Lamb Dysentery

Also known as: Clostridium perfringens type B Enterotoxaemia

Description

Lamb dysentery is a peracute and fatal enterotoxaemia of young lambs caused by the beta and epsilon toxins of C. perfringens type B. Enterotoxemia is characterized by proliferation of and exotoxin production by Clostridium perfringens in the lumen of the gastrointestinal tract. Although limited tissue invasion by the causative organism does occur, most local and systemic lesions result from the effects of potent exotoxins produced by certain genotypes of this bacteria. Clostridium perfringens is a large, Gram positive, anaerobic bacillus that exists ubiquitously in the environment and in the gastrointestinal tract of most mammals [1,2]. There are five defined types, or genotypes, of C. perfringens: A, B, C, D and E. These genotypes are identified based on the lethal toxins that they produce: alpha, beta, iota, epsilon and/or enterotoxin [3]. All genotypes produce alpha toxin, although isolates differ significantly in the amount of alpha toxin produced [4,5]. Additionally, the recently discovered beta2 toxin may be produced by type A, as well as by some isolates of types B, C, and E [6]. Strains of C. perfringens that carry the beta2 toxin gene have been isolated from a variety of species of domestic animals, including horses, camelids, cattle, and swine [6,7].

The enterotoxaemias are a group of diseases caused by members of the Clostridium perfringens family; of the five distinct types of C perfringens, three are of major importance to sheep: types B, C and D. The C perfringens family produces 12 recognisable toxins, some of which are lethal and others of minor significance. The C perfringens types causing enterotoxaemias in sheep each produce different toxins in varying amounts, as reviewed by Rood and Cole (1991).

. Clostridium perfringens is a normal intestina commensal of the sheep which can cause enteroroxaemia under certain conditions. 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 t 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

Presentation of lamb dysentery is usually peracute, with sudden deaths occuring before treatment can be implemented. Even if animals are seen in the stages of disease preceeding death, treatment is usually ineffective. Suggested drugs include oral antibiotics and specific hyperimmune serum^Merck.

Lamb dysentery can be controlled through vaccination against clostridial diseases. Before ewes enter the breeding flock, they should be given two vaccinations separated by an interval of 4-6 weeks. An annual booster should be given about six weeks before lambing to afford passive protection to lambs until around sixteen weeks of age. Lambs born to unvaccinated ewes should themselves be vaccinated at between 3 and 12 weeks old, with a second injection given at least four weeks later. Good husbandry is also critical to the control of lamb dysentery. Lambing is a particularly important period where supervision and hygiene should be maintainted and adequate colostrum intake should be ensured. Care should be taken when introducing animals to an improved plane of nutrition.

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.
4. Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. Proceedings of the North American Veterinary Conference 2006
5. Lewis, (1998) C Aspects of clostridial disease in sheep. In Practice, 20(9), 494-499.