Introduction

• Cause: toxin produced by Clostridium 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 by Clostridium tetani.
• Bacterium found in soil and intestinal tract (thrive in anaerobic environments). 
• Usually enters the body through deep puncture wounds. 

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 tetani enters body usually via penetrating wound.
• The spores of Clostridium tetani are unable to grow in healthy tissue or even in wounds if the tissue remains at the normal oxidation-reduction potential of the circulating blood. 
• The spores can germinate if appropriate needs of low redox potential, low oxygen tension, pH, and bacterial nutrients are met. Typically a small amount of soil or foreign object causing tissue necrosis provide suitable conditions for multiplication to occur. 
• As bacterial cells undergo autolysis, the potent neurotoxins are released.  
• Two different toxins are produced: 
  • Tetanospasmin: enters motor nerves and travels in a retrograde fashion to the inhibitory spinal interneuron. 
  • Blocks release of acetylcholine (by destroying synaptobrevin, a component of the synaptic vesicle docking apparatus) reducing inhibition of motor nerve function → muscle extensor rigidity (spastic paralysis). 
  • Tetanolysin: promotes anaerobic conditions for multiplication of Clostridium tetani by causing local tissue necrosis. 

Timecourse

• Signs occur from one to several weeks but usually occur within 10-14 days of bacterial infection of wound. 
• Recovery usually over weeks to months. 

Diagnosis

Treatment

Prevention

Outcomes