CHART BB. AMERICAN BISON (Bison bison). Tuberculous.

]

[Illustration:

CHART CC. SAMBUR DEER (Cervus equinus). Tuberculous.

]

[Illustration:

CHART DD. VIRGINIA DEER (Mazama virginiana). Non-tuberculous.

]

[Illustration:

CHART EE. AMERICAN ELK (Cervus canadensis). Non-tuberculous.

]

SECTION XVII—PART 2

MYCOSIS

This is a general term applied to the infections with Hyphomycetes, but

in the zoological material discussed here it refers chiefly to the

growth of aspergillus in the air sacs and viscera of birds. A few cases

of cutaneous mould growth have been seen in mammals but are of trifling

importance; brief mention will be made of them on a later page.

Under the names of Aspergillosis and brooder pneumonia, the infection

with _Aspergillus fumigatus_, _A. glaucus_ and others is well known to

breeders of chickens, ducks and ostriches. Literary references to its

occurrence in zoological collections are numerous, but there seems to be

no record indicative of its frequency in the various orders nor

discussion of the pathological types best exhibited by different birds.

There has indeed been some discussion of the actual entity, mould

disease, the picture found at autopsy being referred to secondary

contamination with fungi in the presence of bacterial infection.

Experiments by DeLong and others have been indifferently successful in

the production of the disease by inhalation of mould spores. The

appearance of groups of cases in breeding places, apparently all

exhibiting the same organism, in the absence of other varieties of avian

epizoötics seems to warrant the conclusion that the hyphomycetes can at

least be associated with a fatal morbid lesion of quite uniform

character whether or not they be the original invaders.

Judging by our experience it would seem probable that the aspergillus

can, under conditions not fully explained, cause inflammation of the

avian air sac and tubercles in viscera, in the absence of other evident

causes of illness and death. Over three-fourths of our cases have no

other diagnosis than “mould disease”; this may be in part due to

overlooking other things, but to a much greater extent to the very

extensive mould growth which obscures all other changes. That

unexplained preparatory conditions may exist is indicated by general

observation and some experimental work. Whereas in breeding

establishments this disease occurs in epizoötics, or in groups of cases,

with us it is enzoötic, constantly present, never, however, bursting

forth in virulent form with high mortality. Nor is the condition highly

contagious.

In an attempt to explain its source I examined over forty varieties of

feed and found therein several strains of aspergillus and of mucor; the

latter occurs occasionally in the avian air sac. The infective material

is therefore constantly present, and it would seem that if it were

capable of initiating a fatal disease many more cases should come to our

attention. Perhaps these moulds do gain access to the avian air sac and

are killed off, or only assume a pathogenic rôle when they are in large

numbers or a preëxisting disease assists them. Since our records do not

support the idea that a preceding condition must exist for a growth of

mould to be successful, and yet pathological and experimental

observations suggest that something helps its colonization in the air

sac, what are such conditions? Moulds grow on feed and litter in which

birds pick; from this it is quite possible for a piece of grain or even

inorganic matter laden with spores to be inhaled and lodged in a

secondary alveolus near the air sac whence extension into the air spaces

could occur. In addition I think it quite conceivable that a whole

colony of mould might be inspired with the same result, the mechanical

obstruction being sufficient physical damage to incite inflammation. The

continuous moist surfaces of the bronchial passages and air sacs afford

conditions favorable to the growth of mould and as inflammation is not

vigorous, little resistance is presented to its spread.

The mode of operation of these hyphomycetes has usually been assumed to

be a mechanical one, local colonization replacing healthy tissue or

spreading along surfaces so that function is physically impossible. A

support of this idea is to be found in the fact that inflammation, as

produced by schizomyces, is trifling or absent; the necrosis that occurs

is due to choking off of tissue by the intricately tangled masses of

mycelia and blocking off of air or blood supply. The existence of an

infiltrating and necrotizing form in some parrots and gallinaceous

birds, suggested to me that a toxin might be responsible for some part

of mould action. Proof for this speculation was sought by injecting into

the pectoral muscles of pigeons an emulsion of a dead mould and a

filtered broth culture. Necroses occurred but only to an extent which I

interpreted as due to the physical destruction of muscle by the injected

material; they were larger with the dead mould than with broth filtrate.

I concluded therefore that aspergillus perhaps has no toxin as usually

described for bacteria.

TYPES OF MYCOSIS.

