Part 54

The animal appeared in generally good condition but close inspection revealed a “running nose,” a purplish mottling along the gingival margin of one lower jaw below which was a doughy swelling; no internal ulceration had appeared nor was there a visible change in the external contour of the jaw. Within a few days a small fusiform lump appeared along the body of the lower maxilla which spread gradually backward, the nearby soft parts becoming involved very shortly. This particular animal died without ulceration but with evidences of septicemia. Usually at the time that the lump is noticeable the animal loses appetite, becomes inactive and seems depressed; no especial change in the coat need be perceptible although it may be lusterless or at times ruffled. In the cases with great involvement of the cervical tissues, dyspnœa is an early sign but I lay this more to pulmonary disease than to mechanical obstruction of the upper air passages. The loss of appetite is in large part due no doubt to the discomfort of chewing and swallowing in the presence of an inflammatory mass in the neck. The eyes usually remain normal until quite late. No change in the character of the droppings is recorded.

A slightly different course is followed by the cases that have the primary lesion in the “hare lip” and nose; from these the masses along the jaw may be entirely missing. After an initial stage of “running nose” with or without swelling of the upper lips and alæ of the nose, the animal rapidly goes down hill, with dyspnœa, loss of flesh, perhaps loose stools, lusterless eyes and a “dead” coat, a series of signs indicative of a septicemic state not pronounced in the first variety; any form of this infection may however present course and pathology of a septicemic character. If the beast live long enough ulceration may appear on the upper lips or a large area of necrosis between them may be discovered.

There have been in our series two cases, believed to be due to the same virus, which gave a picture of septicemia with pulmonary localization; they will be discussed in detail later but are of interest here because they were not known to be sick until the day before their death. A similar failure to evince signs of sickness is found in the gastrointestinal cases, those with ulcerations in the stomach and perhaps an accompanying catarrhal intestinal inflammation. At most the report will be that the specimen was “off its feed.”

The signs of Kangaroo disease with exception of those applying directly to the nose and jaw are therefore very vague and one is limited to observation of the contour of the head and of the discharge from the nostrils. Because of the indefinite nature of the earliest changes, the duration of the disease cannot be stated with accuracy but from the time that the swellings are perceptible it is not very protracted if no treatment be given. Some cases die in four or five days while others may last up to three weeks and we believe that two of our cases may have been existent longer than that. It is impossible to estimate the duration of the septicemic and gastric forms although the latter, judging by the appearance of the ulcers, are believed to be chronic. We believe that frequent inspection and the precautions as to the character of fodder are the only special hygienic measures indicated.

THE INCIDENCE OF THE DISEASE.

Not the least puzzling character of the disease is the variability of its appearance. There have been groups of cases in our records; for example the following periods showed several while the intervening years lacked them entirely—1905, 1907–8, 1911–2, and 1920–1. The second and fourth outbreaks were definitely related to a new arrival but the records do not show that such was the case for the other two. Mr. Joseph who supplied us with many specimens, tells us that he has had an experience of fifty-four cases in 200 kangaroos and then failed to encounter the disease for years. Perhaps this irregularity of appearance has something to do with the character of food supplied to the animals.

Among seventy deaths of Macropodidæ we have had thirty-three cases of the varieties which I have included in this infection, made up of the following forms: cases limited to the jaws, pharynx and neck, six; cases of this sort with extension to lungs and stomach, ten; cases of this sort with general spread suggesting septicemia, five; gastrointestinal and hepatic, eight; nasal and sinus infection without necrosis in the jaw and with general spread including the lungs, four. The total incidence in Kangaroos is therefore 47 per cent., the necrotizing forms being 30 per cent., the gastrointestinal 11.4 per cent.

THE PATHOLOGY.

