SOUTH AFRICAN HORSE SICKNESS. ŒDEMA MYCOSIS. DUNPAARDZIEKTE. DIKKOPZIEKTE.

Definition: Geographical distribution: S. Africa; enzoötic or epizoötic on damp soils; damp, humid atmosphere. Pathogenesis: horses, and more mildly mules and asses, quagga; (cattle and goats?). Causes: green forage, from rich, damp lands, eaten dewy; cut and fed with dew on; dried in sun safe; so of horses stabled or corralled; in hot summer only; inoculable; penicillium; cultures cause the disease; debility. Forms: lung sickness—head sickness—blue tongue. Symptoms: incubation 8 days. Fulminant form asphyxiates in an hour. Acute lung form has rigor; remittent hyperthermia; prostration; dyspnœa; cyanosis; serous nasal discharge; frothing; gurgling breathing; cough; death in 3 or 4 days. Head œdema; general swelling and oozing of serum. Blue tongue: great lingual swelling; cyanosis; coldness; projection from mouth; salivation; stertor; asphyxia. Three forms combined. Mortality. Lesions: serous exudate coagulates with heat or blood; intermuscular exudates; whole head densely infiltrated; excessive bloody pleural effusion; punctiform petechiæ; lungs pale, yellow, great interlobular infiltration; or, if worked, hepatization; dark, congested mucosæ; blood diffluent; heart pale; spleen enlarged, blood-gorged; kidneys infiltrated; gastro-intestinal congestions; cerebro-spinal effusion. Prevention: keep indoors during summer and autumn; allow no fresh damp forage; or cut only after dew is off; check rein or muzzle; pastured horses must be stabled at night or in damp weather. Immunization: by protective inoculations; recovered horse is re-inoculated until a high grade of resistance is secured and his blood used to immunize.

Definition. An ectogenous, infective disease of solipeds in South Africa, characterized by intense vascular congestions, destructive changes in the blood and the profuse exudation of liquor sanguinis into the tissues of the affected parts.

Geographical Distribution. The affection is not known out of South Africa, where it has been observed since 1780. It appears yearly in certain areas in the Transvaal, Orange River Colony, Natal, and adjacent States, but only in certain years in Cape Colony and especially in its southern portion. In certain years it makes wide extensions so that it has appeared to become epizoötic instead of enzoötic. The habitual enzoötic prevalence is in the areas that are relatively lower, damper and richer than the surrounding country, where the vegetation is luxuriant and the surface of the ground moist. Thus it is a disease of low meadows, basins, river bottoms, drying marshes or ponds, and the Boers have been in the habit of protecting their horses by sending them to high, dry tablelands, from the first appearance of the disease until the first frost. Yet elevation in itself is no protection, thus Johannisburg, 6000 feet above the sea, is habitually ravaged and Rhodesia loses 90 per cent. annually. A humid atmosphere, mist, or rain with a high temperature are directly connected with the outbreaks.

Animals susceptible. Horses take the disease in its most fatal form. Mules suffer like horses, while in asses the disease is relatively somewhat more benign, and the virus after having passed through the ass, has lost part of its potency. A disease of a similar nature is seen in cattle and goats. The quagga is also alleged to suffer (Edington).

Causes. The disease has been traced to the green forage, grown in damp, hot seasons on the rich moist bottom lands, in basins, gullies, etc., and which has been consumed while damp with night dews or fog. Few suffer that are only turned out to pasture after the sun has dried up the dew, and that are shut in the stable or kraal before sunset. Coley who witnessed a loss of 60 per cent. of the stabled horses at Eshowe, Zululand, found that the deaths were among horses that had been allowed to eat their fodder wet. The Guinea or Ubaaba grass and Indian corn were cut at night and fed to the horses next day. The horses that ate this wet from the bundles were attacked, while those that had it only after it had been opened and dried in the sun escaped. Race horses that receive no green fodder very rarely suffer. Horses that are corralled (in kraal) at night escape.

The hot season is the season of greatest prevalence, the disease beginning in November and proving especially fatal from the end of December to the first of March. It appears in a modified form until May when the first frosts appear.

Though the disease can be fatally inoculated by transferring the blood from one horse to another, it is the rarest possible occurrence to have it propagated in this way. It can be absolutely prevented therefore by attention to the diet.

The real cause of horse sickness is a mold having the general characters of a penicillium, and which enters the system with the moist, dewy food. Edington, who discovered this cryptogam, has found it in the blood in all his necropsies of horses dying of horse sickness. Why this should be no longer infecting when dried does not clearly appear. It has been alleged that the disease has gradually extended to the higher grounds which were formerly free from it, and the introduction of diseased or infected horses has been advanced as the cause, but in the unfenced state of the veldt and the former abundance of wild animals this should have ensured such extension long ago, if it is really a permanent one. The deadly prevalence of the malady in particular areas in given years, and its entire absence from such localities in others may explain the instances of apparent extension. The dryness and cold of winter is the factor which usually extinguishes the poison in a given district. We have as yet no absolute proof of a progressive acclimatisation of the germ in a colder and drier region. Wittshire observes that it will prevail on one side of a narrow river, while the other at an equal elevation is practically free from it. There is no mention of shade which might have explained such a difference in the growth of cryptogams on the right and left banks.

Such limitations, together with the activity of the infection in damp seasons, and during damp hours of the day, and its inactivity in dry air and vegetation, would strongly suggest a microbe which is conveyed in the body of some invertebrate, but this appears to be nonessential because Edington has cultivated his mold in vitro and inoculated its products on horses so as to secure immunity.