Synonyms. Definition: Acute protozoan remittent fever, of rainy season or after, with destruction of red globules, anæmia, emaciation, dropsy, icterus and cutaneous or mucous eruption or discharge. Distribution: India, Burma, Cochin China, Persia, Phillipines, etc. Trypanosoma Evansi: a fusiform flagellate infusorian with undulating membrane, attacking the red globules: agency of flies as carriers, infection of dogs; of crows; feeding, licking; rats; open sores; stables; yards; pastures; pickets; stagnant water; manure or rubbish heaps; abattoirs. Lesions: anæmia; trypanosoma swarms during relapses; leucocytosis; œdemas; effusions; blood extravasations; splenic enlargement; emaciation; gastric and intestinal congestions; gastric ulcers; kidneys petechiated, swollen; brain effusion. Incubation, 2 to 8 days. Symptoms: local swelling, 2 to 4 inches by 4th day; decreases to 14th day; the general symptoms; hyperthermia 102° to 104° F., night highest; dulness; sluggishness; inappetence; icterus; cutaneous eruption; remission in 1 or 2 days; exacerbation after 3 to 10 days; catarrhs; petechiæ; stocked legs; pectoral swelling; encreasing anæmia and emaciation; ulcers on mucosa or skin; generative excitement; fœtid diarrhœa; urine profuse, bilious, albuminous or with casts; thirst; intestinal rumbling; debility; marasmus; hair erect; skin dry, rigid. Duration variable. Diagnosis: based on above, confirmed by finding blood parasites, constantly fatal in horses. Surra in camel, ox, buffalo, rabbits, rats, mice, dogs, cats, apes. Treatment: unpromising; mercurials, iodides, chromates, arsenates, terebinthinate, phenic acid, santonin. Dry, clean, airy stable, dry grain, tonics. Prevention: keep horse and mule from infecting locality; use oxen rather: stables, pickets, etc., apart from marshes, pools, manure and rubbish heaps; disinfectants, insecticides, seclude all surra-affected animals: smudges. Sanitary police.

Synonyms. Sar, Zahrbad, Gumzahrbad, Kushkzaharbad, Sokra, Sokhra, Tap, Tapdik (Punjab): Phitgya, Purana (Meerut): Berbag (Bombay): Tarai, Tebersa, Wabai-ki-bokhar, Pernicious Anæmia, Trypanosomosis, Relapsing Fever, etc.

Definition. An acute, relapsing, protozoan fever of equines, camels and elephants, inoculable on other animals, occurring during or after the rainy season, and characterized by hyperthermia which is liable to be intermittent, remittent or relapsing, anasarcous swellings, petechiæ of the mucosæ, icterus, cutaneous eruption, nasal, ophthalmic, vaginal and other mucous discharges, rapidly advancing anæmia, emaciation and debility, and above all, by the presence in the blood, at intervals from one to six days, of swarms of protozoa, analogous to those found in dourine or nagana.

Geographical Distribution. Surra has long been known to the English veterinarians in India, occurring during or just after the rainy season, and especially on the low flooded lands, along canals, rivers, lakes, etc., and later in Burma, Cochin China, the Persian Gulf, Persia. Lingard claims its existence in East Africa, North and South America, Australia and Southern Europe, but he has evidently confounded it with nagana and other affections. The discovery of the disease by Dr. Slee in 1901, among American, Australian and Chinese ponies in the Philippines is suggestive of a very wide diffusion of the infection in Southern Asia and adjacent islands, with which an American work on veterinary medicine must deal.

