackhead” and “quail disease” in birds; it is to the latter conditions that attention is now directed. The chapter upon the cause of these diseases has yet to be completed, although many reams have been written about it, while the transmission is fairly well understood and the pathology well described. My purpose here is to discuss our experience with the two above mentioned diseases which, while far from conclusive, may assist somewhat in explaining their etiology. There is also reproduced our original report upon quail disease from the Society’s Report of 1915, giving data and figures. Blackhead has been found in five wild turkeys. An unusual case in a Berwick’s Swan is recorded since it bears a striking resemblance to the disease.

The points at issue in the determination of the etiology of blackhead are the importance of _Heterakis papillosa_ in the ceca and the frequency and activity of ameba or histomonas. In three of the five cases of the disease in turkeys the nematode was found macroscopically in the ceca, in two it was not; in one its absence was confirmed microscopically. In two of the turkey cases, forms corresponding to the ameba or histomonas were discovered while the descriptions of the hepatic lesions in two birds use the term coccidia which, from a revision of the slides, is probably incorrect although some of the parasites seem to be possessed of a doubly contoured refractile margin. The larger, more diffuse and ameba-like forms in the intestinal wall suggest that the hepatic inclusions belong to the same group. In only one case was exhaustive search made for coccidia, and without success; the material was not preserved. In two turkeys entirely free of lesions distinctive of blackhead, cecal nematodes (one heterakis, one unknown) are recorded, and in the intestinal wall of another, also free from the disease, forms indistinguishable from ameba could be discovered.[106]

The protocol of the Berwick’s Swan is interesting because the full fledged disease is not known in this bird. While this case is not by any means typical, the chronic cecitis and ameba-bearing necroses in the liver stamp it as of a kind with the true infection of turkeys. Perhaps the resistance offered by the swan effected a modification of the disease, preventing the usual necrotizing enteritis and turning it into a chronic interstitial variety.

Berwick’s Swan (_Cygnus berwicki_). About a month before death passed several large clots of blood. Acute catarrhal enteritis, mural endocarditis, chronic colitis, chronic nephritis, passive congestion and necroses in liver, acute follicular splenitis, edema of lungs, chronic pericarditis, chronic salpingitis, hydrothorax, hydropericardium, hydroperitoneum. Tissues generally are slightly yellow. In serous cavities of thorax is about three ounces of clear fluid. Lungs are distended, subcrepitant, pale red and gray, highly edematous. The pericardium contains about one-half ounce of clear watery fluid. Epicardium is glistening, congested, irregularly thickened especially near the blood vessels. The heart is contracted, slightly large, pale brown-red muscle. On the posterior surface of the right ventricle extending from the auricular opening to the pulmonary valve is an irregularly curved line of grouped, recent red vegetative granulations. Valves negative, they and chambers competent. Aorta negative except heavily blood stained. Liver is slightly large. What of the liver remains undamaged is homogeneous deep purple. Major portion of right lobe badly contused; this seems to have been partly antemortem because there is blood staining and mottling under capsule. In view of colon finding and history of possible injury it is probably the result of degenerations in the liver plus slight trauma. There are several small, pale gray, well outlined, homogeneous areas probably necroses in the liver. The spleen is slightly large, soft, egg-shape, capsule smooth. Section surface shows bright red homogeneous pulp with clearly cut, large follicles. The kidney capsule is smooth, surface smooth brown, consistency firm and tough. The section surface gives a dull gray-brown appearance, seemingly from connective tissue. Markings indistinct. Oviduct is negative except over a distance of an inch near the cloacal opening. Here there is a compound curve with constriction to almost obliteration of lumen. This does not seem to be connected with the colonic trouble. The stomach is negative containing only a few small pebbles. Beginning at the pylorus and extending through the whole of the small gut is a recent, moderately severe catarrhal enteritis with so much exudate as to form almost a cast of the tube. Colon and cloaca show an infiltration of submucosa with areas of hemorrhage. Mucosa swollen as if by edema, glistening and covered by bloody mucus. Ceca negative except that they seem to have been closed as their contents are scanty and firm. Histological section of cloaca shows it to be the seat of a chronic inflammation which has constricted and distorted the tubules into simple masses of nuclei. Marked polynuclear and round cell infiltration of mucosa and submucosa. This is apparently due to ameba-like bodies—a large vacuole with a delicate limiting membrane and a piece of diffuse chromatin in the centre—a few of which may be found deep in the mucosa. Liver shows marked passive congestion, here and there areas of necrosis with some fatty infiltration. Small groups of ameba-like bodies can be found apparently lying in sinusoids of liver and in neighborhood of necroses.

Quail disease, since the careful work of Morse in 1907, has been thought by most observers to be due to an organism of the colon group, but I am informed recently by the Pennsylvania State Board of Animal Industry that coccidia have been found often enough in the droppings and in the morbid lesions to warrant a suspicion of their etiological importance. Although they were not especially sought in the work about to be reported, their presence probably would not have escaped detection during that investigation. I have recently had occasion to examine three birds with lesions identical with those accepted as characteristic of quail disease, one of which was subjected to the proverbial “fine tooth comb” methods; no coccidia were found in the liver or intestinal lesions.

The idea that quail disease, with its ulcerative typhlitis and necrotizing hepatitis, is identical with blackhead or at least that if the latter be due to protozoa, the former is also, requires no special stretch of imagination to one familiar with the morbid lesions. A decision is the more difficult because of one’s inability to reproduce quail disease at will and the none too great certainty of the intentional production of blackhead. At all events the transmission is potentially the same, ground or food soiled with droppings, indicating that hygienic measures should take the form of segregation and disinfection. Here follows the report of our original observation:

“An epizoötic disease has decimated three newly imported lots of quail, Scaled quail (_Callipepla squamata_), Gambel’s quail (_Lophortyx gambeli_) and Texas bobwhite (_Colinus texasus virginianus_). On January 5, 1915, the first lot of twenty-four quail arrived from northern New Mexico _via_ Kansas City; on January 11th a second lot of twelve bobwhite arrived from Brownsville, Texas, _via_ Kansas City; the first of this lot died the day after arrival with lesions of this infection. From this lot of birds the first lot was probably infected, the first death occurring on January 20th, no other deaths having occurred in the first lot since arrival. On January 21st the third lot of twelve quail arrived direct from Mexico. The first of this lot died of the disease on January 24th. Some birds were also sent at the time of the arrival of the third consignment, to Doctor Kalbfus of the State Game Commission. It is to be emphasized that to date no cases of infectious enteritis have occurred in the lot sent to Doctor Kalbfus. The first case appeared at this Garden on January 12th, more than a week before the third lot arrived. It would seem that the disease was brought to the Garden by the second lot of birds, and that they picked it up on the way from Texas to Kansas City to Philadelphia. The birds made a stop at Kansas City. The birds died at long intervals for the first two weeks, but late in January and early in February several died each day. The last death with characteristic lesions occurred February 11th. After the epidemic reached its height it subsided very quickly.

“During the illness the birds exhibited very few symptoms, indeed some of them were not known to be sick. A few sat huddled in a corner with ruffled feathers and drooping head; the stools were little if any altered as far as could be determined among so many in the enclosure. At death the birds were in good condition, feathers fairly smooth, skin clear, body plump and fat in good amount—not abundant, nor were the animals emaciated. The principal lesions were enteritis, degenerative necroses and abscesses in the liver, congestion of all the viscera and plastic peritonitis in a few. A small number showed congestion of the lungs and two had patches of pneumonia. Many but not all of the birds had Heterakis in the ceca. The process seemed to start as a focal necrotizing lesion in the mucosa or submucosa of the ileum just above the ceca and colon; many had lesions in the ceca and as far down in the colon as the cloacal dilatation. Among the animals dying late in the epidemic several showed lesions involving the whole small intestine, a few indeed with greater involvement of the duodenum than of the lower parts.

“Judging from the gross and microscopical appearances it seems that the virus causes at first a cellular infiltrate in the mucosa or submucosa upon which necrosis shortly supervenes. The overlying mucosa soon degenerates, and the surface is covered with an indefinite slough. In other cases, especially early in the epidemic, the process extended outward and appeared as muscular or subperitoneal necrotic areas before the mucosa was much involved. At all events necrosis was an early change in every case. The blood vessels were usually thrombotic. In the cases that spread toward the peritoneum a plastic peritonitis of varying severity was present. The focal liver lesions were not present in every case. They took the form of focal necroses or abscesses. Some fatty or parenchymatous degeneration was always present. The liver lesions probably started as inflammations of the veins from which necrotizing or infiltrative lesions spread. The splenic lesions were those of lymphoid hyperplasia, only distinctive in the enormous number of large lymph cells. Typical microscopical changes are as follows, quoted from one of the autopsy protocols: The lung showed moderate congestion with here and there a little epithelial swelling and a mild bronchitis and peribronchitis. The type of bronchitis is infiltrative rather than catarrhal. The heart muscle showed granular degeneration of the fibres with breaking up or irregularity of the striæ. Some increase in interfibrillar nuclei and especially those of the capillaries. There is moderate congestion. Epi- and endocardia are slightly raised as if by edema. Here and there slight fragmentation of fibres. The liver cells are granular and some show fat droplets. There is moderate congestion and more than the normal number of round nuclei between the columns. Here and there are focal necroses of varying sizes without circumferential reaction. Here and there are also some small collections of round cells near to which the liver nuclei are large and show attempts at regeneration. In these collections but not in the necroses, bacillary forms may be found. There is no reaction on the part of the bile ducts. The larger vessels are thrombotic, and in one section a thromboangiitis was found. One stretch of early plastic perihepatitis was found. The kidney showed slight granularity with slight cloudy swelling of the epithelium. The nuclei of the glomeruli are prominent. There is moderate congestion. The spleen showed distinct large lymph cell hyperplasia with relative inconspicuousness of small round cells. The follicles are very diffuse, their centres filled with large lymph cells. The cords are hyperplastic and the sinuses compressed. Moderate congestion; no unusual blood destruction; one area of hyaline necroses found. The proventricle and gizzard are negative with the probable exception of active desquamation on the surface of the former. The outer coats of the duodenum are negative except for slight richness in nuclei. The deep mucosa is very rich in nuclei and red blood cells. The outer parts of the villi are either swollen with a cellular infiltrate or by an area of granular necrosis, or have disappeared. It would seem that the surface of the mucosa rapidly degenerates and desquamates. Bacteria are very numerous. The adjacent pancreas is negative. The ileum showed round cell infiltration of the deep mucosa, swelling of the villi and a desquamation of the surface. One ulcer was found having its base on the swollen muscularis and being covered with necrotic slough. Adjacent peritoneum is slightly infiltrated, but chiefly congested and edematous. This ileum lesion seems to be the characteristic one of the disease. Bacteriological observations were made upon cultures obtained from the intestinal mural lesions, the peritoneal exudate, the liver necroses, and the heart’s blood in eleven cases. In seven cases I was able to isolate a motile rod like the _B. coli communis_ and in four cases a non-motile rod of the _Bact. aerogenes_ type. The former is quite similar to the _B. scoticus_ (Migula) reported in Grouse disease.

“We obtained from Doctor Kalbfus of the Pennsylvania State Game Commission, four perfectly healthy birds for experimentation. A culture of the isolated germ was injected into two of them and mixed with the food of the remaining two. It does not seem profitable to cite the details of the work as the results were entirely negative, no lesions resulting that bore the slightest resemblance to the spontaneous disease. The birds either lived indefinitely or succumbed to wholly foreign conditions. This negative experiment is of course no proof that the organism is not the cause of quail disease, for the methods employed might not be the correct ones to propagate the virus or the germ may have lost its virulence during the laboratory culture work. However, as some observers have not reported this bacillus in the disease this germ loses something in importance by the negative inoculation experiment.

“Judging from reports and based upon the observations of Morse upon Grouse disease it would seem that the incubation period of the disease is about eight to ten days. However, one of the third lot of our birds died within three days of its arrival at this Garden, and therefore within three days of its exposure to the second arrivals; if it be correct that this second lot brought the disease and the third lot did not have it, it would seem that the incubation period can be as short as three days; how long it may be is only suggested by the fact that some of the third lot did not die for three weeks after arrival and exposure. All the Gambel’s and scaled quail succumbed to the disease, but two of the twelve bobwhite survived. It would seem that although these last birds probably introduced the disease, they still possessed more resistance than the others, for the second death among them occurred seventeen days after the first death. The epidemic as we have seen it here seems to be the same as Grouse disease of Scotland and as the Grouse disease in this country as reported by Morse (Bureau of Animal Industry Report 109, May 18, 1907).

“The means of transmission of the disease is not exactly known, but is in all probability by a pollution of the food, the water supply or the ground. Since the lesions are so marked in the lower ileum, cecum and colon, a possible transmission by cohabitation must not be entirely overlooked. There does not seem to be any means of limiting the epidemic in a flock by segregation or sacrifice of the infected birds, because symptoms are few and do not appear until shortly before death. Each bird would have to be put into a separate cage until proved infected. Scrupulous cleansing of the enclosure is desirable, but its efficiency is difficult to estimate.”

SECTION XVIII THE ANIMAL PARASITES, THEIR INCIDENCE AND SIGNIFICANCE

FRED D. WEIDMAN, M. D.

It is quite to be expected that animal parasites would be found in the animals of zoological gardens, garnered as these beasts are from all parts of the world, tropical and otherwise. It inevitably follows that many of the forms should be strange and new, enticing one to the fascinating determination of their identity, life history and hygienic importance; and, developing from all this, one can easily imagine how limitless the opportunities are for scientific work in parasitology in a laboratory like ours.

