Chapter C: F. Dawson, in investigating a wasting disease of well fed Brahma (9)

_Microbiology._ The parasite is formed in the red globules and blood serum of the affected sheep and closely resembles the microbe of Texas fever. In the blood globules the parasite is seen in different forms, round, oval, oblong or curved and from one tenth to one sixth the diameter of the red globule. A single red globule may show from one to four of the microörganisms. They may at times show indications of division, and at others, automatic amœboid movements, from one portion of the blood globule to another, or from the periphery toward the centre. The affected blood globules are usually enlarged, having lost their biconcave outline, and become biconvex or spherical, with irregular crenated surface, and a dull, lustreless appearance instead of a clear red or yellow aspect. The protozoön stains readily in anilin red or methylene blue.

_Lesions._ The condition of the carcass was good or even high, in sheep attacked when in good flesh, and in which the affection ran a rapid and fatal course. In sheep attacked while in low condition on the other hand, the case tended to be milder and more prolonged, and the body was emaciated and anæmic. Dropsical swellings were common on the ears and sides of the head and neck.

The skin, connective tissue, fat, and other normally white tissues were usually of a yellow color, varying from sulphur to lemon color. The muscles were pale and soft with a yellowish tinge.

The blood was pale, thin and watery, especially in protracted cases, formed a loose coagulum, or remained fluid with a grayish red color. There was marked leucocytosis (1:4 or 5).

The stomach and intestines were more or less icteric, and contained little ingesta.

The liver was congested, softened, shrunken in protracted cases, colored of a deep yellow especially in the interior, and with gorged biliary radicles so that the acini stood out very prominently. The gall bladder was usually well filled with a thick, flocculent bile, yellowish green, blackish green or chocolate color.

The spleen appeared shrunken, somewhat spherical, 2 to 3 ozs., firm, and with a dark, reddish brown pulp.

The kidneys were greatly enlarged, weighing 12 to 16 ozs., dark red or bluish black, friable, and on section exuding freely a bloody or chocolate-colored liquid. The capsule was easily detached. The bladder contained a bloody or chocolate-colored urine, but was sometimes empty.

The heart cavities were empty or contained small diffluent blood clots. Petechiæ were common on pericardium and endocardium.

Yellowish or yellowish green gelatinoid effusion was often present, not only on the head and neck, but also on the inner side of the thighs, and in one or other of the serous cavities.

_Symptoms._ The first indications noticed are dulness, listlessness, a dragging behind the flock, ceasing to graze, arched back, and stiff or unsteady movements. There is moderate fever, yellowness of the visible mucosæ and skin, and rosy, bloody, or reddish brown urine.

Puffy dropsical swellings are noticed, especially on the ears, sides of the face, on the neck or thighs, and the patient lies down most of the time.

The patient usually dies in a state of collapse which has lasted for several hours, yet in certain cases it is preceded by a convulsive agony.

It is certain that the affection may appear in a mild form, as sheep slaughtered in apparent health are found to show the general icterus, the congested liver, and the leucocytosis with crenation of the red globules which characterize the disease. The icteric carcasses are said to be recognized and condemned at Kansas City and Omaha.

The _duration_ of the affection is from 1 to 5 days, though it may last longer, and severe attacks usually end in death.

The _prevention_ of this disease can, as yet, be based only on the same principles that guide us in the case of Texas fever. Search should be made for an invertebrate host of the protozoön, by the extinction of which infection may be stopped. The spring outbreak could be opposed by feeding hay on safe ground until the higher pastures furnish sufficient vegetation. To counteract the autumn attack, the sheep might be fenced out from the alkaline bogs, and the forage supplied in the form of hay or soiling crops. If it should appear that any wild animals harbor or transmit the parasite, a campaign of extermination upon them would be in order. If, as seems to have been the case in the early nineties, the movement of sheep from the infected flocks and pastures tends to cause the disease, this should be legally interdicted. Finally, the complete extermination of the sheep on infected areas could be practiced, and their place supplied by the immune Angora goat.

PALUDISM IN DOGS. MALIGNANT PROTOZOAN JAUNDICE.

