Clostridium tetani is an obligate anaerobic spore-forming bacillus. Mature organisms develop spores that are widely distributed in soil and dust as well as in the intestines and feces of animals. While the bacteria are sensitive to heat and aerobic conditions, the spores are resistant to ethanol, phenol, and formalin. However, they do not survive treatment with iodine, glutaraldehyde, hydrogen peroxide, or autoclaving at 121°C and 103 kPa (15 psi) for 15 minutes [1].

The vegetative form of C. tetani produces two types of zinc metalloproteinase toxins, tetanospasmin and tetanolysin, with tetanospasmin playing more of a prominent role in pathogenesis. Unlike the toxin produced by Clostridium botulinum, the C. tetani neurotoxin is of a single antigenic type and specifically targets the central nervous system (CNS), including the peripheral motor end plates, spinal cord, brain, and the sympathetic nervous system [1,2]. Although this toxin can exert an excitatory effect, it acts primarily by blocking the release of neurotransmitters such as glycine and γ-aminobutyric acid (GABA), which normally acts to inhibit the transmission of motor nerve impulses. Specifically, the toxin degrades synaptobrevin, a protein required for contact of inhibitory neurotransmitter vesicles with their release site on the presynaptic membrane [3].

Antitoxin is of therapeutic value only in protecting neurons that have not already bound the toxin. As the effect of the toxin on a synapse does not appear reversible, recovery from tetanus depends on the generation of new nerve terminals and new synapse formation.

Tetanus is endemic in the developing world with neonatal tetanus accounting for the majority (> 50%) of deaths due to tetanus [4]. Tetanus is a rare disease in the developed world with morbidity and mortality in the United States declining
steadily, due to the availability of tetanus vaccines, improved wound management, and the use of tetanus immunoglobulin for postexposure prophylaxis [5]. According to the 1998 to 2000 surveillance data, an average of 43 tetanus cases occurred yearly in the United States with the majority of cases related to acute injuries such as puncture wounds, lacerations, and abrasions [6]. The highest incidences were reported in individuals ≥60 years old, persons of Hispanic origin, older adults with diabetes, and intravenous drug users. No deaths were reported in those individuals who received adequate immunization.

Tetanus usually occurs in the setting of necrotic or infected tissue in which anaerobic bacterial growth is facilitated. However, in up to 30% of cases, no acute injury is reported [6]. The incubation period for tetanus varies from 3 to 21 days, with the length of the incubation period dependent on how far the injury site is from the CNS [7]. The first nerves affected are the shortest, accounting for the early symptoms of facial distortion and neck stiffness. It has been found that the shorter the incubation period, the worse the prognosis [8].

Clinical tetanus can present in three forms—local, cephalic, and generalized—with 80% of cases being generalized. Local tetanus presents as a focal region of muscle contraction at a site of spore inoculation [1]. Symptoms may persist but usually resolve spontaneously. Cephalic tetanus develops after a traumatic head injury, but has been reported after otitis media when C. tetanus was present in the middle ear [9]. Typically, there is involvement of the cranial nerves, especially cranial nerve VII in the facial area.

Generalized tetanus typically presents with involvement of facial musculature, starting with masseter rigidity (lockjaw or trismus) and risus sardonicus (orbicularis oris), and then progresses in a descending fashion with difficulty swallowing and abdominal rigidity [1]. Spasms, which are often triggered by sensory stimuli, are common and may resemble seizures with flexion of the arms and the extension of legs (opisthotonus). The patient does not lose consciousness and severe pain usually accompanies the spasms. Laryngospasm and respiratory compromise may result from vocal cord or diaphragmatic spasms and upper airway obstruction. In addition, fractures of the spine or the long bones, dislocations, and rhabdomyolysis may occur as a result of spasms. The course of this illness occurs over 2 weeks, reflecting the time it takes for intraaxonal toxin to travel to the CNS. Spasms occur within the first 2 weeks of illness followed by autonomic disturbances such as extremes in blood pressure and cardiac arrhythmias including sinus tachycardia and cardiac arrest [10,11]. Individuals with tetanus are at high risk for nosocomial pneumonia with an incidence of approximately 35%. Autonomic dysfunction is an independent risk factor for pneumonia in patients with tetanus [12].

Neonatal tetanus, more often seen in developing countries, is a form of generalized tetanus that commonly arises when an unhealed umbilical stump becomes infected after an incision with an unsterile instrument and if the mother has not been adequately immunized [1,7].