Tetanus is due to a toxin-secreting clostridium: C. tetani. The organism is found in soil, and illness usually results from a contaminated wound. The injury itself may be trivial and disregarded by the individual. It has also complicated intravenous drug misuse. In developing countries neonatal tetanus follows contamination of the umbilical stump, often after dressing the area with dung.

The organism is not invasive, and clinical manifestations of the disease are due to the potent neurotoxin, tetanospasmin. Tetanospasmin acts on both the α and δ motor systems at synapses, resulting in disinhibition. It also produces neuromuscular blockade and skeletal muscle spasm, and acts on the sympathetic nervous system. The end result is marked flexor muscle spasm and autonomic dysfunction.

Clinical features

The incubation period varies from a few days to several weeks. The most common form of the disease is generalized tetanus. General malaise is rapidly followed by trismus (lockjaw) due to masseter muscle spasm. Spasm of the facial muscles produces the characteristic grinning expression known as risus sardonicus. If the disease is severe, painful reflex spasms develop, usually within 24-72 hours of the initial symptoms. The interval between the first symptom and the first spasm is referred to as the 'onset time'. The spasms may occur spontaneously but are easily precipitated by noise, handling of the patient, or by light. Respiration may be impaired because of laryngeal spasm; oesophageal and urethral spasm lead to dysphagia and urinary retention, respectively, and there is arching of the neck and back muscles (opisthotonus). Autonomic dysfunction produces tachycardia, a labile blood pressure, sweating and cardiac arrhythmias. Patients with tetanus are mentally alert.

Death results from aspiration, hypoxia, respiratory failure, cardiac arrest or exhaustion. Mild cases with rigidity usually recover. Poor prognostic indicators include short incubation period, short onset time, and extremes of age.

Localized tetanus is a milder form of the disease. Pain and stiffness are confined to the site of the wound, with increased tone in the surrounding muscles. Recovery usually occurs.

Cephalic tetanus is uncommon but invariably fatal. It usually occurs when the portal of entry of C. tetani is the middle ear. Cranial nerve abnormalities, particularly of the seventh nerve, are usual. Generalized tetanus may or may not develop.

Neonatal tetanus is usually due to infection of the umbilical stump. Failure to thrive, poor sucking, grimacing and irritability are followed by the rapid development of intense rigidity and spasms. Mortality approaches 100%. One aim of the WHO Expanded Programme on Immunization (EPI) is to eliminate this condition by immunizing all women of childbearing age, providing clean delivery facilities and strengthening surveillance in high-risk areas.

Diagnosis

Few diseases resemble tetanus in its fully developed form, and the diagnosis is therefore usually clinical. Rarely, C. tetani is isolated from wounds. Phenothiazine overdosage, strychnine poisoning, meningitis and tetany can occasionally mimic tetanus.

Management

Any wound must be cleaned and debrided if necessary, to remove the source of toxin. Human tetanus immunoglobin 250 units should be given along with an intramuscular injection of tetanus toxoid. If the patient is already protected a single booster dose of the toxoid is given; otherwise the full three-dose course of adsorbed vaccine is given (see below).

Established tetanus management is supportive medical and nursing care. Improvement in this area has contributed more than any other single measure to the decrease in the mortality rate from 60% to nearer 20%. Patients are nursed in a quiet, isolated, well-ventilated, darkened room. Benzodiazepines are used to control spasm and sedate the patient; if the airway is compromised intubation and mechanical ventilation may be necessary.

Antibiotics and antitoxin should be administered, even in the absence of an obvious wound. Intravenous metronidazole is the drug of choice, although penicillin is also effective. Human tetanus immunoglobulin (HTIG) 500 IU should be given by intramuscular injection to neutralize any circulating toxin. If HTIG is not available, immune equine tetanus immunoglobulin 10 000 IU should be given intramuscularly: this is probably as effective as HTIG, but there is a high incidence of severe allergic reactions. If the patient recovers, active immunization should be instituted, as immunity following tetanus is incomplete.

Prevention

Tetanus is an eminently preventable disease and all persons should be immunized regardless of age. Those who work in a contaminated environment, such as farmers, are particularly at risk and should have regular booster injections. Active immunization with the alum-adsorbed toxoid should be given. Initially two doses of 0.5 mL of the toxoid are given intramuscularly with an 8-week interval. The third dose is given 6-12 months later as a booster. Subsequent boosters are required at 5-year intervals. Infant immunization schedules in all countries include tetanus. Protection by passive immunization with either the equine or human antitetanus immunoglobulin is short-lived, lasting only about 2 weeks.