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.
Debility doubtless renders an animal more susceptible, yet the disease usually kills nearly all horses attacked, excepting such as have been immunized. This is the same for casual and inoculated cases. When, however, the virulence has been lessened by culture or by passing through the body of an unsuitable animal the results are very uncertain; some horses it will kill, while in others it produces a slight and harmless fever.
Forms. Two leading forms of the disease are known: 1st, the lung sickness (Dunpaardziekte), and 2nd, the head sickness (Dikkopziekte). A variety of this last is blue tongue (Blautong), which has been confounded with gloss-anthrax.
Symptoms. The lung sickness may appear as a fulminant affection following on the usual incubation of about eight days. Suddenly, in the midst of apparently full health and vigor, the breathing becomes accelerated and dyspnœic; this encreases for about an hour, then the patient staggers, falls, ejects a mass of white froth from mouth and nostrils and dies. When death is more delayed, there may be noted a rigor, and in the evening a rise of temperature to 103° F., lowering a little next morning and rising again toward night, yet making an encrease day by day until near the end, when it becomes subnormal. Death in such cases occurs on the third or fourth day, preceded by great prostration, hurried, labored breathing, dark red or cyanosed mucosæ, loud rattling over the large bronchia or lower end of the trachea, coughing and dropping of a serous fluid from the nose, or accumulation of white froth around nostrils and mouth. The froth soon condenses in part into a straw-colored liquid, which collects in considerable quantity. The abundance of froth blocking the air passages produces death by suffocation.
In the head œdema, the muzzle, lips, head and neck become the seat of excessive exudation, the swelling of the face drawing back the lips so as to expose the teeth of the lower jaw. The skin is rendered tense and exudes the straw-colored serum, as do also the buccal and pituitary mucosæ.
In blue tongue the exudate is concentrated in the lingual organ, which swells to an enormous size, forcing the jaws and lips apart, and hanging out as a dark blue, cold mass. A foul, liquid mixture of saliva and exudate drivels from the mouth. The pressure on the larynx may cause marked stertor, advancing to asphyxia.
While these three types may seem to be distinct and uncomplicated in some cases, more commonly the exudation appears to a slight extent in all three situations, and it is only the predominance of the symptoms in one particular part that assigns the attack to one type rather than another. All are very fatal, but the lung sickness is preëminently so, very few such surviving.
Lesions. There is usually a mass of white froth around the mouth and nostrils. The serous exudate coagulates readily in the presence of minute traces of blood, and forms a solid mass of clot when heated. A yellow gelatinoid exudate is found in streaks or patches, subcutaneously and between the muscles, but especially along the jugular furrow. In the head sickness the whole subcutaneous and intermuscular tissue in the head and neck are infiltrated, and the straw-colored liquid escapes abundantly when the part is scarified. The same is true of the tongue, which is stained throughout with blood that has gravitated into it.
The pleuræ contain an abundant exudate more or less deeply stained with blood. The same is true of the pericardium. In the latter Edington has found 140 fluid ounces. On the surface of the lungs and pericardium are extensive yellowish exudates. They are covered with petechiæ mostly small or punctiform. If the horse has stood at rest throughout the illness the lungs seem pale, yellowish, yet swollen and indisposed to collapse. The interlobular tissue especially is infiltrated with serum so that toward the free margin the lobules may be separated by intervals of half an inch in breadth as in lung plague of cattle. In horses that have been worked during the illness the whole organ is congested and firm, resembling the condition of croupous pneumonia. The trachea and bronchia show dark congestion of the mucosæ and a mixture of froth and serous exudate. The large blood vessels contain diffluent blood clots of an intensely dark color. In the vascular furrows of the heart and along the large vessels are yellow exudates or blood extravasations. The muscular tissue of the heart appears normal or rather pale, and under the microscope the striæ are found to be obscured by cloudy swelling, and minute blood extravasations and hæmatin are met with. The endocardium is cloudy, with blood extravasations, and exceptionally ante-mortem clots are found. The spleen is usually swollen, very dark, blood gorged and covered with petechiæ. On section there are found extensive extravasations, with masses of blood pigment and crystals. The kidneys are enlarged, the capsule easily detached, the epithelium of the glomeruli and convoluted tubes swollen and their nuclei multiplied. A gelatinoid exudate is usually present in the renal pelvis. Congestions have been found in the right gastric cul-de-sac and less frequently in the intestines. Exudations have also been found in the cerebro-spinal nervous system, the laryngeal mucosa and the conjunctiva. The latter is usually cyanosed.
Prevention. The first consideration is to keep work horses indoors or in a kraal during the summer or sickly season. Here they must be fed on dry hay and grain only, grass being strictly withheld. If it becomes absolutely necessary to feed green fodder of any kind it should not be cut until all dew or rain has completely dried off in the heat of the sun, and if kept over night should be kept under cover and again dried before feeding. When taken out to work the animal should wear a check rein or muzzle so that he cannot by any chance reach the green vegetation. This rule must be most strictly adhered to at night or during damp weather.
For horses turned to pasture a fair amount of protection may be secured by shutting them in a stable or kraal before sundown, and until the vegetation has been thoroughly dried by the sun the next morning.
Immunization. A horse that has recovered from the sickness has been long held to be immune and will bring from six to ten times its former price. As any disease is liable to be called the sickness this enhanced value is too often insubstantial. Wiltshire even says that all “salted” horses eventually die of horse sickness if allowed to live long enough. Be this as it may Edington appears to have established a reasonable measure of immunity by his protective inoculations. He takes a recovered (‘salted’) animal and reinoculates it at intervals with encreased doses of virulent blood. After the last of these inoculations the subject is allowed to rest for a long period of time, and is then re-inoculated with a small dose of virulent blood. A definite amount of this horse’s virulent blood is mixed with 50cc. of serum and injected subcutaneously; some days later 30cc. of the same serum with the same dose of blood is injected; at a later date the procedure is repeated, with a reduced dose of serum, and fourteen days later pure virulent blood is injected.” The result has been perfectly satisfactory.