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Tetanus is a severe neuromuscular disorder characterized by sustained muscle spasms caused by the bacterium Clostridium tetani.

It is caused when Clostridium tetani spores enter the host through wounds and germinate under anaerobic conditions in damaged or necrotic tissue.

The germinated vegetative cells remain localized at the infection site and proliferate.

These cells secrete tetanospasmin, a two-chain neurotoxin linked by a disulfide bond.

The toxin spreads to motor nerve endings and enters the motor neuron by endocytosis.

It then travels by retrograde axonal transport to the spinal cord in the central nervous system, where inhibitory interneurons take up the toxin.

After endocytosis, the toxin’s chains separate within the vesicle, and the light chain enters the cytoplasm.

The light chain cleaves synaptobrevin, a vesicle protein needed to release inhibitory neurotransmitters such as gamma-aminobutyric acid, or GABA, and glycine.

This prevents the release of inhibitory neurotransmitters. Without inhibition, motor neurons remain overactive, causing sustained muscle contraction or spastic paralysis, which manifests as muscle rigidity, facial spasms, and lockjaw.