Avian mycosis occurs in three different forms, two of which are probably

of similar nature and two are frequently combined. The first variety,

most often seen in gallinaceous and anserine birds, consists of

thickening and opacity of the air sac walls, upon the surface of which

either a curd-like pseudocoagulum or a velvety or fluffy mould growth

appears. This variety usually begins about the anteroinferior pulmonary

stoma on the right side extending thence to the related sac, upward

toward the wing and downward to the abdominal spaces. Occasionally the

middle thoracocervical space is involved, probably _via_ the opening in

the syrinx. Extension takes place by the way of normal passages, but

when the growth is dense it also seems to occur by continuity through

tissue. This variety may or may not be associated with the second, an

infiltrative type of lesion best seen in the lung. Under what seems to

be a true picture of mycotic pneumonia, dirty gray consolidated areas

will be found around the bronchial space, infiltrating in all directions

and without definite boundaries. A similar lesion has been seen also in

the liver on rare occasions, but the lung is its usual seat. Judging

from microscopic appearances this is a process complicated by the

addition of bacteria.

[Illustration:

FIG. 59.—NODULAR OR TUBERCULAR MYCOSIS IN THE LUNGS OF A DUCK. ONE-

HALF OF THE LUNG IS CUT AWAY AND LAID ON THE INTESTINES TO CONTRAST

THE PLEURAL AND SECTION SURFACES.

]

The third variety is nodular or tubercular mycosis, a process of

probably more chronic nature since around the isolated lesions

connective tissue is perceptible, it being absent or inconspicuous in

the other types. The formation of gray or yellow-white nodules from a

few millimetres to a centimetre in cross section, is the characteristic

production in this variety. Lungs, liver, spleen, intestines and air

sacs are involved in about this order. Attempts at explanation of this

peculiarity of growth were made in the direction of identification of

the species of mould, kind of bird and probably degree of resistance. No

conclusions could be drawn since the same variety of mould was found in

this as in other types; no bird showed a special susceptibility or

resistance to it. It is quite difficult to obtain a culture from nodular

mycosis, it being necessary to crush or grind the solid masses before

making cultural implants. This variety should always be differentiated

from tuberculosis by staining for the organisms.

Histologically studied these three types are not as easily separated as

the gross appearances would warrant one to expect. The original mould

nodule begins in essentially the same manner in all, a small

colonization of mycelia and spores which grow centrifugally, but ever

becoming more intricately wound in their first location. As the tissue

is invaded, total necrosis takes place, no recognizable cellular

architecture being left. When fully formed the mycotic tubercle consists

from the centre outward of a necrotic mass, in which spores and mycelia

stain indifferently well, surrounded by a dense zone of fully formed

mould beyond which mononuclear cells and a few loose fibrils may be

found. The circumferential tissue of the viscus supplies a mild

congestion and perhaps a moderate connective tissue capsule. Giant

cells, as known for tuberculosis, do not appear.

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.

[Illustration:

FIG. 60.—MICROSCOPIC APPEARANCE OF ONE OF THE NODULES. NOTE THE

CENTRAL NECROSIS AND THE CLOSE FIBROCELLULAR PACKING IN THE

RESTRAINING CAPSULE.

]

[Illustration:

FIG. 61.—MYCELIAL GROWTH IN AN ALVEOLUS IN THE RAPIDLY SPREADING

VARIETY OF PULMONARY MYCOSIS. SEVERAL FRUIT-HEADS ARE VISIBLE.

]

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.

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.”

[Illustration:

FIG. 62.—KANGAROO STREPTOTHRICOSIS. ULCERATIVE AND NECROTIZING PROCESS

IN “HARE LIP” AND IN MUCOSA AND BONE OF ANTERIOR PORTION OF HARD

PALATE; TEETH HAVE FALLEN OUT ON LEFT SIDE.

]

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.

[Illustration:

FIG. 63.—KANGAROO STREPTOTHRICOSIS. ANTEROPOSTERIOR SECTION OF HEAD,

SHOWING MASSIVE TUMEFYING PROCESS IN LOWER JAW BONE.

]

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.

[Illustration:

FIG. 64.—KANGAROO STREPTOTHRICOSIS. STOMACH, SHOWING TWO ULCERATIONS

AND DEEP INFILTRATIONS OF THE WALLS.

]

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.

[Illustration:

FIG. 65.—KANGAROO STREPTOTHRICOSIS. ULCERATION IN GASTRIC WALL AND

MASSIVE NECROSES IN LIVER.

]

[Illustration:

FIG. 66.—KANGAROO STREPTOTHRICOSIS. SECTION OF LUNG SHOWING EARLY

ABSCESSES AND NECROSES, ONE WITHIN A BRONCHUS, ONE IN

SEMICONSOLIDATED PULMONARY TISSUE. NOCARDIAL STRANDS COULD BE FOUND

IN BOTH AREAS.

]

Thigh striped Wallaby (_Macropus thetidis_). Streptothricosis of soft

tissues of jaw. Early bronchopneumonia. Acute fermentative gastritis.

Acute general infiltrative enteritis. Cloudy swelling of myocardium.

