Difference between revisions of "Clostridium tetani"

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*Causes [[Tetanus|tetanus]]
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*Causes [[Tetanus - Horse|tetanus (maily in horses)]]
 
*Acute, potentially fatal intoxication affecting many species
 
*Acute, potentially fatal intoxication affecting many species
 
*Horses and man particularly susceptible; carnivores fairly resistant
 
*Horses and man particularly susceptible; carnivores fairly resistant
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**Debridement of wounds in horses
 
**Debridement of wounds in horses
  
[[Category:Neurotoxic Clostridia]][[Category:Cattle]][[Category:Dog]][[Category:Horse]]
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[[Category:Neurotoxic Clostridia]][[Category:Cattle Bacteria]][[Category:Dog Bacteria]][[Category:Horse Bacteria]]
 
[[Category:To_Do_-_Bacteria]]
 
[[Category:To_Do_-_Bacteria]]
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[[Category:To Do - Major]]

Latest revision as of 16:48, 9 May 2011

  • Causes tetanus (maily in horses)
  • 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
    • Endospores 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