Changes

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.  

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 D causes sudden death in sheep of any age, particularly well-grown lambs of between 4 and 10 weeks of age and fattening lambs of 6 months to 1 year old³. Rams are also susceptible when they are subjected to an incraesed plane of nutrition prior to mating. The condition is associated with a change in diet, for example to include lush grass or high proportions of concentrate. This leads to rapid multiplication of the bacterium and excessive production of its ε toxin. ε toxin causes loss of epithelial integrity and first increases the permeability of the intstinal mucosa to facilitate its rapid absorptions¹. It then gives degeneration of vascular endothelium elsewhere, particularly in the brain, leading to increased capiliary permeability and oedema formation^{2, 4}. Hepatic glycogen is mobilised by ε toxin and so hyperglycaemia and glycosuria are frequently seen¹, and the endothelial damage reulsts in protein-rich effusions. The incidence of pulpy kidney declined over the past 25 years or so, due to the widespread use of clostridial vaccines⁵, but the condition is now becoming a problem again as complacency reduces the use of vaccination. At its most extreme, pulpy kidney can cause losses of 10-15% of the lamb crop. The disease can also occur in cattle, but this is rare².

Enterotoxaemia due to ''Clostridium  perfringens''  type D causes sudden death in sheep of any age, particularly well-grown lambs of between 4 and 10 weeks of age and fattening lambs of 6 months to 1 year old³. Rams are also susceptible when they are subjected to an increased plane of nutrition prior to mating. The condition is associated with a change in diet, for example to include lush grass or high proportions of concentrate. This leads to rapid multiplication of the bacterium and excessive production of its ε toxin. ε toxin causes loss of epithelial integrity and first increases the permeability of the intstinal mucosa to facilitate its rapid absorptions¹. It then gives degeneration of vascular endothelium elsewhere, particularly in the brain, leading to increased capiliary permeability and oedema formation^{2, 4}. Hepatic glycogen is mobilised by ε toxin and so hyperglycaemia and glycosuria are frequently seen¹, and the endothelial damage reulsts in protein-rich effusions. The incidence of pulpy kidney declined over the past 25 years or so, due to the widespread use of clostridial vaccines⁵, but the condition is now becoming a problem again as complacency reduces the use of vaccination. At its most extreme, pulpy kidney can cause losses of 10-15% of the lamb crop. The disease can also occur in cattle, but this is rare².

==Signalment==

==Signalment==