Part 39

SECTION XIII-PART II THE EYE

INFLAMMATIONS.

Conjunctivitis is rather rare but does occur in all varieties of animals, seldom however, to the extent that the specimen has to be sacrificed. So far as the daily reports can be relied upon we have had no epidemic inflammations of the eye. The parrots and monkeys are the only animals that can be handled enough for treatment, and in them the applications have not seemed very efficacious. Two cases of conjunctivitis and iritis have had a tuberculous basis and two other specimens have had tuberculosis in the eye. Two parrots had, in association with generalized tuberculosis, semisolid masses in the orbit which dislocated the bulb, thickened the lids and presented as yellowish granulating tumors under the conjunctiva; a Swainson’s long-tailed jay (_Calocitta formosa_) had this lesion on both sides. The only case in a mammal concerned an Anubis baboon (_Papio anubis_) in which one eye had been enucleated, two weeks before death, for purulent ophthalmitis. The other eye became affected shortly after the extraction and the animal was killed; it was found to have caseous pneumonia. The tuberculous process had probably begun in the region of the optic nerve and involved the whole bulb. Secondary infection with pyogenic cocci had been superimposed upon the original process. Keratomalacia, encountered on a few occasions, will be discussed by Doctor White.

Iridocyclitis was found in a white browed guan (_Penelope superciliaris_) the notes of which are condensed as follows:

The internal organs show nothing of value pathologically. The right eye shows moderate conjunctivitis and a marked thickening of the cornea with complete opacity. The lens is destroyed and the retina infiltrated by gelatinous material. Humors are watery, non- suppurative, but the fundal portion of the retina shows several poorly circumscribed, yellowish white, gelatinous collections. Microscopical section of cornea shows replacement of normal bundles by wavy ones intermixed with small numbers of nuclei. These are never of inflammatory type, but always of connective tissue type. Conjunctival mucosa defective in centre, puckered but shows no subjacent inflammatory features. Ciliary body richly infiltrated by lymphocytes and vessels distinctly congested. This condition extends over whole anterior surface of iris and for a short distance over posterior. Sclera shows much bone formation. Chronic interstitial keratitis, subacute interstitial iritis and cyclitis.

CATARACT.

Opacities of the cornea are quite common among our specimens, most often due we believe, to local trauma; ungulates exhibit them more than other varieties. Cataractous opacities of the lens are frequently observed in senile animals but, while I have no figures for the statement, I believe they are not as common among our specimens as can be observed in domestic horses and dogs. No record has been made of streaky clouds or spots in the lens but only of complete opacities. There are three only, an aoudad (_Ovis tragelaphus_) a macaw (_Ara macao_) and a summer duck (_Aix sponsa_) the last of which alone is interesting. This bird, a fully developed adult female, was killed because of total blindness and found to have a low grade chronic pancreatitis and a bilateral Morgagnian cataract, the lens capsule containing a thin cloudy fluid with the nucleus quite freely movable in it.

AMBLYOPIA.

A very interesting case of amblyopia in a young monkey was studied and reported by Dr. H. M. Langdon and Doctor Cadwalader in the _Journal of Comparative Pathology and Therapeutics_, Vol. XXVIII, Part 4. Because of its unusual character and careful investigation, the report is reproduced here:

Pigtailed macaque (_Macacus nemestrinus_) was born June 9, 1913, in the monkey house, a well developed baby. He thrived and was as good as any for his age. He was never known to have anything wrong with him until on the morning of June 3, 1914, when he was found on the bottom of the cage in the monkey house. He had clenched hands and feet, jaws tightly closed, lips drawn back, eyes staring and glassy, with convulsive shaking of the extremities. At intervals he would become limp, with fists still clenched, and with only occasional jerks in the extremities. This would last about a minute, and then convulsive movements would be resumed. The entire “fit” lasted about ten minutes. He was immediately removed from the large cage in the monkey house to a small one in the back room of the laboratory. When put in the small cage he staggered as if dazed, and groped about apparently blind. He never recovered his sight entirely, but at times seemed to see better than at others. He was not seen in a “fit” in the laboratory. On June 24th, a small piece of banana was offered by a person who stood directly in the sunlight. The monkey came to the front of the cage, reached out and grasped very firmly the thumb of the hand holding the banana but did not take the banana although he very plainly wanted it. The banana was thrown into the cage, hitting the monkey on the back. He turned very quickly, then smelled over the floor of the cage until he found the banana. On June 30th, he was examined by Doctor Langdon and the following condition was noted:

“Pupils react to the light of the ophthalmoscope. Optic discs are normal. Arteries possibly a little small. No other fundus changes.” On July 1, a cloudy day, he was laid facing a window. A coat sleeve was laid over his eyes for a minute and then quickly removed. His pupils were seen to react slowly but distinctly to the light. His gaze would not follow a finger moved in front of his eyes. When put back in the cage he climbed up on the wire at the back and then tried to climb the plain sheet-iron side. He groped and felt for a support and then fell. This he did several times. About August 1, when the eyes were examined, there seemed to be more visual perception and very distinctly prompter pupillary reflex, which condition remained about the same when examined October 1. He died October 10, 1914, of a compound fracture of the right femur inflicted by a monkey in the adjoining cage.

