Tetanus is an acute, often fatal disease caused by wound contamination with Clostridium tetani, a motile, nonencapsulated anaerobic gram-positive rod. Clostridium tetani exists in either a vegetative or a spore-forming state. The spores of this organism are ubiquitous and extremely resistant to destruction, surviving in soil or on environmental surfaces for years. Clostridium tetani is usually introduced into a wound in the spore-forming, noninvasive state but can germinate into a toxin-producing, vegetative form if tissue is compromised and tissue oxygen tension is reduced. Any factor that lowers the local oxidation-reduction potential, such as the presence of crushed, devitalized tissue, a foreign body, or the development of suppuration, favors the development of the vegetative, toxin-producing form of C. tetani.5

Once converted into the vegetative form, C. tetani produces two exotoxins: tetanolysin, which appears to be clinically insignificant; and tetanospasmin, a potent neurotoxin that is responsible for all the clinical manifestations of tetanus. Although the infection caused by C. tetani remains localized at the site of injury, tetanospasmin reaches the nervous system by hematogenous spread of the exotoxin to peripheral nerves and by retrograde intraneuronal transport. Bloodborne tetanospasmin does not cross the blood-brain barrier, but retrograde intraneuronal transport of the exotoxin enables tetanospasmin to gain access to the central nervous system.1

Tetanospasmin acts on the motor end plates of skeletal muscle, in the spinal cord, in the brain, and in the sympathetic nervous system. This extremely potent exotoxin prevents the release of the inhibitory neurotransmitters glycine and g-aminobutyric acid (GABA) from presynaptic nerve terminals, releasing the nervous system from its normal inhibitory control.6

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