eMedicine Specialties > Infectious Diseases > CNS Infections

Tetanus

Author: Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Contributor Information and Disclosures

Updated: Jan 26, 2010

Introduction

Background

The word tetanus comes from the Greek tetanos, which is derived from the term teinein, meaning to stretch. Tetanus appears in military medical documents throughout the ages. Slapping infected dung on the umbilical cords of newborns (ie, as part of ritualistic ceremonies) caused rampant tetanus neonatorum or trismus nascentium in the West Indies and in Africa. Osler's textbook describes the "eight days sickness" caused by umbilical sepsis, which killed 84 of 125 children within a fortnight of birth in St. Kilda, Scotland. During World War I, tetanus occurred in 1.47 per 1000 British wounded and in 12.5 per 1000 persons involved in the Peninsular campaign. Nicolaier discovered the anaerobic bacillus Clostridium tetani in 1885. In 1889, Koch's pupil, Kitasato, obtained the bacillus of tetanus in pure culture and associated the disease to animals.

Although rare, the disease has not been eradicated, and early diagnosis and intervention are life saving. Prevention is the ultimate management strategy for tetanus. The 4 clinical types of tetanus are generalized, local, cephalic, and neonatal.

Neonatal tetanus is a major cause of infant mortality in underdeveloped countries, but this form is rare in the United States. Infection results from cord contamination during unsanitary delivery conditions, coupled with a lack of maternal immunization. At the end of the first week of life, infected infants become irritable, feed poorly, and develop rigidity with spasms. This form of tetanus has a very poor prognosis for survival.

Cephalic tetanus is uncommon and usually occurs following head trauma or otitis media. Patients with this form present with cranial nerve palsies. The infection may be localized or may become generalized.

Patients with local tetanus present with persistent rigidity in the muscle group close to the injury site. The muscular rigidity is caused by a dysfunction in the interneurons that inhibit the alpha motor neurons of the affected muscles. No further CNS involvement occurs, and this form has very low mortality rates.

Approximately 50-75% of patients with generalized tetanus present with trismus secondary to masseter muscle spasm. Nuchal rigidity and dysphagia also are early complaints that cause risus sardonicus, the ironic smile of tetanus, resulting from facial muscle involvement. As the disease progresses, patients have generalized muscle rigidity with intermittent reflex spasms in response to stimuli (ie, noise, touch). Tonic contractions cause opisthotonus (ie, flexion and adduction of the arms, clenching of the fists, extension of the lower extremities). During these episodes, patients have intact sensorium and feel severe pain. The spasms can cause fractures, tendon ruptures, and acute respiratory failure.

Pathophysiology

Tetanus results from infection with C tetani, a mobile, spore-forming, anaerobic, gram-positive bacillus. This bacillus is found in or on soil, manure, dust, clothing, skin, and 10-25% of human GI tracts. The spores need tissue with the proper anaerobic conditions to germinate; the ideal media are wounds with tissue necrosis.

Under anaerobic conditions, the spores of C tetani germinate and produce 2 toxins: tetanolysin (a hemolysin with no recognized pathologic activity) and tetanospasmin, which is responsible for tetanus. The action of the latter helps explain the clinical manifestations of the disease.

Tetanospasmin is synthesized as a single 151-kd chain and is cleaved to generate toxins with 2 chains joined by a single disulfide bond. The heavy chain (100 kd) is responsible for specific binding to neuronal cells and for protein transport. The light chain (50 kd) blocks the release of neurotransmitters.

These processes are accompanied by autonomic nervous system instability. The toxin binding may be irreversible; recovery depends on the sprouting of new axonal terminals. Once the toxin is synthesized, it moves from the contaminated site to the spinal cord in 2-14 days. When the toxin reaches the spinal cord, localized or cephalic tetanus may occur initially, followed by generalized tetanus.

Frequency

United States

Incidence has declined with the advent of active immunization. Reports indicate that 560 cases occurred in 1947; 101 cases occurred in 1974; 60-80 cases occurred each year during the 1980s; and 47 cases occurred in California in 1997. Almost all cases occur in persons who are partially immunized or nonimmunized. The incidence of patients who contract tetanus despite full immunization is extremely rare (ie, ~4 per 100 million persons who are immunocompetent and vaccinated).

International

Reports show up to 1 million cases annually, mostly in underdeveloped countries. Neonatal tetanus accounts for 50% of the tetanus-related deaths in developing countries.

Mortality/Morbidity

• Tetanus results in approximately 5 deaths per year in the United States.
• Mortality in the United States resulting from generalized tetanus is 30% overall, 52% in patients older than 60 years, and 13% in patients younger than 60 years.
• Residual neurologic sequelae are uncommon. Mortality usually results from autonomic dysfunction (ie, extremes in blood pressure, dysrhythmia, cardiac arrest).

Age

In the United States, 59% of cases and 75% of deaths occur in persons aged 60 years or older.

Clinical

History

Most cases in the United States occur in patients with a history of only partial immunization. Persons who inject drugs also constitute a high-risk group.

• Symptoms usually begin 8 days after the infection, but onset may range from 3 days to 3 weeks.
• Patients may report a sore throat with dysphagia (early sign).
• Localized tetanus causes muscle rigidity at the site of spore inoculation.
• The initial manifestation may be local tetanus, in which the rigidity affects only 1 limb or area of the body where the clostridium-containing wound is located.

Physical

Common first signs of tetanus are headache and muscular stiffness in the jaw (ie, lockjaw), followed by neck stiffness, difficulty swallowing, rigidity of abdominal muscles, spasms, and sweating.

• Patients often are afebrile.
• Severe tetanus results in opisthotonos, flexion of the arms, extension of the legs, periods of apnea resulting from spasm of the intercostal muscles and diaphragm, and rigidity of the abdominal wall.
• Late in the disease, autonomic dysfunction develops, with hypertension and tachycardia alternating with hypotension and bradycardia.

Causes

The source of infection usually is a wound (~65%), which often is minor (eg, wood or metal splinters, thorns). Chronic skin ulcers are the source in approximately 5% of cases, and in the remainder of cases, no obvious source is identified.

• The US Centers for Disease Control and Prevention (CDC) statistics from 1982-84 are as follows:
  • Infected lacerations or puncture wounds (69%)
  • Infected chronic wounds and abscesses (20%)
  • Exposure via intravenous drug abuse (3%)
  • Neonates (1%)
  • Other or no identifiable cause (7%)
• Possible causes not usually associated with tetanus
  • Otitis media
  • Burns
  • Intranasal foreign bodies
  • Corneal abrasions
  • Foreign bodies
  • Dental or surgical procedures

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