INFECTIVE ULCERATION OF ANUS AND VULVA IN CATTLE.
This curious affection is recorded as having prevailed in the winter of 1897–8 in different localities in Iowa, Missouri, Kansas and Nebraska. In 1900 and 1901 it was again reported in different parts of Iowa.
Causation. No bacteriology of the disease has been given, and its appearance in isolated herds which had no known communication with other herds, and even in the young cattle on a farm to the exclusion of the older ones, seems to suggest an enzoötic origin, perhaps in food or water, or in some toxin determined by a fermentation of organic matter out of the body.
On the Rodkey farm at Blue Rapids, Marshall county, Kan., eight heifers from ten to fourteen months old, suffered, while the seventeen steers of the same age and the milch cows escaped. (Steddom). Near Shelby, Ia., a bull, from a healthy herd, broke into an affected herd and served cows there, and was afterward returned to his own herd and served cows there, but did not communicate the disease. (S. T. Miller). No case is recorded to show that any bull serving affected cows or heifers contracted ulcer or other disease of sheath or penis.
In one herd near Shelby, Ia., nineteen head of cows and heifers suffered, while the four steers in the herd escaped. In another herd of twenty-six head, in the same district, the four cows and eight of the twenty-two steers suffered. It is not, therefore, confined to the females. (S. T. Miller).
In all cases the disease appeared in the cooler months, from October to April inclusive, and while the cattle were secluded in muddy yards.
In different cases they occupied the yards in common with swine which were charged with wounding the vulva, until the general character of the outbreak forbade this conclusion. At Blue Rapids it was sixty-two days after they had been yarded with the hogs before the disease was observed.
In this case the lot was small, poorly drained and very muddy most of the time. Calves and hogs drank from the same troughs until the disease appeared. The water supplied to the calves and hogs was from a well sixteen feet deep. The cows, which escaped, were supplied with water from the Blue River.
Cows, heifers and steers were fed on a ration of shelled corn 6 parts, rye 1 part, oats 1 part, and had an abundance of fodder, consisting of prairie hay and millet in equal parts. They were in good condition, some of them fat, and nearly all dehorned. A second herd had shelled corn, kafir corn and cane, with water from a shallow well, and all (cows and heifers) suffered.
As showing the localized nature of the cause, C. Muller adduces the case near Ottumwa, Ia., in which a herd of 30 calves were attacked, and sold out, the owner filling the same yard a few days later with 30 more bought in the surrounding country, and which he put on the same rations. In about 10 days the disease appeared in the second lot.
On the Rice farm, Blue Rapids, were 60 yearling heifers, bought in Kansas City, and two home cows. In the first week after arrival 5 heifers suffered, in the second week 20, in the third week 40, and in the fourth week all the 60. The two cows mingling with them were only slightly affected.
In the Rodkey farm, Blue Rapids, cases, all of the young cattle (which alone suffered) had been raised on the farm and had not been exposed to outside cattle.
Symptoms. “The ulcer, in almost every case, started as a mere abrasion, the size of a pinhead, usually on the inner surface of the labia, near the border of the inferior commissure, gradually eating its way through until it appeared as a much larger denuded surface on the outside” (C. Miller). S. T. Miller says: “The first noticeable symptom was serous exudate, rapidly forming into a brown scab, under which was very fœtid pus, with extensive inflammation. The affection usually occurred on the lower portion of the lips of the vulva, in heifers and cows, and in steers around the anus or root of the tail. The scabs which formed seemed to spread very rapidly, destroying more and more of the underlying tissue and forming a thicker and thicker scab. The scab, if pulled off, would expose a raw surface which would bleed very readily. In a short time a new scab would be formed.”
Steddom says: “The vulvar lips thickened and continued to discharge for four or five days. In the meantime certain pustules appeared, 0.1 to 2.5 centimeters in diameter. About the fifth day these ruptured and discharged yellowish pus.” The mucous membranes of the vulva and vagina were dry and slightly congested. The ulcers were covered with brown leathery scabs, which adhered tenaciously and when detached left an angry, red, purulent, granular, elevated and pitted surface. In some of the more severe cases, one or both lips of the vulva had sloughed off, and the sore had extended 10 to 15 centimeters on the skin of the escutcheon. The pus from this sore did not corrode the adjacent skin.
The more severe cases showed loss of appetite, constipation, hurried breathing, tucking up of the abdomen, with general dulness and dejection, and great tenderness of the affected skin with stiff, straddling gait.
Pathology. This is very obscure. The primary cause of the sores is not evident, though their occurrence on the anus and vulva only, and especially on the latter would suggest an elective affinity of the poison (microbian or chemical) for these structures and their products. If we assume a pathogenic microbe in the fæces, the question arises as to the cause of the habitual immunity of the steer, and of the margin of the anus in the majority of the affected heifers. The susceptibility of heifers rather than cows may imply a previous exposure and acquired immunity on the part of the mature animal.
Again if we suspect the existence of a necrobiotic agent of organic origin (like ergotin, secalin, sphacelin) we must assume a superadded microbian infection, implanted in the primary sore and rapidly extending it. The prompt recovery under antiseptic treatment shows that no mere chemical poison maintains the destructive process, for it is manifestly the microbicide which puts a prompt limit to the disease, and under such treatment no sphacelating agent in the blood or tissues keeps up the advance of the ulceration or prevents healing.
Treatment. The ulcers healed rapidly under cleanliness and antiseptic applications. The tail, anus, and vulva were washed with tepid water, and then dressed with a solution of creolin (5:100), or carbolic acid (3:100), or mercuric chloride (1:500 or 1000). The ulcers were touched with a pencil of silver nitrate. S. T. Miller followed the sublimate lotion by the subjoined ointment: iodoform 20 grains, eucalyptol 40 minims, phenic acid 20 minims, petrolatum enough to make 2 oz. C. Miller in addition to the carbolic acid lotion applied the common white lotion (zinc sulphate 1 oz., lead acetate 1 oz., water 1 qt.) and used silver nitrate on the ulcers. Four dressings on four successive days were given and in the milder cases healing was completed in 10 or 12 days.