ISSN 2398-2969      

Tetanus

icanis

Introduction

  • Cause: toxin produced byClostridium tetani Clostridium tetani.
  • Signs: generalized or localized muscle spasms.
  • Diagnosis: clinical signs and history.
  • Treatment: supportive.
  • Prognosis: good provided animal is supported through critical period.

Pathogenesis

Etiology

  • Toxin produced byClostridium tetani.

Pathophysiology

  • Bacteria enters body → toxin production → enters motor nerves → extensor rigidity of all muscles.
  • Dogs are relatively resistant to effects of toxin (as compared to man and horses).
  • Clostridium tetanienters body usually via penetrating wound.
  • Three different toxins produced:
    • Tetanospasmin: enters motor nerves and travels in a retrograde fashion to spinal cord along nerve axons.
    • Reduced inhibiton of motor nerve function → muscle extensor rigidity.
    • Hemolysin: promotes anaerobic conditions for multiplication ofClostridium tetaniby causing local tissue necrosis.
    • Nonspasmogen: has poorly defined role.

Timecourse

  • Signs within 1 week of bacterial infection of wound.
  • Occasionally signs delayed up to 3 weeks.
  • Recovery usually over weeks to months.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Adamantos S & Boag A (2007) Thirteen cases of tetanus in dogs. Vet Rec 161 (9), 298-302 PubMed.

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