Enterotoxemia Caused by Clostridium perfringens Type A

Type A strains of C perfringens are commonly found as part of the normal intestinal microflora of animals and lack some of the powerful toxins produced by strains of other types. C perfringens enterotoxin (CPE), is the principal toxin involved in C perfringens foodborne illness and is associated with non-foodborne diarrheal disease in different animals. C perfringens also produces a necrotizing toxin associated with necrotic enteritis in poultry (see Necrotic Enteritis) and dogs, colitis in horses, and diarrhea in pigs. C perfringens type A is implicated in a rarely occurring hemorrhagic diarrhea in dogs and has been associated with nosocomial and acquired acute and chronic diarrhea in dogs. The acute form is characterized by a necrotic enteritis in which there is massive destruction of the villi and coagulation necrosis of the small intestine. Many large, gram-positive rods are visible in fecal smears, and large numbers of C perfringens type A are recovered on anaerobic culture of feces of dogs with acute diarrhea. Fecal tests are not useful in determining the cause of diarrhea, however, because of a high number of false-positive results. A commercial ELISA for CPE in dogs is quite specific. PCR for CPE gene expression in dogs is currently being evaluated. Type A strains from pigs with diarrhea have produced enterotoxin in vitro, and anti-enterotoxin antibodies in sows indicate that enterotoxin is produced in vivo. Enterotoxin has also been demonstrated in the feces of pigs with diarrhea but not in feces of healthy animals. C perfringens isolated from pigs with diarrhea are typically nonenterotoxigenic but produce the cytotoxic β2 toxin, which possibly plays a role in disease. Experimental disease has been produced in pigs challenged orally with C perfringens type A.

Enterotoxemia Caused by Clostridium perfringens Types B and C

Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals (see Clostridial Diseases: Enterotoxemia Caused by Clostridium perfringens Types B and C). Types B and C both produce the highly necrotizing and lethal beta toxin that is responsible for severe intestinal damage. This toxin is sensitive to proteolytic enzymes, and disease is associated with inhibition of proteolysis in the intestine. Sow colostrum, which contains a trypsin inhibitor, has been suggested as a factor increasing the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats.

Table 1
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Enterotoxemia Caused by Clostridium perfringens Types B and C Disease C perfringens Type Host Lamb dysentery Type B Lambs ≤3 wk old Calf enterotoxemia Types B and C Well-fed calves ≤1 mo old Pig enterotoxemia Type C Piglets in first few days of life Foal enterotoxemia Type B Foals in first week of life Struck Type C Adult sheep Goat enterotoxemia Type C Adult goats

Clinical Findings

Lamb dysentery is an acute disease of lambs <3 wk old. Many may die before clinical signs are seen, but some newborn lambs stop nursing, become listless, and remain recumbent. A fetid, blood-tinged diarrhea is common, and death usually occurs within a few days. In calves, there is acute diarrhea, dysentery, abdominal pain, convulsions, and opisthotonos. Death may occur in a few hours, but less severe cases survive for a few days, and recovery is possible. Pigs become acutely ill within a few days of birth and there is diarrhea, dysentery, reddening of the anus, and a high fatality rate; most affected piglets die within 12 hr. In foals, there is acute dysentery, toxemia, and rapid death. Struck in adult sheep is characterized by death without premonitory signs.

Lesions

Hemorrhagic enteritis with ulceration of the mucosa is the major lesion in all species. Grossly, the affected portion of the intestine is deep blue-purple and appears at first glance to be an infarction associated with mesenteric torsion. Smears of intestinal contents can be examined for large numbers of gram-positive, rod-shaped bacteria, and filtrates made for detection of toxin and subsequent identification by neutralization with specific antisera.

Treatment and Control

Treatment is usually ineffective because of the severity of the disease, but if attempted includes specific hyperimmune sera and oral anti-biotics. The disease is best controlled by vaccination of the pregnant dam during the last third of pregnancy: initially, 2 vaccinations 1 mo apart, and annually thereafter. When outbreaks occur in newborn animals from unvaccinated dams, antiserum should be administered immediately after birth.

