The disease is caused by Clostridium tetani, an anaerobic bacterium that exists in both vegetative and sporulated forms and has been isolated from soil, feces of humans and animals, dust, wounds, intact skin, catgut, and talcum powder. During unfavorable conditions the organism exists in the sporulated form, which can remain viable for several months. It is resistant to boiling and antiseptics but is killed by autoclaving at 121°C for 15 minutes. Clostridium tetani is not locally invasive and does not provoke an inflammatory response, and inoculation of spores into viable tissue does not produce tetanus. However, tissue necrosis, foreign bodies, or concurrent anaerobic or facultative anaerobic infections lower the normal oxidation-reduction potential of the tissue, which allows conversion to the vegetative form with subsequent toxin formation. The toxins produced include tetanolysin, which is capable of causing local damage to viable tissue, thereby optimizing conditions for bacterial multiplication, and production of tetanospasmin, which is a potent neurotoxin responsible for the clinical disease state.5 Toxin formed in a skin wound enters the underlying muscle and may spread to adjacent muscles. It then accumulates in the nerve endings of motor fibers. Retrograde transport of the toxin then occurs via intra-axonal and periaxonal pathways from nerve endings to the ventral horns of the spinal cord or motor nuclei of the cranial nerves. If toxin is produced in larger amounts, it also accumulates in the lymphatic system of the invaded muscle, enters the bloodstream via the thoracic duct, and is disseminated throughout the body. Toxin passing from blood to skeletal muscle then accumulates in the nerve endings of the motor fibers and proceeds to the ventral horns (or cranial nuclei), or is taken up by the lymphatic system and recirculated in the blood. The rate of accumulation of toxin in the ventral horns of the spinal cord depends on the length of the neural pathway and the activity of the muscles involved.6 Since jaw muscles and spinal postural muscles have short neural pathways to the ventral horns and are continually active in the awake human, this is the likely explanation for trismus and neck stiffness early in the course of the illness.