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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 vaccines<sup>3</sup>, 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 lambs<sup>3</sup> because these animals consume the largest quantities of milk, which functions as a growth medium for ''C. perfringens''.
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 vaccines<sup>3</sup>, 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 lambs<sup>3</sup> because these animals consume the largest quantities of milk, which functions as a growth medium for ''C. perfringens''.
Pulpy kidney disease, which is caused by C perfringens
type D, is by far the commonest of the enterotoxaemias.
It is usually encountered in growing lambs of four to 10
weeks of age, and in finishing lambs of six months of
age and above. However, it is not unusual for adults to
be sporadically affected. Rams, in particular, appear to
be susceptible when they are on a rising plane of nutrition
in preparation for mating.
C perfringens elaborates a non-toxic protoxin, which
is converted to the lethal epsilon toxin by the action of
Very congested small intestine and ecchymosal
haemorrhages on the abomasum of a three-month-old lamb
with acute pulpy kidney disease (Picture, Shrewsbury VIC)
Congested small intestine in
a lamb under 14 days of age
with lamb dysentery
(Picture, Carmarthen VIC)
trypsin. The disease is peracute and the majority of cases
are found dead. In the rare instances that animals survive
for a short time, diarrhoea is a feature, as are CNS signs
due to the development of focal symmetrical encephalomalacia;
typcially, there is ataxia, progressing to
recumbency, opisthotonos, convulsions with or without
nystagmus, and death.
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].