Cause. Parasite. Trypanosoma Evansi. The essential cause of the disease, Trypanosoma Evansi, discovered by Dr. Griffith Evans, Inspecting Veterinary Surgeon, British Army, in 1880, is a flagellate infusorian, pointed at one end, near which is a dark centrosome, and from this a flagellum running along the free border of the broad undulating membrane to the extreme opposite end of the parasite and extended beyond this as a waving lash. The length of the Trypanosoma Evansi is 20 to 50μ, (10 to 14μ, Smith and Kinyoun, Manila), its breadth 1 to 1.5μ. By reason of its large size and active motion it is easily detected in a film of fresh blood under ⅙th inch objective, and no less easily when dried and stained on a cover glass. It must be borne in mind that the mature parasite appears in the blood at intervals in swarms, so that examination at one time of day, or on a particular day, may fail to detect it, while examinations made earlier or later are successful. The general structure and successive stages of growth of the parasite appear to be the same as described for the Trypanosoma Equiperdum of Dourine, to which accordingly the reader may turn for description. The distinction from that parasite is to be found mainly in the pathogenesis. In this respect it should be noted that the parasites are strongly attracted by the red globules, upon which they fasten themselves by the blunt ends, shaking the cell in the most vigorous manner and even breaking pieces off and carrying them away. They are most strongly attracted by the concave part of the disc, and when there are rouleaux they will bore between the globules and even push them apart (Evans).

The appearance of the disease at the conclusion of the rainy season when the waters dry up and become foul, has led to the idea that the parasite lives in waters, but as this is also the time of the great swarming and activity of flies, and as the trypanosoma is found in the bodies of tabanidæ and hippoboscidæ that have bitten affected animals (Lingard), and as horses crowded together so that the fly with piercing apparatus still wet can pass from horse to horse (Evans), the opinion has grown that it is a compulsory parasite which is transmitted through the bites of insects. In 1880, Griffith Evans found that the native Hindoos attributed the disease to the bites of a very large brown fly which was active in July (probably a tabanus), in 1897, Pease identified the incriminated fly as the tabanus tropicus. Finally, Rodgers, in 1901, took flies that had been on surra horses, kept them 4 days or longer and found that their bites failed to produce surra; whereas those that were allowed to go directly from the sick to the healthy animal produced the disease in the latter. The direct experimental inoculation from horse to horse infallibly conveys the disease so that the flies are not needed to pass the parasite through an intermediate stage of its existence, but merely to carry it. It follows that no particular fly is the bearer but any insect may carry the infection from a bite or sore to inoculate it on a sore or by a bite on a fresh animal. Different observers have noticed the tendency to the infection of dogs and other animals that fed from rubbish heaps, or upon the carcasses of animals dead of surra, suggesting at once the intervention of the swarms of flies that congregate at such places. This is probably another example of the shrewd insight of the common mind, as in the case of the tick-borne Texas fever.

Lingard finds another bearer in the crow which sits on the backs of affected horses, pecking at the wounds, and passes at once to other healthy horses to peck their sores.

Experiments in feeding the infested blood to sound animals, have apparently succeeded, and the observation that dogs and cats suffer from eating the carcasses is in favor of this view. Horses that lick the infested sores, or the blood drawn by the flies may readily infect themselves, and especially if the mouth bears scratches caused by fibrous food, leech bites, or sores from bits, or if the pharynx or stomach has been wounded by bots or spiroptera.

The water and food are blamed by the natives in some quarters, but Pease’s observations on the Bombay tramway horses, which all perished though kept on boiled water and carefully picked fodder from sound regions, would suggest that this if a channel of infection at all, is not the main one.

The bowel excretions of rats harboring trypanosoma, when mixed experimentally with the food of the horse, have been charged with causing surra, but there are objections to the acceptance of this as a common cause. The alleged period of incubation in the horse in such cases was 40 days in place of the usual 7 or 8 days, when inoculated from a horse first affected in this experiment on a second the usual incubation of 7 or 8 days was shown, and though the horse fed on rat’s dung in the infected region of Bombay contracted the disease, the experiment failed when the same dung was fed in a high dry region unaffected by surra. The natural inference is that Bombay experimental horses contracted the affection in the usual way, probably through insects.

In the rainy season the Indian rats swarm with the Trypanosoma Lewisi, an entirely different species, and though they can be successfully inoculated with the T. Evansi of Surra, the T. Equiperdum of Dourine, the T. Brucii of Nagana, and it is alleged the T. Equinum of Mal de Caderas, yet these are not their common parasite. The presumption is that the rat affected with Trypanosoma Evansi could transmit the disease to the horse through one of the many possible insect channels or otherwise.

Neither condition, sex nor age appears to affect receptivity. Open sores especially open the way for infection.