Distribution: Senegal, Lyons, E. Africa, Paris, Pas de Calais, Cape
Colony. Microbiology: piroplasma: differentiation from that of Texas
fever: pathogenesis: tick-borne. Symptoms: incubation 3 to 5 days;
dulness, prostration, apathy, drowsiness, anorexia, thirst,
hyperthermia, icterus, hæmoglobinuria, offensive odor, emaciation,
protozoön in globules, loss of globules. Death in collapse. Lesions:
body shrunken, emaciated, fœtid; dark tissues, mahogany yellow,
petechiæ, enlarged congested liver and spleen; muco-enteritis; bloody
urine. Treatment unsatisfactory. Prevention: keep from tick infested
land; clear and cultivate land; smear dog with insecticide ointment
when hunting.

In certain malarial districts dogs suffer severely and even fatally from a febrile affection in which violent shivering is followed by great hyperthermia and yellowish or brownish red discoloration of the visible mucosæ. It was frequently attributed to malaria, and even sought to be identified with intermittent fever in man. Marchoux in 1899 studied this disease on the malarious seaboard of Senegal, and recognized the existence of hæmoglobinuria and the presence in the red globules of a hæmatozoön. Leblanc, about the same date, found a protozoön in the blood of dogs at Lyons, suffering from “red water,” and Koch later found a double piroplasma in the red globules of suffering dogs in East Africa, both considering the disease analogous to Texas fever in cattle. Nocard and Almy in 1901, at Charenton, Paris, met with a similar affection in a dog which had just returned from a fox hunt, and was covered with ticks. Its urine was brownish red, like coffee-grounds, and highly charged with albumen and hæmoglobin. Many of the red globules were affected and contained minute, spherical refrangent bodies which, when stained with carbolized thionine, appeared like those of Texas fever. There were but 2,800,000 red globules in a cubic millimetre of blood.

The injection of 5 grammes of the blood into the jugular of an aged bitch caused in the 3d day hyperthermia (105° F.) and an extensive invasion of the red globules which still counted 6,100,000 per mm. On the 4th day the animal was thoroughly prostrated, refused to eat, had hæmoglobinuria, and many individual red globules enclosed from 4 to 8 hæmatozoa each. On the 5th day the count of the red globules was but 4,400,000 per mm. By the 6th day the urine was nearly normal, and appetite returned, but the red globules counted but 3,500,000 per mm. Menveux went to Pas de Calais with an Irish setter to hunt rabbits. The dog came in every night covered with ticks. In 5 days he sickened, with extreme prostration, diarrhœa and red urine and died on the 25th day.

Wm. Robertson describes the disease in Cape Colony. The piroplasma was first identified at Grahamstown by Purves and successfully inoculated by Spreul. By intravenous inoculation symptoms appeared on the fourth day and death followed about the sixth, while by subcutaneous inoculation the course was slower and the animal died about the eleventh day. Robertson inoculating from animal to animal carried it through a succession of thirteen dogs all of which perished. He found the blood to be infecting on the third day after inoculation subcutem, and the globules invaded on the fourth. They were especially numerous in blood taken from the spleen.

_Microbiology._ The protozoön resembles that of Texas fever, but is larger, longer, less pyriform, and more like an oat seed, staining slightly in the centre which shows one clear spot, and more deeply at two or three places in the margin. It stains well with carbol thionine blue or methylene blue, but not readily with hæmatoxylin. The dog’s blood, containing abundance of parasites, failed to infect horse, sheep, ox, cat, fowl, Guinea pig, rabbit, rat or mouse (Robertson).

Robertson found the ticks on every affected dog which had contracted the disease by simple exposure and which came under his observation. Specimens sent to Neumann were identified as Hæmaphysalis Leachi. Mature ticks from an infected dog were preserved and their eggs hatched in an incubator. The resultant six-legged larvæ, placed on susceptible puppies a month old proved harmless and no protozoa appeared in their blood. This was repeated when the same generation of ticks had reached the stage of nympha, and it was after two months from the hatching that the ticks, now mature, when placed on the same puppies conveyed the disease. On the thirteenth day the temperature reached 105° F., and the red globules swarmed with parasites, many single globules containing no fewer than eight. They were of various shapes, spherical, pyriform or cloveshaped many tapering finely toward the ends like an oat. The puppies died respectively 14 and 18 days after infection.

