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
  • 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