Part 53

Where the process involves loose tissue like the lung, especially when growing rapidly, the sporulating heads of the mycelia stretch out in advance of the main mass and resemble rays. So too in a rapidly growing nodule radiating mycelia are sometimes seen but never with the regularity of arrangement typical for actinomycosis. Diffuse and irregular mycelial spread is characteristic of the second or infiltrative type of lesion and between the mould stalks one may discover well preserved tissue cells and at times bacterial forms like cocci or bacilli. This picture, suggesting as it does bacterial admixture and more active inflammation, leads one to the conclusion that the morbid process in which it is found does not represent mould disease _per se_, but a mixed infection. Whether or not the bacterial disease exists first and paves the way for the mould I am unprepared to say; I am inclined to the view that mycosis can start by itself.

INCIDENCE IN AVIAN ORDERS.

Mycosis may be said to occur in all birds although the appended list fails to show cases in a few of the orders included in this study; the sum total of autopsies from missing orders is only 45, so that they may be ignored.

═══════════╤═══════════ │ per cent. Passeres │ 3.7 Picariæ │ _1.2_ Psittaci │ 3.9 Striges │ 6.7 Accipitres │ 5.1 Columbæ │ .6 Galli │ 2.7 Fulicariæ │ _8.6_ Alectorides│ _2.7_ Gaviæ │ _10._ Impennes │ _40._ Herodiones │ _2._ Anseres │ 6. Struthiones│ _9.4_ ───────────┴─────────── For meaning of italics see foot note Table 1.

These figures hardly permit conclusions as to relative vulnerability unless the large percentage of cases for the small number of Impennes, Gaviæ and Struthiones be permitted to stand. Judging from orders upon which there are at least one hundred autopsies, owls, ducks and eagles are most likely to suffer with mycosis. The percentages are, however, not very convincing, and it would seem better with these data to conclude for the present that any variety of bird is susceptible to mould. Ostriches have long had the reputation of succumbing to this affection, so that their outstanding position in the list is more easily credited.

It was to be hoped that the various susceptibilities would assist in an explanation of the genesis of mould disease, but the result of the analysis is suggestive only in one direction which can be stated quite briefly. Ostriches, owls, shore and swimming birds have large stomata between the lungs and the lateral air sacs and show a high mould disease incidence. The natural thought is that access of mycelia and spores to the air sacs is facilitated. More comparative data is being assembled upon this point. Water birds are more susceptible to mould than land birds; the percentages based upon cases and totals for orders is 5.4 to 3.7.

The hygiene of mycosis is that of scrupulous cleanliness. Being hampered by incomplete knowledge as to its genesis one can only apply common sense measures. The germs having been found upon all the vegetable feeds, it naturally follows that they cannot be eradicated, but their colonization in large numbers can be prevented by repeated cleansing or sterilization of bins and pans so that no mouldy or musty material is given to the animals. At times of serious outbreaks sterilization by burning all old feed, starting fresh with good material in bins painted or saturated with disinfectant and then deodorized, is the only salvation. Where the blast lamp can be applied, it is the safest procedure. Autoclave sterilization should be thorough if practiced. By constant vigilance we believe that our large exhibition house is protected, but the sanitation of the pond, where many ducks have the disease, can never be so satisfactory.

Mycosis among mammals as an organic pathological entity is certainly a rare condition, indeed almost always to be considered an accidental or secondary one. In so far as human pulmonary disease is concerned it is among the pathological curiosities deserving of individual report. Moulds of several varieties have been found in intestinal ulcers, in cranial sinuses and in the ear, while generalized mycosis from thrush and favus are reported (cases of thrush in kites with fatal outcome has been described on page 168). Cutaneous infestation with mould is quite another matter for ring worms and similar conditions are now believed to be due solely to the penetration by spores and mycelia into the superficial dermis and into hair follicles. Numerous small lesions have been detected on dogs and cats that correspond to the ring worms described for them; to these we have devoted little study, because when discovered the animal is removed, treated or killed to protect others. Doctor Weidman has discovered several varieties of hyphomycetes which he will report upon at a later time. No case of generalized mould disease has been found in mammals, but Doctor Weidman has discovered a hitherto undescribed mould in ulcers and cutaneous abscesses of seals; no extension beyond subcutaneous areolar tissue occurred in these cases.

Botryomycosis, while not strictly belonging to the foregoing group, may be mentioned here because of its nodular tumor-forming superficial growths. The case to be cited certainly belongs to this illy defined group of diseases even if the organism was not isolated. It cannot be accepted as wholly demonstrated that the disease described under this name is always the same or that it has a single cause.

