ABSTRACT
Tetanus toxin is a protein neurotoxin produced by Clostridium tetani. This organism is a common environmental bacterium that has been identified in soil samples taken from all over the world (Hatheway, 1990). Unlike many pathogenic bacteria that produce a number of different virulence factors, all of the clinical effects seen in animals that have contracted tetanus can be attributed to this one toxin. Spores of C. tetani that are introduced into an animal through wounds will grow in a sufficiently anaerobic environment and produce toxin. After tetanus toxin is produced at a wound site, it is taken up by peripheral nerve endings and delivered to the central nervous system by the process of retrograde axonal transport and transsynaptic transport. In the central nervous system, tetanus toxin acts to inhibit the release of inhibitory neurotransmitters. The unopposed release of excitatory neurotransmitters results in the clinical symptoms seen in tetanus, such as muscle stiffness, trismus, opisthotonus, and reflex spasms. Symptoms of tetanus can become apparent as quickly as 48 h after exposure to C. tetani or may not appear for up to 3 weeks (see Bleck, 1989, for a review). The disease can remain localized to muscles near the entry site of the bacteria (localized tetanus) or affect the entire body (generalized tetanus). The effects of tetanus toxin on neuronal cells are extremely long-lasting, making recovery from tetanus a slow process. Recovery is thought to result at least in part from nerve sprouting and establishment of new synaptic contacts rather than the recovery of intoxicated cells.