The essential features of the necrotizing variety of this disease are similar to those of actinomycosis—an inflammation giving rise to much fibrous tissue overgrowth enclosing pockets of softening, the whole process causing a deforming tumefaction. While primarily developing in the soft parts, this streptothricosis behaves like the ray fungus in that it spreads not only along clefts of tissue but directly through muscles and organs and even bones. Rarefying osteitis with irregular attempt at repair in the form of productive periostitis may be found in both infections. There is however a greater tendency to ulceration and general disease in the marsupial form, variations which seem referable to secondary invaders. When however the massive tumorous, necrotic and ulcerative characters of this streptothrix disease are insignificant or absent, the pathology is modified to the extent of obvious bacterial mixed infection, there then being catarrhal and fibrinous inflammations with degenerations of the viscera.

BACTERIOLOGY.

Since the pathology varies with the bacteriology as seen at this laboratory, it is well to pause at this time in a discussion of the former subject to introduce a brief statement of our findings in the latter, leaving however a full description thereof for later paragraphs. It is relatively easy to find in smears from necrotic masses threads of streptothrix, straight or curved with heavy blunt, but not bulbous, ends and never branched. Similar forms may be found in the necrotic tissue, both free in the softened area and near the margin of the healthy tissue, as irregular colonies growing in a tangled mass from the edge of which radiating threads may be seen. It has not been possible to find a “ray” growth with anything like the regularity so characteristic of the actinomyces nor do the ends present the bulb distinctive of that organism. Branching has been found once only, it being very uncommon in tissues although beautifully developed in cultures. While not especially sought, cocci and bacilli have not been seen, by Gram stains, within or immediately around the streptothrix colonies. Surrounding the mycelial groups is a necrotic zone about which is a loose connective tissue full of mononuclears and a few polynuclears. The centre of the colony is made up of tangled mycelial threads and necrotic debris. From uncontaminated necrotizing masses we have obtained cultures three times out of very many attempts.

When ulceration or suppurative softening has taken place mixed infection with lower bacterial forms naturally occurs and the whole picture changes. Pulmonary complications, with or without evident ulceration in the pharynx, also admit other bacteria. Streptothrical forms are often easy to detect in stained smears and in cultures but the very extensive bacterial flora soon overgrows them and attempts at isolation are fruitless. Under the best of conditions their colonial development is slow and tiny until they are well accustomed to saprophytic life. The complicating bacteria that have been identified are _Streptococcus pyogenes_, pneumococcus, pyocyaneus and colon bacilli to which may be added moulds of the Aspergillus group but these all have been variable in numbers and appearance; the most frequent and therefore probably most important secondary invader is an organism we have not been able to identify.

This germ, a tiny, Gram-negative, non-motile rod with a tendency to bipolar staining, will appear in smears from an ulcerated necrotic mass, from the nasopharyngeal exudate and from pulmonary lesions and may develop upon agar or blood media for the first generation but refuses to grow after that despite our best efforts. At present we hope to have it by growing material a long time in blood broth. Microscopical examination has not revealed it in the tumor-forming variety but on one occasion it was found in the lung; its Gram-negative characters make its detection in tissue very difficult. For obvious reasons the importance of this germ cannot be estimated but it seems from the frequency with which it is encountered that in some manner the streptothrix may be aided by this unidentified bacillus especially in the ulcerative and septicemic varieties of Kangaroo disease.

In so far as the diagnosis of this infection in the uncomplicated form, like lumpy jaw, is concerned the finding of streptothrix by stain seems adequate and its presence in the gastric ulcers and hepatic necroses identifies this variety. The most difficult question to decide is the identity of the cases without one or the other of these distinctive features but with mucocatarrhal or purulent nasosinusitis followed by pneumonia or septicemia, and of cases of primary pulmonary involvement. These instances have been diagnosed as belonging to the same category because of the presence of streptothrix in the exudate at the site of the important lesions and because the type of lesion is similar to that which complicates accepted characteristic cases. Inability to reproduce experimentally any of these infections limits our criteria for judgment in the matter. I am inclined to view these septicemic cases therefore as initiated by the streptothrix, growing in the nose and sinuses or inhaled into the lungs, aided by lower bacteria, an unidentified Gram- negative bacillus being the most important.

