Lamb Dysentery

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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

Prognosis

Links

References