As in other biological fields, the taxonomic range of parasites here is wide. It extends from the lowly protozoa to the insecta, and, dropping to the smaller subdivisions, includes not only most of the genera familiar to human parasitology but many known only among the lower animals. From the standpoint of the host, the biologic state of parasitism extends from the lowest protozoa to homo.

The above will suffice to indicate the wide range of parasitism in animals, but the extent of work actually done thus far in wild animal material is a different story. Collated, consistent studies, so far as I am aware, have been undertaken only at the London Garden, here at Philadelphia, and at Washington, D. C., by Dr. Charles W. Stiles and Albert Hassal. The data, collected by the last mentioned workers are incidental to the Index Catalogue of Veterinary and Medical Zoology, and embrace only the (index) phase indicated by the title, but it is so valuable, and withal so altruistic, that it must be credited. What other work there is is scattered where—not in literature—general biological, medical and veterinary. That at London has been conspicuous through the observations of Plimmer and of Beddard on filariæ and cestodes respectively, while the work of Nicoll must not fail of mention.

That the reader may the better appraise the sections of our own work which are to follow I wish at once to indicate their material basis. Ordinarily only the larger parasites are looked for at the autopsy table and there must be special indications to demand search for the finer ones. Those of microscopic size, or so minute as to be overlooked in the guise of seeds, vegetable fibres, etc., have not, both here and elsewhere, been routinely studied as have macroscopic ones.[107] From our autopsies there have accumulated records of nearly 900 parasites— some determined generically, others but as to order. The parasites have in greatest part been preserved and are available for further study; in the past, special groups have been culled out from time to time and examined. Where conditions have been pressing, as in certain epizoötics, investigations have amounted to more than observations and descriptions, and received detailed laboratory examinations with more or less animal experimentation as the occasion demanded.

The foregoing may suffice to apprise the reader that the subject of wild animal parasites has been but broached so that data are especially incomplete on life histories—a phase most important in relation to hygiene; but in spite of this and although the statistics are only approximate, as is the case in most parasitological work, these data have attained to sufficient proportions to justify at least a beginning in the matter of collating and generalization. At any rate the time has arrived to establish at least a nucleus for the accretion of data, which can be later subjected to confirmation or correction. We draw just a grain of comfort from the knowledge that the more fully worked field of human parasitology is also vulnerable to criticism of very much the same order.

THE VALUE OF PARASITOLOGICAL STUDIES IN ZOOLOGICAL GARDENS.

The foregoing chapters have made clear two fields of practical usefulness of any study in such gardens. These—hygiene in relation to the animals and comparison in relation to human beings—need therefore only to be mentioned at present since it is obvious that both benefit by our parasitological work. But there is yet a third—a scientific phase of parasitology which may be considered purely academic. It consists in morphological and other studies necessary for the identification of the parasite, the determination of its life history, etc. These last studies may still in a restricted sense include a modicum of the practical in so far as they have a bearing on the disease with which they are associated. But on the whole they are a source of danger for us since such things as studies on the finer structures of worms, taxonomic arrangements, descriptions of new species of commensals, etc., being alluring, are likely to lead one so far afield that eventually an attitude of stubborn resistance will have to be assumed in order to conserve that precious, volatile laboratory asset—time—for the more crying, practical problems ever reaching out to us.

However, in parasitological investigations as in other scientific work, immediate abstract information may at some time prove to be of greatest practical value. Thus for example if we can discover the exact facts concerning one phase of the life history of a certain parasite, it may be possible by hygienic measures, to break the cycle of development of the parasite at one point thereby preventing its completion. This information is perhaps obtained most readily in experimentation upon the rôle of lower animal forms in the pathogenesis of disease but where reliable evidence is lacking, help may be had by comparison with others in the same taxonomic group. Undoubtedly systematic classification will go far to help solve many of these riddles.

PATHOGENICITY OF ANIMAL PARASITES IN GENERAL.

The first question which arises in this connection concerns the actual ability of animal parasites to produce disease in wild animals. At once it will be seen that this must be a relative matter, for no one on one side would contend that every symbiont in an animal is harmful—parasites _sensu stricto_—nor on the other that none could possibly be, _i.e._, that all are always commensals. It is evident that the issue boils down to questions as to the extent to which they are harmful. Before attempting the answer let us consider the means by which the parasites may conceivably produce disease.

MODES OF DISEASE PRODUCTION (PATHOGENESIS).

The medical reader is familiar enough with the pathogenic powers of some animal parasites, but may be sufficiently interested to glance over specific wild animal instances illustrating them while they are being listed for those less familiar with this subject.

1. MECHANICAL OBSTRUCTION.

I refer here particularly to simple blockage of normal body passages as the result of bulk or mass. This occurs more commonly in the intestines than elsewhere on account of the greater frequency, greater numbers and larger size, in general, of parasites inhabiting this tract. Thus, we have recorded a liothrix (_Liothrix luteus_)[108] where the combination of a small host and consequently narrow gut and comparatively large parasite induced obstruction. Plimmer[109] records microfilaria clogging the brain capillaries. Shipley[110] mentions two specimens of _Ascaris lumbricoides_ obstructing the nares of a chimpanzee (_Pan niger_). Blockage may also be produced secondarily to the presence of the parasite, even in the absence of notable numbers of them, and quite apart from the element of verminous bulk. This occurs through inflammatory swellings which the worms excite. We saw many serious grades of this in our spiroptera epizoötic, the lumen of the proventricle being narrowed by swelling of the mucosa and more or less occluded by exudate and necrotic mucous membrane.

Yet another direction wherein a mechanical rationale pure and simple obtains is by the production of diverticula. Worms encysted in the gut wall may, by weight alone or by excitation of peristalsis, cause the wall to bulge outwards (or inwards even) like a pocket. Such a diverticulum has been noted in the gut of a Pale Cebus (_Cebus flavescens_)[111] parasitized by acanthocephalus, but in this case there were adhesions to the nearby stomach, and it is possible that in this individual case the diverticulum was a traction one, _i.e._, pulled out by the anchorage of adhesions externally.

[Illustration:

FIG. 71.—ACANTHOCEPHALUS (THREE SPECIMENS) PROJECTING FROM THE INCISED INTESTINES OF A PIGMY MARMOSET. COMPARE THE SIZE OF THE PARASITES, WHICH MAY BE DISTINGUISHED BY THEIR ANNULATIONS, WITH THAT OF THE INTESTINES. ]

[Illustration:

FIG. 72.—BLOOD-RED NEMATODES PROTRUDING FROM FRONTAL SINUSES OF COMMON OPOSSUM (DIDELPHYS VIRGINIANA). THE SKULLCAP HAS BEEN LIFTED OFF AND THE POSTERIOR WALLS OF THE SINUSES BROKEN. ]

2. MECHANICAL IRRITATION.—In those instances where inflammation is the manifestation which reflects the simple mechanical effects of parasites it will be difficult indeed to prove, in the present state of our knowledge, that it is not rather the effect of associated toxic substances or excreta elaborated by the parasite. But instances of a purely mechanical irritation there must be, although one can scarcely put the finger upon them and say that this or that individual inflamed mucosa did not become so from a toxic cause. Omitting these then, the more certain, purer, more unequivocal examples will be those where physiological processes become exalted as the result of the parasitic irritation. An example in point is a case of volvulus in a Screech Owl (_Otus asio asio_).[112] Here it is probable that the parasites excited the gut to undue peristaltic action, and that during this process it became twisted. Worms in such passages as the nose and nasal sinuses (I have seen blood-red filariæ in the frontal sinuses of an opossum) undoubtedly produce nervous effects by their presence and movements. Those in the subcutaneous tissue (filariæ of wild cats) probably also do so. It is difficult to judge those cases where doubtfully sensitive parts are the ones affected. Probably the intestinal and intraperitoneal worms, and less certainly the generally-migrating ones analogous to _Filaria loa_, produce no nervous effects mechanically.

3. PRODUCTION OF HEMORRHAGES.—Hemorrhages large enough to kill suddenly are theoretically possible, since worms occasionally produce aneurysms which may rupture; we have seen such an accident in a Paradoxure (_Paradoxurus leucomystax_). But certainly it is the long continued, wasteful small hemorrhages that are important, inducing an anemia often of severe and fatal grade. The hookworms are the shining offenders here, yet we have seen very much the same effect from Acanthostoma in the intestine of monkeys. Œsophagostomum has also been incriminated at the London Garden in young Rhesus Macaques (_Macacus rhesus_)[113] where the young forms of the parasite did the damage as they burrowed into the wall of the gut.

4. OPENING UP AVENUES OF INFECTION.—This may be accomplished either by passage of parasites from one position normally containing bacteria to another which is susceptible to infection, or by devitalizing a tissue which is ordinarily resistant to infection; _i.e._, creating a _locus resistentiæ minoris_. The intestinal tract is the most common organ concerned, but the illustrations to follow will give variety. Thus, the mature examples of œsophagostoma in young rhesuses just referred to above burrowed into the gut wall and led to both local and general peritonitis. In one of our “spiroptera” parrots the worm had passed through the proventricular wall and a chronic fibrosis resulted around it. At the autopsy on a Rhesus Macaque Doctor Fox found a localized abscess adjacent to the gut wall, and in it a whipworm was imbedded. Passing from these examples of intestinal worms, I can mention the loss of a valuable Philippine Spotted Deer (_Cervus alfredi_) as the result of secondary infection of a cysticercus cyst of the lesser omentum which led to a nearby peritonitis. Lung infections are not uncommon. Murray[114] records that forty-four out of eighty-five young rhesus monkeys dying from pneumonia showed an acarian, and he ascribed the pulmonary irritation to certain crystals in the excreta of the mite. I have studied a case of bronchopneumonia in a prairie dog where great numbers of an arachnid were present. The reports of the London Zoological Society are replete with notes of round worm pneumonias of reptiles. These pulmonary cases must result from decreasing of tissue resistance by the presence of the worms, and are easy to understand, much more so than the intestinal infections when one recalls how sensitive lung tissue is to foreign bodies, and that there seems to be no indication that this tissue becomes accustomed to infestation such as may be argued for the gut. All these citations must convince us that parasites are most important predisposing agents to infection, and that this is one of the most sinister phases of animal parasitism.

5. DESTRUCTION OF TISSUE.—This heading does not refer to the comparatively trivial effects that accompany the more acute inflammations secondary to parasites, albeit certainly the absorption of their disintegrative tissue products has some effect on the economy; but our ideas of such are so vague as to justify their being disregarded here. What I refer to is the more massive destruction such as may occur in the blood, for instance, from the action of protozoa. There is also loss of mucosa in those chronic infestments of the stomach where we find excessive fibrous tissue overgrowth. The most striking example of tissue destruction we have seen was in the cirrhotic livers of prairie dogs affected by _Hepaticola hepatica_, where in extreme cases, the amount of functionating liver substance was reduced to a very small fraction of its normal bulk.[115]

6. TOXINS.—We have no direct evidence to offer that noxious products of parasites are concerned in producing disease in wild animals. The local effects of such toxins are not distinctive enough—individual enough to toxins or to the animal body—to separate them from the effects of such accompanying factors as bacterial inflammations; nor can we separate the general effects of these toxins from what might have been, for instance, the effects of an accompanying anemia of hemorrhagic or other origin. From a knowledge of what happens in human prototypes though, there is scant doubt that some one of the multitudinous species must be capable of producing toxins, but just which varieties are concerned cannot be listed by anyone. By analogy we can at most only suspect the hookworms and the dibothriocephalidæ. Under this same category of the toxins come the worm-products which are reputed to have a destructive effect upon the digestive enzymes in the gastrointestinal tract of the host, and which would thereby interfere with the proper assimilation of pabulum, resulting in malnutrition. For the same reasons as above indicated for the toxins one is unable to speak for or against these “anti-enzymes.”

7. PRECLUSION OF NUTRITION.—This must be a very unimportant phase of the activity of intestinal parasites, when one compares the bulk of food which passes through the bowel and the average number of worms present; and the same holds good for some interstitial parasites like the adult filariæ. Even in amazingly heavy infestments of the intestines one will be constrained to dismiss this idea when he compares the bulk of parasites with that of the host, and recalls what the physiologist terms the “factor of safety” inherent in this tract as elsewhere. But in the case of blood parasites the matter may be different. Here we are concerned with the withdrawal of refined foodstuffs—those which have been worked over and over by subtle internal metabolic processes; and we are not so sure, especially on recalling the enormous numbers of parasites usual to blood infestments, that there is the capacity on the part of these internal processes to meet increased demands that we count upon for the intestinal functions. It is much more serious to be deprived of the finished product than of the crude because it means the undoing of “digestive” work all along the line, from gut to tissue cell. Furthermore, a blood infestment guarantees that the parasite has been feeding upon and depriving the animal of the precise foodstuffs the cells require, and not by any chance upon, even in part, intestinal substances that were wastes or residues. If we except the blood parasites, then, it seems safe to conclude on the whole that the amount of pabulum used by parasites is unimportant to the animal.

Having reviewed the manner in which parasites may conceivably be harmful, it is time to return to the question of the actual exercise of these powers.

The older appraisal of parasites in animals, namely that they were rather innocent of disease production, was suggested by and borrowed from the veterinarian, probably being engendered in him by their frequency in what appeared to be normal domestic specimens. Yet it is only proper to add that one of our former pathologists, and sometime professor of veterinary pathology, Dr. C. Y. White, is a medical man and is of much the same opinion. Older writers regarded worms even as “guardian angels” of children. Very recently Schwartz[116] reviews some work in this connection showing that, _in vitro_, some cestode extracts were inhibitory to certain bacteria (_B. anthracis_, _B. pyocyaneus_ and _B. dysenteriæ Shiga_). This relationship is so different from natural conditions as to need no further comment.

