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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.
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.
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].
Type D enterotoxemia in sheep is typically a peracute illness, with many cases simply being found dead. If a live ovine case is detected, neurologic signs predominate. Lethargy and ataxia are evident early on, with collapse, hyperesthesia, lateral recumbency, convulsive paddling, and opisthotonus following within hours. Diarrhea is inconsistently seen. Glucosuria is frequently present [29].
At necropsy examination, the peritoneal, pleural, and / or pericardial spaces are filled with variable volumes of straw- or red-colored fluid that may contain fibrin clots. Petechial hemorrhages are often visible on the visceral surfaces. Pulmonary and mesenteric edema may be evident. Gross lesions of the intestinal tract are frequently absent in affected sheep. Dipstick analysis of urine collected from the bladder frequently reveals the presence of glucose. The renal cortex may be softened (hence the term "pulpy kidney"), although this is a nonspecific autolytic change seen on occasion in small ruminant cadavers. The thalamus and cerebellum may be appreciably soft, with scattered hemorrhages therein. Occasionally, no gross lesions are seen in ovine cases of type D enterotoxemia [24].
* Caused by [[:Category:Clostridium species|''Clostridium welchii'' / ''Clostridium perfringens'']] type D.
* Caused by [[:Category:Clostridium species|''Clostridium welchii'' / ''Clostridium perfringens'']] type D.
** The organisms are found everywhere cannot be got rid of.
** The organisms are found everywhere cannot be got rid of.