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

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%.