Tetanus is an acute, often fatal, disease caused by an exotoxin produced by the bacterium Clostridium tetani (2). It is characterized by generalized rigidity and convulsive spasms of skeletal muscles, commonly the masseter muscle is effected which is known as lockjaw and infection with tetanus can often become fatal (10).
The bacterium causing tetanus is C. tetani, a gram-positive, spore forming, anaerobic rod and the spores are resistant to destruction by most methods (7). Tetanus occurs worldwide but is most frequently encountered in densely populated regions in hot, damp climates with spores often found within manure treated soil, the gastrointestinal tract and feces of many domestic and barnyard animals (8). Tetanus infection also may follow surgery, burns, puncture wounds, otitis media, dental infection, animal bites, abortion, and pregnancy(6). The incubation period ranges from 3 to 21 days, generally injuries closer to the central nervous system have shorter the incubation periods and higher mortality rates (2). The rate that symptoms occur depend the concentration of toxins present, the last date of vaccination, and present health status of the infected individual (1).
When the proper anaerobic conditions are present, such as in a wound, the spores germinate and produce the two toxins, tetanolysin and tetanospasmin, which spread systematically via axons, blood circulation, and lymphatics to reach peripheral motor end plates, central nervous system, and the sympathetic nervous system (7). While the mechanism of tetanolysin has not been clearly demonstrated, tetanospasmin is an extremely potent neurotoxin that results in the symptoms and pathology associated with tetanus (6). Tetanospasmin is a two chain polypeptide composed of a heavy chain and light chain linked by a protease sensitive loop (4). The original inactive form of tetanospasmin is exposed to protease and cleaved, exposing the disulfide bridge linking the two chains and allowing the heavy chain to bind to neural membranes for uptake into the neuron (4). The light chain prevents neurotransmitter release from the infected neurons by cleaving synaptobrevin, a membrane protein that transports inhibitory neurons like glycine and gamma-aminobutyric acid (GABA) causing a situation in which gamma-aminobutyric acid (GABA)-containing and glycine-containing vesicles are not released, ultimately causing the loss of ability to inhibit motor and autonomic neurons (6).
Tetanus can present in four different ways. Local tetanus, is an uncommon form in which patients have s contraction of muscle spasm of rigidity in close proximity to the anatomic area that is injured (2). These contractions may persist for many weeks before gradually subsiding. Local tetanus may precede the onset of generalized tetanus but is generally mild (2). Cephalic tetanus is rare and is seen with otitis media or injuries to the head that become infected with C. tetani and cause pathology of cranial nerves and muscles...