The position of stables, yards, pastures or picket grounds near stagnant water, manure or rubbish heaps, abattoirs or other places that breed or attract flies, is a much more important consideration. Foul stables, or those having light from both sides are more exposed to flies.

Pathology and Lesions. The pathology of the disease consists in the rapid destruction of the red blood globules by the trypanosomata. It is a form of rapidly advancing pernicious anæmia due to the great and active voracity of the trypanosoma. The swarming of the trypanosoma in the blood at the period of the relapse and the absence of the mature form in the intervals is remarkable. The trembling movement in the blood at the period of swarming results from their prodigiously active movements. The red globules may assume various forms, crenate, echinated, (Ranking), and more or less broken up or disintegrated, their numbers steadily decrease, leaving the blood thin and watery with rusty serum and yellow (icteric) staining of the white tissues, even the bones. Encrease of white globules, actual or relative, has been a marked feature (always present in typical cases, Burke).

Petechiæ are especially common on the conjunctiva, vaginal mucosa, endocardium, and less marked in the nose, mouth, and serosæ.

Œdemas are common, yellowish, gelatinoid exudate at the base of the heart, subcutem, between the muscles of the limbs or elsewhere, and as effusions into the pleuræ, pericardium or peritoneum.

Distinct blood extravasations have been noted beneath the endocardium.

The spleen is often enlarged, excessively so if death occurred during a paroxysm. The lymph glands are swollen and appear dropsical.

The whole body is emaciated and shrunken, the visible (unpetechiated) mucosæ are pale and bloodless, often yellow, yet rigor mortis is well marked.

Gastric ulcers are common (Steel, Burke, G. W. Evans) apparently preceded in many cases by capillary embolism, congestion and degeneration. Intestinal congestions are frequent (Steel, Burke), but ulcers are rare (Geo. H. Evans).

The liver may be normal (Griffith Evans), or especially during a paroxysm (Lingard) congested, inflamed and enlarged. The pancreas is usually normal.

The kidneys are petechiated, congested, œdematous, or the seat of blood extravasations.

Instances have been noted of cerebral and meningeal œdema (Steel, Lingard), encrease of fluid in the arachnoid or lateral ventricles, or in the spinal cord, with gelatinoid exudation in the lumbar portion (Lingard). Like other tissues, in advanced stages the nerve centres are usually anæmic (Geo. H. Evans).

Incubation. As made out by inoculation cases this extends from two to eight days, according to the dose—five to seven days being the most common. Infection by inoculation subcutem in mules showed a hyperthermia on the fifth day; or by ingestion (feeding the virus) on the sixth day (Steel). Longer (alleged) incubation depends mainly on the first slight paroxysms having been overlooked, or set down for the frequent bilious and icteric condition which is common in mules and horses in India (Steel), or to a later infection by insects or otherwise.

Symptoms. In experimental cases a small raised swelling in the seat of the inoculation, appears in 24 hours, encreasing to 2 to 4 inches in diameter, and 1 to 1½ inch high by the 4th day, and loosely connected with the parts beneath. From the 4th to the 14th day it decreases in size and softens and general symptoms set in.