At the London Garden the view appears to be different. In the 1910 report they charge five deaths against perforation by worms of the stomach and intestines; in the 1911 report they record giant toads dead from lung infestment; in 1912 “eighteen cases of enteritis were due to worms”; and in 1917 they mention pneumonia in a toad and perforation of the stomach of a puma. These reports represented evidently the more striking, unequivocal examples of death from parasites which had outspoken anatomical expressions, and omitted those in which the more subtle agencies of parasitic pathogenesis were concerned. Their experience has apparently been much the same as ours.

The ideal approach to a decision in reference to the importance of parasites would appear to be a mathematical one, something as follows: First, to determine what species infest animals and how commonly, then to decide which ones are pathogenic and thirdly to estimate the severity of the disease induced; so that finally, by an analysis and comparison of the three results—a comparison and analysis judicial in the broadest sense—we might hope to come to an opinion. Let us consider the three avenues in order. At the first glance it must be evident that a list of all possible parasitic varieties does not exist and may never be compiled. The most that can be done is to tabulate the findings in scattered laboratories, data usually recorded in terms of the individual observer’s studies and often inadequate to give the compiler all the facts desired. The same remarks apply to the percentage incidence of parasitism. Not to prolong the academic discussion, suffice it to say that very much the same obstacles present in the second avenue—that of pathogenicity of the individual species. Our own data referring to this second heading will be presented later, but after the failure of the first avenue, the second and third lose greatly in value. At best, statistics can be only suggestive. Unless critically and suspiciously interpreted, and with a full appreciation of their limitations from a foreknowledge of the way in which they were compiled, they would only delude the reader and offend science, and so we abandon this line of reasoning.

At present the best results of the study of pathogenesis by animal parasites will probably be reached by a combination of methods, as follows:

1. Direct. How commonly do we see clinical symptoms and morbid anatomical changes that are incontrovertibly due to the parasite? We restrict ourselves here to a narrow group of infestments indeed, and think of such diseases as trichosomiasis in prairie dogs and spiroteriasis in parrots.

2. By comparison with analogous infestments of domestic animals and man— more thoroughly studied and therefore more accurately appraised, in general, as to pathogenicity; a comparison from the standpoint of disease production rather than natural habits of the parasite. Example, coccidiosis and hookworm disease in foxes and dogs.

3. By inference through deduction. This is the most unsatisfactory consideration of all, and should be well checked up and discounted. Here we would evaluate the known propensities of the parasite first, such as its size, motility, anatomic position in the host and the general pathological traits of the genus and family to which it belongs, etc., and then compare these verminous properties with those of the host—its size, temperament, physical stamina, etc. This third consideration must necessarily overlap with or be supplementary to the first two. For example, this consideration would have to be resorted to in many cases of ascaris infestment where anatomical changes are generally not demonstrable.

Acting on these three considerations, and after twelve years of observation on parasites here in the Garden, a fresh review of our records, and a recent review of the accessible relevant parasitological literature I have come to the conclusion that, considering wild animal collections the world over, there is no justification for an unqualified, definite answer to the question of pathogenic parasitism that will meet all conditions. We lack data on too many species that are not sufficiently represented in collections or indeed not represented at all. It is the liability to infestment of each order or family of beasts that will have to be determined, and, depending on the assortment each garden has on exhibition, will the importance of parasites to the garden as a whole vary.

Speaking for the Philadelphia Garden, I have come to the conclusion that on the whole parasitism does play an important part of our annual losses. The financial loss which could be charged against spiroptera alone is in the four figures, to say nothing of the difficulty of replacement of rare species. And while touching the financial phase let it be added that scientific work done now, it must be remembered, is not restricted to the present time or place, but is to be measured in dollars and cents with the yard stick applied to the future, and in other places than that where the initial work is done. Even if we cannot answer the question of the matter of importance the world over we can guarantee that it is sufficiently so in the Philadelphia and London Gardens to warrant a rigid supervision for parasitism; and since the other larger collections are probably made up of similar animals, albeit in different proportions, we surmise at least that it is likewise so with them.

IMPORTANCE OF PARASITES IN OTHER FIELDS.—In addition to their importance to exhibitions, animal parasites of wild animals are important first to man. The animal hosts may serve as porters of infestation, and interfere with attempts at eradication of the disease. The experience of the European with African sleeping sickness attests to this. Not to go farther than immediate examples I wish to note in this connection the occurrence in this Garden of scabies in an orang which was transmitted to a keeper, and of amebic dysentery in monkeys. Leiper[117] has called attention to a guinea-worm in a leopard.

Parasites are important to certain wild animal industries. The ones that have come to my attention are the fur seal (_Otoes alaskanus_) industry of the Pribiloff Islands and fox-farming in Newfoundland. In both of these instances the hookworm was concerned and entailed losses of thousands of dollars. Lucas, who conducted a United States Government commission to the seal grounds and after whom Stiles named the parasite, has left very full notes of the former disease. I have identified the same infestment in a young California hair seal (_Zalophus californianus_) which was born and died in this Garden. This indicates that the parasite might perhaps be found farther down the Pacific coast than hitherto suspected.

To hunters parasitism of animals must be important, but to an unknown and undoubtedly unimagined extent. The grouse plague of Scotland[118] is an example to point. Who knows but that the disappearance of some of our game animals, particularly birds, was not due more to disease than to the ravages of man? There is at least food for thought here.

OCCURRENCE OF ANIMAL PARASITES IN THE WILD.—It would be unbelievable that parasitism did not exist in the wild. It seems proper, however, to record some evidence. Diesing’s _Systema Helminthum_ is replete with references to Natterer’s Brazilian expedition. Nicoll speaks of a German expedition to Spitzbergen in 1898, and a Swedish one to Egypt in 1901, in both of which large numbers of parasitic forms were collected. Nicoll[119] found _Trichosoma hepaticum_ in a hare shot in the wild, and liver-flukes[120] in a kestrel shot on the coast of Scotland. Leiper[121] found nine species of worms in hippopotami during an expedition to Uganda, and[122] states that thirty-seven species of helminths were collected on an Antarctic voyage by Surgeon Atkinson. In an investigation of Grouse disease in Scotland, Fantham found many different blood and intestinal parasites. Dr. Charles B. Penrose tells me that all of the white-tailed deer he shot in the valley of the Swan River, Montana, were infested with liver-flukes, so much so that the liver was literally riddled by the disease, and yet the deer were fat. The black-tail deer of the same valley were not thus parasitized and were not as fat. In our own Garden we have found many tapeworms in wild cats[123] which had been too recently captured for the worms to have developed in captivity. Such instances might be still further multiplied.

A more important consideration is the fate of the parasites thence introduced into our Garden. Do they disappear of themselves? Naturally we can never make sweeping predictions, for future events will depend upon the life history of the individual parasite concerned. But by and large, once introduced it is better to assume the attitude of pessimism, and resign oneself against spontaneous disappearance and, what is worse, realize that the parasitism is likely to become indigenous. We have several pieces of evidence, however, that the infestment may occasionally quite disappear. Thus, I have seen _Coccidium bigeminum_ spontaneously disappear from a Swift Fox (_Canis velox_) and _Spiroptera incerta_ from a Macaw as proven at autopsy. Nicoll[124] remarks that certain trematode infestations were heavier in newly arrived animals than in ones long resident in the Garden. This is conceivable on the basis of individual worms dying out, _i.e._, fulfilling their life spans without the host becoming reinfested with fresh parasites. Precise information on the subject is supplied by Ackert[125] who found that cestodes disappeared from chickens in six to eight months when the birds were confined, _i.e._, protected from reinfestment. Moreover, it is known that worms can escape during acute infections, the infectious state of the economy producing conditions obnoxious to the parasite. We hear of many instances of their expulsion in human feces and vomitus during malaria and the exanthemata of childhood and know of similar discharge from animals during the death agony. I cite these data largely because they explain the scarcity or absence of parasites at autopsy in animals which were known to have been clinically infested.

FREQUENCY OF PARASITISM IN WILD ANIMALS

There can be little doubt that wild animals are more frequently infested than man, and furthermore with a larger number of parasites. I have no statistical basis for these opinions—they rest on personal observations of human and animal autopsies, and reports of findings in the tropics and elsewhere. They have therefore but the value of an individual opinion. I should estimate rather cautiously that wild animals are infested at least two or three times as frequently as man and much more heavily.

The first step in the discussion of the incidence of parasites must be that respecting the (host) classes and smaller taxonomic divisions—of course as they have been studied in this Garden. Certain statistical limitations were experienced and can be summarized as follows:

Data are not available on a sufficiently large number of animals to justify conclusions as far down as genera and species, except for such commonly and generously exhibited forms as monkeys and parrots. I have therefore in tabulating and reviewing our records, distributed the animals only as far as families—not into genera and species. The table (24) to follow will be found not to contain every family because to do so would needlessly enlarge it. Accordingly I have followed the policy of only indicating those genera and species showing either frequent or important infestment. I shall refer to those groups later as “susceptible” groups. If no family is recorded in the table it means that we have had no important numbers of infestments in it. The “remarks” column shows the individual parasite that has been particularly frequent or otherwise important. If there are no remarks it means that the species of parasites found have been scattering.

RESULTS OF REVIEW AND TABULATIONS.

We now pass to an analysis and discussion of the findings brought out in the previously mentioned review of our records and in Table 24. Viewed broadly we find that there is a wide variation in the susceptibility of different families to infestment. Those that are susceptible may be located by consulting the table, and each will therefore not be separately culled out and subjected to needless repetition. A few points are however worthy of separate mention. While there is a familial or generic susceptibility within certain orders it is unwise to generalize too broadly. Thus for example the Corvidæ have a high percentage in incidence for tropidocerca, syngamus and periproventricular worms, many families of Ungulata harbor echinococcus, and Carnivora are prone to show ascarids. On the other hand, among the copious exceptions to this may be cited the irregular liability to infestment exhibited by the Galli. Four varieties of these birds are represented but there are missing such important kinds as curassows, guans, guinea fowl and peafowl.

