Difference between revisions of "Category:Clostridium species"

Overview

• Organisms present in the soil, alimentary tract and faeces
• Endospores may be present in liver and may be reactivated to cause disease
• Neurotoxic clostridia, Clostridium tetani and Clostridium botulinum affect neuromuscular function but cause no tissue damage
• Histotoxic clostridia cause localised lesions in tissues and may cause toxaemia
• C. perfringens cause inflammatory lesions in the gastrointestinal tract and enterotoxaemias in sheep

Characteristics

• Large Gram-positive rods
• Obligate anaerobes
• Fermentative, catalase negative, oxidase negative
• Straight or slightly curved
• Motile by flagellae
• Require enriched media for growth
• Produce endospores which vary in shape and location and cause bulging of mother cell

Pathogenesis and pathogenicity

• Produce extracellular digestive enzymes and toxic substance known as exotoxins
• Exotoxins cause necrosis, haemolysis and death
• Collagenase, hyaluronidase and DNase enymes facilitate spread through tissues

Diagnosis

• Anaerobic transport medium
• Culture on blood agar enriched with yeast extract, vitamin K and haemin
• Anaerobic culture with hydrogen supplement and 5-10% carbon dioxide for 48 hours
• Colonies of C. perfringens are 5mm diameter, circular, flat and grey and surrounded by a zone of double haemolysis
• Positive cAMP test with Streptococci agalactiae
• Biochemical tests
• Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
• Nagler reaction to detect alpha toxin - plate neutralisation test
• Fluorescent antibody tests for histotoxic clostridia
• ELISA, PCR for toxin detection
• Sudden death in unvaccinated farm animals may suggest C. perfringens types B, C and D
• Post mortem
• Gram positive rods present on intestinal smears suggests clostridial enterotoxaemia

Histotoxic Clostridia

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 A

• Necrotising enterocolitis in pigs and necrotic enteritis in chickens (alpha toxin with lecithinase activity)
• Canine haemorrhagic gastroenteritis (cytotoxic enterotoxin)
• Typhlocolotis in horses, possibly associated with Colitis X

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

C. piliforme

• Spore-forming filamentous Gram negative intracellular pathogen
• Only grows in tissue culture or embryonated eggs
• Causes Tyzzer's disease - severe hepatic necrosis
• Sporadic disease in foals, calves, dogs, cats
• Foals under 6 weeks, found dead or comatose
• Incubation period up to 1 week
• Depression, anorexia, fever, jaundice, diarrhoea
• Hepatomegaly and necrosis on post mortem
• Diagnosis: Warthin-Starry silver impregnation technique demonstrates organisms in hepatocytes

C. difficile

• Dogs with chronic diarrhoea
• New born foals with haemorrhagic enterocolitis
• Possibly associated with acute colitis in adult horses following antibiotic therapy or grain overload

C. colinum

• Enteritis in poulty and game birds
• Shed in faeces of clinically affected and carrier birds
• Intestinal ulceration and hepatic necrosis
• Therapeutic antibiotics in drinking water

C. spiroforme

• Spontaneous and antibiotic-induced enteritis in rabbits
• Enterotoxaemia, fatal within 48 hours
• Oral antibiotics upset the intestinal flora, allowing overgrowth of clostridia