Tetanus Toxin

Tetanus Toxin first described in the fourth century BC by Hippocrates of Kos (Greece) as a neuroparalytic disease. The disease leading to rigidity and tetanic spasms is characterized by voluntary muscle hyperactivity. Tetanus caused by a bacterium was demonstrated in 1884 by Carle and Rattone and later isolated by Kitasato and named Clostridium tetani. In 1889, it was demonstrated that the bacterium C. tetani produce a potent neurotoxin that causes tetanus.

Worldwide, the spores of C. tetani are present in the environment, which can contaminate minor abrasions, wounds, and the umbilical stump in neonatal tetanus. The spores of C. tetani in anaerobic conditions produce vegetative bacteria, which cause tetanus by expressing the tetanus toxin. Although tetanus affects all mammals, the disease susceptibility varies; primates and horses are more susceptible than carnivores. Tetanus neurotoxin (TeNT) is synthesized as a single-chain polypeptide of molecular weight 150K Daltons. The toxin is activated proteolytically by clostridial proteases in the extra-bacterial medium or by exogenous proteases from the host. The teNT is not generally detectable in biological samples, and identifying toxins is often difficult. The identification of characteristic spastic paralytic signs and a suspected wound can help in the diagnosis of tetanus. Isolation of C. tetani from contaminated wounds is not always feasible. The primary treatment of tetanus is to control spasms and reduce cardiovascular instability and consists of antibiotics, antitoxin, wound debridement, and supportive care. Tetanus is not transmissible; vaccination with tetanus toxoid can prevent the disease. Tetanus eradication is impossible because of the environment's extensive occurrence of the causative agent. Therefore, a strategy should be taken to eliminate the disease rather than eradicating it to reduce the incidence of tetanus. [AKM Mahbub Hasan]

See also diphtheria toxin, toxin