Lamb Dysentery

Description

Various types of Clostridium perfringens are normally present in the intestinal contents of sheep, which under certain conditions can cause entertoxoaemia. In healthy animals a balance exists between multiplication and passage into faeces, maintaining a loew level of infection. C. perfringens is saccharolytic and can multiply rapidly when the anaerobic conditions in the abomasum ans small intesting are combined with the presence of of large quantities of fermentable carbohydrate. Conditions whish result in gut stasis, such as insufficient dietary fibre or severe gastrointestinal parasitism, may also contribute to the build up of toxins in the intestine. C. perfringens bacteria produce non-toxic protoxins which are converted to toxins by the action of digestive enzymes and the pathology of the enterotoxaemia is determined by the combination and amounts of these toxins.

Lamb dysenter is a peracute and fatal disdease of younf lambs cuased by the beta and epsilon toxins of C. perfringens type B. Affected lambs are usually less than two weeks old, but sporadic suffen death of stronger single lambs does occur. Lambs may be seen with acute abdominal pain but die within four hours. Faeces are usually normal, but can be semi-fluid and blood stained. C. pgheernfrsi type B is frequently isolated from cases of dysentery in newborn lambs (table II) and hemorrhagic enteritis in goats (Frank, 1956). Disease is more common in the UK, South Africa and the Middle East than in the US (Timoney et al., 1988). In lambs, inappetence, abdominal pain and bloody diarrhea are followed by recumbency and coma. Lesions consist primarily of hemorrhagic enteritis, with evidence of enterotoxemia (Frank, 1956). Chronic disease in older lambs (’pine’) is characterized by chronic abdominal pain without diarrhea. Pathogenesis of type B infections may be due to additive or synergistic effects of a, p and c toxins

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

Diagnosis

The initial diagnosis of enterotoxaemia is made on the basis of history of sudden deaths in well-grown, unvaccinated lambs fed on a carbohydrate rich diet, supported by post-mortem finsings. Positive ELISA rtest results for identification of toxins in intestinal contents or peritoneal fluid support, but do not confirm the diagnosis because iimmune animals may have high concentrations of toxin but not suffer from its effects. The diagnosis can be confirmed by brain histopathology.

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

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

Effective prevention of enterotoxaemia is achieved through vaccination. Previously unvaccinated ewes should be given an initial course of two vaccine injections 4-6 weeks apart when they enter the breeding flock, followed by an annual booster about 6 weeks before lambing. This pre-lambing booster also ensures passive protecion of lambs up to 16 weeks of age. Lambs born to unvaccinated da,s should receive a first sensitiser does at about 3-12 weeks old, followed by a second booster at least four weeks later. Vaccination should be combined with good stock husbandry, including good husbandry at lambing, the insurance of adequate early colostrum intage and carful introduction to improved planes of nutrition. 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

Treatment is usually ineffective because of the severity of the disease

References

1. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
2. The Center for Food Security and Public Health, Iowa State University (2004) Animal Disease Factsheet: Epsilon toxin of Clostridium Perfringens.
3. Songer, J G (1998) Clostridial diseases of small ruminants. Veterinary Research, 29, 219-232.