The general condition of coat and of nutrition is good. The jaws are

wide and the maxillocervical region full, both due to an indurative

inflammation of the gums, tongue, floor of mouth and upper cervical

tissues. At either side of the tongue and running around body of

maxilla both sides, the inflammatory tissue becomes softer and there

is an area about one inch long where it is soft, gray and contains

yellow gray bodies in a grumous matrix. The teeth seem sound as do the

external buccal tissues. The nasopharynx is free from induration. The

bone on the left side shows a periosteitis with involvement of the

superficial layers of bone, while on the right side the periosteum is

swollen and opaque but the bone is free. The thyroid is imbedded in

the edematous infiltration of the lower cervical tissues. The pleuræ

are free of fluid and adhesions. Lungs are collapsed, uniformly pink

somewhat emphysematous at places but give the impression of being

lumpy. On palpation numerous nodular areas are detected. These prove

to be peribronchial areas of gray-red solidity which swell out on

section. The bronchus contains a gray and bloody thick mucoid matter.

There is distention of the mesenteric vessels especially near the

enteric insertion. The liver surface is smooth, edges very sharp,

consistency firm, tough, resilient, color deep red, the section

surface is glistening, moist, opaque, architecture probably normal.

The gall-bladder is distended with viscid green bile; the common duct

is patulous. The spleen has a rough, thin capsule, consistency tough

and resilient, the section surface is mottled red with purple points;

on section two small, pale objects seem to be squeezed out. The kidney

capsule is smooth, strips easily leaving a smooth, deep red surface,

the consistency is soft, the cortex is deep red, then a purple line

between it and the red medulla, striæ invisible. The stomach contains

frothy grayish mush. The mucosa is finely mammillated, deep pink until

the last third when it becomes deep red, deeply injected and somewhat

thickened. The pylorus is closed. Externally the gut is congested, in

places translucent but for most part seems thickened by reddish

swelling of both external layers and mucosa. The mucosa is granular or

pebbly with here and there a small bloody suffusion. The histological

section of lung shows alveoli open, septa relatively thin but somewhat

congested, bronchi mostly open and connective tissue not increased.

Some few bronchi, especially the larger, show a slight catarrhal

bronchitis but mostly an infiltrative peribronchitis. The nearby veins

and arteries show the most striking change, there being in nearly all

of them a distinct thrombosis without circumferential pneumonia. In

one place a distinct peribronchial pneumonitis was found. The kidney

shows very marked congestion of all parts, causing compression,

cloudiness and granularity of the epithelium. Glomeruli and connective

tissue about normal. The intestinal serosa is negative save for

congestion. Submucosa is densely infiltrated with mononuclears, some

in definite groups. Section does not show areas mentioned in notes but

these could be accumulations of cells with congestion. No streptothrix

forms. Section from the infectious focus of face consists of active

granulation tissue, densely injected and filled with mononuclears of

two types, one the lymphoid cell, the other of the young connective

tissue type. Areas of grouping like abscesses are seen and some

necroses. Streptothrix in small numbers in the cellular collections.

Nail tailed Wallaby (_Macropus unguifer_). Kangaroo disease of nasal

region. Necrotizing bronchopneumonia (Aspergillus fumigatus and

Micrococcus albus). Acute diffuse splenitis. Congestion of liver and

kidney. The general condition of coat and nutrition is good. The face

is wide just below the eyes. About the “hare lip” and the nose the

soft tissues are soft, gray, necrotic. All the internal nasal tissues

seem swollen, gray-red. There is subcutaneous edema, bloody in places,

around the right face, eye and jugular angle. Tissues of nasopharynx

swollen, deeply injected and covered by a thick mucus. Pharyngeal and

buccal cavities negative. Tonsillar areas pink and flat. Larynx and

trachea slightly swollen but pale on mucosa. Salivary glands and

cervical glands normal in size and pale pink. Pleuræ pale and empty.

Lungs swollen out uniformly, quite cottony except at lower right base

where there is a nodule about 3 × 5 cm. firm and doughy. On section it

is found to be a peribronchial consolidation of pale reddish gray

color and indefinite outline. The bronchus itself is deeply congested

and contains a grumous mass. The peribronchial lymph nodes are small,

soft, pink, homogeneous. The heart is negative. The liver is large,

surface smooth, edges sharp, color deep purple, consistency soft.

