Hyperkeratosis

AUBREY M. LEE.

A NEW and strange disease of cattle was first seen and reported by Dr. Peter Olafson, of the New York State Veterinary College, in 1941. It was called hyperkeratosis, or X-disease-"X" being a symbol for the unknown and "hyperkeratosis" indicating the increased amount of keratin, or horny material, that develops on skin of the neck, shoulders, and withers in chronic cases.

This ailment was reported in 10 States in 1946. A year later it was known to exist in 27 States. Officials of the Department of Agriculture and of Southeastern States in 1948 investigated 26 affected herds in 20 counties in Alabama, Florida, Georgia, Tennessee, and Virginia. They found an average loss of 4,200 dollars per herd.

The disease was causing an estimated loss of 2 million to 4 million dollars a year by 1949. Deaths were highest up to 80 percent in calves less than 6 months old. About 50 to 60 percent of older calves died. The mortality in adult cattle was 10 to 35 percent.

In Texas the disease was diagnosed in 53 counties by 1950. In Wisconsin in June 1952 we had reports of 1,085 cases among cattle on 268 premises; an estimated 10,000 calves died in the winter of 1952. In Illinois 33 herds were affected. Tennessee reported more than 3,000 cattle had died or had to be slaughtered before 1952 because of the hyperkeratosis. About 20,000 animals were affected in Texas and 5,000 in Oklahoma in the winter of 1952-1953.

The disease then had been diagnosed and reported in 35 States, and in 4 more States it had been suspected in a herd or two. No new cases of hyperkeratosis of cattle were reported to the Department of Agriculture in 1954 or 1955 an indication that it had been eradicated or reduced to the extent that it was no longer important to the livestock industry.

SYMPTOMS usually start with listlessness, depression, excessive secretion of tears, drooling of saliva and a watery discharge from the nose, and loss of flesh. A rapid drop in blood plasma vitamin A often to very low levels may occur.

Often there also develops loss of condition, emaciation, a variable appetite, intermittent diarrhea, and a dry, scurfy skin. Raised areas, or wartlike lesions, often are found on the floor of the mouth and on the dental pad, hard palate, lips, tongue, gums, and the inside of the cheeks. They have been found also on the muzzle, the margins of the nostrils, and the lining of the esophagus.

If the animal survives those systemic effects and does not die from secondary bacterial infection, pneumonia, or inflammation of the intestines, the typical skin hyperkeratosis develops slowly. Then there develops gradually an accumulation of hard, keratinous material, which makes the skin thick, inelastic, and wrinkled. The deep fissures and bold folds formed in the skin become so hard that they are not reducible by stretching with the hands. The skin feels more like a hide than a skin. Hair on the affected skin gets thin or disappears entirely. The sides of the neck, shoulders, and withers are affected most commonly. Skin on the inner surface of the thigh, the udder, and scrotum, the convex surface of the ear, the dewlap, and the sides also may be affected. Almost all the skin of the body and sometimes the skin of the legs may be affected in extreme chronic cases.

A few herds, free of brucellosis but severely affected with bovine hyperkeratosis, have had abortions and stillborn calves and greatly reduced milk secretion. In some experimentally produced cases of hyperkeratosis in pregnant cows, abortion took place and milk flow dropped markedly. The extreme lowering of blood plasma vitamin A in hyperkeratosis could predispose to secondary bacterial infections, such as abscess formation, and inflammations of some of the internal organs.

The symptoms vary according to the amount of the toxic or poisonous substance the animal eats or touches and the duration of the exposure. The concentration of the toxic substance in the feed or in the compound that the animal comes in contact with will also cause variations in some symptoms. Other factors, such as age, individual differences, rations, and the material in which the toxic principle is suspended, may determine which symptoms are shown and which form the disease takes.

Research workers applied known hyperkeratosis-producing substances in diluted form locally to the skin of cattle. Little or none of the general systemic effects were produced, but a typical definite hyperkeratosis of the skin developed. The scientists found, however, that the systemic effects developed if the material were fed or given internally and that the skin hyperkeratosis developed from this internal administration, although usually it took 6 weeks to 2 months or longer. Calves died with the acute rapid form of the disease before skin changes appeared.

THE INTERNAL changes or lesions in the internal organs that are most characteristic of hyperkeratosis are swellings on the inside lining of the gall bladder, gall duct, and the large bile ducts. Characteristic changes of the small bile ducts of the liver commonly occur. The pancreas, liver, kidneys, and reproductive organs may be affected. The intestines, may become inflamed, and the inside lining of the fourth, or true, stomach, especially near the intestinal opening, may have reddened areas, flat erosions, and small ulcers.

SCIENTISTS in 18 States in 1949-1953 undertook research in a cooperative project with the Department of Agriculture to find the cause of hyperkeratosis. They had to start from scratch. They had only a few theories to begin with.

They had to study practically the whole environment of the affected cattle soils, plant life, fertilizers, bacterial flora of the rumen, livestock feeds, viruses.

Drs. A. G. Johnson and W. O. Robinson, of the Department of Agriculture, established that soil, plants, and fertilizers were not factors.

Dr. W. O. Gibbons, of Alabama Polytechnic Institute, did extensive survey work and proved that DDT did not cause the disease.