Part 57

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.