Causes. The microbian cause of the disease has not been definitely ascertained, so it is idle to speculate whether we have to deal with a saprophyte which has taken on deadly pathogenic properties, or whether the infection was carried to the island by winged insects or birds attracted by the decaying carcasses.

Certain conditions may be named as accessory or favoring causes. The wild horse often escapes so long as he is on the pasture, but when lassoed, taken to the corral and broken, he will die in four to six days. This suggests that the infection is laid up and preserved in the corrals or stables, the mangers or racks, or possibly in the water supplies. The contact with even the reins (harness) of other horses is alleged to be a prominent cause of infection. Another significant point is that around every hacienda, within a radius of a mile, there are numbers of carcasses, so that there is every opportunity for the infection of the wild and susceptible horses caught and brought in. Near the buildings, too, are accumulations of horse and cattle manure and rubbish heaps of all kinds, the breeding places of the flies, which are probably important factors in conveying the infection. Again, the attacks are more numerous and severe and death earlier in the hot, dry summer weather, while there is a pause and a lesser intensity in the cool or rainy season. All domestic animals, save when kept up for breaking or work, live in the open field day and night and subsist on the green food (capine, gramineæ), and are thereby exposed to all climatic changes.

Symptoms. At the first appearance of the disease (1830) it proved fatal in a few hours, but after a year’s prevalence, when the more susceptible animals had been killed off, the progress of the malady became slower, death being deferred to the 8th or 15th day, so that the symptoms could be more definitely followed. From 7 to 14 days before the more obvious symptoms, there were lifelessness, tardy movement, hurried breathing, debility, weakness and emaciation without work or other obvious cause. Exercise caused difficult breathing, dilated nostrils and great agitation of the flanks.

One of the most constant symptoms was the loss of power of the hind limbs which would sway and stagger, the femurs turning inward, as if dislocated, and on uneven ground the animal could not walk without falling. When down, he could not rise without assistance. In the earlier experience of the malady (1835) only 8 to 16 per cent. failed to show these paraplegic symptoms, whereas in recent years 50 per cent. or more escape them. In these cases the emaciation goes on alone, gradually encreasing until the patient appears like a living skeleton. Some retain an appearance of liveliness, yet all stand on three limbs, and change from one hind limb to the other every six or eight seconds.

The retraction of the abdomen is a marked feature, yet expulsive contraction is defective, the patient fails to put himself in the position for urination or defecation, and there is more or less detention of urine or fæces, the latter being dry, moulded, covered with mucus and of a reddish yellow color. After a time the urine escapes in fine jets, so small that in the absence of stretching to urinate, or raising of the tail, they are easily overlooked. The urine may be normally clear, or dark colored. The penis hangs out of the sheath several inches farther than in health.

Appetite is sometimes impaired, or completely lost, but usually the patient eats and drinks to the last, but without proper digestion or assimilation. It does not check the advance of marasmus. Thirst often becomes excessive and in such cases, there is diuresis together with frequent and excessive rumbling of the bowels. The loins are very sensitive to pinching.

About sixty to seventy per cent. in different outbreaks show œdema, in the epigastric region it may be six inches in diameter, or it may extend from the sternum back so as to include the abdomen, sheath, or mammæ, and perineum, and even the hind limbs. Considerable serous oozing takes place from this for four or five days after which it dries up.

In about seven to fourteen per cent. the head became œdematous and swollen, with an abundant fœtid purulent discharge from the nose and eyes, and extensive ulceration of the pituita and conjunctiva. Such cases became completely blind prior to death. In other cases extensive ulceration of the skin set in with the formation of most repulsive sores.

The nervous symptoms assumed various forms; in some there was stupor with head resting on the ground; in others extreme debility and paraplegia with phenomenally rapid emaciation; in a few hemiplegia, or even delirium was shown; in all there was a marked paresis of the digestive organs and especially impairment of peristalsis. The blood assumed a dark gluey aspect.

The most constant symptoms appear to be dyspnœa under exercise, paresis of the hind limbs and intestines, genital atony, a wonderfully rapid and extreme emaciation, œdema, and a tendency to impaired nutrition or ulcerous degenerations of the pituita, conjunctiva or skin.