Difference between revisions of "Category:Enteropathogenic and Enterotoxaemic Clostridia"
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Revision as of 11:05, 12 May 2010
- General:
- Clostridium perfringens types B, C and D
- Found in soil, feaces and intestinal tract
- Survive in soil as spores
- Husbandry, changes in diet and environment predispose to proliferation in the intestine
- Abrupt changes to rich diets and intestinal hypomotility due to overeating
- Pathogenesis and pathogenicity:
- Clostridial replication and overgrowth in the interstinal tract of sheep
- Production of potent exotoxins which cause local and systemic effects of enterotoxaemia
- Type of toxins produced determine clinical syndrome
- Haemolysins, collagenases and hyaluronidases also produced
Clostridium perfringens type B
C. perfringens type C
- Acute enterotoxaemia in adult sheep, 'struck'
- Sudden death or terminal convulsions in sheep at pasture
- Beta toxin (lethal, necrotising) plays major role in pathogenesis of the disease - increases intestinal and capillary permeability
- Also alpha toxin (lecithinase)
- 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, goats
- Peritonitis in cattle - sudden death in feedlot cattle
C. perfringens type D
- 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
- Epsilon toxin increases intestinal and capillary permeability; also alpha toxin
- 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
- ALpha and iota toxins
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
Pages in category "Enteropathogenic and Enterotoxaemic Clostridia"
The following 5 pages are in this category, out of 5 total.