Difference between revisions of "Category:Clostridium species"

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(Created page with '===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, ''…')
 
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===Histotoxic infections===
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===[[Histotoxic Clostridia]]===
  
*Exotoxins cause local tissue necrosis and systemic effects which can be fatal - toxaemia
 
*''C. chauvei'' and ''C. septicum'' present in muscle as latent spores which can germinate to cause infection
 
*''C. novyi'' type B and ''C. haemolyticum'' have latent spores in the liver
 
*When inoculated into wounds, cause malignant oedema and gas gangrene
 
*Endospores persist in the soil
 
*Most ingested spores excreted in faeces, but some become dormant in tissues
 
*Tissue injury leads to reduced oxygen tensions allowing germination and replication of bacteria
 
*Exotoxins cause local necrosis
 
*Activated spores in the liver and muscles cause endogenous infections including blackleg, infectious necrotic hepatitis and bacillary haemoglobinuria
 
*Inoculation of wounds causes exogenous infections including malignant oedema and gas gangrene
 
  
 
===''Clostridium chauvei''===
 
 
*[[Muscles Inflammatory - Pathology#Black leg|Black leg]]:
 
**Acute disease of cattle and sheep
 
**Endogenous infection in young cattle with latent spores in muscles, activated by trauma
 
**Exogenous infection via wounds in sheep of any age
 
**Gangrenous cellulitis and myositis caused by exotoxins leads to rapid death
 
**Skeletal muscle damage with lameness, swelling and crepitus due to gas accumilation
 
**Dyspnoea due to lesions in tongue and throat muscles
 
**Myocardial and diaphragmatic lesions can cause sudden death
 
**Fluorescent antibody test for diagnosis
 
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]], along with [[Clostridium species#Clostridium septicum|''Clostridium septicum'']]
 
 
 
===Clostridium septicum===
 
 
*Causes malignant oedema:
 
**Infection via wounds
 
**Cellutis with minimal gangrene and gas formation
 
**Tissue swelling die to oedema; coldness and discoloration of overlying skin
 
**Toxaemia with depression; death may be rapis if extensive lesions
 
*Causes braxy:
 
**Abomasitis of sheep
 
**Disease occurs during winter
 
**Rapidly fatal; anorexia, depression, fever
 
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
 
 
 
===Clostridium novyi===
 
 
*Infectious necrotic hepatitis/black disease:
 
**Acute disease of sheep, occasionally cattle
 
**Hepatic necrosis caused by exotoxins of ''C. novyi'' type B in liver damaged by ''Fasciola hepatica''
 
**Rapid death
 
**Dark discoloration of skin caused by subcutaneous venous congestion
 
**Fluorescent antibody test diagnostic
 
* Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]].
 
*May be involved in [[Bacterial skin infections - Pathology#Systemic bacterial infections|cutaneous lesions]]
 
*Causes big head in rams - oedema of subcutaneous tissues of the head, neck and cranial thorax; necrotising lethal alpha toxin
 
 
 
===''Clostridium perfringens'' type A===
 
 
*[[Necrosis - Pathology#Gas Gangrene|Gas gangrene]] and [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]]
 
**Extensive bacterial invasion of damaged muscle
 
**Gas production causing subcutaneous crepitus
 
**Similar manifestations as malignant oedema
 
 
 
===''Clostridium haemolyticum''===
 
 
*Causes bacillary haemoglobinuria in cattle, occasionally sheep
 
*Endogenous infection - endospores dormant in liver
 
*Fluke migration allows germination
 
*Beta toxin causes intravascular haemolysis and hepatic necrosis
 
*Haemoglobinuria due to destruction of red blood cells
 
 
 
===Clostridium sordelli===
 
 
*Causes [[Necrosis - Pathology#Gas Gangrene|gas gangrene]], [[Muscles Inflammatory - Pathology#Gas gangrene|myositis]] and abomasitis (lambs)
 
 
 
===Treatment of histotoxic infections===
 
 
*Early penicillin
 
*Vaccination with bacterin or toxoid at 3 months and booster after 3 weeks, then annually
 
  
  

Revision as of 10:50, 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



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

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.