Tetanus

Descriptive text is not available for this imageBASICS

DESCRIPTION

  • Tetanus is characterized by muscle rigidity and spasms due to production of a neurotoxin in infected wounds by Clostridium tetani, an anaerobic spore-forming gram-positive bacillus.
  • There are four clinical forms of tetanus: generalized, neonatal, localized, and cephalic.

EPIDEMIOLOGY

  • Tetanus is rare in the United States, with approximately 17 to 34 cases reported to Centers for Disease Control and Prevention (CDC) annually (2016 to 2020). Nearly all cases are in unvaccinated individuals. Rare cases have been reported in patients with protective levels of antitetanus antibodies.
  • Tetanus continues to occur in countries in which mothers are not immunized and in which nonsterile care of the umbilical cord is practiced. Worldwide, it is estimated that 73,000 total tetanus cases including >27,000 neonatal tetanus infections occurred in 2019. Generalized tetanus is the most common form of disease.

ETIOLOGY

  • Tetanus is caused by C. tetani, a spore-forming, anaerobic gram-positive bacillus.
  • C. tetani is a normal inhabitant of soil and animal and human intestines and is ubiquitous in the environment. Under anaerobic conditions, spores become vegetative and produce tetanospasmin; anaerobic conditions in wounds are promoted by extensive necrosis, foreign bodies, or other suppurative infections.

RISK FACTORS

  • Inadequate immunization
  • Neonate born to unimmunized mother
  • Elderly with declining immune status
  • Injection drug use
  • Chronic wounds
  • Acute traumatic injury
  • Foreign bodies
  • Nonsterile delivery conditions and practice of applying mud or feces to umbilical cord

GENERAL PREVENTION

  • All wounds should be cleaned with soap and water, and foreign bodies should be removed.
  • Universal immunization with tetanus toxoid (for details and information on catch-up schedules, refer to CDC Web site)
  • Tetanus postexposure prophylaxis should be initiated at the time of injury:
    • For clean minor wounds:
      • If patient has had ≥3 prior doses of tetanus toxoid (DTaP, Tdap, or Td) and it has been <10 years since the last dose, no prophylaxis is indicated; if it has been ≥10 years since last dose, give tetanus toxoid.
      • If patient has had <3 prior doses of tetanus toxoids, give tetanus toxoid.
    • For all other wounds:
      • If patient has had ≥3 prior doses of tetanus toxoid and it has been <5 years since the last dose, no prophylaxis is indicated; if it has been ≥5 years since the last dose, give tetanus toxoid.
      • Patients with <3 prior doses of tetanus toxoid should receive tetanus immune globulin (TIG) and tetanus toxoid at separate sites.
      • Patients with HIV or severe immunodeficiency should receive TIG regardless of prior immunization history.
    • In neonates or infants <6 months of age who have not received 3 doses of DTaP, the decision to use TIG should be based on mother’s tetanus immunization status; if unknown or inadequate, give TIG.
    • Type of tetanus toxoid to use for prophylaxis:
      • For children <7 years old, use DTaP; if pertussis vaccine is contraindicated, use DT.
      • For a child 7 to 10 years old, use Tdap.
      • For an adolescent 11 to 18 years old who has not received Tdap, use Tdap; for those who have received Tdap or for those whom pertussis is contraindicated, use Td.
    • TIG dose is 250 U IM for wound prophylaxis (regardless of age or weight); if TIG is unavailable, use IV immunoglobulin (IVIG) or tetanus antitoxin (TAT).
      • Because TAT is equine in origin, test patient for sensitivity prior to use.
      • TAT is no longer available in the United States.

PATHOPHYSIOLOGY

  • C. tetani produces tetanospasmin, a powerful metalloprotease neurotoxin.
  • Tetanospasmin can be absorbed directly into skeletal muscles adjacent to the injury.
  • Tetanospasmin can travel to the central nervous system (CNS) via retrograde axonal transport through peripheral nerves or via lymphocytes.
    • In the CNS, tetanospasmin prevents the release of γ-aminobutyric acid (GABA) and glycine in inhibitory nerve terminals, resulting in sustained excitatory discharges (motor spasms and increased muscle tone) and autonomic instability; tetanospasmin does not directly affect cognitive processes.
    • In the peripheral nervous system, tetanospasmin may block inhibitory impulses to motor neurons.
    • Loss of regulation of adrenal catecholamine release precipitates tachycardia, hypertension, and sweating.
  • Infection does not confer immunity; all patients need to be immunized during recovery.

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