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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 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.

[[Image:clostridium perfringens.jpg|thumb|right|200px|Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)]]

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 affects 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 vaccines³, but the condition is now becoming a problem again as complacency reduces the use of vaccination. 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''.

Clostridium perfringens type D causes enterotoxemia in small ruminants of all ages; [1,10] disease in cattle appears to be very rare [27]. Clostridium perfringens  type D is not considered to be a common inhabitant of the gastrointestinal tract of normal ruminants, although it can be carried sporadically by healthy animals [10]. As for type C enterotoxemia, passage of soluble carbohydrates or protein into the small intestine is thought to induce rapid replication and elaboration of epsilon toxin from this organism [24]. Unlike beta toxin, however, epsilon toxin is activated by intestinal and pancreatic proteases [1]. Once absorbed into the bloodstream, epsilon toxin causes loss of endothelial integrity, increased capillary permeability, and edema formation in multiple tissues [28].

Clostridium perfringens type D causes enterotoxemia in small ruminants of all ages; [1,10] disease in cattle appears to be very rare [27]. Clostridium perfringens  type D is not considered to be a common inhabitant of the gastrointestinal tract of normal ruminants, although it can be carried sporadically by healthy animals [10]. As for type C enterotoxemia, passage of soluble carbohydrates or protein into the small intestine is thought to induce rapid replication and elaboration of epsilon toxin from this organism [24]. Unlike beta toxin, however, epsilon toxin is activated by intestinal and pancreatic proteases [1]. Once absorbed into the bloodstream, epsilon toxin causes loss of endothelial integrity, increased capillary permeability, and edema formation in multiple tissues [28].