Toxins produced by Clostridium Tetani

Toxins produced by Clostridium Tetani-Delaram



Clostridium tetani is gram positive, rod-shaped, anaerobic bacterium of the genus Clostridium. C. tetani is found as spores in soil or as parasites in the gastrointestinal tract of animals.

C. tetani usually enters a host through a wound to the skin and then it multiplies. Once an infection is established, C. tetani produces two exotoxins- tetanolysin and tetanospasmin.

Tetanospasmin is the key toxin of tetanus. The genes that produce toxin are encoded on a plasmid which is present in all toxigenic strains, and all strains that are capable of producing toxin produce identical toxins.

Tetanolysin serves no known function to C. tetani, and the reason the bacteria produce it is not known with certainty.

Tetanospasmin is a neurotoxin and causes the clinical manifestations of tetanus. Tetanus toxin is generated in living bacteria, and is released when the bacteria lyses, such as during spore germination or during vegetative growth. A minimal amount of spore germination and vegetative cell growth are required for toxin production.

On the basis of weight, tetanospasmin is one of the most potent toxins known.

The clinical manifestations of tetanus are caused when tetanus toxin blocks inhibitory impulses, by interfering with the release of neurotransmitters, including glycine and gamma-aminobutyric acid. This leads to unopposed muscle contraction and spasm. Seizures may occur, and the autonomic nervous system may also be affected. Tetanospasmin appears to prevent the release of neurotransmitters by selectively cleaving a component of synaptic vesicles called synaptobrevin II.


Treatment: (Not required for this SAQ but retained due to its usefulness.)

When a tetanus infection becomes established, treatment usually focuses on stopping toxin production, and neutralizing the effects of the toxin. Treatment includes administration of tetanus immune globulin (TIG), which comprises antibodies that inhibit tetanus toxin (also known as tetanus antitoxins), by binding to and removing unbound tetanus toxin from the body. Binding of the toxin to the nerve endings appears to be an irreversible event, and TIG is ineffective at removing bound toxin. Recovery of affected nerves requires the sprouting of a new axon terminal. Large doses of antibiotic drugs (such as metronidazole or intramuscular penicillin G) are also given once tetanus infection is suspected, to halt toxin production.

Prevention of tetanus includes vaccination, and cleaning the primary wound. Prophylaxis is effective, in the form of a tetanus toxoid vaccine, which is given with or without passive immunization with tetanus immune globulin- DPT vaccine (diphtheria-pertussis-tetanus) is given at 2, 4, 6, and 15–18 months of age, followed by a booster before entry to school (4-6 years). This regimen provides protection from tetanus for about 10 years, and every 10 years thereafter, a booster shot of tetanus vaccine is recommended.