Having reviewed briefly the bacteriology of Kangaroo disease, its strict pathology may be discussed more definitely in terms of the type of infection. Reference has already been made to the method of pathogenesis employed by the streptothrix and its congeners. Whether or not a toxin is elaborated by these organisms is an unsettled question, especially for the marsupial variety because as yet it cannot be made to produce lesions in other animals. It is highly probable that all these organisms find colonization easy in the animal’s body once they get well settled, and that they act mechanically, producing necroses by their growth and by attracting leucocytes in such large numbers that digestion of devitalized tissue occurs, to an extent that resembles pus. The inflammatory tissue is not distinctive, except in so far that fibrosis enclosing pus pockets is peculiar to it. In softer tissue, like the liver, fibrosis is not so prominent, whereas diffuse and irregular spread is more pronounced. At the margin with the healthy tissue, reactive, that is resistant, inflammation is no more in evidence than within the tumor growth itself and as a matter of fact the tissues do not seem to put up a good fight against the spread of the inflammation.

Histologically, aside from the finding of the streptothrix colonies, there is nothing distinctive, the peculiar expressions of the disease being most manifest in their gross characters. For the purpose of describing the pathological features, the cases have been divided into the necrotizing form around the jaw, a similar process in the stomach and liver, necrotic cervical cases followed by lung involvement, the nasal variety upon which pneumonia succeeds and a septicemic form arising from any locality. Illustrative cases will be cited for each of these forms, a method of presenting the pathology thought to be superior to a general discussion.

The first illustrative case is one localized in the tongue and pharyngeal wall; it is quoted because of its strict localization.

Great Gray Kangaroo (_Macropus giganteus_). Sick four days, tongue swollen so he could not eat.

DIAGNOSIS.—Necrotizing process of floor of mouth and pharyngeal wall, dilatation of heart, passive congestion of liver, acute diffuse nephritis, inflammatory edema of lungs. General condition good. Jaws and teeth negative. Floor of mouth firm in places, boggy in others, but generally infiltrated. Anterior two-thirds of tongue purple and green as if gangrenous. Root of tongue and adjacent floor of mouth yellowish, wet as if from recent coagulation necrosis. In the muscle of the tongue a line of demarkation is shown at end of hemorrhagic zone behind which muscle is fairly good. Sides of pharynx, palate, tonsillar region show superficial pseudomembranous inflammation and yellowish gray, wet infiltration of muscles. Epiglottis purple and swollen to twice normal size. Laryngeal mucosa deeply injected, swollen and covered with tenacious gray mucus. Trachea and bronchi deeply injected and slimy. The lungs are uniformly deeply injected and along course of bronchi in lower lobe, lung tissue is distinctly more boggy than elsewhere. On section this area is slightly paler and more granular than the rest of the lung. Lung is everywhere slightly edematous. The bronchial lymphatics are swollen, pale pink and edematous. The heart is dilated acutely judging from the left ventricle wall which is nowhere over 1 cm. The liver is slightly enlarged, surface smooth, edges sharp, color deep purple, section surface very bloody. The spleen is soft, capsule smooth, pulp homogeneous purple, follicles not visible, trabeculæ normal. The kidney is slightly large, capsule smooth, strips easily leaving purple surface. The cut surface swells out, has irregular striæ, congested lines between, glomeruli visible and large. Smear from centre of tongue muscle shows staphylococci in some places in colonies, and long, slender rods.

The following case is one of gastric, intestinal and hepatic involvement, apparently primary, the last possibly arising by a hematogenic or lymphogenic route. Judging by the slides of the gastric wall the process started deeply and broke through the mucosa. This cannot be asserted definitely since kangaroos are susceptible to gastritis so that the streptothrix may have been implanted upon a preëxisting inflammation.

