Difference between revisions of "Clostridium species"

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<br>
 +
===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
 +
 
 +
===Neurotoxic clostridia===
 +
 
 +
 
 +
===''Clostridium tetani''===
 +
 
 +
*Causes [[Tremors and Movement Disorders (Nervous System) - Pathology#Tetanus|tetanus]]
 +
*Acute, potentially fatal intoxication affecting many species
 +
*Horses and man particularly susceptible; carnivores fairly resistant
 +
*Found in horse faeces
 +
*Characteristics:
 +
**Terminal, spherical endospores give mother cells a drumstick appearance
 +
**Enodospores resistant to boiling and chemicals but susceptible to autoclaving
 +
**Swarming growth and haemolytic on blood agar
 +
**Many serotypes but all produce same neurotoxin, tetanospasmin, therefore antibodies neutralise all
 +
*Pathogenesis:
 +
**Endospores introduced via damaged tissues e.g. penetrating wounds
 +
**Damaged tissue creates an anaerobic environment, allowing germination of spores
 +
**Tetanospasmin made by bacteria replicating in damaged tissue
 +
**Absorbed toxin affects neuromuscular junction distant from site of toxin production
 +
**Neurotoxin binds irreversibly to ganglioside receptors on motor neurons and is transported to nerve cell body
 +
**Toxins transported across synapse to terminals of inhibitory neurons where they block transmission of signals
 +
**Spastic paralysis by constant tensing of muscles results
 +
**Toxin can be blood-borne and bind to motor terminals throughout the body as well as in the CNS
 +
*Clinical signs:
 +
**Incubation period 5-10 days
 +
**Stiffness, localised spasms, altered heart and respiratory rates, dysphagia, altered facial expression, lock-jaw from mastigatory muscle spasm
 +
**Tonic muscle contraction easily stimulated
 +
*Treatment:
 +
**Antitoxin IV or into subarachnoid space on 3 consecutive days
 +
**Toxoid subcutaneously to promote active immune response
 +
**Penicillin to kill vegetative cells
 +
**Debridement and flushing of wound with hydrogen peroxide
 +
**Fluids, sedatives, muscle relaxants
 +
*Control:
 +
**Toxoid vaccine for farm animals
 +
**Debridement of wounds in horses
 +
 
 +
 
 +
===''Clostridium botulinum''===
 +
 
 +
*Ubiquitous organism
 +
*Oval, subterminal endospores; spores survive boiling for hours
 +
*Causes [[Muscles Degenerative - Pathology#Botulism|botulism]], a potentially fatal intoxication
 +
*Germination of endospores, growth of bacterial cells and toxin production in anaerobic conditions e.g. decaying carcasses and vegetation
 +
*Disease in animals consuming rotting carcasses and in herbivores through contamination of feed
 +
*Pathogenesis:
 +
**Intoxication on ingestion and absorbtion of toxin from GIT into the blood
 +
**Occasionally germination of spores in wounds or GIT
 +
**Neurotoxin carried to peripheral nervous system
 +
**Toxin binds gangliosides irreversibly at the neuromuscular junction
 +
**Blocks release of acetylcholine
 +
*Clinical signs:
 +
**Dilated pupils, dry mucus membranes, decreased salivation, tongue flacidity, dysphagia in farm animals
 +
**Incoordination and knuckling followed by flacid paralysis and recumbency
 +
**Paralysis of respiratory muscles leads to death
 +
**Flacid paralysis of legs and wings in birds
 +
*Diagnosis:
 +
**Mouse inoculation with infected serum
 +
**Toxin detection by PCR, ELISA
 +
**Toxin neutralisation tests in mice
 +
*Treatment: polyvalent antiserum neutralises unbound toxin
 +
*Toxoid vaccine used in endemic regions
 +
*Implicated in [[Intestine Physical Disturbances - Pathology#Equine dysautonomia, or grass sickness|equine grass sickness]]
 +
 
 +
 
 +
===Histotoxic infections===
 +
 
 +
*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 [[General Pathology - Necrosis#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 [[General Pathology - Necrosis#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 [[General Pathology - Necrosis#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===
 +
 
 +
*[[General Pathology - Necrosis#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 [[General Pathology - Necrosis#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
 +
 
 +
 
 +
===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
 +
 
 +
 
 +
===''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

Revision as of 18:42, 11 August 2009

 This article has been peer reviewed but is awaiting expert review. If you would like to help with this, please see more information about expert reviewing.