Experiments made on other dogs with the larval and mature ticks, fully confirmed the conclusion that the immature insect was harmless. A 14 days old puppy infected by mature ticks died on the 11th day so that the immunity of the other puppies cannot be due to a milk diet, as in the case of calves and Texas fever. Intravenous inoculation with the infected blood invariably conveyed the disease.

_Symptoms._ On the third day after inoculation the dog is dull, prostrate, apathetic and drowsy, refuses food and shows thirst. Temperature may reach 103° to 106° F. On the fourth day the mucosæ assume a yellowish tinge, and by the fifth this has encreased to a deep chrome yellow, which involves any white portions of the skin as well. Hæmoglobinuria is now well developed, the liquid being often as dark as claret, and the patient may lie perfectly prostrate, giving off an offensive odor from the skin, lungs, and especially from the mouth. The tongue is furred, the teeth dirty, and the gums may be congested or even ulcerated. Emaciation advances rapidly. The temperature may oscillate from day to day or it may rise steadily to a climax, and then descend suddenly when collapse occurs. In all cases the protozoön is found in the red globules, or free in the blood. In the worst cases the red globules may be so reduced in number that they can scarcely be found. Death comes usually by collapse. In some instances the hæmoglobinuria may be absent yet the disease advances to a fatal result.

_Lesions._ The carcass is usually shrunken and emaciated and exhales a fœtid odor. The mucosæ, white skin, and all naturally white structures (fat, connective tissue, fascia, tendons, ligaments, brain, spinal cord, etc.), are stained of a deep yellow. The muscles, liver and other darker tissues are of a mahogany yellow; petechiæ appear on the heart and serosæ; the liver is greatly enlarged and friable (10 lbs.) the spleen is swollen, gorged with blood and a soft, black, bloody pulp; the stomach and small intestines are empty, yellow and sometimes congested. The large intestines show muco-enteritis throughout with an abundant rusty red exudate. The kidneys are yellowish with cortex somewhat pale. The bladder also yellow contains dark colored urine. The red blood globules are greatly diminished in number, many are crenated, broken up and distorted and they contain the piroplasma in large numbers.

No system of _treatment_ has proved successful. Essays would naturally be made with quinia and other antiperiodics.

_Prevention_ would naturally be sought in keeping dogs off from the uncultivated land and brush during the tick season (summer, autumn), in clearing and cultivating the tick infested pastures, in drainage, or in smearing the coat of the dog with the oil of tar liniment or other insecticide when he goes hunting.

PALUDISM IN HORSES.

Alleged identity with ague. Geographical distribution. Points of
difference from ague. Causes: low, damp, undrained, inundated
localities, hot seasons; inoculation, congenital. Symptoms: restless,
drowsy, stiff, shivering, hyperthermia, tremors, cough, frothy, rusty
expectoration, excited breathing and pulse, anorexia; puffy,
petechiated eyelids; epiphora; dyspnœa: albuminous, yellow or red
urine with casts: hæmoglobinæmia: colics, constipation, fœtid
diarrhœa. Death in a few hours to 6 days, or months. Lesions:
reduction in blood globules, crenation, watery blood: petechiæ:
enlarged, blood-gorged liver and spleen; congested, swollen, softened,
kidneys; congested lungs with extravasations: in chronic—anæmia,
dropsies, lung hepatization and suppuration. Prevention: keep
susceptible horses from low, infected lands from June to November and
from their water: protect from insect enemies. Treatment: quinia
sulphate or bromide, hot baths, etc.

Cadeac and others describe an intermittent or remittent febrile affection of the horse, as identical with ague, and due, they allege, to the presence in the blood of the _plasmodium malariæ_ of Laveran.

_Geographical Distribution._ It has been observed on the low marshy grounds of Sicily, the Danube bottom lands, Algiers, Tonkin, Madagascar, Soudan, Senegal and Cochin China (Dupuy, Lenoir, Pierre, Colin). Dr. Gelston informs me that in the American cavalry in the Philippines extensive losses are sustained from this disease.

