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[[Image:clostridium perfringens.jpg|thumb|right|200px|Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)]]
 
[[Image:clostridium perfringens.jpg|thumb|right|200px|Clostridium Perfingens. Source: Wikimedia Commons; Author:Don Stalons (1974)]]
Pulpy kidney is a common, peracute and usually fatal enterotoxaemia of sheep of all ages, caused by the &epsilon; toxin of ''Clostridium perfringens'' type D. ''C. perfringens'' is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals<sup>1</sup>. 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<sup>2</sup>. 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.
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Pulpy kidney is a common, peracute and usually fatal enterotoxaemia of sheep of all ages, caused by the &epsilon; toxin of ''Clostridium perfringens'' type D. ''C. perfringens'' is a large, gram positive, anaerobic bacillus that is ubiquitous in the environment and commensalises the gastrointestinal tract of most mammals<sup>1</sup>. 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<sup>2</sup>. These are produced as pro-toxins, and are converted to their toxic forms by digestive enzymes such as trypsin. 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.  
 
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.  
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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 old<sup>ref</sup>. 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 &epsilon; toxin. &epsilon; toxin causes vascular damage, particularly of the capillaries in the brain<sup>merck</sup>. The incidence of pulpy kidney declined over the past 25 years or so, due to the widespread use of clostridial vaccines<sup>3</sup>, 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 rare<sup>ref 2?</sup>.
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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 old<sup>lewis</sup>. 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 &epsilon; toxin. &epsilon; toxin causes vascular damage, particularly of the capillaries in the brain<sup>merck</sup>. The incidence of pulpy kidney declined over the past 25 years or so, due to the widespread use of clostridial vaccines<sup>3</sup>, 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 rare<sup>ref 2?</sup>.
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lewis: Pulpy kidney disease, which is caused by C perfringens
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type D, is by far the commonest of the enterotoxaemias.
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It is usually encountered in growing lambs of four to 10
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weeks of age, and in finishing lambs of six months of
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age and above. However, it is not unusual for adults to
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be sporadically affected. Rams, in particular, appear to
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be susceptible when they are on a rising plane of nutrition
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in preparation for mating.
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C perfringens elaborates a non-toxic protoxin, which
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is converted to the lethal epsilon toxin by the action of
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Very congested small intestine and ecchymosal
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haemorrhages on the abomasum of a three-month-old lamb
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with acute pulpy kidney disease (Picture, Shrewsbury VIC)
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Congested small intestine in
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a lamb under 14 days of age
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with lamb dysentery
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(Picture, Carmarthen VIC)
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trypsin. The disease is peracute and the majority of cases
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are found dead. In the rare instances that animals survive
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for a short time, diarrhoea is a feature, as are CNS signs
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due to the development of focal symmetrical encephalomalacia;
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typcially, there is ataxia, progressing to
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recumbency, opisthotonos, convulsions with or without
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nystagmus, and death.
       
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