In casual cases these general symptoms are the first to be observed. There is a transient fever 102° to 104°, highest toward night and without preliminary chill, hot mouth and skin, dulness, sluggishness, inappetence, yellowness of the mucosæ, petechiæ on conjunctiva or vulva, and sometimes nodules like those of urticaria on the skin. After a day or two these symptoms subside, the temperature is 101° F., or below, the mucosæ clear and pale, and spirit and appetite nearly normal. These slight first paroxysms are rarely seen by the veterinarian, having been looked upon as one of the oft-recurring bilious attacks of a hot climate. The remission lasts for 3 to 10 days when the second paroxysm sets in, like the first but often more marked: temperature 102° to 104°, eyes especially the membrana nictitans petechiated, epiphora, slight catarrh from nose or vulva, it may be stocking of the legs, or pitting swelling under the breast bone, or abdomen, or in the sheath. Like the first, the second paroxysm subsides, and after another interval a third sets in, to be followed in like manner by a fourth, a fifth and so on, if the patient survives. With each the symptoms become more pronounced, the mucosæ are left more pale and bloodless, debility and weakness are greater, emaciation is more marked, œdema of the limbs or body more extensive, hyperthermia may reach 105° or more, the pulse is weaker and the heart more liable to palpitation, and the respirations may reach 50 or 60 per minute. Yet in sparely built animals dropsy may be entirely absent (Steel). Steel often found superficial, circumscribed ulcers on the tongue, inner sides of the lips, nose, eye, or vulva, beginning as epithelial degeneration, followed by superficial erosion and early healing. Sometimes, similar erosions appeared on the skin. Generative excitement may be present, the mare appears to be in heat, while the horse has erections, which are supposed to depend directly on the implication of the generative centre in the lumbar myelon. The submaxillary glands sometimes swell and even suppurate and discharge a gluey pus (Griffith Evans). The bowels are usually costive at first, the fæces may be glazed, but in advanced stages they become soft, pultaceous and fœtid. The urine at first normal in amount, becomes later abundant or even profuse (Griffith Evans, Ranking, Nariman and Vaz, Lingard). It is at first yellow and turbid, later of a dingy green or greenish yellow. Sometimes it diminishes as the disease advances. It may contain bile, albumen, or even casts (G. H. Evans), though the latter appear to be exceptional. The reaction varies, sugar is absent, and the parasite has not been found in it. Appetite though interfered with during the paroxysms, remains fair or even voracious in the intervals and the animals may eat to the last (Burke). Thirst usually encreases with the advance of the disease, in keeping with the free urinary secretion. Rumbling and gurgling of the bowels are common and even tympany at times (Lingard).

In the advanced stages the picture is one of great anæmia, marasmus and general debility. When moved the animal will stumble over the slightest obstacle, even the litter, recovering himself with effort and difficulty. If he should fall he is liable to remain down indefinitely, the side next the ground becoming drenched with sweat though there is no general perspiration. The hair becomes encreasingly dry, withered and erect, the skin dry, powdery, rigid and more and more firmly adherent to the bones and muscles, losing all its natural pliancy and mellowness, and becoming like that of a dead animal. It is bloodless, and sloughs readily over the prominent bones, where compressed or bruised in lying, owing to the lack of nutritive and reparatory action. The visible mucosæ are absolutely bloodless. The muscles as a whole are wasted to an extreme degree, but this atrophy is most marked in the back and loins, along the longissimus dorsi and in the quarter in the gluteal muscles. The patient may remain recumbent, from sheer weakness, for a length of time at the last, or he may get up after a long recumbency and stand to the end.

Death may occur early with general anasarca and extreme hyperthermia (110° F.). In the great majority it appears to result largely from perforation of the stomach, clots in the heart, or general debility and heart failure.

Diagnosis. With symptoms such as are above described the discovery of the trypanosoma in the blood completes the diagnosis. Trypanosoma is found in dourine, nagana and other affections so that the discovery of it alone would not be conclusive as to the existence of surra. Nor can the discovery of the parasite always be made at the first or second attempt. The swarm of mature trypanosomata is found with the advent of a paroxysm, and as the veterinarian is often called during the decline of the attack the parasites have already retired and elude his investigation. It becomes needful to take the temperature and examine the blood daily sometimes for eight or ten days, and when with a sudden rise of temperature he finds also a swarming of the mature trypanosomata, the diagnosis is perfect. A drop of blood placed on a cover glass, pressed down upon the slide, and placed under the microscope, will show the parasite with eel-like movements among the blood globules. There may be very few during the first or second paroxysm, but they become numerous and very obvious as the disease gains its height. Evans recommends to use defibrinated blood.

They may be dried rapidly on a cover glass, fixed in absolute alcohol one or two minutes, then stained ten minutes in a mixture of the two following liquids united just before using:

The plasma of the trypanosoma appears blue, the flagellum red and the chromatin of a different shade of red. It may be permanently mounted in balsam.

Mortality. The disease is constantly fatal in horses, though the animal may survive for months.

SURRA IN CAMELS.