_Microbiology._ The causation of the disease is attributed to the _plasmodium malariæ_, which is carried by the Anopheles and inoculated in the skin of man, in malarious regions at night, but we are confronted with the difficulty, that accepting the alleged identity, the disease in the horse should be coextensive with that occurring in man. Yet we have in the New World many areas characterized by the all but universal prevalence of intermittent fever in man, and at the same time by its entire absence in the case of the equine races. It may further be considered that protozoa, found in the red globules of birds, were at one time considered identical with those of malarious fever, but have been demonstrated to be entirely different so far as pathogenesis is concerned. There is every presumption that the protozoa of the red globules found in the horse in this disease are also distinct pathogenically.

Laveran has sought in vain for his plasmodium in the blood of the affected horses, while Pierre found in the blood globules of the Soudan victims refrangent, crescent shaped bodies, thickened and staining deeply in the centre, which in his opinion represented the growing hæmatozoa of Laveran. Gelston found the rounded and crescent shaped forms abundant in the red globules. The disease in the horse is said to be conveyed by direct contact, which would again distinguish it from intermittent fever of man. If the protozoön is the cause, and not a mere sequel or attendant on the disease of the horse, the indications are that it is peculiar to the equine race and distinct from the germ of human malaria.

_Causes._ Like malarial diseases in man, it is confined to low, damp, undrained or inundated localities, and shows in the hot seasons when the surface dries out. The elevated plains and tablelands which are habitually dry or well drained are exempt. Cadeac alleges that infection is usually inhaled in the floating dust. The mortality of Algerian horses taken to the Soudan is 90 per cent., while but 25 to 35 per cent. of the native horses in the Soudan or in Senegal suffer. This difference is manifestly the result of the survival of a comparatively immune strain of blood, or of immunity resulting from a previous invasion. Subcutaneous inoculation on a soliped failed, while transfusion of blood from the affected horse to a sound mule produced the disease. It is also claimed that it is transmitted from the affected mare to the fœtus in utero, which showed characteristic visceral lesions after birth.

_Symptoms._ Premonitory symptoms of restlessness, drowsiness, or stiffness, are followed by violent shivering, elevation of temperature (104° or 106° F.), muscular tremors, rapid breathing, hacking cough with expectoration of frothy mucus, tumultuous heart beats, and small irritable pulse. There is complete anorexia, an opaque, infiltrated, petechiated, mahogany colored, conjunctiva, epiphora, and sometimes blood extravasations into the vitreous. The lungs may become intensely congested, with rapid, panting breathing, dyspnœa, a frothy, rusty expectoration, and extended head and limbs. This may prove fatal in a few hours. Otherwise there may be remissions of the fever and dyspnœa at somewhat irregular intervals. Sooner or later are observed urinary changes, the liquid becomes albuminous, yellow, or red, or it shows distinct casts. These indicate the destruction of the red globules and the escape of hæmoglobin. In other cases there are slight colics and constipation alternating with a greenish yellow fœtid diarrhœa. The early nervous prostration and drowsiness may merge into vertigo, or paralysis. Vertigo is a very prominent feature in the Philippine cases (Gelston). The skin which, at first, may often be pricked without response, sometimes becomes tender, itchy and congested, with erection of the hairs and the formation of pustules, or small abscesses like hazelnuts.

_Course. Duration._ In very acute cases death may take place in a few hours. More commonly illness lasts from three to six days. In certain instances it becomes chronic and may last two or even three months, the early congestion of the mucosæ giving place to pallor and anæmia with advancing emaciation, dropsies and finally marasmus and death.

_Lesions._ These are mainly in the blood, red globules being distorted, crenated, massed in clusters and greatly diminished in numbers so that the liquid appears thin and watery. The mucosæ, internal organs and serosæ are petechiated and the serous cavities contain a yellowish serum. A yellowish tint pervades the white tissues generally. The liver is congested, virtually gorged with blood, enlarged and yellow or yellowish brown. The spleen is greatly enlarged, blood gorged, and shows irregular, rounded swellings indicating the seats of extravasation of blood. In some instances rupture has taken place. The kidneys are congested, enlarged, softened and of a brownish red or black color, with circumscribed extravasations especially in the cortical area. The lungs are violently congested, with many areas of blood extravasation, and they do not collapse when the chest is opened. The heart is petechiated, with a parboiled aspect and shows areas of commencing necrosis or fatty degeneration.

