INTRODUCTION AND EPIDEMIOLOGY
Tetanus is uncommon in the United States, but worldwide estimates are approximately 100,000 cases per year, with a mortality rate of 35% to 40%.1,2 The Centers for Disease Control and Prevention defines tetanus as a syndrome of acute onset of hypertonia and/or painful muscular contractions (usually of the muscles of the jaw and neck) and generalized muscle spasms without other apparent medical cause.3 In the United States, tetanus is a reportable disease, aggregated through the National Notifiable Diseases Surveillance System.
Improved childbirth practices, widespread immunization programs for children, decennial tetanus boosters for adults, mechanization of agriculture, and use of chemical fertilizers rather than animal manure have all resulted in a >95% decline in the annual incidence of tetanus in the United States since 1947.4 From 2009 to 2015, 197 tetanus cases were reported in the United States, with 16 deaths.4 Most patients who develop tetanus have inadequate immunity to the disease. Due to waning immunity and failure to receive routine boosters, only 31% of Americans >70 years old have adequate tetanus immunity.5 Tetanus among children and neonatal tetanus are uncommon. The case fatality rate is approximately 8%, and patients >55 years of age account for all deaths.3,4
Most cases of tetanus in the United States are associated with an acute wound. Puncture, contaminated, infected, or devitalized wounds account for approximately 70% of tetanus cases. Although less common, chronic wounds and dental abscesses are also associated with the disease. Diabetics and injection drug users have an increased risk of contracting tetanus.3,6
Two thirds of patients who develop tetanus do not seek medical care for their initial wound. Of those who do seek initial treatment and later develop tetanus, up to 95% do not receive appropriate therapy.3
Clostridium tetani is a motile, nonencapsulated, anaerobic gram-positive rod; it produces toxins that cause tetanus. C. tetani exists in either a vegetative or spore-forming state. The spores are ubiquitous in soil and animal feces and can survive on environmental surfaces for years. In agricultural areas, adults may harbor the organism; spores are found in many places, including on skin or in contaminated heroin.6,7 C. tetani is usually introduced into a wound in the spore-forming, noninvasive state but can germinate into the toxin-producing, vegetative form if tissue oxygen tension is reduced. Crushed or devitalized tissue, a foreign body, or the development of infection favors the growth of the toxin-producing form of C. tetani.7,8
C. tetani produces two exotoxins: tetanolysin, which facilitates growth of the bacterial population; and tetanospasmin, a powerful neurotoxin responsible for all of the clinical manifestations of tetanus. Tetanospasmin reaches the nervous system by hematogenous spread of the exotoxin to peripheral nerves and by retrograde intraneuronal transport. Tetanospasmin does not cross the blood–brain ...