Tetanus: Debilitating Infection

Tetanus is a devastating disease that can be prevented by proper immunization and wound care. Although the incidence is low in the United States due to widespread routine vaccination, immunization coverage remains below target, especially in older adults. Since outcome is influenced by the clinician's ability to make a timely diagnosis and initiate appropriate care, continued appreciation of tetanus is warranted.

Tetanus is a neurologic disorder resulting from infection by the gram-positive, spore-forming anaerobic bacillus Clostridium tetani. The bacterium, in spore form, typically enters the body through a contaminated soft-tissue wound. Ubiquitous in the environment, C tetani spores are found throughout the world—in soil as well as in animal feces and saliva—and are resistant to temperature extremes and antiseptics. Tetanus is infectious but not contagious (not transmitted person-to-person).¹ Wounds with devitalized tissue or those supporting anaerobic conditions, such as bites, puncture wounds, burns, and gangrene, are conducive to the development of tetanus. Infection can also occur following dental extractions, abortions, and illicit drug injection.¹ Although vaccination programs have decreased the incidence of tetanus in the United States, C tetani infection remains an ongoing clinical concern because the spores are omnipresent, universal vaccination coverage has not been achieved, and vaccine-immunity wanes over time, placing individuals at risk.

PATHOPHYSIOLOGY

C tetani produces two toxins: tetanolysin and tetanospasmin (tetanus toxin). Tetanolysin may have a role in promoting the diffusion of tetanospasmin in soft tissues.² Tetanospasmin is a highly potent toxin, with a lethal dose in humans of less than 2.5 ng/kg of body weight.³ The toxin enters the peripheral nerve at the site of injury and migrates to the central nervous system (CNS). There, it causes unopposed α-motor neuron firing by preventing the release of inhibitory neurotransmitters such as γ-aminobutyric acid (GABA), resulting in muscle spasms and excess reflexive response to sensory stimuli.⁴ It also leads to excessive catecholamine release from the adrenal medulla.¹

Tetanospasmin binds to neurons in the spinal cord and brainstem. Because toxin binding is irreversible, resolution of tetanus requires the neurons to grow new axon terminals. The effects of tetanus can persist for six to eight weeks until new terminals develop.^3,5 Patients often require several weeks of ventilator support during this time.³

EPIDEMIOLOGY

Tetanus continues to be a serious cause of morbidity and mortality worldwide. The majority of cases (80%) occur in Africa and Southeast Asia.⁶ Incidence is much lower in the United States (0.1 cases per million persons annually) because of widespread vaccination, with only 233 cases of tetanus reported between 2001 and 2008.⁷ However, in the absence of confirmatory tests, the diagnosis is a clinical one; furthermore, there is no laboratory reporting program for tetanus. As a result, more cases may occur in the US than are detected or reported.

In developed countries, tetanus is primarily a disease of the elderly or the unvaccinated. Older persons, especially non-veterans, are less likely to have received the primary series. Because immunity decreases with age, even those who completed the primary series but have not received booster doses are at increased risk.⁸ Home-schooled children, who are not subject to school-entry vaccination requirements, are also at risk if unvaccinated.⁹

Neonatal tetanus is an ongoing problem in undeveloped countries that lack maternal vaccination programs. (Maternal immunization successfully reduces neonatal tetanus via passive immunity, and maternal tetanus via active immunity.) Unvaccinated women who undergo nonmedical abortions or unhygienic childbirth are at increased risk for tetanus.^3,10

Other risk factors for tetanus include wound contamination with soil, saliva, or devitalized tissue; injection drug use; and exposure to anthropogenic or natural disasters.¹ C tetani spores can contaminate heroin and may grow in abscesses of heroin users.⁴ Small outbreaks of tetanus among injection drug users have been reported, even among younger adults who had some immunity from childhood vaccination.^7,11 In addition, patients with diabetes are at increased risk for tetanus. These patients may have chronic wounds due to slowed healing and poor vascularity, which can lead to lower oxygen tension in their wounds and create an environment conducive to anaerobic infection. These chronic wounds are often ignored as a potential nidus for tetanus; instead, focus is placed on plantar puncture wounds or lacerations.⁷

Though tetanus risk is greatest for those who were never fully immunized, cases have been reported in persons who were immunized in the remote past but had not received a recent booster. Such cases show that tetanus immunity is not absolute and does wane over time.^12-14 Among the 233 tetanus cases reported in the US during 2001-2008, vaccination status was reported for 92. Of these, 24 patients had a complete series and 31 patients had at least one prior dose of tetanus vaccine.⁷ Furthermore, six cases occurred in patients known to have had the four-dose series and a booster within 10 years of diagnosis. Similarly, a 14-year-old boy who was fully vaccinated developed cephalic tetanus from a stingray wound.¹⁴ Given these data, clinicians should not assume that a patient who reports having had “a tetanus shot” is completely protected; a full series and regular boosters are required, and, in rare cases, tetanus can occur despite full vaccination.