Clinical meaning
Tetanus is caused by Clostridium tetani, an anaerobic, spore-forming, gram-positive bacillus found in soil, dust, and animal feces. Spores enter the body through wounds (puncture wounds, lacerations, burns, surgical wounds, injection drug use sites, umbilical stump in neonatal tetanus). In anaerobic wound conditions, spores germinate into vegetative bacteria that produce tetanospasmin, one of the most potent toxins known (lethal dose for humans ~2.5 ng/kg). Tetanospasmin undergoes retrograde axonal transport from the wound site to the spinal cord and brainstem. At the presynaptic terminal, the toxin cleaves VAMP/synaptobrevin (SNARE protein) in inhibitory interneurons, blocking release of GABA and glycine — the primary inhibitory neurotransmitters in the CNS. This loss of inhibitory input to motor neurons causes unopposed excitatory activity, resulting in sustained muscle contraction (spastic paralysis). The clinical hallmark is 'descending tetanus' — symptoms typically begin in the jaw (trismus/lockjaw from masseter spasm) and progress caudally to neck stiffness, dysphagia, back rigidity (opisthotonus — extreme spinal hyperextension), abdominal rigidity, and extremity spasms. The incubation period is 3-21 days (shorter incubation = more severe disease). Autonomic dysfunction occurs in severe cases: labile blood pressure, tachycardia, diaphoresis, cardiac arrhythmias — a major cause of death alongside respiratory failure from laryngospasm and respiratory muscle spasm. Tetanus does NOT confer natural immunity — recovered patients must still be vaccinated.