Description

  • Lamb dysentery is usually seen in lambs under 2 weeks of age.
    • Related to being kept in a cold, dirty environment, with build-up of infection during the lambing season.
  • Lambs may produce bloodstained diarrhoea before death, but they often die before this effect is apparent.
  • Diagnosed by culturing contents of gut.

Infection with Clostridium perfringens types B and C causes severe enteritis, dysentery, toxemia, and high mortality in young lambs, calves, pigs, and foals. Types B and C both produce the highly necrotizing and lethal β 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 in the susceptibility of young piglets. Type C also causes enterotoxemia in adult cattle, sheep, and goats. The diseases are listed below, categorized as to cause and host. C perfringens also has been associated with hemorrhagic enteritis in dogs. (See also intestinal diseases in horses, Intestinal Diseases in Horses and Foals: Introduction.) Lamb dysentery: type B in lambs up to 3 wk of age

Signalment

Diagnosis

Clincal Signs

Lamb dysentery is an acute disease of lambs <3 wk old. Many may die before 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

Laboratory Tests

Pathology

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 antiserum

  • The gut is blown and distended with foamy ,bloody contents.
  • Sometimes ulceration with perforation and fibrinousperitonitis is seen.
  • Focal or diffuse congestion and haemorrhage
  • Coagulative necrosis of villi.
  • Oedema.
  • Haemorrhage.
  • Influx of inflammatory cells in the lamina propria and submucosa.

Treatment

Treatment is usually ineffective because of the severity of the disease, but if available, specific hyperimmune serum is indicated, and oral administration of antibiotics may be helpful. 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.

Prognosis

Links

References