Background

Enterotoxemia is caused by Clostridium perfringens through the production of exotoxin in the lumen of the gastrointestinal tract. However, the bacteria perform limited invasion of the tissue, and most of the lesions are produced by the local and systemic effects of enterotoxins produced by different genotypes. Clostridium perfringens is Gram-positive bacteria ubiquitously present in the environment and gastrointestinal tract of mammals. There exist five defined genotypes of C. perfringens (A-E) based on the production of toxins: alpha, beta, iota, epsilon, and enterotoxin. All five genotypes produced alpha-toxin in different amounts. The beta toxin is produced by type A, as well as some isolates of type B, C, and E. Genotyping of C. perfringens is performed by the gene sequence of alpha, beta, beta2, epsilon, and iota toxins and enterotoxin. C. perfringens type A generally exists in the intestine and can grow in the gut lumen. Gastrointestinal tract infection by Clostridia is a common problem in ruminants, despite the presence of a large number of immunoprophylactic products. C perfringens type C is a widespread neonatal infection and colonizes rapidly in the absence of normal flora. Neonatal calves of less than ten days of age develop haemorrhagic, necrotic enteritis, and enterotoxemia with abdominal pain. Death can be peracute or maybe after several days of clinical course. In type C infection, beta-toxin is the dominant player in pathogenesis The organism. is attached to the jejunal mucosa by causing damage to the micro-villi, terminal capillaries, and mitochondria. After that widespread mucosal necrosis occurs, the number of bacteria increases and can be seen all over the mucosa. Ultimately, death is due to beta toxaemia. The protection can be achieved by antitoxin and toxin alone cannot reproduce the disease. C.septicum also causes enteric infection as braxy and organism attached to the abomasum causing fatal bacteremia. The infection mainly occurs by the ingestion of frozen food, which damages mucosal function leading to organism dissemination and bacteremia. The organism produces mostly alpha-toxin along with other toxins, and protection can be primarily by antitoxic. C. perfringens type A causes enterotoxemia in lamb and is also known to cause fowl necrotic enteritis and necrotizing enteritis in neonatal pigs. The type A bacteria occurs as normal flora in animals, making it difficult to assign it as an etiologic agent of enteric disease. However, the disease is reproduced by type A cultures experimentally. Excess amount of sugar, starch, or soluble protein in the stomach increases the development of enterotoxemia. Thus, controlling these amounts is pivotal in preventing enterotoxemia. Therefore, control of diet, fiber content, feeding frequency, carbohydrate overload, and time of grazing can help in controlling the disease. Vaccination of the animals is considered to be the critical procedure in preventing clostridial illness in livestock. C. perfringens type C and D administration to cattle induce protective titers against beta and epsilon toxin in animals

Cause

A disease caused by Clostridium perfringens type A, B, C, D and E

Host Species

Cattle, sheep, goat, pigs, and horses

• Lambs on well-fed, heavy-milking ewes are particularly susceptible.
• Feeder lambs are most commonly affected soon after they are introduced into feedlots.
• The husbandry conditions in which the disease occurs include grazing on lush, rapidly growing pasture or young cereal crops, and heavy grain feeding in feedlots.
• Insufficient cleaning and disinfection of farrowing pens, the housing of pigs on concrete are the risk factor for enterotoxaemia.

The clinical signs depend on the type of organism and species affected.

Clostridium perfringens Type A

• It causes acute hemorrhagic enteritis in calf, lamb and foals.
• There will be acute onset of severe depression, collapse, mucosal pallor, jaundice, hemoglobinuria, dyspnea, and severe abdominal pain.
• Temperature remains in normal range and, most affected animals dying within 12 hours of the onset of illness.
• The disease in adult cattle occurs most commonly in the period shortly after calving.
• In pigs, diarrhea is common.

Clostridium perfringens Type B, C and E

Lamb

• In per-acute cases, lamb die without showing any premonitory signs.
• In acute form, loss of sucking reflexes and severe abdominal pain identified by bleating, stretching, and looking at the abdomen.
• The dysentery is manifested by brown, fluid feces with or without blood and painful straining.
• Death usually occurs after a period of recumbency and coma and within 24 hours of the onset of illness.
• In chronic form, animals show abdominal pain and reluctance to suck but no diarrhea.

Pig

• In the herd, young pigs die very rapidly whereas, more prolonged disease is seen in slightly older piglets.
• Affected pigs become dull and depressed and exhibit watery diarrhea, dysentery, and gross reddening of the anus.
• Some piglets will show diarrhea with hemorrhagic and red-brown color, and contain necrotic debris.
• In less than 24 hours, they rapidly become dehydrated, hypoglycemic, hypothermic, and comatose.
• Piglets affected at an older age have a fluid, yellow colored diarrhea and blood may not be evident.

Foal

• Foals will show the signs of severe depression, pronounced toxemia, and marked abdominal pain.
• The young foals will have an acute attack of collapse with bloody feces, subnormal temperature, fast pulse and respiratory rate, and death within a few hours.

Calves

• In calves, the signs include diarrhea, dysentery, and acute abdominal pain with violent bellowing and aimless running.
• Sometimes, the nervous signs with tetany and opisthotonos are seen.
• In very acute cases, death occurs in few hours, sometimes without diarrhea being evident.

Clostridium perfringens Type D

• Usually, sudden deaths in the best-conditioned lambs are the first indication of enterotoxaemia. 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 per-acute 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. Sub-acutely 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 enterotoxaemia occasionally is seen in young horses that have overeaten.

Management

• In individual cases the disease is often too acute for effective therapy.
• Fluid and supportive therapy are indicated.
• Hyperimmune serum is the specific therapy and the major therapy of value.
• Oral and parenteral administration of penicillin.

Preventive measures

There are three major control measures available:

• Reduction of the food intake
• Administration of antitoxin
• Vaccination

These may be used individually or in combination

Control

Vaccination is the only effective way to control the disease

Type of vaccines

Inactivated C.perfringens type D bacteria vaccine

Vaccine Schedule

The vaccination is recommended to sheep and goat at the age of 4 months of age and booster after 15 days and to be repeated annually.

Dose: 2mL S/C route or following manufacturer's instructions

Note: Deworming is must at least 15 days before vaccination

Source/manufacturer of vaccine in India

Indian Immunologicals, Hyderabad (Telangana)

Biovet Pvt Ltd, Kolar (Karnataka)

Brilliant Bio Pharma Ltd, Hyderabad (Telangana)