**2. Pathophysiology**

The *C. tetani* bacterium is a spore-forming, gram-positive, slender, anaerobic rod. It is heat sensitive and cannot survive in the presence of oxygen. The spores however are extremely resistant to heat and they can survive autoclaving at a temperature up to 121°C for 10–15 min. The spores of *C. tetani* are widely distributed in the environment and they reside in soil, faeces and dust. Once the spores enter the body through a wound, they germinate in the presence of an anaerobic condition. In some patients, no entry site is seen. Spores of *C. tetani* can also gain entry into the body through burns, surgery sites or childbirth. It has an incubation period of 2 and 21 days with an average 8 days. The further the injury site is from the central nervous system the longer the incubation period. Shorter incubation periods are associated with severe form of the disease and a higher chance of death. *C. tetani* produces two exotoxins, tetanolysin and tetanospasmin. Tetanospasmin is a neurotoxin and it is responsible for the clinical presentations of tetanus. This is an extremely potent neurotoxin and it is estimated that the minimum human lethal dose is 2.5 ng/kg of body weight (a nanogram is one billionth of a gram). The toxin spreads into the nervous system by binding to the neuromuscular junction and then being transported backwards into the cell body. Further spread occurs trans-synaptically to adjacent motor and autonomic nerves. The effect of tetanospasmin is by cleaving synaptobrevin which is a vesicle-associated membrane protein which is essential for the release of neurotransmitter. The inhibitory pathways is the most affected there by preventing the release of glycine and g-amino butyric acid (GABA). When interneurones inhibiting alpha motor neurones are affected, there is failure to inhibit motor reflexes [3]. This causes increased muscle tone and rigidity, interposed by sudden and potentially devastating muscle spasms. Muscles of the face are affected early because of their short axonal pathways. Sympathetic neurones become affected later in the disease. Disinhibited autonomic discharge leads to loss of autonomic control, resulting in sympathetic overactivity and increased catecholamine levels. Neuronal binding of the toxin is irreversible. Recovery requires the growth of new nerve terminals, which explains the prolonged duration of the disease.
