Enterotoxemia of Sheep

B. R. MCCRORY AND C. L. DAVIS.

ENTEROTOXEMIA is a highly toxic and usually fatal disease of suckling and feeder lambs. Mature animals are less susceptible to it. Investigators in different countries have described it under the various names of enterotoxemia, overeating, pulpy kidney, apoplexy, milk-colic, and braxy-like disease. It has been very costly to the sheep industry of the world, but effective control has resulted from good management and the use of biological products for immunization.

Most investigators agree that enterotoxemia is of nutritional and bacterial origin, the predisposing cause being the overeating or gorging by the animal of highly nutritive feed ingredients, which causes a digestive disturbance and creates an ideal environment for the multiplication of the organism, Clostridium perfringens Type D. This organism is commonly present in the stomach and intestinal tract of normal warm-blooded animals and in the soil. The immediate cause of the disease is the absorption into the blood circulatory system of the toxin liberated by the organism. The mechanism by which the toxin is absorbed from the intestines has not been determined.

Invariably the lambs affected by the disease are the largest, thriftiest, and greediest feeders. Nursing single lambs that consume too much milk are similarly affected, as are older animals that are given access to a good, lush grass pasture or winter-wheat pasture. The practice of "lambing down" corn and other grain fields has been discontinued in many districts because the death loss from enterotoxemia makes it unprofitable. Severe losses occur every year in feeder lambs that are being finished for market on a grain ration.

Symptoms of illness are manifested by most of the affected lambs a few hours before death. It is common to find dead animals in the pens in the morning even though all appeared healthy the night before.

Many lambs may suddenly jump, fall to the ground in a convulsive seizure, and die. Others show symptoms of a brain disturbance by holding the head to one side and walking in a circle, holding the head high and extended or thrown back and staggering about the pen, or standing with the head down and pushing against the fence, feed bunker, or other objects.

Extreme excitement may be shown by a lamb. It may run blindly about the pen for a few minutes, then collapse, and go into a coma or die. The temperature may be raised 2 to 3 F. Loss of appetite, depression, vomiting, paralysis, constipation, diarrhea (which may persist for several days), and a rapid loss of weight are some of the symptoms frequently observed.

I. E. Newsom, in experiments at the Colorado Agricultural Experiment Station, determined that sugar in the urine may run from 2 to 6 percent and should be regarded as characteristic of acute cases of enterotoxemia.

Characteristic lesions revealed at Postmortem examination are many large, blotchy hemorrhages along the wall of the intestines, in the diaphragm, and in abdominal muscles. Small hemorrhages frequently are observed under the covering of the heart. An accumulation of straw-colored fluid containing small clots may be found in the sac surrounding the heart. When the animal lives for a few days after symptoms are noticed, it is usual to find an inflammatory reaction in the tissue lining the fourth stomach and especially in the first few feet of the small intestine attached to it. Often no lesions are visible when lambs die suddenly. Pulpy kidney is considered a postmortem change that occurs 3 or 4 hours after the lamb dies.

Enterotoxemia must be differentiated from such infectious diseases as listeriosis, anthrax, paratyphoid, coccidiosis, and hemorrhagic septicemia and from plant poisoning.

A diagnosis of enterotoxemia is justified when some of the most vigorous and fattest lambs on full feed show signs of brain disturbance; dead lambs are found in the pens a few hours after they were seen to be normal; symptoms and losses stop abruptly when grain is removed from the ration; nursing lambs stop dying when the ewes are placed on sparse pasture or a less nutritive feed; during postmortem examination, large blotchy hemorrhages are found along the intestinal wall, in the diaphragm, and in abdominal muscles; there is no evidence of pneumonia; Clostridium perfringens Type D toxin occurs in the contents of the intestines.

GOOD MANAGEMENT is an essential part of the program for preventing the disease in fattening lambs because they vary considerably in their individual abilities to assimilate grains or concentrated feeds. Lambs that are received from the range may be placed on pasture or sorted according to size and penned. If they are penned, it is advisable to feed only hay or other good roughage for a few days. Water should always be available to the lambs. There should never be any extra feeding space left at the grain trough. The grain should be spread evenly the length of the trough to assure a more uniform consumption of feed.

The ration for lambs that are being started on feed should consist mostly of hay or other good roughage and a small amount of grain. The grain allowance is raised gradually as they become accustomed to it. Sudden or radical changes of ingredients in the ration or in feeding time should be avoided.

When enterotoxemia develops in lambs nursing ewes that are on lush pasture or rich feed, the flock should be placed on sparse pasture or penned in a dry lot for a part of the day to restrict grazing.

It requires close observation, especially for the inexperienced feeder, to detect the lambs that are about to go off feed and those that show early signs of scouring. When lambs show either tendency, an immediate reduction of one-half to three-fourths of the daily grain allowance for 4 or 5 days will prevent other lambs from gorging and dying, but it will also reduce the rate of gain.

Following the reduced-feed period, the daily allowance of grain or concentrate should be increased gradually until the lambs are on full feed. It is important that close observation of the lambs be maintained.

A. W. Deem and his colleagues at the Colorado Agricultural Experiment Station have shown by several feeding experiments that the addition of sulfur to the daily grain ration greatly reduced (but did not completely prevent) the death loss from enterotoxemia. The addition of one-third ounce of the sulfur (325-mesh commercial ground), added to the daily grain ration of each sheep, was an effective control that did not affect appreciably the rate of gain.

Losses can be prevented near the end of the feeding period by sorting out and shipping to market the fat lambs that are ready for slaughter and by reducing the amount of ration and trough space to the requirements of the remaining sheep.

The administration of antitoxin and bacterin has given excellent results in preventing enterotoxemia.

ANTITOXIN gives an immediate immunity that lasts 2 or 3 weeks. It is used to stop death losses in lambs of all ages in the face of an outbreak of enterotoxemia and may also be used to immunize feed-lot lambs on short-term (21 days) feeding.

Bacterin is intended to stimulate the development in healthy animals of an immunity that will last at least 5 or 6 months. About 10 days are required to develop a protective immunity. Bacterin therefore should be administered at least 10 days before sheep are placed on full feed.

There may be a reaction in the tissues at the site of injection. Because it may persist for at least 30 days, it is inadvisable to use bacterin if the animals are intended for slaughter within that time. Bacterin should not be injected into lambs under 2 months.

Antitoxin and bacterin should not be injected at the same time, because the immediate immunity established' by the antitoxin will prevent the body tissues from reacting to the bacterin.

The antitoxin or bacterin is injected by aseptic means, usually under the skin in the wool-free area back of the place where the foreleg joins the body. Injection there helps to prevent unnecessary lameness.

B. R. MCCRORY is a veterinarian of the Animal Disease Research Laboratory in Denver, Colo. He was graduated from Colorado Agricultural and Mechanical College and received an advanced degree from Ohio State University. He served as associate Professor of pathology at the Colorado Agricultural and Mechanical College and Colorado Agricultural Experiment Station, and later became professor and head of the Department of Veterinary Medicine and Anatomy. Dr. McCrory joined the Department of Agriculture in 1953.

C. L. DAVIS in 1955 joined the Laboratory Section, Animal Disease Eradication Branch, of the Department of Agriculture.