At autopsy the viscera appeared normal throughout. The animal was fairly well nourished. There was about 5 cc. clear, pale yellow fluid under the dura. It escaped upon removal of the brain. There were adhesions of the dura over the temporal lobe (inferior surface), posterior and external to the optic tract, so firm as to remove some periosteum and superficial bone. Rest of dura seemed normal.

Examination of the brain. Sections were made from different parts of the cerebral cortex, all of which were more or less alike. There was swelling of the endothelium of the pial lymph spaces, with some separation of the fibres of the pia itself which extended into the sulci. The perivascular lymph spaces of the larger arteries of the cortex were dilated, and the adjacent cerebral tissue was edematous. A well marked endothelial swelling and hyperplasia affected a number of the arteries and capillaries producing marked general or nodular thickening in some places. Accompanying these hyperplastic changes there was a marked calcification of some of the arteries. This was not confined to one tunic, but in some instances it extended almost completely through the vessel wall, and here and there the lumen of a vessel was nearly obliterated. The main features were endothelial hyperplasia, edema of the pia and of the subpial cortex with some calcification of the vessels. It was perhaps less well marked in the occipital lobes than in other parts. The optic nerve and other portions of the brain appeared to be normal.

MOON BLINDNESS.

It seems also profitable to repeat here a report Dr. H. M. Langdon and I made in 1911 upon a horse with periodic ophthalmia or “moon blindness,” a widespread condition and one upon which there is even to-day little known and much contradictory theorizing. It is worthy of record that Dr. J. H. W. Eyre of Guy’s Hospital, had a case to study at the same time as ours. He did not find the protozoön-like body discussed below, but laid weight upon the isolation of St. aureus, an organism often mentioned in the literature about this disease. I cite the whole report since our publication in the 1911 Report of this Garden seems not to have been quoted in any of the reference articles on “Moon blindness.” Those who are interested in the clinical and pathological sides of the question will find a good summary in _Veröff. aus der-Jahres. Vet. Berichten der beamt. Tierärzte Preussens_, 1908, and the bacteriology of the equine eye by Karsten, _Inaug. Disser._ Giessen, 1909.

“During the latter part of 1909 and first part of 1910 we had a horse referred to us suffering with recurrent ophthalmia or moon blindness. This affection, suggested by its name, is supposed to have some relation to the lunar periods. Some points in our work showed that such may be the case. Attacks appear not infrequently at the time of the full moon, and in our only experimental infection twenty-eight days elapsed between inoculation and a general ocular inflammation.

“This affection manifests itself as a conjunctivitis early in the attack, but rapidly progresses to an iridocyclitis and lastly to a panophthalmitis. After each attack the ball is smaller until it is so shrunken as to be sightless from chronic thickening and opacities. The causation is not known. The disease behaves not unlike an infectious one, remaining in a stud for years at a time. Not every horse may be affected. It has been connected with dampness, bad fodder, overwork and the like. Again others have connected it with malaria or rheumatism. Potapenke, Vigezzi, Koch and others have found various microörganisms, no two of which seem to be the same. Even an animal organism like malaria has been described. (Whether or not malaria has anything to do with the disease, it must be said that our horse was favorably affected in regard to temperature as well as to the eye condition by repeated subcutaneous injections of Quinine Bisulphate, Grain xx daily.) The attacks last five to nine days. One or both eyes may be attacked and not uncommonly do they alternate. One eye may cease to have attacks while the other continues. The experiments here recorded were made with the idea of transmitting the disease to other horses. They were only partially successful. During eight months the affected animal referred to us had six attacks of ophthalmia. The attack was observed for study on the first occasion, but during the second his anterior chamber was entered by a needle attached to a syringe, the exudate aspirated and injected into the eye of a horse with apparently healthy eyes. The history of this second horse will be given later. The attacks of the first horse ranged from six to twelve days. Five of the six affected the left eye and one the right. In January, 1910, the left eye was used for further inoculation, and following this traumatism complete recovery never took place. The corneal scar left by the needle tract almost disappeared, but an inferior anterior synechia formed and was followed by a spreading opacity of the cornea, much wrinkling of the iris and opacity of the depths. After the fourth attack in this eye it was completely blind. Material was obtained from this eye during its last attack, but it was merely serous fluid containing a few blood cells and epithelium, but no bacteria.

