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INTRODUCTION

Tetanus is a noncommunicable, toxin-mediated disease caused by Clostridium tetani, an organism that is ubiquitous in the environment. The disease is characterized by muscle rigidity and spasms, and medical treatment requires hospitalization and costly intensive care management. The case-fatality rate remains high (>10%), even among patients treated in modern care facilities. In developed countries, the disease has become uncommon following the implementation of universal childhood vaccination programs using safe and effective tetanus toxoid-containing vaccines (TTCVs); however, tetanus remains a public health problem in developing countries.

Etiological Agent, Pathogenesis, and Diagnosis

The causative agent, C. tetani, is an anaerobic, gram-positive rod that exists in both vegetative and sporulated forms. The vegetative form of C. tetani is sensitive to heat and does not survive in the presence of oxygen. Tetanus spores are ubiquitous in the environment and are found in soil, dust, animal and human feces, and on human skin. Spores can survive in the environment for years and are resistant to dry environments, most household disinfectants, ethanol, phenol, and hydrogen peroxide, and can survive boiling for 20 minutes, but are destroyed by autoclaving at 121°C and 103 kPa (15 psi).1

Spores enter the body through skin abrasions or breaches. Tetanus can occur in association with a number of acute and chronic conditions and exposures, including puncture wounds, compound fractures, abrasions, avulsions, burns, crush injuries, animal bites or scratches, surgery, injections, dental and ear infections, chronic skin ulceration, abscesses, gangrene, abortions, childbirth, and infections of the umbilical stump. Puncture and deep wounds, especially those associated with devitalized tissue, are more prone to tetanus infection than superficial abrasions. However, skin breaches may be trivial and not recalled in 7–21% of cases.1

After entry into the body, the spores vegetate and multiply under anaerobic conditions such as occur in necrotic tissue, purulent accumulations, and deep puncture wounds. The bacilli produce two known powerful exotoxins—tetanolysin and tetanospasmin. While the role of tetanolysin is not well understood, it may promote tissue necrosis and bacterial proliferation at the injury site. Tetanospasmin is one of the most potent neurotoxins, and the minimum human lethal dose is estimated to be 2.5 ng/kg of body weight.2 Tetanospasmin travels along nerves toward the central nervous system by retrograde intra-axonal transport, binds to gangliosides at the neuromuscular junction, and proceeds to the ventral horns of the spinal cord or motor horns of the cranial nerves. The toxin blocks the release of neurotransmitter substances such as γ-aminobutyric acid (GABA) and glycine and increases unopposed motor activity that results in spasms or convulsions that are characteristic of generalized tetanus.3 Similarly, disinhibition of autonomic nerve fibers can cause cardiovascular instability. The toxin does not cross the blood-brain barrier.

The diagnosis of tetanus depends on symptoms and clinical signs rather than laboratory confirmation. Isolation of C. tetani from infected wounds is neither sensitive nor specific for ...

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