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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].

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].

. ''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.

. ''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.