Vegetative cells of Clostridium tetani are usually rod-shaped and up to 2.5 μm long, but they become enlarged and tennis racket- or drumstick-shaped when forming spores.

If inoculated into a wound, C. tetani can grow and produce a potent toxin, tetanospasmin, which interferes with motor neurons, causing tetanus.

[4] While C. tetani is frequently benign in the soil or in the intestinal tracts of animals, it can sometimes cause the severe disease tetanus.

[5] In deep wounds, such as those from a puncture or contaminated needle injection the combination of tissue death and limited exposure to surface air can result in a very low-oxygen environment, allowing C. tetani spores to germinate and grow.

[6] In the nervous system, tetanospasmin acts by blocking the release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid at motor nerve endings.

[1] Clostridium tetani is susceptible to a number of antibiotics, including chloramphenicol, clindamycin, erythromycin, penicillin G, and tetracycline.

[1] This is made commercially by growing large quantities of C. tetani in fermenters, then purifying the toxin and inactivating in 40% formaldehyde for 4–6 weeks.

[6] This is given in several doses spaced out over months or years to elicit an immune response that protects the host from the effects of the toxin.

[6] In 1889, C. tetani was isolated from a human victim by Kitasato Shibasaburō, who later showed that the organism could produce disease when injected into animals, and that the toxin could be neutralized by specific antibodies.

In 1897, Edmond Nocard showed that tetanus antitoxin induced passive immunity in humans, and could be used for prophylaxis and treatment.