In the chronic form the watery condition of the blood is remarkable, the serous cavities (peritoneum, pleuræ, pericardium, arachnoid) contain considerable effusion, dropsical conditions of the limbs and dependent parts of the body are common, the lungs show hepatization and minute centres of suppuration, and other viscera may show fibroid degeneration.

_Prevention._ It is advisable to keep susceptible horses from the low marshy infected lands from June to November and to avoid especially water that is drawn from such lands. It is not needful to take the stock to any very marked elevation provided the land is dry and free from wet or swampy areas. The native horses or those that have been long in the marshy district and have thus secured a partial immunity may profitably replace the more recently imported and susceptible horses during the dangerous summer months.

The habit of the paludal protozoa of securing their transfer from one of the higher animals to another through the intermediation of insects in which they undergo developmental changes essential to their survival, would further suggest the adoption of especial precautions against such invertebrate enemies in the affected district.

_Treatment._ Pierre employed quinia sulphate or bromide 45 grs. in distilled water 1 oz., intravenously, Gelston, creolin, subcutem. Hot baths, 95° to 100° F. are claimed to lower the temperature and contribute to the arrest of an attack. Other complications are treated according to indications.

SURRA: ROT.

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:

A.—ONE PART OF THE
MIXTURE.

Methylene blue 1 Grams.
Borax 2.5 „
Distilled water 100 „

B.—FOUR PARTS OF THE
MIXTURE.

Eosin .1 Grams.
Water 100 „

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.

NAGANA. TSETSE FLY DISEASE.

Trypanosoma Brucii: attacks horse, ass, mule, cattle, buffalo,
antelope, camel, hyena, dogs, etc. Elephants and zebra, pigeon and hen
immune. Tsétsé fly. Inoculation only certain channel; virulence in
dead body 24 hours; in vitro 3 to 4 days, or when dried or heated
(122° F.) Symptoms: hyperthermia; anæmia; leucocytosis; buffy coat;
œdemas; catarrhs; wasting; debility. Lesions: as in surra; trypanosoma
in blood at intervals, bone marrow, lymph glands, spleen. Immunizing
unsuccessful. Prevention as in surra.

This is an infective disease caused by the _Trypanosoma Brucii_, which has been supposed to be identical with _Trypanosoma Evansi_ but differs in its morphology and in its infectiveness toward a greater variety of animals. It is 25 to 30μ long by 1.5 to 2.5μ broad, less pointed at its posterior (nonflagellate) end, broader undulating membrane, more deeply staining protoplasm, and more sluggish movements. It invades the blood of horses, asses, mules, cattle, buffaloes, antelopes, camels, hyenas, and dogs, and can be inoculated on cats, rats, mice, rabbits, hedgehog, boshbok, zebra hybrids, Guinea pigs, goats, sheep, weasel, and monkey (Macacus rhesus). Elephants are immune though they suffer from T. Evansi, and the zebra is immune though a soliped.

The _tsetse fly_ (glossina morsitans) is credited with being the main agent in transmitting the parasite to mammals, (see _Diptera_).

Kauthack, Durham and Blandford found that Guinea pigs were more resistant than rabbits, surviving the inoculation for a longer time. Bruce also found the native South African sheep and goats more refractory than others, yet their hæmatozoön was as deadly to other animals as that of horse or dog. Pigeons and South African hens proved refractory. Manifestly in Africa the present races of some animals are the products of the survival of the fittest.

_Inoculation._ The disease has been produced experimentally by inoculation only. Feeding experiments on rabbits, cats and Guinea pigs, the sucking by puppies of an infected dam for 14 days, coitus, and even the careful dropping of infected blood under the eyelid failed to convey it. Lousy rats with sores on face, one cat doubtless scratched by a bone, and one rabbit supposed to be infected by sexual congress (Rouget) offer exceptions, which in the light of the general results must be looked on as probable inoculations through wounds.

Successful inoculations were made with blood, lymph gland, spleen, bone marrow, aqueous humor, serum, œdema fluid, and testicular juice. The effectiveness of inoculation did not vary materially with the different fluids used, with the amount, nor with the point selected for its insertion, subcutaneous, intravenous, intraperitoneal, or on a mere scratch.

Virulence is lost in the dead body in 24 hours or less; when the infected blood is kept aseptically _in vitro_, in 3 or 4 days at most; or when completely dried. Heating to 122° F. for 30 minutes sterilized, while at 114.8° F. for half an hour the trypanosoma became nonmotile, but not quite non-virulent.

