Clinical Information

Tetanus results from contamination of wounds or lacerations with Clostridium tetani spores from the environment. The spores germinate to actively replicating bacterial cells localized within the wound and produce the heat-labile toxin tetanospasmin. Tetanospasmin attaches to peripheral nerve endings and travels to the central nervous system where it blocks inhibitory impulses to motor neurons and leads to severe, spastic muscle contractions, a classic characteristic of tetanus.

The disease is preventable by vaccination with tetanus toxoid (formaldehyde-treated tetanospasmin), which stimulates development of antitetanus toxoid antibodies. In the United States, tetanus toxoid is administered to children as part of the combined diphtheria, tetanus, and acellular pertussis (TDaP) vaccine.

Two to 3 weeks following vaccination, a patient's immunological response may be assessed by measuring the total antitetanus toxoid IgG antibody level in serum. An absence of antibody formation postvaccination may relate to immune deficiency disorders, either congenital or acquired, or iatrogenic due to immunosuppressive drugs.