Difference between revisions of "Category:Enteropathogenic and Enterotoxaemic Clostridia"

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===''[[Clostridium perfringens type B]]===
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===''[[Clostridium perfringens type C]]===
  
  
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===''C. perfringens'' type C===
 
===''C. perfringens'' type C===
  
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*Acute enterotoxaemia in adult sheep, 'struck'
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*Sudden death or terminal convulsions in sheep at pasture
 
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*Beta toxin (lethal, necrotising) plays major role in pathogenesis of the disease - increases intestinal and capillary permeability
 
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*Also alpha toxin (lecithinase)
 
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*Post mortem: jejunal ulceration; hyperaemia in small intestine; fluid accumulation in peritoneal cavity; congestion of peritoneal vessels; petechial haemorrhages
 
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*Haemorrhagic enteritis in piglets
 
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**Peracute enterotoxaemia often of entire litter with mortality rates 80%
 
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**Infection from sow's faeces
 
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**Death within 24 hours in young piglets
 
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**Chronic disease in older piglets
 
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**Dullness, anorexia, bloody faeces, perianal hyperaemia
 
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**Post mortem: necrosis of terminal small intestinal mucosa, caecum and colon and blood-stained contents; serosanguinous fluid in pleural and peritoneal cavities
 
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*Necrotic enteritis in chickens:
 
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**Broilers under 12 weeks
 
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**Acute enterotoxaemia, sudden onset and high mortality
 
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**Necrosis of small intestine
 
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**Predisposing factors include diet changes, coccidial infection and intestinal hypomotility
 
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*Acute enterotoxaemia with haemorrhagic enteritis in calves, lambs, foals, goats
 
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*[[Peritoneal Cavity Inflammatory - Pathology#In cattle|Peritonitis in cattle]] - sudden death in feedlot cattle
 
  
  

Revision as of 11:07, 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 C

C. perfringens type C

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.

C

P

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