Section surface is glistening, smooth, moist, very dark purple with

obscure markings. The gall-bladder contains fluid brown bile; common

duct is patulous. The spleen is soft, tough, capsule pebbly, section

surface is mottled, light and deep pink, follicles and trabeculæ not

distinguished. The kidney capsule is smooth, strips easily leaving a

smooth purple surface, section surface is glistening, deeply

congested, striæ obscure but seem normal, glomeruli not visible, organ

is soft. The gums and teeth are not involved in the mycosis. The

stomach contains mushy digesting food. The mucosa is mottled pink,

soft, digesting, at lower half submucosa is deep pink, a few small

ecchymoses. From pylorus to ileum, serosa is deeply injected,

edematous, mucosa swollen and edematous, deep pink, loosened in

places, but translucent. Below this the mucous membrane becomes

smooth, flat, pink-yellow. Lower ileum and colon contain rather firm

fecal balls. Follicles nowhere prominent. The pancreas is small, soft,

yellow pink. The follicles of the mesentery are small, pink gray and

homogeneous. Smears from the bronchopneumonia show a threadlike Gram-

positive form and a few Gram-negative rods. Cultures from lung show

_Aspergillus fumigatus_ and _Micrococcus albus_. Nose too foul for

culture. Histological section of lung shows the alveoli mostly open

but the septa widened by congestion. Blood vessels are open and

contain recent clots; one vessel near lesion below is thrombotic. The

two large bronchi in section show catarrhal bronchitis and

infiltrative peribronchitis of which the latter is more severe and

advanced. Beside the larger is a necrotizing pneumonitis from which

nearly all the architecture has disappeared. The exudate is chiefly

mononuclear around the edges; centre no cellular identity. Another

mononuclear process not connected with bronchus in section is found

with an early necrosis. Streptothrix strands may be found in the

bronchial exudate and near the margin of the necrotic patch. They do

not grow in colonies however. The spleen shows general congestion

without pigmentation. Follicles large, solidly lymphoid. Connective

tissue about normal. The kidneys show marked congestion everywhere.

Capsule and intrarenal fibrous tissues about normal. Very severe

congestion which seems to have caused compression and granularity of

the epithelium.

The last case, judging by stained smears, is one of pure nasosinusitis

from streptococci and streptothrices. Cultures were not tried because of

the enormous bacterial flora.

[Illustration:

FIG. 67.—KANGAROO STREPTOTHRICOSIS. LOW POWER PHOTOMICROGRAPH OF A

NOCARDIA COLONY WITH NECROSIS WITHIN AND AROUND IT. THIS WAS FOUND

IN A SECTION FROM THE LIP OF THE SPECIMEN SHOWN IN FIG. 62. THE

BLACK BORDER CONSISTS OF PARALLEL THREADS SO CLOSELY PLACED THAT

THEIR SEPARATION UNDER THE CAMERA IS PRACTICALLY IMPOSSIBLE. THIS

TYPE OF COLONY RESEMBLES THE “RAY” COLONY OF ACTINOMYCES.

]

Robust Kangaroo (_Macropus robustus_). Acute purulent ethmoiditis.

General acute purulent anterior cranial sinusitis. Acute necrotizing

glossitis and pharyngitis. Cloudy swelling of kidney. The face seems a

little full and the subcutaneous tissues slightly edematous. The

nasopharynx contains a thick tenacious mucopus. Ethmoid and frontal

sinuses and turbinate spaces contain a thick purulent matter, the

mucosa being densely injected, swollen and velvety. Pharyngeal wall

and right half of posterior half of tongue are involved in a dull

brown and necrotizing process, quite sharply outlined by zone of

congestion. This process is comparable to the necrotizing gingivitis

seen in front of jaw in kangaroos. Larynx, trachea and lungs seem

uninvolved save for slight generalized congestion. Cervical lymph

nodes especially those about the larynx are definitely enlarged, soft,

moist and brown. Mediastinal nodes slightly enlarged, soft and pink.

The heart is negative. Liver normal. Spleen is soft, homogeneous dull

red. The capsule of the kidney is smooth, strips easily leaving a

purple surface. The glistening section surface swells slightly, vasa

recta are congested, striæ wide and pale, glomeruli not visible;

consistency is resilient. The mouth and teeth are not involved in the

process mentioned above. There is a small quantity of properly

digesting food in the stomach. Stomach and intestines negative. Brain

not involved. No extension from anterior cranial sinusitis. Smears

from the mucopus confirm the gross appearance and contain short chains

of streptococci and large diplococci. Smear from cut surface of tongue

shows innumerable small bacilli and diplococci but especially mycelia

with rather heavy clubbed ends but without true branching. One group

was found arranged like ray fungus. It is noteworthy that there is no

aspiration pneumonia and very slight evidences of septicemia.

BIOLOGY OF N. MACROPODIDARUM.

The original discovery of the streptothrical forms was made in stained

smears from necrotizing lesions. They were considered as secondary

invaders until repeated observations of a similar character aroused the

suspicion that they stood in some important relationship to the lesion.

Early attempts at their cultivation were made under anaerobic

precautions, a method now known to be almost certainly doomed to failure

because a strain long under cultivation requires two to three weeks to

make an appreciable growth in the absence of air. Finally in 1911 a

successful cultivation occurred by searing the surface of an unopened

mass in a freshly dead animal and planting bits of the interior upon

aerobic blood serum plates. Colonies grew after three or four days and

from them the first strain was started. It grew for several generations,

long enough for the preparation of a vaccine, which will be described

later, when by mischance it was lost. In 1920 another successful

cultivation occurred, this time by incising a mass in the soft

sublingual tissue and plating in the same manner; upon this culture the

biology is described. Smear preparations offer no more than has already

been mentioned.

