Epidemiology

Etiology

Tetanospasmin: reaches the CNS through retrograde axonal transport
- Toxin binds to receptors of peripheral nerves and is then transported to interneurons (Renshaw cells) in the CNS via vesicles.
- Acts as protease that cleaves synaptobrevin, a SNARE protein → prevention of inhibitory neurotransmitters (i.e., GABA and glycine) release from Renshaw cells in the spinal cord → uninhibited activation of alpha motor neurons → muscle spasms, rigidity, and autonomic instability
Tetanolysin: causes hemolysis and has cardiotoxic effects

Tetanus vs botulism

Both work on SNARE proteins

Incubation period: Days to weeks.
Presents with a descending pattern of muscle rigidity.
Early signs:
- Trismus (lockjaw): Spasm of masseter muscles.
- Risus sardonicus: “Sardonic smile” from facial muscle spasm.
Later signs:
- Opisthotonos: Arching of the back due to severe extensor muscle spasm.
- Painful, generalized muscle spasms, often triggered by minor stimuli (noise, light).
- Autonomic instability: Tachycardia, hypertension, sweating.
Pt remains conscious throughout.

Immediately manage life-threatening and severe symptoms.
Administer passive immunization, e.g., human tetanus immunoglobulin (HTIG), as soon as possible.
Manage acute wounds, e.g., wound irrigation and debridement
Initiate antibiotics, preferably PO metronidazole.
Begin active immunization with the tetanus vaccine once the patient is improving.
Prevention
- Prevention of neonatal tetanus is achieved primarily by vaccination of the mother during pregnancy with an inactivated tetanus toxin (tetanus toxoid) as part of the tetanus-diptheria (Td) or tetanus-reduced diphteria-acellular pertussis (Tdap) vaccine. An appropriately vaccinated woman provides transplacental IgG to the fetus, which decreases the incidence of neonatal tetanus by approximately 95%.