Difference between revisions of "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

C. perfringens type B

• 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
• Also alpha and epsilon toxins
• Haemorrhagic enteritis and ulceration in the small intestine
• Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability (beta toxin)
• 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 (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