Type D Enterotoxemia

(Pulpy kidney disease, Overeating disease)

This classic enterotoxemia of sheep is seen less frequently in goats and rarely in cattle. It has a worldwide distribution affecting animals of any age. It is most common in lambs that are either <2 wk old or weaned in feedlots and on a high-carbohydrate diet or, less often, on lush green pastures. The disease has been suspected in well-nourished beef calves nursing high-producing cows grazing lush pasture and in sudden death syndrome in feedlot cattle; however, supportive laboratory evidence in the latter is lacking.

Etiology

The causative agent is C perfringens type D. Predisposing factors are essential, the most common being the ingestion of excessive amounts of feed or milk in the very young and of grain in feedlot lambs. In young lambs, the disease usually is restricted to ewes with single lambs, because ewes with twins seldom give enough milk to allow enterotoxemia to develop. In the feedlot, the disease usually is seen in lambs switched rapidly to high-grain diets. As starch intake increases, it provides a suitable medium for overgrowth of C perfringens, producing epsilon toxin. The toxin causes vascular damage, particularly in capillaries of the brain. Many adult sheep carry strains of C perfringens type D as part of their normal intestinal microflora, which is the source of organisms that infect the newborn. Most such carriers have nonvaccinal antitoxin serum titers.

Clinical Findings

Usually, sudden deaths in the best-conditioned lambs are the first indication of enterotoxemia. In some cases excitement, incoordination, and convulsions occur before death. Opisthotonos, circling, and pushing the head against fixed objects are common neurologic signs; frequently, hyperglycemia or glycosuria is present. Diarrhea may or may not develop. Occasionally, adult sheep are affected too, showing weakness, incoordination, convulsions, and death within 24 hr. In goats, the course of disease ranges from peracute to chronic, with signs that vary from watery diarrhea with or without blood to sudden death. Affected calves not found dead show mania, convulsions, blindness, and death within a few hours. Subacutely affected calves are stuporous for a few days and may recover. In goats, diarrhea and nervous signs are seen, and death may occur over several weeks. Type D enterotoxemia occasionally is seen in young horses that have overeaten.

Lesions

Necropsy may reveal only a few hyperemic areas on the intestine and a fluid-filled pericardial sac. This is particularly the case in young lambs. In older animals, hemorrhagic areas on the myocardium may be found as well as petechiae and ecchymoses of the abdominal muscles and serosa of the intestine. Bilateral pulmonary edema and congestion frequently occur but usually not in young lambs. The rumen and abomasum contain an abundance of feed, and undigested feed often is found in the ileum. Edema and malacia can be detected microscopically in the basal ganglia and cerebellum of lambs. Rapid postmortem autolysis of the kidneys has led to the popular name of pulpy kidney disease; however, pulpy kidneys are by no means always found in affected young lambs and are seldom found in affected goats or cattle. Hemorrhagic or necrotic enterocolitis may be seen in goats.

Diagnosis

A presumptive diagnosis of enterotoxemia is based on sudden, convulsive deaths in lambs on carbohydrate-rich feed. Smears of intestinal contents reveal many short, thick gram-positive rods. Confirmation requires demonstration of ε toxin in the small-intestinal fluid. Fluid, not ingesta, should be collected in a sterile vial within a few hours after death and sent under refrigeration to a laboratory for toxin identification. Chloroform, added at 1 drop for each 10 mL of intestinal fluid, will stabilize any toxin present. Although immunologic tests have been developed to replace the traditional mouse assay for detection of toxin, they are less sensitive. A PCR for detection of epsilon toxin gene is available for identification of the isolates as either type B or D.

Control

The method of control depends on the age of the lambs, the frequency with which the disease appears on a particular property, and the method of husbandry. If the disease is seen consistently in young lambs, ewe immunization probably is the most satisfactory method of control. Breeding ewes should be given 2 injections of type D toxoid in their first year, a booster injection 4–6 wk before lambing, and each year thereafter.

Enterotoxemia in feedlot lambs can be controlled by reducing the amount of concentrate in the diet. However, this may not be economical, and immunization of all lambs with toxoid upon entering the feedlot likely will reduce losses to an acceptable level. Two injections, 2 wk apart, will protect lambs through the feeding period. When alum-precipitated toxoids or bacterins are used, the injection should be given at such a site that the local cold abscesses, which commonly develop, can be removed easily during normal dressing and will not blemish the carcass.

Last full review/revision March 2012 by Henry R. Stämpfli, DVM, DrMedVet, DACVIM