Difference between revisions of "Clostridium species"

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#REDIRECT[[:Category:Clostridium species]]
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<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
 +
 
 +
 
 +
===''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
 +
 
 +
*Toxoid vaccine
 +
*Implicated in [[Intestines - physical disturbances#Equine dysautonomia, or grass sickness|equine grass sickness]]
 +
 
 +
 
 +
===Clostridium chauvei===
 +
 
 +
* Causes [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]], along with [[Clostridium species#Clostridium septicum|''Clostridium septicum'']].
 +
* Infects muscles giving black leg [[Muscles - inflammatory#Black leg|myositis]]
 +
 
 +
===Clostridium novyi===
 +
 
 +
* 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]]
 +
 
 +
===Clostridium perfringens===
 +
 
 +
* Causes:
 +
** [[Intestines - Fibrinous/ Haemorrhagic Enteritis#Lamb Dysentery (Enterotoxaemia with Blood)|Lamb dysentery]]
 +
** [[Intestines - Fibrinous/ Haemorrhagic Enteritis#Colitis X|Colitis X]].
 +
** [[Intestines - Catarrhal Enteritis#"Pulpy Kidney" Disease|Pulpy kidney disease]]
 +
*** ''C. perfringens'' type D only.
 +
** [[Peritoneal cavity - inflammatory#In cattle|Peritonitis in cattle]]
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**  [[Respiratory system - clinical signs#Dysphagia|Dysphagia in horses]]
 +
** [[General Pathology - Necrosis#Gas Gangrene|Gas gangrene]]
 +
** [[Muscles - inflammatory#Gas gangrene|Myositis]]
 +
 
 +
===Clostridium septicum===
 +
 
 +
* Causes [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles - inflammatory#Gas gangrene|myositis]]
 +
 
 +
===Clostridium sordelli===
 +
 
 +
* Causes [[General Pathology - Necrosis#Gas Gangrene|gas gangrene]] and [[Muscles - inflammatory#Gas gangrene|myositis]]
 +
 
 +
 
 +
 
 +
===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
 +
*''C. perfringens'' colonies are surrounded by a zone of double haemolysis
 +
*Biochemical tests
 +
*Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
 +
*Fluorescent antibody tests for histotoxic clostridia
 +
*ELISA, PCR for toxin detection

Revision as of 19:27, 18 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


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


Clostridium chauvei

Clostridium novyi

Clostridium perfringens

Clostridium septicum

Clostridium sordelli


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
  • C. perfringens colonies are surrounded by a zone of double haemolysis
  • Biochemical tests
  • Toxins identified in body fluids by toxin neutralisation or protection tests in lab animals
  • Fluorescent antibody tests for histotoxic clostridia
  • ELISA, PCR for toxin detection
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