Colonies develop upon blood serum plates as opaque, pale yellow,

circular, discrete masses with a slightly depressed uneven centre, but

without umbilication. They remain smooth and slightly glistening for

several days, then become slightly wrinkled and twisted with a more

definitely raised edge and a tendency to an uneven sinking in of the

centre. Transfers to agar slants show wrinkled continuous opaque, dull

yellow, sharply outlined growths which soon wrinkle, fold, and twist

like certain tubercle bacillus cultures. Spreading occurs, but is slow

after forty-eight hours. As medium becomes drier it is possible to see a

thin, colorless, wrinkled film stretching out from the main growth. If

the medium be dry or old or if only a small portion of seed material be

used and this scattered over the surface of the slant, discrete colonies

arise. These are circular, seldom exceeding 3 mm., dirty yellow-white,

distinctly umbilicated and without clear film of spreading around them.

In nearly all quite old cultures, a white chalky efflorescence appears

over the surface.

The morphology of the young agar culture is chiefly mycelial or

filamentous, whereas from a culture on dried media and those showing

efflorescence, the organisms are short, heavy, deeply granular and of

the mycobacterial type.

Glycerine agar.—Corresponds to agar.

Blood agar.—Similar to agar but much less luxuriant.

Blood serum.—Limited dirty yellow, raised, dull, wrinkled and

granular, tightly adherent to the medium.

Potato.—Spreading, dirty yellow, much wrinkled, friable, tightly

adherent.

Gelatine.—Limited growth as a wrinkled, tough scum only on surface.

[Illustration:

FIG. 68.—KANGAROO STREPTOTHRICOSIS. HIGHER MAGNIFICATION OF EDGE OF

STREPTOTHRIX COLONY, FIG. 67. IT SHOWS THE DEEPLY STAINING MYCELIA

SEPARATING MUSCLE FIBRES WHICH ARE DEGENERATING.

]

Litmus milk.—No change for six days, then beginning slight alkalinity

which increases very little, shows digestion of the caseinogen,

slight, thin filmy growth on surface.

On media such as litmus lactose agar and old Endo it grows slowly on

surface and assumes the color of the medium.

Broth.—Only surface growth appearing during early generations, after

3–6 days as a wrinkled, pale yellow scum very much like the tubercle

bacillus growth; later generations grow perceptibly in one to three

days. Medium perfectly clear. If a large mass be seeded into neutral

broth there is a perceptible increase in the growth after ten days.

The medium thereafter tends to a faint turbidity. Titration of broth

growth after twelve days shows alkalinity requiring 0.3 cc. decinormal

acid, while the control tube incubated same length of time showed an

acidity requiring 0.57 cc. of decinormal NaOH.

On the following sugars there is a slight surface growth without

change in the color, Andrade indicator—dextrose, lactose, saccharose,

maltose, mannite, dextrin, galactose, salicin.

Cultures observed on two per cent. neutral agar.

A.—Stained by Loeffler’s stain.

Twenty-four hours.—Shows threads growing out from a central amorphous

mass, but the whole does not retain the regularity or parallelism of

actinomyces. Threads are poorly stained and rather disconnected but

not jointed. Small number of metachromatic bodies apparently in older

individuals, certainly in the better formed ones. No intercalary

spores, unless the metachromatic bodies be so considered. Individual

threads measure from one-third to one micron in width. Metachromatic

bodies measure on the average one micron.

The threads in the forty-eight hour preparation seem distinctly wider,

up to one micron and possibly become heavier toward the end, but do

not have a distinct bulbous extremity.

In three days the threads are much longer, show distinct branching and

a tendency to transverse segmentation. More than one metachromatic

body may be present in one segment.

Four days.—Still coarser, short segments have appeared separately.

Metachromatic body is coarser and blacker; some of the masses have

gone to pieces and show only a diffusely staining smudge of

metachromatic bodies. The short segments show a tendency to grow out

into threads.

Fifth day.—Condition is much the same plus many young, delicate,

poorly staining threads.

Sixth day.—The same but all seem to be somewhat wider and diffusely

staining.

Seventh day.—More diffuse staining and decidedly fewer metachromatic

bodies.

A.—Stained by Gram’s stain.

Twenty-four hours.—All forms are light purplish. The threads stain

much more clearly than by Loeffler’s and show distinct transverse

segmentation of rather uniformly long bacilliform shape. Metachromatic

bodies not so distinct but seem larger where found. Coarser threads

have swellings in some of the areas which are not segmented and this

type seems to have more branching and metachromatic bodies; in other

words it would seem that this is a form that reproduces by budding or

intercalary spore formation.