California Hair Seal (_Zalophus californianus_) ♀ . Had sore spots on side for several months. Ate well up to three days before death but ate something to time of death.

DIAGNOSIS.—Chronic enteritis with acute hemorrhagic exacerbation. Low grade chronic diffuse nephritis. Botryomycosis. General condition poor, subcutaneous fat practically absent. On the left side of the thorax there is a warty and nodular thickening of the skin overlying diffuse and flat thickening of subcutaneous tissues. There are warty, pustular, fistulous communications in four places between surface and deep mass. They are covered over with light crust. On dissection mass is found to be in subcutaneous tissue well outlined and encapsulated and consisting on section of dense, white, firm trabeculæ forming a mesh around yellow, soft areas which can be squeezed out. An adjoining lymph node is much enlarged, dense, tough, resilient, on section showing great connective tissue increase and solid brown medulla. The thyroids are solid, brown, 3. x 2. x .6 cm. and 3.7 × 1.8 x .6 cm. Trachea and bronchi contain pink froth but mucosa is negative. Anterior edges of lungs are distinctly emphysematous. Remainder of lung is uniformly congested and lobules are quite prominent. No consolidations. Bronchial lymph nodes are slightly large, anthracotic and wet. The heart is dilated, filled with mixed clot, muscle firm and deep brown color. The liver surface is smooth, edges sharp, size normal, color dull brown with greenish cast, consistency firm and tough. Section surface is glistening, smooth, moist, lobules indistinct but probably normal. The gall-bladder is full of fluid yellow bile. The common duct is patulous. The spleen is of normal size and shape, capsule opaque gray. The trabeculæ are prominent, the pulp stippled rusty brown. The kidney is of normal size, capsule is smooth, strips easily leaving a smooth purple surface. The organ is firm. The lobules and lobular markings are distinct. The adrenal has a narrow regular brown cortex and gray homogeneous medulla. The stomach contains whole fish. The mucosa shows digestion, congestion and mucus formation. Beginning at the pylorus and extending to the colon the mucosa is swollen and edematous, yellow brown. In the lower part it is quite firm and opaque. In the upper part it is more translucent except where there are diffuse hemorrhagic mottlings of the submucosa. Here and there are shallow erosions but no ulcers. The lymphatics of the mesentery are definitely enlarged, white, pale and very firm. Smear from the surface of the growth in side fails to show any definite yeasts or moulds by Loeffler’s or Gram’s stains. It is largely made up of polynuclear cells with many large mononuclears, many of which are phagocyting polynuclears and nondescript bodies. Cultures failed to grow. Microscopic section of liver shows marked congestion with slight hydropic degeneration of the epithelium. The kidney capsule is not thickened. Interstitial tissue not grossly exaggerated but connective tissue nuclei fairly numerous. Some tufts have decidedly more elongated nuclei than others and connective tissue around the stalk vessels seems hyaline. Capsule for most part not thickened but space contains cells and detritus in many instances. Epithelium of the tubules for the most part swollen, loosened and without nuclei. Some imperfectly formed casts. The intestine shows distinct congestion of the whole mucosa with here and there definite small hemorrhages well out in the villi. Slight round cell increase but no definite fibrosis. In submucosa around vessels connective tissue is hyaline in many places. The tumor on side consists of dense strands of connective tissue forming alveoli of varying size containing an exudate of fibrin and cells, about three-fourths of the latter being mononuclears. Neither connective tissue nor cells are arranged in a characteristic or peculiar manner so the observer is forced to conclude that this is one of the conditions of the group called Botryomycosis.

SECTION XVII—PART 3 THE STREPTOTHRICOSES

The organisms belonging to the genera Streptothrix, Actinomyces, Discomyces and Nocardia as named by various authors have in common the power to produce local chronic inflammation of gradually spreading character and chronic course. Their most conspicuous representative, the ray fungus, is best known as the producer of lumpy jaw in cattle and as an occasional pathogen in man. Other members of the group cause certain lymph-channel disease in domestic animals and pulmonary disease in man. Pathogenic power, it is believed, lies in the ability of these organisms to colonize and irritate, thus producing continuously enlarging tumefactions, no evidence being at hand that any of them produce a toxin either in their surroundings or within their own bodies. Because of their constant irritation, bacterial mixed infection often ensues so that purulent degeneration may occur at the original site of disease and thence may spread via the blood vessels, or by continuity of tissues or, if the mucous membrane of the pharynx be diseased, by the air passages.