TABLE 24. _Incidence of Parasites in Animal Groups._ ══════════════════════╤═══════════════════════════════╤════════════════════ Animal │ MAMMALIA │ Remarks ──────────────────────┼───────────┬────────┬──────────┼──────────────────── „ │ Number of │ Number │Percentage│ „ │Autospecies│Infested│ │ ──────────────────────┼───────────┼────────┼──────────┼──────────────────── Primates │ [126]538│ 51│ 9.4│ Cercopithecidæ │ │ │ │ Sooty Mangabey │ 34│ 4│ 11.8│ Cercocebus │ │ │ │ fuliginosus │ │ │ │ Rhesus Macaque │ 60│ 6│ 10.│ Macacus rhesus │ │ │ │ Callitrichidæ │ │ │ │ Marmosets │ 43│ 7│ 16.3│ Cebidæ │ │ │ │ Squirrel Monkeys │ 8│ 3│ 37.5│ Other Cebus │ 87│ 10│ 11.5│Eight had Filaria Monkeys │ │ │ │ gracilis. Lemures │ 86│ 6│ 7.│ Carnivora │ 498│ 84│ 16.9│ Felidæ │ │ │ │ American Wild Cat │ 28│ 11│ 40.│Stomach and │ │ │ │ intestines, 22; Felis ruffus │ │ │ │Bronchi, 4; Muscles, │ │ │ │ 7. Spotted Wild Cat │ 5│ 4│ 80.│ Felis ruffus │ │ │ │ texensis │ │ │ │ Canada Lynx │ 10│ 4│ 40.│Ascarids only. Felis canadensis│ │ │ │ Lions │ 10│ 3│ 30.│Ascarids in stomach │ │ │ │ and Felis leo │ │ │ │intestines. Ocelot │ 15│ 5│ 33.│Uncinaria. Felis pardalis │ │ │ │ Canidæ │ │ │ │ Gray Fox │ 28│ 1│ 4.│Cestodes. Canis cinereo │ │ │ │ argenteus │ │ │ │ Red Fox │ 17│ 2│ 12.│Uncinaria. Canis vulpes │ │ │ │ pennsylvanicus│ │ │ │ Swift Fox │ 5│ 2│ 40.│Uncinaria. Canis velox │ │ │ │ Gray Wolf │ 18│ 2│ 11.│Ascarids. Canis mexicanus │ │ │ │ Mustelidæ │ │ │ │ American Badger │ 17│ 7│ 41.│Physaloptera. Taxidea taxus │ │ │ │ Procyonidæ │ │ │ │ Raccoon │ 42│ 2│ 5.│ Procyon lotor │ │ │ │ Ursidæ │ │ │ │ Bears │ 37│ 6│ 16.│Ascarids. Otariidæ │ │ │ │ Hair Seal │ 20│ 1│ 5.│Uncinaria. Zalophus │ │ │ │ californianus │ │ │ │ Rodentia │ 198│ 32│ 16.│ Sciuridæ │ 44│ 4│ 9.│Scattered through │ │ │ │ four Castoridæ │ │ │ │different genera. American Beaver │ 17│ 4│ 23.│In three cases │ │ │ │ oxyuris Castor │ │ │ │and flukes in cecum. canadensis │ │ │ │ Hystricidæ │ │ │ │ Canada Porcupine │ 47│ 17│ 36.│Cestodes 8, filaria │ │ │ │ 11, oxyuris 9, Erythizon │ │ │ │in peritoneal cavity dorsatus │ │ │ │ also intestine. dorsatus │ │ │ │ Hyraces │ 7│ 2│ 28.│Cestodes in bile │ │ │ │ ducts. Cape Hyrax │ │ │ │ Procavia capensis │ │ │ │ Ungulata │ 365│ 44│ 12.│ Equidæ │ │ │ │ Zebras │ 7│ 7│ 100.│Nematodes, │ │ │ │ intestine. Cervidæ │ │ │ │ Axis Deer │ 6│ 1│ 17.│C. tenuicollis. Cervus axis │ │ │ │ Barasingha Deer │ 8│ 0│ │ Cervus duvanceli│ │ │ │ Eld’s Deer │ 6│ 0│ │ Cervus eldi │ │ │ │ Fallow Deer │ 20│ 1│ 5.│Echinococcus cysts. Cervus dama │ │ │ │ Hog Deer │ 21│ 0│ │ Cervus porcinus │ │ │ │ Japanese Sika Deer│ 14│ 0│ │ Cervus sika │ │ │ │ typicus │ │ │ │ Red Deer │ 14│ 0│ │ Cervus elaphus │ │ │ │ Elk │ 29│ 2│ 7.│Trichocephalus. Cervus │ │ │ │ canadensis │ │ │ │ White tailed Deer │ 33│ 2│ 6.│Echinococcus in lung │ │ │ │ (2). Mazama │ │ │ │ virginiana │ │ │ │ Mule Deer │ 8│ 5│ 62.│Four Cyst. │ │ │ │ tenuicollis. Mazama hemionus │ │ │ │ Camelidæ │ │ │ │ Llama │ 14│ 2│ 14.│ Lama glama │ │ │ │ Camels │ 9│ 4│ 44.│Hydatid cysts. Suidæ │ 19│ 2│ 10.│ Edentata │ 16│ 2│ 12.5│ Armadillos │ 10│ 2│ 20.│ Marsupialia │ 175│ 45│ 26.│ Didelphyidæ │ │ │ │ Common Opossum │ 84│ 40│ 48.│Physaloptera, 38; │ │ │ │ oxyuris, 5; │ │ │ │ cestodes, 5; │ │ │ │ nematodes in │ │ │ │ lungs, 3; cysts in │ │ │ │ peritoneal areolar │ │ │ │ tissue, 2; │ │ │ │ trematodes in │ │ │ │ ileum, 1. Didelphys │ │ │ │ virginiana │ │ │ │ Macropodidæ │ │ │ │ Kangaroos and │ 70│ 0│ 0.│ wallabies │ │ │ │ ──────────────────────┼───────────┴────────┴──────────┼──────────────────── │ AVES │ Passeres │ │ │ │ Corvidæ │ │ │ │ Common Crow │ 16│ 7│ 44. }│Tropidocerca and │ │ │ │ occasional │ │ │ │ intestinal │ │ │ │ cestodes. Syngamus │ │ │ │ in crows. Few │ │ │ │ filaria. Corvus │ │ │ }│ brachyrhynchos│ │ │ │ brachyrhynchos │ │ │ }│ Magpies │ 28│ 18│ 64. }│ Jays │ 41│ 22│ 55.│Periproventricular │ │ │ │ filaria, │ │ │ │ strongylus. Pies, choughs, │ 35│ 12│ 33.│There is a striking etc. │ │ │ │ consistency of │ │ │ │ infestment in the │ │ │ │ different members │ │ │ │ of Corvidæ both as │ │ │ │ regards degree of │ │ │ │ infestment and │ │ │ │ species of │ │ │ │ parasite present. Sturnidæ │ │ │ │ Starlings │ 63│ 19│ 30.│Periproventricular │ │ │ │ filaria largely. Turdidæ │ 25│ 8│ 33.│Periproventricular │ │ │ │ filaria largely. │ │ │ │Thrushes and Robins. │ │ │ │ None in American │ │ │ │ thrushes, one in a │ │ │ │ robin. │ │ │ │Finches. Not │ │ │ │ examined closely │ │ │ │ at autopsy, but │ │ │ │ there is a │ │ │ │ scattering of │ │ │ │ periproventricular │ │ │ │ filaria and │ │ │ │ intestinal │ │ │ │ cestodes through │ │ │ │ most of the │ │ │ │ species. Canaries │ 24│ │ │Were free from │ │ │ │ parasites. Picariæ │ │ │ │ Picidæ │ │ │ │ Woodpeckers │ 4│ 2│ 50.│ Rhamphastidæ │ │ │ │ Toucans │ 30│ 9│ 30.│Spiroptera largely. Striges │ 142│ 2│ 7.│Remarkably free of │ │ │ │ parasites. Psittaci │ [127]774│ 124│ 16.│ Loriidæ │ │ │ │ Lorys │ 24│ 5│ 20.│3 spiroptera, 1 │ │ │ │ hemoproteus, 1 │ │ │ │ intestinal worm. Cacatuidæ │ │ │ │ Cockatoos │ 4│ 2│ 6.│2 spiroptera. Crested Ground │ 45│ 4│ 9.│4 spiroptera. Parrakeet │ │ │ │ Calopsitta novæ- │ │ │ │ hollandiæ │ │ │ │ Psittacidæ │ │ │ │ Old World (Totals)│ 453│ 65│ 14.3│ Undulated Grass │ 121│ 2│ 1.6│1 spiroptera, 1 Parrakeet │ │ │ │ coccidium. Melopsittacus │ │ │ │ undulatus │ │ │ │ Pennant’s │ 21│ 6│ 29.│6 spiroptera. Parrakeet │ │ │ │ Platycercus │ │ │ │ elegans │ │ │ │ Rosehill Parrakeet│ 48│ 21│ 44.│20 spiroptera, 1 │ │ │ │ cestode. Platycercus │ │ │ │ eximius │ │ │ │ Other old world │ 86│ 12│ 14.│12 spiroptera. parrakeets │ │ │ │ Old world parrots,│ │ │ │ lovebirds, │ 74│ 13│ 18.│13 spiroptera. eclectus. │ │ │ │ New World (Totals) │ 321│ 69│ 21.5│ Macaws │ 26│ 9│ 34.│9 spiroptera. Conures │ 62│ 16│ 26.│15 spiroptera, 1 │ │ │ │ hemoproteus, 1 │ │ │ │ blood larva. Amazons │ 164│ 27│ 16.5│24 spiroptera, 3 │ │ │ │ nematodes. Other new world │ 69│ 17│ 10.│7 spiroptera. parrots │ │ │ │ Accipitres │ [127]201│ 13│ 6.7│ Falconidæ │ │ │ │ Buzzards │ 55│ 4│ 7.3│ Eagles │ 44│ 1│ 2.3│ Serpentaridæ │ │ │ │ Vultures │ 29│ 1│ 3.4│ Miscellaneous │ 73│ 7│ 9.6│4 were blood │ │ │ │ protozoa. Galli │ 299│ 42│ 14.│ Phasianidæ │ │ │ │ Pheasants │ 95│ 20│ 21.│Heterakis in ceca. Partridges │ 14│ 3│ 21.│ Quail │ 70│ 10│ 14.│Heterakis. Megapodidæ │ │ │ │ Wild Turkeys │ 39│ 7│ 18.│Intestinal cestodes. │ │ │ │ Coccidia twice. Columbæ │ [128]163│ 14│ 9.│Mostly intestinal │ │ │ │ cestodes, but │ │ │ │ several │ │ │ │ spiroptera. Fulicariæ │ [128]38│ 7│ 18.│ Alectorides │ [128]41│ 10│ 25.│ Gaviæ │ [128]21│ 3│ 14.│ Steganopodes │ [128]22│ 1│ 5.│ Herodiones │ [128]105│ 21│ 20.│ Anseres │ [128]319│ 28│ 8.8│ Swans │ 48│ 7│ 14.│No significant │ │ │ │ groupings. │ │ │ │ Parasites │ │ │ │ scattering. Few │ │ │ │ intestinal │ │ │ │ cestodes. Geese │ 83│ 13│ 15.6│ Ducks │ 188│ 8│ 4.│ Struthiones │ 36│ 1│ 2.8│ ──────────────────────┴───────────┴────────┴──────────┴────────────────────

Nor do all members of a genus necessarily show the same susceptibility, and the heterakis infestment in the pheasants illustrates this matter very well. It was limited almost entirely to two species—Amherst’s and Golden, whereas several frequently exhibited species showed none. The following table brings this out in more detail:

TABLE 25. _Heterakis in Pheasants._ ════════════════════════════════════════════╤════════╤════════╤════════ Species │ Total │Infested│ Per │ │ │ cent. │ │ │infested ────────────────────────────────────────────┼────────┼────────┼──────── Golden Pheasant (Chrysolaphus amherstiæ) │ 18│ 12│ 67 Amherst’s Pheasant (Chrysolaphus pictus) │ 16│ 5│ 31 Silver Pheasant (Gennæus nycthemerus) │ 19│ 1│ 5 Reeves’ Pheasant (Phasianus reevesi) │ 16│ 1│ 6 Ringnecked Pheasant (Phasianus torquatus) │ 12│ 0│ 0 Swinhoe’s Pheasant (Gennæus swinhoii) │ 10│ 0│ 0 ────────────────────────────────────────────┴────────┴────────┴────────

Enzoötics and environment played no part in the above figures. We have had no real heterakis enzoötics, for in but two instances did three heterakis deaths occur in a year, and two deaths per year have occurred in but four instances in the past twenty years. During this time there have been sufficient animals on exhibition and subjected to autopsy to indicate definitely that the two species named—Amherst’s and Golden, must be considered as more susceptible than the other varieties. Nearly all of the heterakis in quail likewise occurred in one species—seven of the ten cases occurred in a total of twenty-three Scaled Quail—but in these birds the infestment appeared in enzoötic form and cannot be viewed as indicating a preference for a species.

Psittaci are on the whole, not susceptible to worms. It is true that we suffered a serious outbreak of spiropteriasis a few years ago, but if we consider this a closed chapter we can accept the above generality as stated. Among 774 parrots autopsied we have encountered but one cestode and three intestinal round worms.

The deer, likewise, are singularly free from intestinal parasites. I gave the detailed records of these animals in Table 24 to emphasize the scarcity of parasites even when fairly numerous specimens had been available for examination.

Other interesting features in the table are the outstanding infestments of squirrel monkeys and marmosets among the monkeys, of gastric and intestinal worms in the wild cats, and intestinal worms in the zebras.

The foregoing has had to do with parasitism from the standpoint of the host. The next phase, that of the individual parasite itself, interests more the strict parasitologist than the general zoologist; however, both will see how it may have a very practical value.

TABLE 26. _Distribution of Parasitic Cases According to Parasitic Groups._ ═════════════════════════════════════╤════════════════╤════════════════ Nematodes │ 183[129]│ Spiroptera │ 145│ Filaridæ │ 138│ Ascaris │ 30│ Physaloptera │ 28│ Uncinaria │ 25│ Tropidocerca │ 23│ Heterakis │ 22│ Trichocephalus │ 11│ Syngamus │ 9│ Trichina │ 2│ Hepaticola │ 2│ Other Miscellaneous │ 4│ Total Nematodes │ │ 622 Cestodes │ 165[129]│ Echinococcus │ 9│ Cysticercus │ 7│ Tænia │ 4│ Miscellaneous │ 3│ Total Cestodes │ │ 188 Trematodes │ │ 22 Acanthocephalus │ │ 4 Protozoa │ │ 14 Arthropods │ │ 6 Unclassified │ │ 34 ─────────────────────────────────────┼────────────────┼──────────────── Grand Total │ │ 890 ─────────────────────────────────────┴────────────────┴────────────────

INCIDENCE ACCORDING TO PARASITIC GROUPS.

Inasmuch as it has been physically impossible to determine specifically and classify efficiently the accumulations of verminous material from our autopsies I will not be able to tabulate parasitic groups even as closely as I did in the “animal host” table. Nevertheless sufficient has been done to illuminate in part certain phases of parasitism and to prevent a summary dismissal of the subject. Reviewing our cross index I have distributed the data into the following Table 26, the parasites being listed in the order of their frequency. It may serve only as a panorama of the situation, inasmuch as determinative study of a group amounts to a research in itself, and the multiplicity of them precludes a consistent study of every one. The data are based upon “cases of parasitism.” That is, each and every worm species occurrence has been counted, regardless of whether it was the same species that has been concerned over and over again, or in different anatomical positions (of different individual hosts, of course) or whether it was in association with other parasites.

ANALYSIS OF TABLE 26.

There is a grand total of 890 cases of animal parasitism embraced in the above table, which is a sufficiently large number to give representative value to some phases of the analysis.

In the first place nematode worms occur about three times as frequently as all other forms of parasites. In gardens where spiroptera has not figured so largely the proportion might be reduced to about two to one. Cestodes rank a poor second, trematodes a worse third, and acanthocephali a very bad last. This order agrees with our figures of 1913[130] and with the small series of Nicoll.[131] The latter worker found that the order was not changed when pains were taken to include also such smaller worms as could only be obtained from the host by using sieves, etc. Cestodes were not likely to be overlooked, but very small trematodes and nematodes were easily passed over.

VISCERAL DISTRIBUTION.

As to the individual organs which are most commonly parasitized our records show that with Aves as well as Mammalia the intestines are the parts most commonly affected. The stomach ranks second for both—the proventricle rather than the gizzard of birds corresponding, parasitologically speaking, to the stomach of mammals. We have found but one parasitic species in the gizzard of birds, _i.e._, immature forms of _Spiroptera incerta_ lying under the chitinous lining of the gizzard and only discoverable after the lining has been peeled off. The peritoneum comes third (air sacs of birds) due to the presence of filaridæ, and the blood fourth for the same reason. It is to be emphasized that, in our data, identical organs of mammals and birds should be about equally liable to infestment with the possible exception of the lungs. But in view of the small number of cases available there is no justification for speculating about the reason for this last difference, albeit the radical difference in the anatomy of the two classes is very inviting.