Forty-eight hours.—Much the same, more long threads with transverse

division, somewhat more delicate, generally fewer coarse threads with

swellings and spores. Still pale purple and not distinctly Gram-

positive.

Three days.—Condition much the same.

Four days.—Two forms present—definitely Gram-negative delicate slender

threads, nearly Gram-positive, and heavier, curved and twisted long

bacillary forms, some streptococcoid threads and a few bulbous short

threads. Very few metachromatic bodies.

Five days.—Condition much the same except that the delicate threads

are inconspicuous and the darker purple bacilli have increased.

Metachromatic bodies increased as have swellings in coarser threads.

Six days.—Much the same but for the appearance of young, delicate

definitely Gram-negative threads. There are fewer metachromatic bodies

and internal spores.

Seven days.—The same.

B.—Grown on Loeffler’s blood serum.—Loeffler’s stain.

Twenty-four hours.—Delicate, poorly stained short threads, few tiny

metachromatic bodies.

Two days.—Not well stained, relatively short threads show numerous

metachromatic bodies varying from exceedingly tiny dots to coarse

granules wider than the thread. These may be numerous in the same

segment and form a row from six to ten. Many short bacillary forms.

Three days.—Poorly stained, metachromatic bodies apparently more

numerous but much smaller.

Four days.—Almost entirely short, heavy bacillary forms, some of which

are very like diphtheria bacillus in the irregularity of width; many

metachromatic bodies, distinct branching, some of the small heavy ones

have fusiform swellings; practically no long, heavy threads.

Five days.—Essentially the same, individual elements slightly larger,

fewer but coarser metachromatic bodies, more numerous round forms

suggesting large pale cocci.

Six days.—Much the same but elements shorter, smaller and some more

segmented.

Seven days.—More long forms of uniform staining but still a majority

of coccoid or short bacillary forms with irregular staining and

metachromatic bodies; no long threads.

B.—Gram’s stain.

Twenty-four hours.—Pale purple, almost Gram-negative, long, slender

but well outlined threads, a few coccoid forms, practically no

granules.

[Illustration:

FIG. 69.—KANGAROO STREPTOTHRICOSIS. PHOTOMICROGRAPH SHOWING THE

SEPARATE THREADS OF NOCARDIA IN A SOFT NECROTIC LESION.

]

Two days.—Very pale, almost Gram-negative threads, very many coccoid

forms and short rods, considerable segmentation of the longer threads.

Three days.—Increase in short, heavy bacillary forms with bulbous

ends, deeply stained ones and the granules being lightly Gram-

positive; long, slender threads are disappearing.

Four days.—Almost exclusively short, heavy forms with bulbous ends

with coccoid forms, heavier forms almost definitely Gram-positive,

granules Gram-positive.

Five days.—Much the same but more segmentation in the bacillary forms,

coccoid forms become more numerous.

Six days.—Individuals are somewhat longer but there are many rods with

fusiform swellings containing granules; coccoid forms present in

chains sometimes.

Seven days.—More long rods or short threads, pure coccoid and

bacillary forms.

The morphology upon bouillon depends somewhat on age and upon the

location. Upon the surface the long branching mycelial type appears

early and persists until the whole surface is covered whereupon the

segments divide into coccoid elements with metachromatic bodies. If

heaping-up develop the coarse grains on the mass consist of granular

or coccoid rods. When growing in the depth the coccoid form is the

predominant one, only a few delicate mycelia, usually Gram-negative,

being found.

The Gram character of the organism should be emphasized. The young,

delicate mycelia are negative or take a very feeble blue stain. The

heavy bacillary forms are Gram-positive. Like the ray fungus the heavy

ends are sharply Gram-positive, but unlike it, there has never been

seen a Gram-negative bulbous capsule around this end.

The determination of this organism was undertaken from the

classifications of Petruschky (Kolle-Wassermann), of Castellani in

Castellani and Chalmers’ _Tropical Medicine_, and of the Society of

American Bacteriologists. In the first classification it corresponds in

some ways with _Streptothrix hominis_, and in some ways with

_Streptothrix capræ_. As for the second authority it falls into the

Nocardiaceæ, section parasitica, subsection I, in that a distinct earthy

odor is absent and that there is no liquefaction of coagulated protein.

It resembles several of the species given in this subsection, but does

not correspond exactly with any of them. Consultation of the

classification of the American Bacteriologists would place it among

Mycobacteriaceæ. The facts that it is strongly aerobic, produces whitish

efflorescence which may possibly be aerial hyphæ and breaks up into

short segments, place it in the genus Nocardia. It seems, however, to

belong to a division of Nocardia which is close to the Mycobacterium

since the short elements are swollen, cuneate and usually heavy, which

is unusual in the more typical Nocardia. It is not, however, acid fast

and therefore cannot be classified among the Mycobacteria. This culture

seems to be a variety not heretofore described, and since its

association with the disease is so definite, whether or not it be the

cause, the name NOCARDIA MACROPODIDARUM is proposed, because the

kangaroos belong to the order Marsupialia, family Macropodidæ.

