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Text Book of Veterinary Medicine, Volume 4 (of 5) · James Law — chapter 88 of 154 · ~2,719 words · public domain

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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.

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