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 Clostridium perfringens type B. C. perfringens is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals¹. Five genotypes of Clostridium perfringens exist, named A-E, and all genotypes produce potent exotoxins. There are 12 exotoxins in total, some of which are lethal and others which are of minor significance². These are produced as pro-toxins, and are converted to their toxic froms by digestive enzymes. The enterotoxaemias are a group of diseases caused by proliferation of C. perfringens in the lumen of the gastrointestinal tract and excessive production of exotoxin.

In healthy animals, there is a balance between multiplication of Clostridium perfringens and its passage in the faeces. This ensures that infection is maintained at a low level. However, C. perfringens is saccharolytic and is therefore able to multiply rapidly when large quantities of fermentable carbohydrate are introduced to the anaerobic conditions of the abomasum and small intestine, leading to build-up of exotoxin. Gut statis, for example due to insufficient dietray fibre or a high gastrointestinal parasite burden, can also contribute to the accumulation of toxins.

Enterotoxaemia due to Clostridium perfringens type B causes severe enteritis and dysentery with a high mortality in young lambs (lamb dysentery), but also in calves, pigs, and foals. The β toxin it produces is highly necrotising and is responsible for severe intestinal damage. ε toxin also plays a part in pathogenesis. The incidence of lamb dysentery declined over the past 20 years or so, due to the widespread use of clostridial vaccins³, but the condition is now becoming a problem again as complacency reduces flocks vaccinating for the disease. Outbreaks of lamb dysentery typically occur during cold, wet lambing periods when lambing ewes are confined to small areas of shelter which rapidly become unhygienic. Most cases are seen in stronger, single lambs³, because these animals consume the largest quantities of milk which functions as a growth medium for C. perfringens.

Signalment

Affected animals are unvaccinated lambs of less than two weeks old. The condition is most common in neonates between one and three days of age, and typically affects well-fed singletons^sargison.

Diagnosis

A provisional diagnosis of lamb dysentery can be made on the basis of a history of sudden deaths in well-grown, unvaccinated lambs. This is supported by post-mortem findings, and laboratory testing may also be useful.

Clincal Signs

Lamb dysentery often presents as sudden death of lambs less than 2-3 weeks old^{sargison, lewis, merk, songer}. When clinical signs are seen, these include cessation of suckling, depression and recumbency^merck. Animals suffer acute abdominal pain, and semi-fluid blood-stained faeces may be passed^{sargison, leis merck, sanger}. However, the rapid course of disease means that faeces are often observed to be normal. In 2-3 week old lambs, lamb dysentery may present with non-specific neurological signs^sargison.

Laboratory Tests

Intestinal contents or pertioneal fluid may be collected post-mortem and submitted for an ELISA test to identify clostridial exotoxins. A positive result supports a diagnosis of enterotoxaemia but does not confirm it: animals with immunity to Clostridium perfringens may have high concentrations of toxin with suffering from its effects.

Intestinal smears and scrapings readily reveal gram-positive rods^{sargison, watt}. Culture of intestinal contents can yield almost pure growths of C. perfringens^watt, but this is again supportive rather than diagnostic^sargison.

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

watt: Diagnosis on post mortem examination is usually obx ious with areas of the small intestine markedly hy peraemic and with characteristic ulceration of the mucosa. (Disease presentinig similar lesions has been described involving Cl wet1ihil type C.)

sargison At postmortem examination. localised areaLs ot the intestinies appear dark red and distended, with ulceration otl the mucosa and serous, blood-stained peritoneal fluid. The liver may be pale and friable and the kidnieys enlarged. Numerous Gram-positixe rods are present in smears from intestinal scrapings.

Treatment

Presentation of lamb dysentery is usually peracute, with sudden deaths occuring before treatment can be implemented. Even if animals are found prior to death, treatment is usually unrewarding as organs are irreversibly damaged by toxins by the time signs present^lewis. Instead, a definitive diagnosis should be pursued before great losses occur, and the farmer should be encouraged to submit the carcase for further investigations.

As treatment is so ineffective, much emphasis is put on to the control of lamb dysentery. Vaccination in the face of an outbreak has been shown to be effective^west, and specific hyperimmune serum can also be administered^{Merck, watt}. Oral antibiotics may be given^merck but are regarded as a less appropriate therepautic. Management measures such as removing the flock from a particular pasture or reducing concentrate feeding may be implemented in other clostridial diseases but are of no benefit in lamb dysentery: over-ingestion of the dam's milk combined with poor hygiene are responsible for this disease. Therefore, sufficient supervision should be given at lambing time to ensure adequate intakes of colostrium and the maintenance of good hygiene.

Lamb dysentery can be controlled through vaccination against clostridial diseases. Before the development of modern clostridial vaccines in the 1970s, catastrophic losses of up to 30% of the lamb crop could occur due to lamb dysentery^lewis. The vaccines used today have several components, making them effective against a variety of clostridial diseases and, for some vaccines, Pasteurella. The vaccines consist of toxoids, which are inactivated forms of the toxins produced by clostridial organisms. The principles of vaccination are the same whether a clostridium-only or Pasteurella-combined product is used: a sensitising dose must be given 4-6 weeks before a second confirming does^lewis. As immunity wanes over a period of a year booster doses are required annually. Therefore, ewes should receive the primary vaccination course before entering the breeding flock and an annual booster approximated about six weeks before lambing. This timing of the booster vaccination affords 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.

Links

• The Merck Veterinary Manual: Enterotoxemia Caused by Clostridium perfringens Types B and C
• NOAH: Vaccination of farm animals
• Clostridia.net - Clostridium perfringens

References

1. Van Metre (2006) Clostridial Infections of the Ruminant GI Tract. Proceedings of the North American Veterinary Conference 2006.
2. Lewis, C (1998) Aspects of clostridial disease in sheep. In Practice, 20(9), 494-499.
3. Sargison, N (2004) Differential diagnosis of diarrhoea in lambs. In Practice, 26(1), 20-27.
4. Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial.
5. The Center for Food Security and Public Health, Iowa State University (2004) Animal Disease Factsheet: Epsilon toxin of Clostridium Perfringens.
6. Songer, J G (1998) Clostridial diseases of small ruminants. Veterinary Research, 29, 219-232.
7. Watt, A (1980) Neonatal losses in lambs. In Practice, 2(2), 5-9.
8. Lewis, C (2000) Vaccination of sheep: an update. In Practice, 22(1), 34-39.