The study of the genesis of actinomycosis is by no means a closed one. While it is believed that pastures and fodder carry the organism and that it gains access to the tissues by passing into small wounds that are made by sharp sticks or grain beards, the exact origin of the disease is not understood. The original lesion is certainly trifling and the fully developed one may not be discoverable until it is well under way and causes external deformity. Even when sloughing has occurred, the disease is not very communicable. The method of contraction of lymphatic streptothricosis in cattle is believed to be from other cases _via_ skin wounds or if abrasions be soiled by infective dirt. Just how human beings contract these infections, in the absence of infected cattle is unknown, but for the pulmonary form the route usually followed in tuberculosis is probably taken.

The material of our zoological collection permits few observations of value upon “lumpy jaw” but we have encountered a streptothricosis of kangaroos which may throw some light upon the whole subject and to these cases I shall devote considerable space since no description of it occurs in the literature.

ACTINOMYCOSIS.

This disease has been diagnosed with certainty in two American Tapirs and with reasonable satisfaction in three deer. Two Malayan Tapirs have also had lumpy jaw clinically but the organisms were not found. It is interesting and noteworthy that other zoological collections have observed the disease in this same animal, a fact which suggests the high susceptibility of the tapir to actinomycosis. There are recorded in the protocols a few times sluggish ulcers on the tongue in other ungulates but I am not prepared to label them as actinomycotic since on one occasion smears and sections were studied with great care and nothing found to justify such a diagnosis; nor were there maxillary or pulmonary lesions. Before passing to a discussion of the diagnosis and morbid characters it seems worthy of emphasis that our cases of this disease should appear in one family of Perissodactyla and in one family of Artiodactyla, in the latter not affecting Bovidæ, the family to which domestic cattle belong.

The diagnosis of lumpy jaw depends upon the growth of tumors in the neck and maxillary regions which tend to break down and discharge a thick pus containing “sulphur granules,” little masses of necrotic matter surrounding colonies of the ray fungus. When these conditions are fulfilled, the matter is easily enough settled. This was possible with the tapirs but in the deer the conclusion was not so easily reached and the diagnosis had to be made partly by exclusion. Anatomically the gross and microscopic appearances of lumpy jaw in the tapirs follows the text- book descriptions but our cases in the deer deserve separate comment. Whether or not these differences mean a peculiarity of resistance on the part of the animal or a new variety of streptothrix only further study can settle.

The beginning of the lesion in the deer was in the jaw bone as circumscribed or fusiform swellings appearing on the under surface. Growth usually progressed into the pharyngeal cavity and backward under the ear, but a large tumor stretching down the neck was only observed once. Suppuration and ulceration occurred twice but only once were bacteriological observations possible before death, and then they were negative. The fatal outcome seemed to be due to inanition, possibly because the animal could not eat, for respiratory tract involvement was only present once and then to a trifling degree. At autopsy, actinomyces in ray form were found in one animal only, the diagnosis resting upon histology in the other two. Nor did the degenerated centre of the swelling contain the sulphur granules in any case.

The microscopic characters of the tumors resembled those of giant cell sarcoma and chronic rarefying osteoperiosteitis with areas of round cell infiltration but no granulomata as are occasionally seen in lumpy jaw. I have always felt that a “giant cell sarcoma” with inflammation when seated in the jaw of a lower animal should be looked upon with grave suspicion and be searched diligently for fungi. The organisms could not be found in sections of any of these cases, although present in the pus from a pocket in one. Reference has been made in discussing tumors of the bones in gazelles and opossums to their resemblances to osteofibroma and actinomycosis. The diagnoses were made after long study of the notes and sections. Actinomycosis is usually unilateral while leontiasis ossium is commonly bilateral; the tumors have not broken down nor spread into the neck. In one macerated jaw bone the osteoporosis and hypertrophic periosteitis were comparable to those of the bovine form but the masses were not so extensive as is common for domestic cattle.

Treatment of this disease was attempted in the tapirs but not in the deer; the latter are too nervous to be handled repeatedly with safety to themselves. Following the usual method, potassium iodide was administered in saturated solution on bread, beginning at twenty grains thrice daily and rising in two cases to sixty grains thrice daily. It cannot be stated that any material improvement followed this heavy dosage although in one case the disease was very protracted—some six months, so that it may have modified the progress of the lesion. However, other things were done for the beast so that the effect of any one kind of treatment is difficult to evaluate. It was noted that iodide served to keep the stools quite loose and that its withdrawal was followed by constipation; upon resumption of the drug normal bowel movements appeared. Every soft spot was opened surgically to allow the pus to drain away. A vaccine of _Act. bovis_ was prepared and injected under the hide beginning at 0.5 mg. and rising to 2.5 mg. in five doses after which the animal became so unruly that the injections had to be discontinued. On the whole we are not impressed with the probability of success in the treatment of actinomycosis in tapirs. In the future we propose to try operation and the use of Dakins solution or Dichloramin T.