Black Wallaby (_Macropus ualabatus_). Congestion and edema of lungs, abscess of stomach and liver (streptothrix), ulcerative enteritis, necroses of spleen and lymph nodes, congestion of kidney. The animal is thin, hair loose. The mouth and nose seem to be absolutely healthy. The weight of the lungs is increased by congestion, they are solid, homogeneously red, with no air in any lobe except at edges. A piece cut from centre of lung sinks quickly in water. The trachea contains frothy blood. The heart muscle is soft, flabby and lustreless, chambers dilated, valves normal. The liver is of normal size, firm, smooth surface, sharp edges, red-brown color. The small sublobe of the liver which lies between the gall-bladder and the pyloric end of the stomach shows a large abscess 4 × 3 cm., apparently starting in the substance of the liver _via_ the bile ducts. This is certainly not extension from the stomach abscess as the liver lying against the stomach is nearly normal. The abscess is sharply circumscribed with a zone of congestion about it. Aside from congestion the rest of the liver is normal. The common bile duct is large and freely patulous. The capsule of the spleen is thick, consistency firm, pulp deep red, irregularly mottled by pale areas of necrosis. The kidney capsule is smooth, strips easily leaving a smooth, brown surface. The organ is firm. The section surface is glistening, the cortex wide and congested, the medulla normal. The adrenal medulla is deep purple with congested line between it and the pale cortex. Most of the gastric mucosa seems good. At about the middle of the lesser curvature is an ulcer about 4 cm. across. The shelving edges are covered with apparently normal mucosa. The centre contains bloody pus and nodular masses of the submucosa extending in finger-like projections through the pus. At one point on the greater curvature there is a small pocket of pus on the serous side which has not ulcerated through to the mucosa nor broken into the peritoneum. The large intestine is deep red and the follicles appear from the serosa as darker areas. On the mucus side the follicles have ulcerated, having a necrotic centre and shelving edges. The rest of the mucosa in the neighborhood is swollen and deep red. The colon mucosa is dry and the contents are hard, dry “baked” feces. The main pancreatic duct and the common bile duct form a thick, firm, cord-like mass running through the pancreas and enlarging the papilla of Vater into the duodenum. All abdominal lymph nodes are large, firm and on section mottled with red areas. Culture from the liver abscess failed to grow. Histological section of lung shows moderate congestion, collapse of alveoli or their filling by edema, epithelial and small round cells. There seems to be no fibrin. This could be an early stage of pneumonia. Bronchi are for the most part negative, little peribronchial round cell infiltration. No streptothrix in two areas of round cell infiltration or in bronchi. Liver section shows a part of the liver destroyed by hemorrhage, degeneration and necrosis. The abscess consists of necrotic matter surrounded by a zone of about equal numbers of mono- and polynuclears and around this a loose fibrocellular zone. Streptothrix abundant in the abscess. Lymph nodes show chronic inflammation and coagulation necrosis without abscess formation. No streptothrix in areas of necrosis. Kidney is very much congested with little or no damage to secreting parts. Spleen shows enormous congestion, moderate amount of pigmentation, connective tissue both trabeculæ and through pulp increased, no areas of necrosis. In the stomach the mucous membrane shows slight cellular activity and some degeneration—this amounts to a true catarrhal gastritis especially in view of the submucous cellular infiltration and the granulation tissue which has separated the muscularis and involved most of the connective tissue. The edge of the necrotic part begins abruptly, the mass of necrosis lying on an active fibrocellular submucous and muscular layer. Streptothrix can be seen at edge and in necrosis.

Pneumonia originating either by inhalation or _via_ the blood stream, is illustrated in two stages by the succeeding cases. The first history illustrates the pulmonary involvement as secondary to necrotic streptothricosis around the jaw and tongue while the second animal’s disease began in the nose and related sinuses. These two protocols provide material for a discussion of two phases of the subject.

The character of the early bronchopneumonia in the first is peribronchial, and there is distinct indication of a generalized process suggesting a hematogenic origin, whereas there is but one area of bronchopneumonia in the second—a necrotizing lesion beginning in the bronchus. Streptothrices are rare in the first case but reasonably easy to find in the second. This latter is one of the cases which seem to support the idea that nasosinusitis may have a streptothrix as its basis in the absence of the usual picture of necrotizing “lumpy jaw.” These cases also indicate that pneumonia may originate either by inhalation or by the blood stream, and that perhaps the hepatic lesion may have the latter origin. There have been two instances of necrotizing periarthritis, in one of which the threads could be found. This also suggests that spread through the blood stream can occur, possibly in this respect to places where previous injury prepares for the reception of the organisms.