“In transferring the affection from this animal, the conjunctival sac was washed with 1–5000 bichloride of mercury solution and well rinsed with salt solution. The anterior chamber was then entered with an aspirating needle and the exudate removed. This consisted of 0.4 cc. slightly turbid straw colored fluid containing a few shreds of lymph. Bacteriological cultures, moist and dry preparations were made from a part of this, while the remainder was introduced into the anterior chamber of the second horse. This animal’s eye showed the effects of the traumatism for eight days, and then was normal save for a small opaque spot in the cornea left from needle puncture. After twenty-three days a small patch of lymph collected in the pupil. This increased slowly accompanied by lacrymation until the twenty-seventh day, when a sudden and violent conjunctivitis arose. The lymph in the anterior chamber likewise suddenly increased and rapidly became pus, forming a hypopyon. The conjunctivitis became purulent. The violent stage lasted five days and slowly subsided, leaving an ectropion with a densely injected bulbar conjunctiva, almost complete corneal opacity and an irregular contraction of iris, apparently due to several small synechiæ. The depths could not be seen because of the corneal condition. This stage of affairs remained during the rest of the animal’s life, two months. He was permitted to live to see if an exacerbation of this chronic process or involvement of the other eye would appear. Such not occurring in two months, he was killed and the eyes removed. Fluid removed from the left eye of the first horse when killed during the last attack was injected into the anterior chamber of a third horse. This animal’s eye received the operation well and the trauma had entirely disappeared when the animal died on the eighth day.

“LABORATORY EXAMINATIONS.—From fluid removed from horse eye (No. 1) anaerobic cultures made on milk and blood serum, blood agar, glycerine agar; cultures were made directly from the fluid, while the coagula were dried upon slides and stained as follows: Loeffler’s, Gram’s, Giemsa. In all there are very few recognizable bodies. They are red blood cells, polynuclears and a very few small mononuclear cells. In regard to microörganisms three structures present themselves. A well staining Gram-positive, rounded end rod of fairly uniform size but tending to grow in pairs and stain rather irregularly with Loeffler and Giemsa. These forms are sometimes called ‘dumbbell’ in that they are bipolar, or even seem to have a constriction in their centre. Another form is peculiar and cannot be said to be recognized as a bacterium. It is circular, of fairly regular size and contour and in many places looks like a very large coccus. In Loeffler’s stain it is colored deeply in the centre with a paler marginal zone and an unstained halo about it, which, however, is not like a capsule. In the Gram and Giemsa method it is deeply blue or purple with a retractile centre and very sharply outlined contour. These forms varied from 3 to 5 microns. The third form is a wavy delicate short mycelium-like thread. Smears from the cultures as made above showed chiefly a Gram-positive, rounded end rod but which did not grow on planting out. It grew on aerobic media, but was not found on anaerobic. The Gram-positive organism would not grow beyond the fourth generation. It was not identified with any known species by the characters manifested during the short time we were able to keep it alive but could be placed in the Hog Cholera group. The mycelium was found to be an aspergillus. In regard to the large coccus-like body, little can be added to the above description. Further examination did not reveal characters permitting us to place it among the protozoa. No evidences of division were seen. The body is quite uniform in appearance, varying only in size. Whatever this is it seems to be an organized body.”

“Cultures from pus in the anterior chamber of the second horse showed the palely staining rod, an aspergillus and Micrococcus aquatilis. The first was planted on horse serum bouillon, but did not grow after the first generation. These cultures were made after death, but the cultures made during the acute attack direct from conjunctival sac contained such a host of organisms that no judgment could be formed of their relative importance. The polar staining rod was found in smears. No large coccus- like bodies were observed in the second horse. Fluid taken from the first horse’s eye at death was sterile.”

“These observations are at variance with those of others but such results are not unique in this respect. It seems as if the polar staining rod deserves some consideration, and we expect to devote some attention to it if another horse suffering from recurrent ophthalmia come to our notice. The large coccus-like bodies are very interesting and may be protozoa. The finding of the amœba in the cases of Potapenke, increases their importance. Before, during and after the fourth attack of the first horse twenty grains of quinine bisulphate were given hypodermically daily for twenty days. The attack was very mild. Before the drug was given his temperature had ranged from 99° to 101° F. Immediately after the first dose the temperature fell to below 99° F., and remained at a very regular level during the entire twenty days. No malarial organisms were found in the blood.”

The ear is without special interest except as a place of localization of sarcoptes, demodex and fly larvæ. A few cases of acute catarrhal otitis media have been found in association with nasopharyngitis both of the nonspecific variety and that which resembles distemper. One case which led to meningitis has been mentioned.