Haggar describes this as having remissions or intermissions as in the horse, the trypanosoma disappearing during the intervals to reappear with the hyperthermia. The temperature may rise to 106° F. and the animal wastes away to a veritable skeleton. A remarkable feature of the disease is the formation of immense abscesses containing a thick, cream-colored pus on the sides of the chest in the vicinity of the pad, and in the sheath and scrotum or udder near to the stifle pad. The mortality is nearly as great as in the horse or mule, yet the camel drivers say that a small percentage recover.

SURRA IN BOVINES.

The domestic ox, the sacred cow of India (Lingard) and the water buffalo (caribao) of the Philippines contract Surra. It is interesting to notice that in these animals the disease is relatively mild and recoveries are frequent.

In the Indian buffalo it causes dulness; advancing emaciation; slight temperature variations; muco-purulent inflammations of the conjunctiva, cornea, and pituita; and occasionally eruptions under the breast or belly.

Among lesions were atrophy, softening of lymph glands, enlarged liver and spleen (slight), petechiæ and blood extravasations on the pericardium, epicardium and other serosæ, and on the intestinal mucosa which sheds its epithelium in patches.

Stall enzoötics in cattle do not seem to affect horses casually. The disease is easily conveyed to rabbits, house rats and mice, dogs, cats and apes. Goats and ducks appeared to be immune (Penning).

TREATMENT OF SURRA.

In well established cases in the horse, ass or mule no treatment has succeeded in saving the patient. Almost every germicide has been called into requisition but without good effect. Among these may be named: mercuric chloride subcutem, iodine and potassium iodide intratracheally, iodoform subcutem and intravenously, oleum terebinthinæ subcutem and intravenously, potassæ bichromas by veins and stomach, cinchona alkaloids and arsenic, phenic acid and iodine, quinine, hydrargyri biniodidum, santonin, potash. The claims of different agents, notably arsenic and phenic acid, have been supported by the manifest improvement of condition under their use and the disappearance of the trypanosoma, but both these conditions may often appear during intermissions, without medication. The usual outcome is that the animal dies and the only claim that can be made is a slight extension of life. This is favored by dry, clean, airy stables, change of water, rich grain and succulent food (oats, rice, linseed, barley, gram sorghum, bran, middlings, salt, etc.), with iron, arsenic, and other tonics, yet the best that can be said for them is that they have deferred somewhat the inevitable death.

Prevention of Surra. The first consideration is to avoid placing equines and especially horses and mules, or camels in the infecting localities in the rainy season and just after it. Oxen and buffaloes can be used in such places with greater impunity. If they must be used in such localities, place the stables or pickets in dry locations well apart from marshes, and stagnant water. Keep the stables dark during the surra season, open to light on one side only and with screens in the windows. Make a deep pit for the manure, keep it well darkened and screened and turn every particle of manure into this several times a day so that the stable shall be perfectly clean. All rubbish heaps should be similarly dealt with. The flies breed in the manure and decaying organic matter. After each sweeping of the stable sprinkle the manure in the pit with some disinfectant, phenic acid, tar water, copperas, etc. Smear the skins of the animals with tar water, coal tar water, naphthalin, daily if necessary to prevent the attacks of the flies. Other suggestions in this line can be found under parasites.

An important consideration would be to seclude every animal attacked with surra. The flies can only carry and inoculate the poison when there is some source from which they can obtain it. Until we shall learn how many animals, tame and wild, casually contract the Trypanosoma Evansi we cannot speak of how effective this may be made, but it is at least a substantial advance in the line of restriction, since the infected horse or mule in the vicinity of healthy ones is a constant peril, and as given insects attack by preference, given favorite genera, the horse flies, coming from the diseased animal are much more likely than other flies to attack the sound horses. In a surra season it would be a wise economy to destroy the infected equine at once, as according to all past experience, sentence of death has already been passed upon him, and his preservation even for a hour is hopeless for him, but full of the gravest danger for others. The carcass and all pertaining to it, blood especially, should be promptly and deeply buried and the place thoroughly disinfected.

In the same way smudges made by burning green grass or other vegetation, tar, leather or other material producing empyreumatic products offensive to the fly may be employed.

Sanitary Police. The Department of Agriculture forbids the landing in the United States or its dependencies of any animal from the Phillipines. If the infection should by any accident be imported no cost should be considered too high to secure a prompt and thorough extinction of it.