Enterotoxemia: overeating disease of sheep and goat

Enterotoxemia is also known as overeating or pulpy kidney disease. Causative agent of disease is clostridium perfringens, is Gram positive, anaerobic, spore forming and rod shaped.

Enterotoxemia: overeating disease of sheep and goat

There are five strains of C. perfringens, designated as A, B, C, D and E. Each strain produces a unique type of toxins. The epsilon toxin is produced by types B and D. Clostridium perfringens type B causes severe enteritis in young calves, lambs and piglets. While Type D causes enterotoxemia in sheep and goats and rarely in cattle.

Toxins produced by Clostridium perfringens type C is alpha and beta toxins and while type D produce alpha and gamma toxins. This toxin is a pore-forming protein, causes potassium and fluid leakage from cells. Disease is caused by the absorption of a large amount of toxins from the intestine.

Clostridium perfringens types C & D are bacteria present in the microflora of gastrointestinal tract of a healthy sheep and goats and also in the soil. In some conditions, these bacteria can rapidly reproduce and producing large quantities of toxins. These toxins cause inflammation of the intestine, increase blood vessels permeability and become absorbed in the blood.

They circulate in the blood and cause swelling in lungs and kidneys. Young animals are more susceptible. Sudden and high mortality rate is seen in lambs and kids. While adult animals are also prone to enterotoxemia, they develop immunity due to frequent exposure to these toxins.

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Factors Associated with Enterotoxemia Outbreaks

Clostridium perfringens types C & D are more likely to produce in the gut of goat and sheep causing enterotoxemia, in such conditions as following:

  • When lambs and kids consume more milk or feed with high quantity of grains.
  • While recovering from an illness
  • when natural immunity is compromised
  • If there is heavy infestation of gastrointestinal parasites i.e. nematodes etc.
  • When animals have any condition that slows motility of the gastrointestinal tract.

Clinical Signs and lesions of Enterotoxemia

Clinical signs are common in young animals. Per acute form of disease is characterized by sudden death that occurs in 12 hours after the appearance of first signs. Loss of appetite, abdominal discomfort, shown by kicking at the belly are the signs of disease.

Profuse diarrhea is the common sign. Sudden death occurs after the onset of central nervous system signs. These signs include incoordination, convulsion and excitement, followed by death. Hyperglycemia and glycosuria is also seen.

Necropsy of the animal shows hyperemic areas on the intestine and pericardial sac is fluid filled. This is common lesion of young lambs. In Older animals, hemorrhage around myocardium as well as petechiae and ecchymosis of abdominal muscle is seen.

Bilateral pulmonary edema and congestion also occur. Microscopically, edema and malacia in the basal ganglia and cerebellum is observed. Autolysis of kidneys lead to pulpy kidney. Necrotic or hemorrhagic enterocolitis also seen in lambs and kids.

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Diagnosis is based upon history and clinical signs, that can be confirmed by necropsy. Diagnosis can be confirmed by identification of enterocolitis. Clostridium perfringens types C & D from the gut and feces content. Presence of glucosuria indicate enterotoxemia.

Postmortem examination of the small and large intestines can identify a high collection of watery blood, fibrinous clots, and numerous ulcers on the mucosa. The brain and kidney may show softening of tissues. Specific DNA testing can help to detect enterotoxemia.

Different diagnostic tests like mouse neutralization test, enzyme linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) are also used.


Recommended treatment includes: Inject C & D Antitoxin according to the manufacturer’s recommendation. Kids are treated with 5 mL of C & D Antitoxin through subcutaneous route. Administration of penicillin, pain killer thiamine (vitamin B1) intramuscularly. Antacids are given orally.

Infusion of intravenous fluid and use corticosteroids. Use probiotics after treating with antibiotics to support repopulation of the microflora in the gut and rumen.

Vaccination Protocol

Vaccination of pregnant animals with C and D toxins during the fourth month of pregnancy. It will enhance the colostrum (first milky secretion produced between one and three days after birth) with antibodies (specific proteins) that will protect the newborn against enterotoxemia.

Vaccinate young animals at four weeks of age and then 30 days later. Booster dose is administered at the time of weaning. All adult animals and bucks are vaccinated once a year.

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Vaccination Procedure

While vaccinating, following things must keep in mind:

  • Do not vaccinate goats 21 days before slaughter.
  • Avoid vaccinating sick animal, only vaccinate animals that appear healthy. Sick animals may not respond well to the vaccine because of their weak immune systems.
  • Record keeping of the herd is also important.
  • Use a new needle for each animal.
  • Disinfect the injection site with alcohol.
  • Don’t cause stress to the animals during vaccination. Handle the herd in a peacefully, avoid accidents and noise while working with goats.
  • In case of anaphylaxis caused by a vaccine, use epinephrine.
  • For product use and storage refer to label instruction before vaccinating.
  • Consult with veterinarian before using product in an extra-labeled manner.

Enterotoxemia is a fatal disease of sheep. To avoid this disease, vaccination is very important Vaccination is very important Vaccinate the animals on time. Some vaccinal products are not approved by the United States Food and Drug Administration for use in meat or dairy goats.

So, their use is considered as extra-labeled. Don’t feed more grains in diet. Disease is transferred by eating contaminated feed or water. If any of the above clinical sign observed, then consult with local veterinarian.

This article is jointly written by Muhammad Hunain Ahmed, Muhammad Usman Naseer, Muhammad Kashif Javaid.

Muhammad Hunain Ahmed

Muhammad Hunain Ahmed

Student of M phil Pathology.

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