Now that our spiroptera enzoötic has subsided, the order above given will be changed, and in view of like disturbing factors other gardens should not expect the same order to hold invariably for their collection, since their enzoötics will depend somewhat on the preponderance of animals of one or another family which are likely to compose their exhibits. A single such enzoötic may suffice to disarrange the whole fabric, and if two or three are taken into account the order of organ involvement can be quite disrupted. To attempt to construct statistically an “order of frequency involved” which would stand for every garden would only lead to interminable adjustments on the basis of animals exhibited and of parasitic enzoötics, so that I have finally been reduced to a combination of our Garden statistics and the bloodparasitic ones of the London Garden. Doing this I have arranged in Table 27 the frequency of organ involvement as follows and estimated the percentage of animals infested. These figures are computed upon a different basis from that of Table 24. They naturally cover all animals and not the “susceptible” ones as in Table 24.

[Illustration:

FIG. 73.—HUGELY DISTENDED PROVENTRICLE OF PARROT DYING WITH SPIROPTERIASIS. COMPARE ITS SIZE WITH THAT OF THE HEART WHICH IS ABOVE AND TO THE LEFT, AND THAT OF THE GIZZARD BELOW AND TO THE LEFT. ]

TABLE 27. ═══════════════════════════════════╤═══════════════════════════════════ Mammalia │ Aves ───────────────────────┬───────────┼───────────────────────┬─────────── │ per cent. │ │ per cent. Intestines │ 9.0│Blood │ 6.5 Stomach │ 3.7│Intestines │ 3.5 Peritoneum │ 2.3│Proventricle │ 1.7 Blood │ 1.5│Air sacs │ 1.3 Lungs │ 1.0│Liver │ 0.3 Muscles │ 1.0│Gizzard │ 0.3 Liver │ 0.5│Scattering │ 0.4 ───────────────────────┼───────────┼───────────────────────┼─────────── Total │ 20.0│Total │ 14.0 ───────────────────────┴───────────┴───────────────────────┴───────────

The effect of this is at first sight startling in that it places the blood parasites of birds so far in the fore, but it must be at once recalled that the inquiries upon the blood parasites were much more searching—microscopic, than in the case of the other organs. If similar methods were applied to the others their percentage of parasitism might be notably raised—particularly that of the intestines.

SPECIAL PARASITOLOGIC CONSIDERATIONS.

At this point the statistical considerations of parasitism will give way to descriptions of certain specific infestments that have given us more or less concern.

The occurrence of single parasitic varieties or of well known species in an isolated host may occasionally be of practical importance, but usually they amount to little more than an academic study, whereas the repeated discovery of single parasitic kinds, or infestment of similar hosts, especially when grouped, raises the matter to a very practical level demanding attention. Such findings being not infrequent in our experience, it has been possible to study our material in a manner designed to show the frequency of various parasites in a certain host, the susceptibility of certain animals to parasites in general and the infestment of dissimilar hosts by the same parasite. The more important of these now follow.

AVIAN SPIROPTERIASIS.

This disease concerned parrots particularly but toucans, pigeons, and such widely separated species of birds as the starling, quail, thicknee and barbet have been occasionally affected. To the naked eye the parasite resembles the human hookworm, but differs in location, being a resident of the proventricle where it produces a swelling of the mucosa which interferes with the passage of food. Up to a hundred worms may be present in the one bird, and immature forms are occasionally found under the chitinous lining of the gizzard. The parasite burrows into the mucous membranes, occasionally penetrates quite through the wall into the air sacs, and on one occasion induced an adenomatous hyperplasia of the mucous membrane, and an adjacent “peritonitis.” Mucus is sometimes present in the droppings. Death may occur either acutely, or with emaciation. Spiroptera incerta Smith[132] is the common parasitic species of parrots, but I have found at least one other as yet unidentified species in the toucan, and there are probably more. In the eight year period 1906–1913 from 25 to 50 per cent. of our dead parrots showed this parasite every year, the total loss being 113 birds for this period—a most important infestment.

[Illustration:

FIG. 74.—HISTOLOGIC SECTION THROUGH PROVENTRICULAR WALL OF PARROT, SHOWING SECTIONS OF SPIROPTERA IN THE LUMEN AND MUCOSA. THERE IS SOME GLANDULAR HYPERPLASIA (ADENOMATOID) AND NECROSIS OF THE LUMINAL PORTIONS OF THE MUCOSA. ]

[Illustration:

FIG. 75.—INFLAMMATORY ROUND CELL INFILTRATION AROUND NERVE TRUNK IN WALL OF PROVENTRICLE. PARROT DEAD WITH SPIROPTERIASIS. ]

We approached the problem by diagnosing and isolating the infested birds through a microscopic examination of droppings, finding that by boiling the droppings in 5 per cent. NaOH solution we clarified them and made examination easier and more certain without at the same time destroying the parasitic ova. The result of the examination of all our parrots was the isolation of 14 per cent. of the parrot population; and as these died off the diagnosis of infestment was found confirmed at autopsy in every case. The parrot house was thoroughly renovated and no newly arrived parrots were admitted until after quarantining and examining droppings for ova. The toucans and other species, being housed elsewhere, were not quarantined. Following this, we were gratified to experience no more spiroptera deaths in parrots for seven years. Then, in 1920 and 1921, a new outbreak occurred in four toucans and several other scattering species, including two parrots; but none of these came from the main parrot house and probably represented a fresh importation. We attempted to cure the isolated verminous birds by medication but were unsuccessful. Likewise attempts at determining the life cycle of the parasite brought us no farther than that the ova developed larvæ in moist sand in six days. Feeding of ova, freshly passed and larvated did not produce infestment in parrots or pigeons. On the whole we can quote our experience with spiroptera as a most satisfactory example of the value of hygiene and as a result which could never have been accomplished by medication.

HEPATICOLA (TRICHOSOMA) HEPATICA IN PRAIRIE DOGS.

Bancroft[133] and Hall[134] have given us details concerning this parasite and the disease it causes. It is threadlike, several inches long, and permeates the livers of the gray rat, white rat and wild hare.[135] We first saw it in the more or less cirrhotic livers of several prairie dogs; later we observed it in a beaver and the gray rats of the Garden. In the prairie dogs and beaver the liver resembled that of fatty cirrhosis and was so considered on naked eye examination at our first autopsy. We were only set right when we came to the histological examination. It was remarkable how well conditioned some of the prairie dogs were in in the face of very extensive liver destruction; but on the other hand some were emaciated and a few of the spontaneously diseased showed at autopsy an enormous ascites. The outstanding features at autopsy were the large size of the liver and its pallor and hardness; and fine yellow lines could sometimes be made out twisting over the surface.

The disease affects wild rats differently from prairie dogs. In both the spontaneous and experimental disease the infestment was insignificant, amounting to perhaps three or four foci the size of a split pea near the anterior margins of the liver. Diagnosis may be easily confirmed by crushing the yellow infested portions of the liver between glass slides and examining microscopically for ova.

We have seen such a small number of cases of this disease because so few prairie dogs reach the autopsy table, yet there must be some important mortal factor in our prairie dog enclosure, for the Superintendent states that the population there does not increase in spite of the frequent births and additions from dealers. The animals almost invariably die under ground and their bodies are not recovered.

In order to test out the origin of the infestment we trapped two of our exhibition specimens, and the liver of both was found infested on surgical examination whereas six newly purchased ones had normal livers. The latter were secured fresh from their native habitat in the West, and their livers were examined through long surgical incisions and found free of infestment. Later we fed the ova (embryophores) from rat livers to these prairie dogs and on destroying them found them infested. We were also successful in transmitting the disease in the opposite direction, _i.e._, from prairie dog liver to white rat. From all this we feel sure that the prairie dog disease in our Garden was transmitted from the rat and that here is another reason for rat extermination in a zoological garden.

[Illustration:

FIG. 76.—OVA OF HEPATICOLA HEPATICA IN LIVER OF PRAIRIE DOG. THEY HAVE BIPOLAR OPENINGS. THERE IS DESTRUCTION OF LIVER TISSUE AND A LITTLE INFLAMMATORY REACTION OF CELLULAR CHARACTER, BUT NO IMPORTANT FIBROSIS. ]

[Illustration:

FIG. 77.—UNCINARIA SMITHI COILED IN INTRAHEPATIC BILE DUCTS OF GIRAFFE. NOTE MARKED PERIDUCTAL FIBROSIS IN THE NEIGHBORHOOD OF THE PARASITES. ]

The adult _Hepaticola hepatica_ of prairie dogs I have not seen in sufficient entirety to compare with the rat species and therefore cannot affirm that the two are identical species. It is presumably like that of the rat, being threadlike and most difficult to separate from the liver substance through which it ramifies. At maturity it dies and disintegrates, leaving the ova distributed more or less in tracts through the liver substance, so that we are limited to a certain period wherein to obtain the mature form. The ova are not passed into the intestine, but remain _in situ_, just as in the case of hydatid disease, and therefore diagnosis cannot be achieved by examination of feces. For the disease to be transmitted the host must die and its carcass be eaten or otherwise so disintegrated that the ova are distributed abroad. Another interesting observation is the long incubation period of the ova. Confirming Bancroft, we found that the ova only became larvated after they had lain in water at least three months.

HOOKWORMS.

These important parasites have been taken from several foxes: Gray Fox (_Canis cinero argenteus_), Arctic Fox (_Canis lagopus_), Swift Fox (_Canis velox_), Red Fox (_Canis vulpes pennsylvanicus_), a Gray Wolf (_Canis mexicanus_), divers members of the Felidæ-Eyra (_Felis eyra_), Jaguarundi (_Felis jaguarundi_), American Wild Cat (_Felis ruffus_), Spotted Wild Cat (_Felis ruffus texensis_), Ocelot (_Felis pardalis_), from two Giraffes (_Giraffa Camelopardalis_, _Giraffa capensis_), a Malayan Tapir (_Tapirus indicus_), and a young California Hair Seal (_Zalophus californianus_). It has been a most serious infestment in American wild cats (_Felis ruffus_ and _Felis ruffus texensis_)—animals which generally also harbor other species of worms. In view of the petechial hemorrhages of the intestines and analogous circumstances in dogs and human beings, it must be conceded that this worm is pathogenic.

At this point it is fitting to note the infestment as it affects hair seals. The parasite concerned, _Uncinaria lucasi_, has long been a scourge among the fur seals (_Otoes alaskanus_) of the Pribiloff Islands. Its punctures are bloodless, being signalized instead by small edematous plaques in the intestinal mucosa, The animal we autopsied was a young California Hair Seal born in the Garden, and is singularly the only hair seal in which we have seen it. The natural habitat of the hair seal is the coast of California which means that the range of _U. lucasi_ may extend farther southward than at first suspected. We have none of the northern variety.

I point out two giraffe cases only because they are unique as to the organ (liver) affected. So far as I know, mature hookworms have never been reported from other organs than the intestines.

From the prophylactic standpoint it will be advisable to have as little moist earth as possible, particularly sandy ground, in and around the enclosures for the above mentioned susceptible animals because it is in such soil that the earlier stages of the life cycle of the parasite are passed.

We have never found any of the human hookworm species in our animals, but it must be recognized that transmission is possible to a certain degree. _Anchylostoma ceylanicum_ Lane[136] was found in man, cats, dogs, and a lion; Leiper[137] reports _A. duodenale_ in a dog, and von Linstow[138] states that the latter parasite also occurs in the chimpanzee.

AMEBIC DYSENTERY IN MONKEYS.—We recently lost six monkeys in a small outbreak of this disease—four black spider monkeys (_Ateles ater_), a Pinche marmoset (_Leontocebus edipus_), and a woolly monkey (_Lagothrix lagotricha_). Except for non-characteristic looseness of stools, there were no symptoms until the usual terminal lethargy set in. Living amebæ were found in feces. At autopsy only the colon was found to be anatomically affected. It was hugely distended, fully an inch in diameter, and there were numerous confluent ulcers of the mucosa covered by a thick slough. The liver showed no abscesses. In the histological sections amebæ were found in the interstices of vital gut tissue just as they are in corresponding human lesions. I have not diagnosed the species yet, but can vouch that it is not _Endameba histolytica_ or _coli_.

[Illustration:

FIG. 78.—MICROSCOPIC SECTION OF LIVER OF GIRAFFE, SHOWING SECTIONS OF UNCINARIA SMITHI IN BILE DUCT AND MARKED FIBROSIS AROUND THE DUCT. ]

[Illustration:

FIG. 79.—COLON OF MONKEY DYING WITH AMŒBIC COLITIS. HIGHLY ELEVATED SLOUGHS COVER THE ULCERS. ]

According to Leidy’s recommendation, grated nutmeg was administered and was followed by an improvement in symptoms. The animals became brighter and the stools firmer, but the amebæ were not eradicated. Emetin hypodermically and by mouth had no obvious effects on the disease or the amebæ. One monkey thus treated with nutmeg recovered, but died the next year of another affection and disclosed the scars of the old ulcers in the colon. Our experience with this disease, however, is not unique. At Washington, D. C.,[139] eight spider monkeys were affected, and sporadic cases come to light from the West Coast[140], Manila, Khartoum and Ceylon. Prowazek’s report concerned a young orang[141]. Liver abscesses in addition to the intestinal lesions were found by three different observers.

As to the transmissibility of monkey amebiasis to man, reporters are divided. Both sides are probably right, in as much as _Endameba histolytica_ was concerned in some cases and non-human species in others. It is an infestment to be feared, and calls for examination of stools from such newly arrived animals as are known to be susceptible (spider and woolly monkeys, orangs).