The discovery of these organisms within tissues is by no means easy even

though the larger colonies may be located by staining. If Loeffler’s

method be used the central mass stains quite diffusely and the spreading

mycelia around the edge stain faintly. For study purposes this stain is

preferable to Gram-Weigert, since despite the positivity of the

cultures, the blue dye can be removed very easily from sections and only

with great care will enough remain to permit tracing of the separate

threads; with Gram stain no detail can be made out in the centre of the

colony, it being a diffuse blue. Careful search near the edge of these

necroses will usually succeed in the discovery of a few mycelia

stretching in between the mono- and polynuclears of the low grade

inflammation. This is best seen in the margin of gastric ulcers, but may

also be found in the cervical masses. When searching in the pulmonary

tissues the organisms are to be found in the bronchial exudate or at the

edge of pneumonias. In one nasal mucosa the mycelia were dispersed, not

growing in colonies as in localized inflammations.

EXPERIMENTS AT THE REPRODUCTION OF THE DISEASE.

When the first culture was isolated it was injected into guinea-pigs;

its loss stopped further work because it could not be regained from the

animals. The present culture had been injected into guinea-pigs,

rabbits, opossums—all with negative results; such an experience is not

unknown for actinomyces. Intraperitoneal, intravenous methods having

failed, inoculation was made into the gums of rabbits and of opossums

with no result, even after traumatizing the mucous membrane. The

injection of about 5. mg. of a twenty-four-hour agar culture was made

directly into the masseter muscle of an opossum without producing even a

lump at the site. Atomizing a culture into the nose and throat of an

opossum seemed also without effect. Injection of cultures into the nose,

gums and labial tissues of a wallaby have been negative; nor has any

perceptible effect followed the atomizing of a heavy nocardial

suspension in broth into the trachea of this animal.

The results of these experiments are in accord with those of many

similar attempts to reproduce actinomycosis. Perhaps in Kangaroo disease

the small Gram-negative bacillus is a necessary factor.

SPECIFIC PREVENTION AND TREATMENT.

Encouragement that we were upon the right track was, however, found in

another direction. Improvement in human and bovine actinomycosis having

followed the use of vaccines, it occurred to me to try this method as

treatment and prophylaxis. The first culture to be isolated was just at

hand, so that it could be used at once. Five injections were given under

the skin of the thigh to a recently developed case of the ulcerative

gingival variety, a noticeable improvement occurring almost at once, and

at death there was an apparent cure of the local lesion. However, the

accompanying protocol made at the time tells the whole story, no

adequate explanation being at hand.

Red Kangaroo (_Macropus rufus_). Disease of the mouth first noticed

March 31, 1912, died September 13, 1912. Necrotizing osteitis,

arthritis and periarthritis of left ankle, subacute fibrinous right

pleuritis, hemorrhagic bronchitis with atelectasis in right middle

lobe, abscess of right middle lobe; passive congestion of lungs,

liver, kidney, chronic splenitis, chronic general lymphadenitis. The

animal is in general good condition except for a fusiform swelling

about the left heel with evidence of fracture. The necrotic process in

the hare lip, nose and palate has entirely disappeared. One front

incisor has gone and the other is loose. There is a scar on the under

part of the soft palate in a small healed channel between palate and

floor of nose. There is no evidence of pyorrhœa. Cervical and axillary

lymph nodes are much enlarged, pale yellow, firm and of the appearance

like early stages of Hodgkin’s disease. Fascias of cavities congested.

The lungs are mottled purple, air content decreased, section surface

purple, exuding frothy blood. The whole right lung is covered with a

thick fibrinous exudate, most intense over middle lobe at site of

atelectasis. There are light scattered adhesions. The anterior margin

of the lung is adherent to the pericardium which is covered in the

front by exudate. Upper and lower lobes show hypostatic congestion.

Middle lobe has separate bronchus filled with necrotizing blood clot

extending into a smaller bronchus with complete occlusion. The alveoli

supplied by the last show atelectasis like hemorrhagic infarct. There

is a small subpleural abscess near the margin of this atelectatic

area. The bronchial lymph nodes are slightly enlarged, mottled yellow

and pink, firm with large, diffuse follicles. The pericardium contains

2–3 cc. clear fluid. The heart muscle is pale, purple and soft. All

the vessels are full of currant jelly clot. On the posterior surface

of the aorta internally about an inch above the valves there is a

patch of roughening with a suggestion of thickening and opacity. It is

comparable to the early stages of syphilitic aortitis. The liver is

normal in size, surface smooth, edges sharp, consistency firm and

friable, color purple. The section surface is glistening, smooth,

moist, and shows passive congestion. The gall-bladder contains fluid

brown bile and the common duct is patulous. The spleen is slightly

enlarged, firm and tough, capsule wrinkled. Section surface is mottled

red and purple with irregular gray trabeculæ and faint scattered

follicles with diffuse margins. The kidney capsule is smooth, strips

easily leaving a smooth brown surface. Organ is firm. The section

surface is glistening with a line of passive congestion with distended

vessels between the cortex and medulla which are of normal widths.