SECTION XIV CONSTITUTIONAL DISEASES

There is a long list of diseases including among others such conditions as hyperthyroidism, osteodystrophies, diabetes and gout which are spoken of as constitutional but which in reality are usually dependent upon some lesion peculiar to a definite organ. Several have been discussed under systemic diseases so that there remain for consideration in this section only two, gout and diabetes.

Constitutional diseases are recognized in wild animals either not at all or by some happy chance which permits of examination direct enough to elicit diagnostic criteria. Gout has been discovered for example in some parrots and herons because of their swollen feet and their movements. In veterinary practice fairly accurate diagnoses are possible but in wild collections they are nearly always hit or miss. Therapeutics naturally follow this rule.

GOUT.

Gout in mammals has been observed in the London Zoological Garden but has not been encountered here or we have overlooked it. Avian gout on the other hand in one of its forms comes to our attention not infrequently. It occurs most often in parrots, gallinaceous and anserine birds and herons; occasionally accipitrine birds will suffer with it, an observation more often recorded in European collections than with us. The figures show no predominance of percentage for any order but the records indicate that the most beautiful examples of internal uratic deposits occur in the anserine birds and parrots, while the best specimen of general gout, including the joints, was found in a boat- billed heron (_Cancroma cochlearia_) quoted below.

In so far as etiology of this disease is concerned in domestic stock, too rich food, especially in protein, and restriction of activity seem to be credited with the greatest influence. These factors, while doubtless of importance for birds as they are believed to be for man, do not seem to fill all the requirements since all our specimens are confined and, because of their lack of exercise, possibly receive too much food. Judging by our observations and by publications from other gardens, carnivorous birds are not conspicuous for the incidence of gout whereas grain- seed- and fish-eaters suffer more often. This suggests that these varieties cannot dispose of dietary protein which might be excessive for their metabolism while in captivity, whereas carnivorous species have a digestive and chemical reserve to take care of excess protein. Some such accommodative power must exist in human beings since not every large meat-eater develops gout. Heredity, often blamed for the human disease cannot help us with these birds. Examination of the diet list at the Garden does not reveal a great percentage of concentrated protein in the feed of the grain- and seed-eaters. The disease occurs too seldom to disturb the accepted dietary for its possible elimination. Studies now going on may indicate appropriate changes in the dietaries that might be responsible.

Arthritic gout appears usually in the pedal joints but may be found in the wings. Irregular, sometimes very deforming swellings appear which must be tender judging by the quietness of the bird and by its behavior if the joints be touched. Most often the swelling seems greater upon the flexor (palmar) surfaces of the toes or in the end of the tarsal articulation. Aside from these few observations there is nothing peculiar about the attack or the specimen during its sickness. Chronicity seems to be the rule and little emaciation may be found. Appetite is normal or excessive, provided the food can be reached.

Internal or serous membrane gout cannot be recognized during life so far as I know. The bird may seem in its usual condition of feather, activity, appetite and elimination, when suddenly it will fade in a day or so and die. At autopsy the serous surfaces of the heart and peritoneum will be white with uric acid crystals and the kidneys a pale yellow brown with markings indicating that the pelves and tubules are choked with urates.

The boat-billed heron (_Cancroma cochlearia_) had had bad feet for three months. The general condition is poor as to plumage and flesh. The tarsal and metatarsal joint areas of both legs are surrounded by firm tough swellings involving skin and periarticular tissue. That on left foot has ulcerated and bled. On section the swelling is found to consist of reddened fibrous tissue around tendons, the latter apparently running through smooth sheaths. At both ankles are urate deposits clearly seen in this inflammatory tissue but at the lower end of the tarsus there are no distinct deposits. The joint surfaces do not seem to be involved. Knee, hip, and wing joints seem uninvolved. Internally all surfaces are opaque by sprinkling of whitish or yellowish dots like urates; this is especially marked over heart. Pleuræ aside from urates are negative. Lungs very slightly uniformly congested throughout. Aorta and branches are stiff, intima smooth. The liver is soft, deep brown color, architecture seems normal. The kidney has a smooth capsule and a smooth pale yellow surface. Organ is firm. Section surface is glistening and opaque, every lobule clear, pelves filled with pale yellow material, cortical areas irregular. Alimentary tract negative. Microscopical section of kidney shows general topography retained, vessels very much injected, some showing thrombosis. Cortex slightly irregular probably by swelling of medulla. Tubular epithelium swollen and granular or desquamating and degenerating. Glomeruli vary in size and shape, mostly fill out the capsule. Capillary cells show some vacuoles. Some urate collections in tubules; practically all pelvic tubules have some urates. Interstitial tissue not increased. Blood vessel walls somewhat loose. Endothelium prominent. No areas of degeneration seen.

DIABETES.