PARASITES OF MARMOSETS AND SQUIRREL MONKEYS.—I give a special place to this subject because Table 24 shows that these monkeys are so commonly infested and because they are so commonly used as household pets. In this connection the questions arising are, first, whether the infestment is a menace to life, and second, whether it is existent outside the Garden or only acquired here. The following lists set forth the parasitic status as shown at autopsy. The figures indicate how long the animal lived in the Garden:

═════════════════════════════════════════╤═══════════════════════════ Marmosets │ Squirrel Monkeys ─────────────┬───────────────────────────┼─────────────┬───────────── Infested │ Not infested │ Infested │Not infested ─────────────┼───────────────────────────┼─────────────┼───────────── 1 day│ 6–15 days ( 4 animals)│ 2 days│ 3 months 1 day│ │ │ 2 months│ 1 month ( 6 animals)│ 14 days│ 3 months 6 months│ 3–5 months ( 9 animals)│ 26 months│ 5 months 12 months│ 6 months ( 2 animals)│ │ 14 months 12 months│ 7 months ( 2 animals)│ │ 15 months 12 months│ 8 months ( 1 animal)│ │ 13 months│ 9 months ( 2 animals)│ │ │ 10 months ( 1 animal)│ │ │ 12 months ( 1 animal)│ │ │ 14 months ( 1 animal)│ │ │ 15 months ( 1 animal)│ │ │ 17 months ( 1 animal)│ │ │ 18 months ( 2 animals)│ │ │ 20 months ( 1 animal)│ │ │ 21 months ( 1 animal)│ │ ─────────────┼───────────────────────────┼─────────────┼───────────── Totals 8 │ 35 animals│ 3 animals│ 5 animals animals │ │ │ ─────────────┴───────────────────────────┴─────────────┴─────────────

Reverting to the questions above raised, the data show that some of the animals were certainly infested on arrival here, and that others probably were; but since these animals were not examined for parasites on arrival in the Garden the duration of infestment remains unknown, and accordingly we are not justified in going farther in our conclusions. In the case of the marmosets, though, if we confine ourselves to the non- parasitized animals, it would appear that the “acclimatization” period is within the first six months. I have attempted to arrive at a conclusion on this basis, but the average lifetime of the four parasitized marmosets which survived this period is the same as that of the sixteen non-parasitized survivors, and we do not know at what time the parasitized ones contracted the disease.

[Illustration:

FIG. 80.—ARACHNID (PNEUMONYSSUS FOXI) IN LUNG OF ADULT MONKEY (MACACUS RHESUS). IT OCCUPIES THE CENTRE OF A CYST WHICH IMMEDIATELY UNDERLIES THE PLEURA SEEN AT UPPERMOST PART OF THE ILLUSTRATION. ]

CYSTICERCUS TENUICOLLIS.—We have noted this bladder worm in the Aoudad (_Ovis tragelaphus_), Red River Hog (_Potamochœrus porcus_), domesticated Angora Goats and several deer (_Cervus alfredi_, _Capreolus capreolus_, _Mazama mexicana_, _M. hemionus_) located with one exception in the peritoneal cavity or membrane. One of the mule deer (_Mazama hemionus_) exhibited the parasite also in the lung and liver. This parasite is discussed because the very valuable Philippine spotted deer (_Cervus alfredi_) died from a peritonitis secondary to an infected cyst in the lesser omentum, and because the parasitism (_Tænia marginatum_) is contractible from canidæ which are also on exhibition in the Garden. It happens that the spotted deer did not become infested from the dogs, but it is quite probable that the goats did, since they passed many times daily in front of the wolf cages, drawing the children’s carriages over the walks, and were stabled nearby. We have not discovered any of the other tapeworm cysts in deer which might be transmitted to them from the canidæ. Camels which are parked directly opposite them have only exhibited echinococcus cysts, yet we have never found its adult form (_Tænia echinococcus_) or its ova in the canine feces. The danger of fatal disease from _C. tenuicollis_, even though the infestment be present, is remote; but we feel that it is better, if possible, not to exhibit the canidæ adjacent to susceptible animals.

PULMONARY ACARIASIS IN MONKEYS.—We have seen but two instances of this affection in the Philadelphia Garden. The offending parasite in our animals was a new species, _Pneumonyssus foxi_ Weidman[142]. It occurred sparingly in small cysts under the pleura and was certainly benign in our cases. The importance of the infestment consists in part in that these lesions may be mistaken for tubercles.

At the London Gardens[143] acariasis was found in forty-four young rhesuses dying of pneumonia, and the observers ascribed the inflammation to irritation of certain doubly refractile crystals which occurred in the excreta of the mite. There are four other recorded instances of such disease in monkeys, all caused by different species of parasites.

As to pathogenesis of these arachnids, the London experience is most illuminating in that it was young rhesuses that were affected. Our specimens were mature, and nothing was stated to the contrary in the other reported cases from various parts of the world. The parasites are perhaps inhaled from the straw used as bedding, since such vegetable material is a common habitat for mites. If the resultant acute pneumonia is weathered the relics might remain only in the form of the subpleural and parabronchial cysts such as we have seen at the Philadelphia Garden.

I am the more willing to accept the possibility that the simian arachnids can induce an acute pneumonia after studying a very definite case of bronchopneumonia in a prairie dog, which was induced by _Cytoleichus penrosei_ Weidman 1916.[144]

PERIPROVENTRICULAR FILARIDÆ OF BIRDS.—Every year we report a number of cases (up to twenty-three) of these worms, probably several species, coiled under the serosa of the air sacs and most commonly around the proventricle. Tentatively we have recognized two forms, a shorter (an inch or so long) and a longer (three to four inches). The latter is most inextricably coiled, but the former may be teased out. Microfilaria occur in the blood of the latter cases, but not in that of the former. The adults have been observed to penetrate from their position in the air sac serosa into the lumen of the proventricle (goose), to have caused rupture of the inferior cava (bulbul), to be associated with subserous cysts of the intestine (weaver) and with profound anemia (liothrix). The birds affected are mostly small, inexpensive ones, but the infestment is important because of its frequency and deserves study of the means of transmission.

[Illustration:

FIG. 81.—ARACHNID (CYTOLEICHUS PENROSEI) IN A BRONCHOPNEUMONIC FOCUS IN THE LUNG OF A PRAIRIE DOG (CYNOMYS LUDOVICIANUS). ]

[Illustration:

FIG. 82.—FILARIAL WORM COILED NEAR PROVENTRICLE OF A FINCH. ]

PHYSALOPTERA IN OPOSSUMS AND BADGERS.—These worms were frequent findings for a period of years and were particularly impressive on account of the large number of parasites present. The stomach often contained scores, more or less securely attached to the mucosa by the head. The worms average an inch or two in length and perhaps an eighth of an inch in thickness. _P. turgida_ is the only species we have identified (three examinations). As to pathogenicity we have not observed that definitely constant lesions are induced by the parasites. In several instances the gastric mucosa has shown the mosaic appearance indicative of chronic gastritis, a condition not necessarily incited by, but certainly aggravated by, these worms; at least significant is the habit of the worm to imbed its head in the gastric mucosa. In one instance the microscope has revealed a most severe fibrosis of the submucosa. The fibrosis was not so much diffuse as it was local or nodular, and in favorable places the ova of physaloptera could be discovered in the centres of the nodules, and thus betrayed the previous presence of the adult worm there. In this individual animal the case against the physaloptera is clinched by direct evidence. In other cases we have circumstantial evidence. Whereas it is not a deeply burrowing parasite, it is still a penetrative one, and this is sufficient to compromise the all important “integrity of the mucosa.” It should therefore be considered pathogenic in all cases, because open to suspicion in several directions—abstraction of tissue juices, irritation by its products or movements and by opening up an avenue for bacterial infection.

TROPIDOCERCA IN BIRDS.—This is a blood-red nematode of the size of a mustard seed to that of a peppercorn which inhabits the depths of the proventricular mucosa. At first sight its spheroidal form suggests that of a fluke, but under the microscope it is found to be a nematode hugely ballooned out by ova, and coiled up into a ball. In spite of its dangerous appearance—being red—it is most likely quite innocuous, for microscopic sections show no sign of inflammation around the worm. Moreover, we know that a Concave Casqued Hornbill (_Dichoceros bicornis_) now on exhibition has harbored the worms, as indicated by ova in the droppings, for eight years and yet seems perfectly well. I have made wax reconstructions of three of the worms and find that the coils are not very intricate and that they assume no regular or constant arrangement.

SYNGAMUS TRACHEALIS.—Our worst experience with this picturesque parasite was in common crows (_Corvus b. brachyrhynchos_). In 1914 and 1915 alone we lost five such birds. Some geese, swans and a pheasant complete the short list of birds affected in addition to the crows. In no case was it a young bird that was affected. Shipley[145] reports this parasite in two grouse at the London Gardens, and Plimmer’s tables show that three deaths were directly charged against them in one year[146].

EXTRA-INTESTINAL TAPEWORMS.—This discovery is worthy of record because it is rare for cestodes to appear anywhere save in the intestines. We have observed three instances where they had backed up into the bile duct—twice in the Cape Hyrax (_Procaria capensis_) and once in a Livingston’s Eland (_Taurotragus oryx livingstonii_). At the London Gardens they were mentioned in the gall-bladder of a wallaby and in Cape Hyraces. Beddard[147] carefully describes four new species of these cestodes from the hyrax.

[Illustration:

FIG. 83.—PHYSALOPTERA IN STOMACH OF COMMON OPOSSUM (DIDELPHYS VIRGINIANA). THIS IS NOT AN EXCEPTIONAL DEGREE OF INVOLVEMENT. ]

[Illustration:

FIG. 84.—ONE OF THE FIBROUS NODULES IN THE GASTRIC SUBMUCOSA OF AN OPOSSUM. AN OVUM OF PHYSALOPTERA IS SEEN PRECISELY IN THE MIDDLE OF THIS ILLUSTRATION. ]

TABLE 28. _Occurrence of Blood Parasites._ (Adapted from Plimmer, nine year period) _Animals examined—12,241 Mammalia—2,924 Aves—6,619 Reptilia—2,698._ ══════════════════════════════════╤══════════════════╤════════╤════════ Parasite. │ Host │ No. │ % │ │Infested│Infested ──────────────────────────────────┼──────────────────┼────────┼──────── 1. Hemogregarines │Reptilia │ 316│ 11.8 2. Microfilaria │Mammalia │ 33│ 1.1 │Aves │ 191│ 3. │Reptilia │ 24│ 1. 3. Hemoproteus │Aves │ 140│ 2.1 4. Trypanosomes │Mammalia │ 1│ 0.003 │Aves │ 28│ 0.4 │Reptilia │ 4│ │Amphibia │ 3│ 5. Plasmodia │Mammalia │ 2│ │Aves │ 39│ 0.6 │Reptilia │ 5│ 6. Leucocytozoa │Aves │ 16│ 0.2 7. Intestinal organisms[148] │Reptilia │ 16│ 0.5 8. Toxiplasma │Mammalia │ 1│ │Aves │ 1│ │Reptilia │ 1│ 9. Spirochæta │Mammalia │ 1│ 10. Babesia │Mammalia │ 1│ 11. Hæmocystidium │Reptilia │ 1│ ──────────────────────────────────┼──────────────────┼────────┼──────── Grand Total │ │ 824│ ──────────────────────────────────┴──────────────────┴────────┴────────

SUMMARY OF TABLE 28. ═══════════════════════════════════╤═══════════╤═══════════╤═══════════ │Parasitized│ Animals │ % │ │ examined │Parasitized ───────────────────────────────────┼───────────┼───────────┼─────────── Mammalia │ 39│ 2,924│ 1.5 Aves │ 415│ 6,619│ 6.5 Reptilia │ 367│ 2,698│ 14.0 ───────────────────────────────────┼───────────┼───────────┼─────────── Total │ 821│ 12,241│ 6.7 ───────────────────────────────────┴───────────┴───────────┴───────────

FILARIASIS IN WILD CATS (_Felis ruffus_).—This parasite was named _Filaria fasciata_ because it coils in the fascia between the muscles— generally those of the thigh and abdomen. The worms are easily detected on skinning the animal and separating thigh and other muscles. Microfilaria were always present in the blood. The grade of pathogenicity is only conjectural.

PERITONEAL FILARIA IN MONKEYS.—Thread worms have been encountered eleven times, largely in Cebidæ. In several instances _F. gracilis_ has been the species identified, always inhabiting the peritoneal cavity, and in one instance also the lung. Microfilaria were always present in the blood. We have never seen lymphangitis or elephantiasis in our filarial cases.

BLOOD PARASITES.—I justify this paragraph on the basis of the usefulness it might have in the clinical direction, for while the taking of blood specimens is not as easy as with man it can still be done with some animals. From time to time we have encountered blood parasites in this Garden, but the large numbers occurring in the experience of special searchers in the London Garden and Plimmer’s particular interest in this direction make their data much the more valuable. In one report of 6,430 animals examined he found 7 per cent. infested with blood parasites of one sort or another. I have constructed the foregoing table (28) from his various reports to show which animal classes were affected by the several blood parasites.

This table (28) brings out that considering them as a whole and without respect to host, just as the animals come day in and day out to the autopsy table, blood parasites will be met in 6.7 per cent. of all cases. They are seen most commonly in the form of hemogregarines of reptiles (2.5 per cent. of all animals and 12 per cent. of all reptiles) while microfilaria run a close second, being found in 2 per cent. of all animals but much more commonly in birds. Hemoproteus of birds while ranking third, should be emphasized on account of its acknowledged blood-destructive properties. The remaining infestations were too infrequent to be useful statistically.

Turning to individual groups of blood parasites, microfilariæ of birds deserve special comment. They occurred four times more often in birds than in other animals, or, put in another way, one out of every twenty- two birds was affected, and only one out of every ninety other animals. The high figure for birds is significant in relation to what we have already said about periproventricular filaridæ in our Garden, indicating that the same infestment probably also exists in London.

