Difference between revisions of "Category:Clostridium species"

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===[[Enteropathogenic and Enterotoxaemic 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 [[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Colitis X|Colitis X]]
 
 
 
===''C. perfringens'' type B===
 
 
*[[Intestines Fibrinous/Haemorrhagic Enteritis - Pathology#Lamb Dysentery (Enterotoxaemia with Blood)|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
 
*[[Peritoneal Cavity Inflammatory - Pathology#In cattle|Peritonitis in cattle]] - sudden death in feedlot cattle
 
 
 
===''C. perfringens'' type D===
 
 
*[[Intestines Catarrhal Enteritis - Pathology#"Pulpy Kidney" Disease|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
 
  
  

Revision as of 11:03, 12 May 2010

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


<ncl style=compact maxdepth=4 headings=bullet headstart=2 showcats=1 showarts=1>Category:Clostridium species</ncl>

Enteropathogenic and Enterotoxaemic Clostridia

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

Subcategories

This category has the following 3 subcategories, out of 3 total.

Pages in category "Clostridium species"

The following 5 pages are in this category, out of 5 total.