Definition. Epizootic manifestations. Faulty hygiene, insanitary stables, impure air, defective drainage, fermenting food, overwork, overfeeding, excitement, heat exhaustion, electric tension. Probably complex. Horse, ox, sheep, goat, dog. Microbian factors in man and rabbit. Lesions: meningeal, brain and spinal congestion, effusion, suppuration, circumscribed necrosis, softening, petechiæ. Blood dark, fluid or a diffluent clot. Symptoms: horse: paresis, anorexia, dysphagia, mucous congestion, reddish brown: in severe cases, chill, stupor, apathy, debility, palsy, tonic spasms of neck, back or loins, hyperæsthesia, twitching, trismus, hyperthermia, delirium, coma, convulsions, and early death. Duration averages 7 to 15 days. Ox, as in encephalo-meningitis. Sheep, microbes. Dog, dulled senses, stupor, coma, palsy, hyperthermia, heat of head, spasms, etc. Diagnosis: by brain and spinal symptoms; cases in groups. More sudden than tetanus, or rabies, and shows no mischievous purpose, nor depraved appetite: from tubercular meningitis. Treatment: Avoid suspected stable, food, water, or suspicious environment, disinfect, correct local diseases, unload bowels, belladonna, atropia, chloral, bromides, ergot, phenacetin, potassium iodide. Bleeding. Cold to head or back. Derivatives. Sling. In convalescence, regulated diet and tonics.
Definition. Concurrent inflammation of the meninges of the brain and spinal cord.
This appears at times in many horses in the same locality, as in New York in 1850 (Large), in Denmark since 1852 (Stockfleth, Bagge), and in Egypt in 1876 (Apostolides). In Cairo alone about 6,000 horses, mules and donkeys perished. Hence the disease is known as epizootic cerebro spinal meningitis. But again it is often seen in scattering or sporadic cases. Add to this that no evidence has ever been adduced that the disease is communicated from one animal to another, and in these days of the parallelism of epizootics and pathogenic microbes, we may well hesitate about continuing to use such a qualifying term. Friedberger and Fröhner claim “that a large number of clinical facts have been erroneously reported under the name of spasm of the neck. Rabies, tubercular basilar meningitis, apoplexy, simple encephalitis, and certain poisonings have been confounded with that disease.” They assure us that “cold, damp, chilly weather, hot stables, clipping and overfeeding are of but secondary importance,” but they fail absolutely to tell us what is of primary importance in a causative sense. American writers who have attempted to account for the disease have groped somewhat blindly for causes in the idea of poison. Large charged it on insanitary conditions, poisonous gases, and defective sewerage in cities, and lack of drainage and deficient stable ventilation in the country. J. C. Michener attributes it to foods undergoing fermentation and considers it as a paralysis due to toxic fungi. W. L. Williams, in Idaho, found the greatest number of cases in winter had been fed hay made from alfalfa (lucerne) and timothy, though some had small grains and native grasses. The soil was dry, porous, gravelly, devoid of humus, and lying on lava rock. The altitude and clearness of the atmosphere were supposed to exclude the idea of cryptogams, yet the crops generally were raised by irrigation. The water was from clear mountain streams. Stables were generally low and full of manure, with thatched roofs, but hardly tight enough to be called close. In these cases the defective stable room, the irrigation, the leafy hay (lucerne), and the probable presence of ferments (bacteria), are the only suggestive conditions. In a fatal outbreak which I saw among the Wilkesbarre, Pa., pit mules, rain-soaked and badly fermented timothy hay, overwork in view of a strike, and a Sunday’s holiday in an unshaded yard under a hot July sun, in contrast with the previous darkness and coolness of the pits, coincided to disturb the general health. In several of the Southern States it is attributed to worm-eaten corn. Trumbower thinks it should be traced to the parasitic fungi that grow on plants, grains, and vegetation. In many instances the disease has appeared simultaneously with the feeding on certain specimens of brewer’s grains, oats and hay, so that to use Trumbower’s words these were the carriers if not the prime factors of the disease.
In recognizing how much cryptogams and bacteria vary under different conditions of life, and what various products they elaborate at different stages of their growth, we can theoretically explain the absence of the disease at one time and its presence at another under what seem to be identical circumstances, as also the variety of symptoms shown in different outbreaks. While this causation cannot be said to be absolutely proved, it is not antagonistic to the facts in many of the best observed outbreaks, and may serve as a hypothetical working theory until actual demonstration can be furnished. The affection suggests a narcotic poison introduced from without, rather than a disease due to a germ propagated in the system.
This need not, however, exclude the operation of attendant conditions such as overwork, plethoric feeding, excitement, close stables, heat exhaustion, etc., which tend to bring about cerebro-spinal congestion. Even the electric tension of Idaho, of the United States generally, and of Egypt, in connection with their comparatively dry atmosphere, should not be overlooked in considering the possible causative factors.
In all probability as we learn more of the true pathology of the disease, we shall come to recognize not one, but several toxic principles, and several different affections each with its characteristic phenomena in the somewhat indefinite affection still known as cerebro-spinal meningitis.
The malady has been described in horses, oxen, sheep, goats and dogs, attacking by preference the young, which are not yet inured to the unknown poison, and by preference in winter and spring, the periods of close stabling, dry feeding and shedding of the coat.
In the absence of bacteriological data from the horse, it may be noted that in man cerebro-spinal meningitis, has been commonly found to be associated with the presence in the meningeal exudates of the micrococcus pneumoniæ crouposæ, (Micrococcus lanceolatus encapsulates). This is frequent in the mouths of healthy persons so that some additional accessory cause must be invoked to increase the susceptibility or lessen the protective power of the tissues. This has been thought to be found in the concurrent presence of other bacteria, the staphylococcus pyogenes aureus, pneumobaccillus of Friedländer and the streptococcus pyogenes. Mosny appears to have established this for the staphylococcus in the case of rabbits. With a given dose of the micrococcus pneumoniæ death was always delayed for a fortnight, while with the same dose thrown into one thigh, and the staphylococcus aureus in the other, the rabbit died in one day. This enhanced potency resulting from the presence of the golden staphylococcus has been invoked to account for the germ making its way from the mouth to the brain in cases of otitis, suppuration of the Eustachian tube, tonsilitis or nasal catarrh. These remarks are intended to be suggestive, rather than conclusive, as we have as yet no certainty that cerebro spinal meningitis in the horse is caused by the same germ as it is in man.
Lesions. The lesions are usually those of leptomeningitis, or congestion of the brain and spinal cord and often effusion into the ventricles, with a serous exudation under the pia mater or into the arachnoid cavity. This may be transparent and yellowish, or grayish and turbid, or milky. In the sheep, Roloff has found purulent products under the pia mater, around the roots of the spinal nerves, and in the surface layers of cerebral gray matter. The marked hyperæmia on the surface of the gray matter is a striking feature, and circumscribed areas of necrotic nervous tissue and softening are not uncommon. Petechiæ are frequent on the meninges, the brain, heart, lungs and kidneys. Granular and fatty degenerations are also met with in these parenchymatous organs. The blood may be dark and liquid or diffluent.
Symptoms in the Horse. The mildest attacks are manifested by paresis, or loss of perfect control over the limbs, or loss of power over the tail, impairment of appetite and some difficulty of swallowing, together with some congestion or reddish brown discoloration of the orbital and nasal mucosæ. In other cases paralysis of one or more limbs may supervene but without marked fever or coma.