[Illustration:

FIG. 85.—ADAPTATION FROM RECONSTRUCTION OF TROPIDOCERCA CONTORTA. THE WORM LAY IN THE WALL OF THE PROVENTRICLE OF A LOUISIANA HERON (ARDEA TRICOLOR RUFICOLLIS). ]

[Illustration:

FIG. 86.—CESTODES (THREE) PROJECTING FROM THE SEVERED END OF THE BILE DUCT OF A CAPE HYRAX (PROCARIA CAPENSIS). ]

A point brought out by Plimmer is to the effect that, of the several blood parasites, the microfilariæ were the least harmful, and that of these the adult forms were the only ones to produce symptoms; yet in one place[149] he records microfilaria as plugging the cerebral capillaries of birds. This is a very important lesion if permanent, and especially so when affecting cerebral capillaries as do the organisms and pigment of malaria. The adult forms were found in one-fourth of the cases where microfilaria were demonstrated.

As to the pathogenicity of these blood parasites in general, it will be unsafe to arrive at a definite conclusion, recalling the pitfalls that I have already outlined in discussing pathogenicity of parasites in general. Keeping in mind the wonderful adaptability on occasion of animals to unfavorable circumstances we must hesitate to declare unqualifiedly the importance of even blood parasites as morbid agents. Where the parasite is known to destroy the blood cells of birds and mammals it is otherwise, but even here experimental work would be necessary to settle the question. The element of “racial” immunity and of phylogeny is the fly in the ointment of our deductions.

TRANSMISSION OF ANIMAL PARASITISM FROM WILD ANIMALS TO MAN.

Examples of direct transmission will be only occasional, due to the relatively infrequent contacts between the two hosts. Pets threaten the most. Several such examples have been touched upon in the preceding pages and it but remains to gather them into one place. There is one concrete instance in the form of clear cut simian scabies being transmitted to a keeper in this Garden[150] and a similar lot fell to the keeper of a wombat at the Paris Garden[151] as well as to the taxidermist who preserved its skin. We know that the skin and feathers of our parrots and pigeons harbor mites[152] (plumicoles of Megnin) and, recalling the occasional cases of poultrymen’s itch, a transient affection might be conceded from pet parrots and other birds. Pediculi are not as numerous on monkeys as popularly supposed—we see very few at the autopsy table. We have seen _Trichinella spiralis_ in the polar bear (_Ursus maritimus_)—an animal whose flesh is edible. The hydatid cysts in the camel appear unimportant, but in the livers of deer it is otherwise. Neither of these infestments is dangerous if the meat is sufficiently cooked before eating.

Hookworm disease points thus far only to _Anchylostoma duodenale_ in the chimpanzee and _Uncinaria ceylanicum_ in the lion and tiger. Both serve as reservoirs of the disease, the ova being discharged by way of the feces. Similarly the _Strongyloides intestinalis_ infestment which we have seen in the orang might be transferred to man. Indirectly, Europeans traveling in Africa have made the crucial test that certain ungulates and other wild animals of Africa are the reservoirs of _Trypanosoma gambiense_, the parasite of the well known African sleeping sickness; for this example the blood stream of the beast is the reservoir and a biting insect the means of transmission.

The above examples are cited to emphasize the possibility that parasites of wild animals may have a pathogenic significance for man. They do not exhaust the subject. Many more instances might be cited but the foregoing bring out the important ones which have come to our attention.

TREATMENT.

The recognition of the existence of parasites during the life of an animal, especially those of the skin and intestinal tract whose discovery is easiest, suggests that some means of combating them should be employed. But we are by now quite satisfied that medicinal and disinfective therapeutic procedures, while they have their field of usefulness, are much less to be depended upon for the protection of exhibits than are preventive measures of general hygienic nature. Under the latter heading come the prompt removal of excreta, frequent changes of drinking water, routine examinations of feces of certain varieties, autopsy examinations and incineration of autopsy remains—all of which are part of the requirements of common cleanliness and general disease prevention. I wish to amplify the matter of disposal of feces and general cage-police. Our ideas as to what constitutes thoroughness in this work have changed considerably since Fulleborn’s recent demonstration that ascarid ova[153] could live in formaldehyde for four or five years, and the older one of Galli-Valerio[154] that those of _Hepaticola hepatica_ lived one month in 2 per cent. formaldehyde solution. Evidently the same substances which disinfect do not invariably disinfest; and if the occasion should arise for the most exacting control in this respect, a special investigation of the susceptibility of the individual ova in question would have to be undertaken.

In addition to these general measures we have put up certain special safeguards against parasites. Thus, each specimen of the large Carnivora (lions, tigers, leopards, etc.), has received routinely a dose of santonin every month over a period of several years. We have no figures on which to base comparison with previous periods, but an examination of feces of all the inmates of the Carnivora house in 1916[155] showed that less than one-third of the animals were infested, and of these all save the jaguars showed either small numbers of ova in the feces or relatively non-pathogenic forms. The jaguars had been badly infested for many years with dibothriocephalus. Prior to this examination we had been under the impression that nearly every one of the felidæ ordinarily was infested and if this impression was well founded, due credit must be given, in company with general hygienic precautions, to the routine santonin dosages. It goes without saying that where animals are detected at autopsy with unequivocal transmissible and dangerous parasites (coccidia, amebæ, etc.), the contacts are isolated, examined and if necessary treated for the affection or even sacrificed.

To continue the preventive measures, it would be most desirable to examine at least the blood and feces of all newly arrived animals, but at present this is not practicable on account of the labor involved in the laboratory and in collecting the material, and because all animals do not stand the restraint involved when blood specimens are being taken. At present we are limiting special examinations to the droppings of newly arrived parrots and toucans for _Spiroptera incerta_ and to the feces of certain monkeys for amebæ.

Further preventive measures will depend on the nature of individual infestments as they crop up. Food inspection, screening, sulphur dips, etc., are but a few examples of what might be found necessary hygienically after investigating or establishing the life cycle of our numerous parasitic groups. However we cannot forbear to emphasize again the value of the blast lamp and of paint in the hygiene of animal enclosures—means we believe to be much more potent and quite as practicable as chemical disinfectants.

[Illustration:

FIG. 87.—TRICHINELLA SPIRALIS IN MUSCLES OF POLAR BEAR (URSUS MARITIMUS). THIS WAS AN OLD INFESTMENT, AS INDICATED BY THE THICK AND HYALOID CHARACTER OF THE CAPSULE. ]

Turning now to the active curative side of the subject, what medical means we have against parasites appertain for the most part to the intestinal ones. The treatment of tapeworms is very hazy and unsatisfactory—areca nut is perhaps more useful in animals than any one other drug. For round worms santonin is most to be depended on although turpentine is useful against the round worm of the Equidæ. The dosage of santonin per month has been—for large bears, ten grains; for lions, tigers, large pumas, six grains; for jaguars, leopards, hyenas, four grains; for wild cats, etc., two grains. The dose of areca nut recommended for Carnivora is two grains per pound of body weight. Since ungulates do not stand areca nut well, iron sulphate may be used. For animals the size of a horse the dosage is two drams, and to this one or two grains of arsenic trioxide may be added. On the basis of very carefully controlled experiments on dogs, Hall recommends carbon tetrachloride for hookworms in these animals—0.3 mils per kilo of body weight, without purging. Its efficacy has been confirmed lately but we have not had the occasion to test it.

From time to time we have broached other lines of medication against worms which may be worth while relating if for nothing more than to illustrate the uncertain ways of our vermifuges when applied to wild animals.

I can speak first of thymol as employed on parrots parasitized by _Spiroptera incerta_. The first thing that impressed us was the large dosage which birds could endure. The lethal dose for pigeons was four grains, suspended in mucilage of acacia. After we had established that certain parrots withstood fourteen grains in mucilage, we administered on one occasion twelve grains and on another sixteen grains, suspended in glycerin. The drug is reputed to be absorbed when exhibited in the latter vehicle and we hoped to get a certain anthelmintic effect on the parasites from the blood side as well as from the lumen of the gut. The bird itself, a very heavily infested cockatoo, showed no ill effects and passed two dead female spiroptera and enormous numbers of ova. But thereafter it passed even greater numbers of ova than before (we estimated 182,000 per day for this bird over a five day period and 288,000 on a single subsequent day), and was obviously unimproved by the treatment. The explanation of failure was clear, for the worms can retire into the protecting mucus or mucous membrane lining the proventricle until the thymol has passed by, and even though paralysed may not be flushed out. In a later test on a toucan which died twenty minutes after thymol administration we found at the autopsy that worms deeply imbedded in the proventricle were translucent and motionless from the effects of the thymol-glycerin mixture, _i.e._, saturated with the medicament and apparently dead. Twenty minutes later they were placed in normal salt solution in the incubator, and next morning were found actively motile. Thymol evidently does not kill—it only stupefies, and in the absence of means for flushing the parasites out, as we do in human hookworm cases, this class of vermifuge will have to be abandoned in work against this parasite.

Not with any serious hope of success, but feeling that arsenic was the most promising drug available for parenteral use, we tried atoxyl hypodermically and arsphenamine intravenously but without success. The only positive results were to emphasize the tolerance of some lower animals to arsenic. Thus in preliminary work pigeons received sixty drops of Fowler’s solution by mouth without embarrassment, but five minims killed a pigeon when administered hypodermically. The organic arsenical, arsphenamine, was withstood intravenously by pigeons in six times the proportional human dosage.

One of our drug trials was instructive in that it worked quite a different effect from that in man, besides being most amusing. In earlier diagnostic work on spiroptera we tested the practicability of examining the vomitus for the worms, hoping thereby to get a greater concentration of ova, which would facilitate the microscopic examination. Hypodermic injections of apomorphine (0.1 grain) into an amazon did not induce vomiting from the gizzard as hoped—only a regurgitation from the crop, but it did cause some dizziness and most ludicrous talking and laughter.

To illustrate further the difficulties of animal medication I quote our experience with four red howling monkeys (_Alonatta seniculus_). One of these died of intestinal obstruction from large ascarids—the case which has been already cited. Ova were found in the stools of the remaining three, and one of the monkeys was treated twice with santonin. It died in thirty hours after the second dose—not of santonin poisoning, for none of the clinical symptoms were present, but most likely from absorption of toxic substances originating in the decomposing ascarids which crowded the gut. It profits not to destroy these parasites, then, unless we feel assured that they may thereafter be removed immediately.

If, for the sake of brevity, I were asked to state in a single sentence the practical status of animal parasitic disease in this Zoological Garden I would put it thus: Since there are various animal parasitic diseases continuously present here of which we know, and since fresh ones are from time to time cropping out, and since these are on the whole of economic importance, it behooves us to continue and extend our efforts against an issue extant—somewhat through therapeutic means, but far more through clinical laboratory examinations, careful autopsy searches, and by rigid general hygienic measures such as cage-police, new quarters, isolation, or if necessary, destruction of the exhibit.

INDEX

Abortion, 305

Abscess of liver, 231 of lung, 155

Acariasis, lungs, 647 of monkeys, 647

Actinomycosis, 138, 568 in deer, 368, 568 tapirs, 568 treatment, 570

Adenoma, 474

Adrenal body, 336

Alimentary tract, 166

Amblyopia, 403

Amœbæ, 606, 644 dysentery from, 644

Amyloid, liver, 227 spleen, 128

Anatomy of labor, 290

Anchylostomum, see hookworms

Anemia, 87 primary, 98 secondary, 88

Aneurysms, 65, 80

Animal Parasitism, hygiene, 656 prevention, 656 treatment, 655

Animal Parasites, 614 disappearance of, 627 frequency, 628 of groups, 633 in blood, 652 incidence, 628–636 modes of action, 617 occurrence in wild, 627 transmission animals to man, 653 visceral distribution, 637

Angina pectoris, 49

Aorta, 72 fatty deposits in, 71

Arteries, 66

Arteriosclerosis, 71

Arteritis, 70

Arthritis, 347 gouty, 347, 411

Ascending nephritis, 276

Aspergillosis, 558

Aspergillus, varieties, 558

Ataxia, 375

Atrophy, acute of liver, 228

Autopsy list, 47

Avian spiropteriasis, 172, 640

Bacterial flora, 418

Basal cell carcinoma, 475

Beriberi, 439

Biliary tract, 225 calculi, 238

Birth canal, 287, 296 comparative anatomy, 287 et seq obstructions to, 306

Blackhead, 206

Bladder, gall, 224, 238, 239 urinary, 286

Blood, diseases of, 83

Blood formation in birds, 98

Blood vessels, 66

Bone marrow, 83, 109, 111

Bones, diseases of, 343 effects of trauma, 343 tumors of, 368

Botryomycosis, 564, 602

Botulism, 604

Brain, 385 tuberculosis of, 378 tumors of, 384 weight of, 385 references to, 387

Breast, 312

Bronchi, 141

Bronchiectasis, 144

Cage palsy, 349

Calculi, biliary, 238 renal, 282

Carcinoma, 476 basal cell, 475

Cataract, 403

Cecum, 211

Cestodes, 637

Cholangitis, 239, 256

Cholecystitis, 239

Choledochitis, 239

Cholelithiasis, 238

Chondroma, 472

Cloaca, 211

Coccidiosis, 606

Cirrhosis of liver, 232

Comparative anatomy of uterus, 287 of pelvis, 297–303

Conjunctivitis, 402

Constipation, 209

Constitutional diseases, 410

Convulsions, 373

Cornea, 403

Coronary arteries, 49

Cowper’s gland, 313

Cretinism, 320, 331

Cysticercus tenuicollis, 647

Cystitis, 286

Cytoleichus penrosei, 647

Deficiency diseases, 438–443

Degenerations of kidney, 269 of liver, 228

Diabetes, 412

Diet, carnivorous, 452 herbivorous, 452 grain, 455 seed, 454 soft, 453 omnivorous, 402 relation to disease, 415 alimentary tract, 417