_Symptoms._ _Hyperthermia_ is marked about the time of the appearance of the infusoria in the blood. (Horse 106.7°; dog 104°; rabbit 105.8°), and in the horse there was a paroxysm with each new swarm of the parasite. In one ass intermissions were not observed. In rabbits there was no constant ratio between the temperature and hæmatozoa, hyperthermia was constant or nearly so. The horse had marked hyperthermia up to death, dogs and cats showed a marked descent even to subnormal, before death.

_Anæmia_ is a marked feature the red globules being greatly reduced, and they show a tendency to clump in masses instead of forming rouleaux. The serum added to healthy blood has the same effect on that. _Leucocytosis_ is not constant nor excessive (15,000 to 34,000 per c.m. at the highest). In clotting the blood may form a buffy coat.

_Œdema_ is common in horse, rabbit, cat and dog especially about the head, legs, belly and genital organs. Rabbits often show swellings, excoriations and sores of the labia, prepuce and penis favoring inoculation by this channel.

_Conjunctivitis_ is common in cats, dogs, rats, rabbits, often in connection with facial œdema, and corneal opacities and ulcers, and turbidity of the aqueous humor may follow.

_Nasal catarrh_ often interferes materially with breathing.

_Muscular wasting_ and _debility_ are prominent phenomena, especially in horse, dog, cat and rabbit, the loss of weight reaching 20 or 30 per cent.

_Lesions._ These are like those of surra. Enlargement of the lymph glands, spleen and liver, firmness, friability and dark color of the spleen; effusions, petechiæ, and even hæmorrhages of the serosæ, lungs and stomach, and great atrophy of the muscles and adipose tissue are prominent features. The liver is always fatty in rabbits. In the shafts of the long bones, the fat is replaced by red marrow. The bone marrow is sometimes red, at others pale.

The _trypanosomata_ in the blood vary greatly. In infected rats and mice they appear 3 or 4 days after inoculation, are almost constantly present thereafter, and as a rule, encrease steadily up to 2,000,000 or 3,000,000 per c.m. In dogs they appear in 4 to 6 days, in cats in 5, in Guinea pigs in 5 to 7, and in horses in 7 days. In rabbits there were found 60,000 per c.m., in dogs 100,000 to 300,000, and in Guinea pigs 200,000 to 500,000. In one Guinea pig they did not appear until 6 weeks after inoculation and then rapidly encreased to a fatal termination. More commonly a few can be found about a week after inoculation, and then they disappear for a variable period. They have been found in the bone marrow when they could not be recognized in the blood. Again, after subcutaneous flank inoculation in the rat, they were found in the corresponding inguinal glands 1 to 3 days before they could be detected in the blood. After death they are found most abundantly in the bone marrow and spleen, but they have not been found in the intestinal contents nor urine except in the case of hæmorrhages or local sores.

_No soluble toxin_ appears to be formed, and _no immunization_ is effected by the serum. Blood serum kept several days until the infusoria had died and then passed through a Berkefeld filter had no apparent effect on the animal economy even in large doses. Blood heated to 122° F. was equally harmless. The same is true of extracts of organs and of bile from infected animals.

Attempts to secure _immunity_ by injecting the blood serum of affected animals, after it had been sterilized by heat, filtration, or standing one week _in vitro_ proved of absolutely no effect. The blood of the fœtus almost at full term proved valueless, and the young born of infected mothers proved fully susceptible when inoculated. The serum of the Guinea-pig, which is naturally somewhat resistant, proved no protection to other animals. Bile mixed with infecting blood _in vitro_, kills the trypanosoma, but such blood has no protective effect on animals. Sewer rats and white rats inoculated and re-inoculated with the common rat trypanosoma (T. Lewisi) until immune from that organism, show a full susceptibility to the trypanosoma of nagana.

_Flesh feeding_ and _vegetable feeding_ have made no difference in the susceptibility in the case of rats. Feeding with the hæmatozoa has produced no immunity.

It is evident that prevention must follow the same lines as in Surra, due consideration being had of the greater number of genera susceptible.

LUNG PLAGUE OF CATTLE.