Intestines seem normal throughout. The pancreas is firm, pale pink,

slightly edematous. The mesenteric lymph glands are moderately

enlarged, yellow, firm, homogeneous with congested centres. About the

left ankle joint there is a necrotizing infection which has involved

the bone causing a pathological fracture of the lower end of the

tibia. Smears from the periarthritis, pleuritis and blood clot in the

bronchus show streptothrix, a short colon-like rod and a coccus in

fours—a picture precisely like that obtained from the jaw bone cases.

In addition to the above there is a very distinct encapsulated

pneumococcus form in smears from the blood clot in the bronchus. This

is the animal which was vaccinated with a culture made from the depths

of a necrotic mass, upon which treatment she rapidly improved and as

seen from the above notes recovered from the palate condition. Why she

should have a second infection apparently with the same organism is

difficult to determine. Possibly the second batch of vaccine was not

sterile, it not having been controlled because the first batch of

vaccine was sterile after one hour at 60° C. Possibly the animal was

sensitized and a few bacteria settled in the leg. It was along this

leg that the inoculations were made.

We permit ourselves the facetious observation that that vaccine

prevented the labial and cervical variety for five years, because during

that period it stood in the icebox, and there was no case of that

particular form to which to give it, although a few of the nasal and

gastric varieties occurred. It was recontrolled and did not show living

organisms. That it should have cured the disease in the jaw and

apparently later permitted a lighting up of a septicemic and pulmonary

form with necroses in the leg is difficult to explain.

Just recently we have used a vaccine from the current culture upon

another case beginning in the gums and jaw bones. This case was detected

early and was treated with ascending doses beginning at 0.3 mg. and

running up to 10. mg. At first there was some improvement, but the

animal finally died from pulmonary complications. The course of the

disease, however, instead of being three weeks, as is the customary

duration, lasted two months, an extension of the course which has made

us hopeful. These two experiments, indefinite though they be, have

offered encouragement and seem to supply a little additional support to

the idea that the organisms stand in etiological relationship to the

disease.

The employment of the vaccine has been extended to its use as a

prophylactic in animals exposed to the disease or specimens that have

slight reddenings or erosions on the buccal mucosæ suggesting possible

early stages of streptothricosis. Five animals have now had a course of

vaccine injections, ranging in number from 5 to 10 and in quantity from

0.3 to 2.4 mg. over a period of a month. Fourteen months have elapsed at

the time of writing and only one case has developed, but this of course

cannot settle the efficacy of the method; perhaps it would be safer to

demand that no case should ever appear in a treated animal, while the

disease did appear in the untreated.

The preparation of the vaccine is by no means a simple matter, since the

surface growth upon solid media is so tenacious. Methods such as are

employed for the tubercle bacillus have to be used. The first two

vaccines were made by scraping off surface colonies from agar and

grinding with glass balls. One successful batch was made recently by

simply triturating the colony directly on the agar slant, but the latest

method seems to offer the simplest and most generally satisfactory way.

Neutral broth is placed in flasks containing glass beads and sterilized

in the incubator. This is seeded with the Nocardia, incubated at 37° C.

until the surface is covered, heated to 60° C. in a steam sterilizer and

tested for sterility. If growth occur it is reheated until dead,

whereupon the broth is syphoned off, the growth emulsified by whirling

the flask, thus grinding the bacterial mass by the glass beads.

Sufficient saline is added to make a workable emulsion, and the fluid

then poured into bottles. Control by reculturing is again done, and if

the fluid be found sterile, 0.5 per cent. trikresol is added to keep it

so. These organisms cannot be counted accurately because of the

variation in length, their budding and coccoid forms. Standardization is

done by weight. A definite equal quantity of the suspension and of the

saline used to make it are evaporated to dryness in weighed vessels and

the whole then weighed. The difference is the weight of the organisms

suspended in the saline. Such a fluid can be diluted so that a given

bulk will contain a convenient weight of germs. The one now in use

contains 8. mg. per cubic centimetre. Dosage as indicated above usually

begins at 0.5 mg., a quantity which does not produce any local

inflammation at the site of injection. It is perhaps well to adopt a

quantity of 0.1 mg. per kilo as the initial quantity.

The Garden has encountered no case of the remaining important chronic

infections, glanders, lymphangitis, and infectious abortion.

SECTION XVII—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.”