Infectious agents and parasitesWikiBugs Banner.png
BACTERIA



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

Neurotoxic clostridia

Clostridium tetani

  • Causes tetanus
  • Acute, potentially fatal intoxication affecting many species
  • Horses and man particularly susceptible; carnivores fairly resistant
  • Found in horse faeces
  • Characteristics:
    • Terminal, spherical endospores give mother cells a drumstick appearance
    • Enodospores resistant to boiling and chemicals but susceptible to autoclaving
    • Swarming growth and haemolytic on blood agar
    • Many serotypes but all produce same neurotoxin, tetanospasmin, therefore antibodies neutralise all
  • Pathogenesis:
    • Endospores introduced via damaged tissues e.g. penetrating wounds
    • Damaged tissue creates an anaerobic environment, allowing germination of spores
    • Tetanospasmin made by bacteria replicating in damaged tissue
    • Absorbed toxin affects neuromuscular junction distant from site of toxin production
    • Neurotoxin binds irreversibly to ganglioside receptors on motor neurons and is transported to nerve cell body
    • Toxins transported across synapse to terminals of inhibitory neurons where they block transmission of signals
    • Spastic paralysis by constant tensing of muscles results
    • Toxin can be blood-borne and bind to motor terminals throughout the body as well as in the CNS
  • Clinical signs:
    • Incubation period 5-10 days
    • Stiffness, localised spasms, altered heart and respiratory rates, dysphagia, altered facial expression, lock-jaw from mastigatory muscle spasm
    • Tonic muscle contraction easily stimulated
  • Treatment:
    • Antitoxin IV or into subarachnoid space on 3 consecutive days
    • Toxoid subcutaneously to promote active immune response
    • Penicillin to kill vegetative cells
    • Debridement and flushing of wound with hydrogen peroxide
    • Fluids, sedatives, muscle relaxants
  • Control:
    • Toxoid vaccine for farm animals
    • Debridement of wounds in horses


Clostridium botulinum

  • Ubiquitous organism
  • Oval, subterminal endospores; spores survive boiling for hours
  • Causes botulism, a potentially fatal intoxication
  • Germination of endospores, growth of bacterial cells and toxin production in anaerobic conditions e.g. decaying carcasses and vegetation
  • Disease in animals consuming rotting carcasses and in herbivores through contamination of feed
  • Pathogenesis:
    • Intoxication on ingestion and absorbtion of toxin from GIT into the blood
    • Occasionally germination of spores in wounds or GIT
    • Neurotoxin carried to peripheral nervous system
    • Toxin binds gangliosides irreversibly at the neuromuscular junction
    • Blocks release of acetylcholine
  • Clinical signs:
    • Dilated pupils, dry mucus membranes, decreased salivation, tongue flacidity, dysphagia in farm animals
    • Incoordination and knuckling followed by flacid paralysis and recumbency
    • Paralysis of respiratory muscles leads to death
    • Flacid paralysis of legs and wings in birds
  • Diagnosis:
    • Mouse inoculation with infected serum
    • Toxin detection by PCR, ELISA
    • Toxin neutralisation tests in mice
  • Treatment: polyvalent antiserum neutralises unbound toxin
  • Toxoid vaccine used in endemic regions
  • Implicated in equine grass sickness


Histotoxic infections

  • 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

  • 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 gas gangrene, along with 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 gas gangrene and 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 gas gangrene and myositis.
  • May be involved in 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

  • Gas gangrene and 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


Treatment of histotoxic infections

  • Early penicillin
  • Vaccination with bacterin or toxoid at 3 months and booster after 3 weeks, then annually


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
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