Dilatation of heart, 54

Diphtheria, 600

Dislocations, 345

Distemper, 599

Diverticula of intestine, 219

Diverticulitis, 219

Dysentery, amœbic in monkeys, 644

Dystocia, 292

Ear, 409

Echinococcus, 647

Emphysema, 161

Encephalomyelitis, 380

Endocarditis, 52

Endometritis, 305

Endothelioma, 165, 474

Enteritis, 177 in Aves, 202, 205 Mammalia, 185

Enterohepatitis, 605

Epithelioma, 475

Esophagus, 169

Exophthalmic goitre, 320, 323, 329

Eye, 402 tuberculosis of, 402

Fallopian tubes, 305

Fat infiltrations of kidney, 268 liver, 226 metabolism, 445

Fibroma, 472

Filaria, fasciata, 651 gracilis in monkeys, 651 in blood, 652 fascia, 651 muscles, 651 wildcats, 651 periproventricular, 648 peritoneum, 651

Food, 415 definition, 415 in relation to alimentary tract, 417

Food, disease, 422 poisoning, 457

Fowl cholera, 598 plague, 598 typhoid, 598

Fractures, 344

Gall stones, 238

Gas-bacillus infection, 602

Gastritis, 204

Gastroenterocolitis in Ungulata, 194 in Marsupialia, 198

Gangrene of lung, 155

Giraffe, hookworm in, 644

Gout, 53, 410

Heart, dilatation of, 54 hypertrophy of, 54 diseases of, 48 effects of, 55 effect of strain, 55–59 weight of, 63 relative vulnerability of, 61

Hemorrhagic septicemia, 598

Hemoglobinuric fever, 603

Hemorrhoids, 218

Hepaticola hepatica, 641

Hepatitis, 228

Hernia, 216

Heterakis in avian ceca, 606

Hookworms, 643, 654 in giraffe, 644

Hypernephroma, 339, 341, 342, 475

Hypertrophic periosteitis, 346

Hyperthyroidism, 320

Hypertrophy of heart, 54 in Aves, 60

Hypothyroidism, 320

Ileus, 213, 261

Infantilism, 433

Infiltrations of kidney, 268 liver, 226

Inorganic salts in diet, 427

Intestinal obstruction, 212 tract, 177 inflammation of, 181 mechanical obstruction of, 212, 617 relation to food, 422

Intestines, diverticula, 219 tumors of, 220

Iridocyclitis, 402

Kangaroo disease, 570 bacteriology, 576, 586 course of attack, 573 pathology, 575 prevention, 572 treatment, 591

Kidney, 263 abscess, 268, 278 calculi, 282 degenerations of, 269 hemorrhages, 271 hypertrophy of, 267 infiltrations of, 268 tumors, 284 weight of, 265

Labor from a comparative standpoint, 290 obstructions to, 306

Laryngitis, 139

Larynx, 138

Leontiasis ossium, 359, 472

Leucemia, 104 in birds, 108 lymphatic, 105 myeloid, 109

Leucocytes, 84–86

Limberneck of ducks, 604

Lipoma, 472

Liver, 222 abscess, 231 acute atrophy, 228 amyloid, 227 cirrhosis, 232 degenerations, 228 fatty changes, 226 infiltration, 226 inflammation, 228 chronic, 232 necrosis in, 230 tumors, 240

Lungs, 146 abscess, 155 congestion, 148 gangrene, 155 infarct, 160 tumors of, 162

Lymphadenitis, 117

Lymphatic leucemia, 105 tissue, 114 hyperplasia of, 115 in pharyngeal wall, 115, 138

Lymph nodes, 114 tuberculosis of, 121 tumors of, 122

Lymphomatosis, 118

Malnutrition, 424

Mammary gland, 312

Marmosets, parasites of, 645

Marrow of bone, 83, 109, 111

Meningitis, 376

Metabolism, carbohydrate, 443 fat, 445 inorganic, 427 protein, 447

Miliary tubercle, avian, 512 bovine, 510 human, 511 monkey, 511

Miscarriage, 305

Molluscum contagiosum, 601

Mönckeberg sclerosis, 74, 76

Monkey’s temperature, 520–528

Moon blindness, 405

Muscles, 370

Mycosis, 137, 558 of esophagus, 168 histology of, 561 hygiene, 563 incidence, 562 of lung, 562 method of action, 560 pharynx, 168, 564 types of, 560

Myelitis, 350, 381

Myeloma, 111

Myocarditis, 52

Myocardium, 49, 50, 65

Myxœdema, 320, 331

Necrosis, liver, 230 spleen, 130

Nematodes, 636

Neoplasms, 462 incidence of, 463, 468 embryonic origin, 471 in captivity, 469 in the wild, 462, 476 metastasis, 471 visceral origin, 477

Nephritis, 271 ascending, 276 effects of, 280 histology of, 279 toxic, 275

Nervous system, 372

Nocardia macropodidarum, 585

Nocardiosis, 570

Obesity, 446

Ophthalmia, periodic, 405

Osteitis, 346

Osteitis deformans, 359, 431

Osteoma, 368

Osteomalacia, 349

Ovary, cysts, 307

Pachymeningitis, externa, 331, 377

Paget’s disease, 359, 431

Pancreas, 244 degenerations, 250 tumors, 259

Pancreatitis, 250

Parasites, see animal parasites, 614

Parovarian cyst, 307

Pasteurelloses, 597

Pearl disease, 491, 501, 505

Pellagra, 441

Pelvis, comparative anatomy, 297–303

Penis, 313

Pericarditis, 53

Pericardium, position of effusion in, 54

Periosteitis, hypertrophic, 346

Periproventricular worms, 648

Perisplenitis, 131

Peritoneum, 260 tumors, 262

Peritonitis, 260

Pharyngitis, 168

Pharynx, 168

Phimosis, 313

Physaloptera turgida, 649 in opossums, 649

Plants, poisonous, 459

Pleura, 163

Pleuritis, 164

Pneumonia, 149 broncho, 152 fibrinous, 151, 153 in Aves, 153 origins of, 154 lobar, 151

Pneumonokoniosis, 159

Pneumonyssus foxi, 647

Poisonous plants, 459

Poliomyelitis, 380

Prostate gland, 313 enlargements of, 314 tuberculosis of, 315 tumors of, 314

Proventricle, 171 worms in, 172, 640

Psittacosis, 208, 597

Pyelonephritis, 277

Quail disease, 608

Rabies, 602

Rachitis, 349, 429

Rectum, prolapse of, 218

Reproductive organs, female, 287 male, 317

Respiratory tract, 134

Rhinitis, 135

Rickets, 349, 429

Renal calculi, 282

Salpingitis fallopii, 305

Santonin, 657

Sarcoma, 471, 474

Scurvy, 440

Seminal vesicles, 315

Sinusitis, 135

Skeleton, 343

Spinal cord, 373

Spiroptera incerta, 638, 640 detection, 640 eradication, 640 in parrots, 172, 208, 640

Spiropteriasis, 172, 640

Spleen, 114, 122 amyloid, 128 congestions, 125 enlargements, 124 hemorrhage, 125 inflammation, 126 in anemia, 130 in hepatic cirrhosis, 130 necrosis, 130 size, 124 tuberculosis of, 132

Squirrel monkeys, parasites of, 645

Starvation, 425

Stomach, 174 tumors of, 176 ulcers of, 175

Streptothricosis, 567

Suprarenal body, 336

Syngamus trachealis, 140, 650

Tænia echinococcus, 647

Tape worms, 637 in liver, 650

Temperature of monkeys, 520–528

Testes, 313 tumors of, 313

Tetanus, 602

Thrombosis, 69

Thymol, 657

Thymus, 120, 336

Thyroid body, 316 atrophy of, 330 hyperplasia of, 325 size of, 318 tumors of, 333

Tonsils, 115, 138

Trachea, 140

Tropidocerca contorta, 649

Tubercle bacillus, types of, 513

Tuberculin test on monkeys, 518 other animals, 549 dose, 529 effect on kidneys, 548 eye, 546 reaction, 530 skin, 546

Tuberculoma, 505

Tuberculosis of brain, 378 avian characters, 503, 512 Carnivora, 498 control, 514–548 diagnosis of, 514 discovery during life, 514 distribution in birds, 504

Tuberculosis of eye, 402 gelatinous, 504 histology, 510 hygiene, 516 in Aves, 503 in Mammalia, 492 in Primates, 492 in various avian orders 506–510 incidence, 489 intestinal in birds, 505 Lemures, 495 lymph nodes, 121, 494 nonsusceptible animals, 490 ordinate characters, 492 frequency, 489 pathological type, 490 Proboscidea, 502 Rodentia, 499 routes of infection, 485

Tuberculosis, sanitation of cages, 516 susceptible animals, 490, 515–517 Ungulata, 500 visceral distribution, 491

Tumors, see neoplasms

Ulcer, gastric, 175

Uncinaria, 643

Uremia, 281

Urethra, 315

Uterus, comparative anatomy, 287 inflammation, 305 tumors of, 308

Vitamins, 438

Waterfowl epizootic, 604

Zoological list, 43

A LIST OF THE PUBLICATIONS FROM THE LABORATORY OF COMPARATIVE PATHOLOGY OF THE PHILADELPHIA ZOOLOGICAL SOCIETY 1909–1923

1. Results of Tuberculin Tests in Monkeys at the Philadelphia Zoological Garden, by C. Y. White, M.D. and Herbert Fox, M.D. _The Archives of Internal Medicine_, December, 1909, Vol. 4, pp. 517–527, Chicago, Illinois.

2. Note on the Occurrence of a Ciliate (_Opalinopsis nucleolobata, n.s._) in the Liver of a Mammal (_Canis latrans_), by Allen J. Smith, M.D. and Herbert Fox, M.D. _University of Pennsylvania Medical Bulletin_, February, 1909, Philadelphia, Pennsylvania.

3. The Tuberculin Test in Monkeys: with Notes on the Temperature of Mammals, by Arthur Erwin Brown, D.Sc., C.M.Z.S., Sec. Zool. Soc., Phila. _Proceedings of the Zoological Society of London_, 1909, pp. 81–90.

4. Observations on the Occurrence of Neoplasms in Wild Animals, by C. Y. White, M.D. and Herbert Fox, M.D. _Proceedings of the Pathological Society of Philadelphia_, February, 1910.

5. Observations on the Comparative Anatomy of the Female Genitalia, by Edward A. Schumann, M.D. _American Journal of Obstetrics and Diseases of Women and Children_, Vol. LXIV, No. 4, 1911, New York.

6. Observations Upon Neoplasms in Wild Animals in the Philadelphia Zoological Garden, by Herbert Fox, M.D. _The Journal of Pathology and Bacteriology_, Vol. XVII. (1912), pp. 217–231. England.

7. A Study of Metazoan Parasites Found in the Philadelphia Zoological Garden, by Fred D. Weidman, M.D. _Proceedings of the Academy of Natural Sciences of Philadelphia_, March, 1913, pp. 126 to 151, Philadelphia, Penna.

8. The Pathology of the Thyroid Gland in Wild Animals, by Herbert Fox, M.D. _Journal of Comparative Pathology and Therapeutics_, Vol. 27, p. 23. Edinburgh, Scotland.

9. The Mechanism of Labor From the Standpoint of Comparative Anatomy, With a Report of Cases of Dystocia in Wild Animals, by Edward A. Schumann, M.D. _American Journal of Obstetrics and Diseases of Women and Children_, Vol. LXIX, No. 3, 1914, New York.

10. Cirrhosis of the Liver in Wild Animals, by Herbert Fox, M.D. _New York Medical Journal_, December 19, 1914.

11. The Dynamics of the Female Pelvis; Its Evolution and Architecture with Respect to Function, by Edward A. Schumann, M.D. _American Journal of Obstetrics and Diseases of Women and Children_, Vol. LXXI, No. 1, 1915, New York.

12. _Pneumonyssus foxi, Nov. Sp_. An Arachnid Parasitic in the Lung of a Monkey (_Macacus rhesus_), by Fred D. Weidman, M.D. _Journal of Parasitology_, September, 1915, Vol. II, pp. 27–45, Urbana, Illinois.

13. _Cytoleichus penrosei_, A New Arachnid Parasite Found in the Diseased Lungs of a Prairie Dog, (_Cynomys ludovicianus_). _Journal of Parasitology_, December, 1916, Vol. III, pp. 82–89, Urbana, Illinois. Fred D. Weidman, M.D.

14. A Method of Obtaining Duplicate Reconstructions from the One Series of Wax Plates, by Fred D. Weidman, M.D. _New York Medical Journal_, March 3, 1917, New York.

15. Papers: Read at the Meeting of the Pathological Society at the Philadelphia Zoological Garden.

Pancreatitis in Wild Animals, by Herbert Fox, M.D.

Report of an Enzootic of Parasitic Proventricular Worms (_Spiroptera incerta_, Smith) of Parrots, with Control of Same, by Fred D. Weidman, M.D.

_Coccidium bigeminum_, Stiles, in Swift Foxes (habitat Western U. S.), by Fred D. Weidman, M.D.

Distribution of Uncinaria Among the Lower Animals, by Fred D. Weidman, M.D.

An Arachnoid (_Pneumotuber macaci_, Landois and Hœpke?) Parasitic in the Lungs of a Monkey (_Macacus rhesus_), by Fred D. Weidman, M.D.

A Note Upon the Lesions of the Female Genitalia in Wild Animals, by Edward A. Shumann, M.D.

Amblyopia in a Young Monkey (_Macacus nemestrinus_), by H. M. Langdon, M.D. and W. B. Cadawalder, M.D.

Remarks on Examinations of a Series of Brains, by W. B. Cadawalder, M.D.

_Journal of Comparative Pathology and Therapeutics_, December, 1915, Vol. XXVIII,