Category:Enteropathogenic and Enterotoxaemic Clostridia

  • 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.