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

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.

sargisonThe diagnosis of lamb dysentery depenids on postmortemii findings.

Clincal Signs

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.

merck: 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

songer: 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

sargison: Outbreaks of lamb dysentery are initially characterised by the sudden death of young lambs, but slower onset disease, manifesting as acute abdominal pain and non-specific nervous signs, is sometimes seen in older, two- to three-\veek-old lambs. Faeces may be semi-fluid and blood stained although, in most cases, they are normal due to the rapid course of the disease.

Laboratory Tests

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.

watt: similar lesions has been described involving Cl wet1ihil type C.) The causal organism is readily demonstrated on1 s.mear anld its cxact identity can be conifirmed in the laboratory.

sargison:Numerous Gram-positixe rods are present in smears from intestinal scrapings. Almost pure anaerobic cultures of C pe):frili,genis from intestinal coIntents, and positixe beta and epsiloni toxin ELISA results fiom intestinal conitents or peritoneal fluid support, but do not confirm, the diagnosis.

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 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.

watt: In the face of ain outbreak each lamb born must be treated with atntiserumii and a programme of ewe % accination instituted be tote subsequent lambings.

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.