Difference between revisions of "Clostridium species"

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#REDIRECT[[:Category:Clostridium species]]
+
<big><center>[[Infectious agents and parasites|'''BACK TO INFECTIOUS AGENTS AND PARASITES''']]</center></big>
 +
<big><center>[[Bacteria|'''BACK TO BACTERIA''']]</center></big>
 +
 
 +
===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 ''Sreptococci 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#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#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 [[Intestines - physical disturbances#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#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#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#Gas gangrene|myositis]].
 +
*May be involved in [[Bacterial skin infections#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#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#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
 +
*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
 +
**Canine haemorrhagic gastroenteritis
 +
**Typhlocolotis in horses, possibly associated with [[Intestines - Fibrinous/ Haemorrhagic Enteritis#Colitis X|Colitis X]]
 +
*''C. perfringens'' type B:
 +
**[[Intestines - Fibrinous/ Haemorrhagic Enteritis#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
 +
**Haemorrhagic enteritis and ulceration in the small intestine
 +
**Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability
 +
**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 plays major role in pathogenesis of the disease
 +
**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
 +
**[[Peritoneal cavity - inflammatory#In cattle|Peritonitis in cattle]]
 +
*''C. perfringens'' type D:
 +
**[[Intestines - Catarrhal Enteritis#"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
 +
**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
 +
*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 10:47, 26 May 2008

BACK TO INFECTIOUS AGENTS AND PARASITES
BACK TO 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 Sreptococci 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
  • 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
    • Canine haemorrhagic gastroenteritis
    • 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
    • Haemorrhagic enteritis and ulceration in the small intestine
    • Fluid in the peritoneal cavity and pericardial sac due to increased capillary permeability
    • 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 plays major role in pathogenesis of the disease
    • 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
    • Peritonitis in 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
    • 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
  • 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
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