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 mammals^ivis. 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 significance^lewis. 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 vaccins^sargison, 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 lambs^sargison, because these animals consume the largest quantities of milk which functions as a growth medium for C. perfringens. In extreme cases, 20-30% of lambs can be lost to lamb dysentery.

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 seen in the stages of disease preceeding death, treatment is usually ineffective. Suggested drugs include oral antibiotics^merck and specific hyperimmune serum^{Merck, watt}.

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.

lewis Treatment of individual cases of clostridial disease is usually unrewarding since the body systems have been irreparably damaged by toxins by the time signs are observed. Usually the first indications of clostridial disease is a dead animal. It is at this stage that a definitive diagnosis should be sought and every effort should be made to persuade the farmer to submit the carcase without delay to the local veterinary investigation centre, before further losses occur. Control of an outbreak of clostridial disease involves a dual approach of management techniques and therapy. In the case of the enterotoxaemias, vaccination in the face of an outbreak has proved effective (West 1993). Alternatively, particularly for lamb dysentery and tetanus, antisera can be administered. Management measures for some of the clostridial conditions include the removal of the remainder of the flock from a particular pasture or a reduction in concentrate feeding. The reduction of stress factors, as well as the gradual introduction of any new feeds or feeding regimens, also reduces the likelihood of disease. The cost of controls can be high in terms of time, labour and possibly further losses due to the stress of gathering the animals for treatment. Of all the diseases that afflict sheep, the clostridials are the ideal candidates for control by vaccination. Vacdction Before the advent of modern vaccines, losses from clostridial diseases could be cata-strophic, on occasion running at over 30 per cent. By the mid-1970s, efficient multicomponent vaccines were widely available and in the mid- 1980s the clostridial components were combined with multicomponent pasteurella antigens. Clostridial vaccines are, except for the C chauvoei component, directed at the toxins produced by the various pathogenic members of the clostridial family. Referred to as toxoids, they are inactivated and require an adjuvant for better stimulation of the immune system. Whether a straight clostridial vaccine or a combined vaccine is used, the principles underlying efficacious vaccination programmes are identical. For effective protection of sheep, of whatever age, a primary course of two doses, administered four to six weeks apart, is required. The first dose can be considered a sensitising dose and, the second, the confirming dose. Immunity wanes over a period of a year and, consequently, booster doses are required annually.

• EWES. Vaccination should be performed

four to six weeks before lambing is due. Where lambing is prolonged, the late lambers should be identified and boosted later, closer to their lambing date.

• LAMBS. By virtue of the ewe's

enhanced ability to concentrate circulating antibodies into the colostrum (Cooper 1967), lambs ingesting sufficient colostrum from adequately fed ewes receive sufficient maternal antitoxins to protect them for about 12 weeks. Such maternal protection is essential to prevent lamb dysentery, tetanus and early enterotoxaemia caused by C perfringens type D. Lambs from fully vaccinated ewes can start their primary course from eight weeks of age, as maternally derived antitoxin does not appear to interfere with the response to the vaccine. The choice and combination of antigens to be used depends on the ultimate fate of the lamb. Those to be retained for breeding require the full complement of antigens. Those for early slaughter may only require protection against pulpy kidney disease and tetanus, while lambs aimed at the store market or autumn finishing require a wider range of antigens to give additional protection against braxy, blackleg and malignant oedema.

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, C (1998) Aspects of clostridial disease in sheep. In Practice, 20(9), 494-499.
6. Sargison, N (2004) Differential diagnosis of diarrhoea in lambs. In Practice, 26(1), 20-27.
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.