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**Type of toxins produced determine clinical syndrome
**Type of toxins produced determine clinical syndrome
**Haemolysins, collagenases and hyaluronidases also produced
**Haemolysins, collagenases and hyaluronidases also produced
===''C. perfringens'' type A===
*Necrotising enterocolitis in pigs and necrotic enteritis in chickens
*Canine haemorrhagic gastroenteritis
*Typhlocolotis in horses, possibly associated with [[Intestines - Fibrinous/ Haemorrhagic Enteritis#Colitis X|Colitis X]]
===''C. perfringens'' type B===
*[[Intestines - Fibrinous/ Haemorrhagic Enteritis#Lamb Dysentery (Enterotoxaemia with Blood)|Lamb dysentery]]
*Up to 30% morbidity and high mortality
*Affects lambs in first week of life
*Abdominal distension, pain, bloody faeces, sudden death
*Bacterial overgrowth in the intestine of the lamb due to immature bacterial flora
*Lack of proteases in the immature gut prevents cleavage of the beta toxin, allowing it to cause disease
*Haemorrhagic enteritis and ulceration in the small intestine
*Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability
*Fatal haemorrhagic enteritis in newborn foals, calves and adult goats
===''C. perfringens'' type C===
*Acute enterotoxaemia in adult sheep, 'struck'
*Sudden death or terminal convulsions in sheep at pasture
*Beta toxin plays major role in pathogenesis of the disease
*Post mortem: jejunal ulceration; hyperaemia in small intestine; fluid accumulation in peritoneal cavity; congestion of peritoneal vessels; petechial haemorrhages
*Haemorrhagic enteritis in piglets
**Peracute enterotoxaemia often of entire litter with mortality rates 80%
**Infection from sow's faeces
**Death within 24 hours in young piglets
**Chronic disease in older piglets
**Dullness, anorexia, bloody faeces, perianal hyperaemia
**Post mortem: necrosis of terminal small intestinal mucosa, caecum and colon and blood-stained contents; serosanguinous fluid in pleural and peritoneal cavities
*Necrotic enteritis in chickens:
**Broilers under 12 weeks
**Acute enterotoxaemia, sudden onset and high mortality
**Necrosis of small intestine
**Predisposing factors include diet changes, coccidial infection and intestinal hypomotility
*Acute enterotoxaemia with haemorrhagic enteritis in calves, lambs, foals
*[[Peritoneal cavity - inflammatory#In cattle|Peritonitis in cattle]]
===''C. perfringens'' type D===
*[[Intestines - Catarrhal Enteritis#"Pulpy Kidney" Disease|Pulpy kidney disease]] in well-fed 3-10 week-old lambs
*Follows overeating high grain diet or luchious pasture
*Starch from partially digested food enterering the intestine from the rumen allows rapid clostridial proliferation
*Epsilon toxin activated by proteolytic enzymes causes toxaemia
*Lambs found dead or with opisthotonos, convulsions, coma in acute phases
*Blindness and head pressing in subacute disease; bloat in later stages
*Hyperglycaemia, glycosuria
*Post mortem: hyperaemia in intestine; fluid in pericardial sac; kidney autolysis with pulpy cortical softening (acute death)
*Subacute death causes symmetrical encephalomalacia and haemorrhage in basal ganglia and midbrain
*Enterotoxaemia in kids and adult goats
===''C. perfringens'' type E===
*Enteritis in rabbits, haemorrhagic enteritis in calves
===Treatment and control of enterotoxaemic infections===
*Hyperimmune serum
*Vaccination - vaccinate ewes with toxoid 6 weeks before lambing to allow passive protection of lambs
*Vaccination of lambs with toxoid before 2 months of age to protect against pulpy kidney
*Avoid sudden dietary changes