Difference between revisions of "Clostridium tetani"
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− | *Causes [[Tetanus|tetanus]] | + | *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 | ||
Line 31: | Line 31: | ||
**Debridement of wounds in horses | **Debridement of wounds in horses | ||
− | [[Category:Neurotoxic Clostridia]][[Category:Cattle]][[Category:Dog]][[Category:Horse]] | + | [[Category:Neurotoxic Clostridia]][[Category:Cattle Bacteria]][[Category:Dog Bacteria]][[Category:Horse Bacteria]] |
[[Category:To_Do_-_Bacteria]] | [[Category:To_Do_-_Bacteria]] | ||
+ | [[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