STREPTOTHRICOSIS OR NOCARDIOSIS OF KANGAROOS.

A fatal disease of Australian marsupials characterized by swellings and ulcerations about the lips, teeth, tongue and cervical tissues is known apparently all over the world by observers of these animals in collections. From commercial shippers of animals, from zoologists and naturalists we have reports that wherever kangaroos and wallabies are exhibited this disease makes its appearance and carries off a considerable percentage of the collection. A fully developed case bears a noteworthy resemblance to lumpy jaw, being called “jaw disease” by non-medical observers. However, it is highly probable that, while the most conspicuous morbid changes occur around the jaw, the agent provocative of the disease is capable of causing different pathological effects and that certain cases of septicemia and gastroenteritis are due to it; Doctor Blair of New York concurs in this opinion. Our study of the problem would inculpate a variety of Nocardia, possibly assisted by certain schizomyces. I have seen in the literature, but unfortunately cannot locate, a reference to an article by a Russian who observed the disease and was convinced that its cause is to be found in a streptothrix[105] obtainable from the necroses in the soft tissues of the jaw, a view entirely in accord with our findings.

The disease is not very communicable because its appearance in a pen need not be followed by secondaries in the mates of the sick beast. It appears chiefly in newly acquired specimens but may develop sporadically in those exhibited a long time and apparently not associated with recent acquisitions. This suggests two or three possibilities. It may be imported by new arrivals, or newcomers may meet a germ to which they are unaccustomed and therefore less resistant, the strange surroundings reducing their opposition to it. Old specimens may have enough resistance to withstand infection entirely or only succumb to large doses. Lastly one comes to the explanation commonly employed for actinomycosis, the presence of the organisms in fodder or pasture, perhaps all the time, but gaining entrance to the animal’s body _via_ wounds made by sharp sticks or the beards of grain.

While circumstantial evidence offers some support to this general idea, it cannot be accepted as proven. I have not made studies of the feed for the purpose of isolation of the streptothrix but cultures from the lips and gingival margin of healthy and infected animals were made for its cultivation. These attempts were fruitless, and without wonder since the germ when isolated from a fully developed case is quite finical in its manner of growth; there are so many kinds of bacterial life that they may easily overgrow the one in quest. So, too, cultures made directly from subcutaneous necrotic areas may not always give a positive growth although smears from the same material may reveal numerous threads under the microscope.

The idea that sharp grasses are responsible for the origin of Kangaroo disease finds a protagonist in Dr. A. S. LeSouef, Director of the Zoological Garden at Sidney, Australia, a gentleman whose judgment carries weight. He writes: “We have found that it is entirely due to getting spear or barley grass in their food; owing to the formation of the mouth, this grass gets wedged in between the teeth and the cheeks, penetrates the flesh and allows the bacteria to get a footing, this in time heaps up on the inside and forms an abscess that bursts exteriorly. Formerly all the Australian Zoos lost animals through this cause, but now, through being very careful not to give any rough spined grasses, we never have the trouble.” Since receiving this letter we have removed straw bedding, and feed only soft alfalfa which is carefully inspected for foreign substances. During this time we have had two cases but the period of observation is too short for final judgment as to the value of feeding grasses without sharp beards and spines. The appearances of cases sporadically without reference to the arrival of new specimens, the low communicability of the disease, its beginning in the jaw in most cases and the prominence of pulmonary and gastric lesions, all seem to support the thought that the virus is received with the fodder or drink. The anatomy of the kangaroo’s buccal cavity favors the collection of material between the gums and cheeks and between the root of the tongue and the molars, while the “hare lip” also affords a crevice in which food particles or foreign bodies may accumulate. These three places seem to be the starting points of most of the cases.

THE COURSE OF THE ATTACK.

Despite careful watching of the exhibition specimens it is often difficult to detect the beginning stages of the disease. Since our last outbreak it has been the practice to examine all kangaroos thrice yearly by catching them, inspecting the buccal membranes, teeth, tongue and nose and by palpating the jugular and sublingual regions. This procedure succeeded in catching one very early case from which the original changes can be described.