USMLE – Tetanus
This disease results from infection with Clostridium tetani, which exists as a commensal in the gut of humans and domestic animals and is found in the soil. Infection enters the body through wounds, often trivial, such as those caused by a splinter, a nail in the boot or a garden fork or following septic infection such as a dirty abrasion. Tetanus is rare in the US and occurs mostly in gardeners and farmers. By contrast, the disease is common in many developing countries where dust contains spores derived from animal and human excreta. If childbirth takes place in an unhygienic environment Tetanus neonatorum may result from infection of the umbilical stump or the mother may develop the disease. Tetanus is still one of the major killers of adults, children and neonates in the tropics where the mortality rate can be nearly 100% in the newborn and around 40% in others.
In circumstances unfavorable to the growth of the organism, spores are formed and these may remain dormant for years in the soil. Spores germinate and bacilli multiply only in the anaerobic conditions which occur in areas of tissue necrosis or if the oxygen tension is low as a result of the presence of other organisms, particularly aerobic ones. The bacilli remain localized but produce an exotoxin with an affinity for motor nerve endings and motor nerve cells. The anterior horn cells are affected after the exotoxin has passed into the blood stream and their involvement results in rigidity and convulsions. Symptoms first appear from 2 days to several weeks after injury-the shorter the incubation period, the more severe the attacks and the outcome may well be fatal with an incubation period of only a few days.
Much the most important early symptom is trismus-spasm of the masseter muscles which causes difficulty in opening the mouth and in masticating, hence the name “lockjaw’. This tonic rigidity spreads to involve the muscles of the face, neck and trunk. Contraction of the frontalis and the muscles at the angles of the mouth gives rise to the ‘risus sardonicus’. There is rigidity of the muscles at the neck and trunk of varying degree. The back is usually slightly arched and there is a board-like abdominal wall.
In the more severe cases violent spasms lusting for a few seconds to 3-4 minutes occur spontaneously, or may be induced by stimuli such as moving the patient or making a noise. These convulsions are painful, exhausting and of very serious significance, especially if they appear soon after the onset of symptoms. They gradually increase in frequency and severity for about 1 week and the patient may die from exhaustion, asphyxia or aspiration pneumonia. In less severe illness convulsions may not commence for about a week after the first sign of rigidity and in very mild infections they may never appear. Autonomic involvement may cause cardiovascular complications such as hypertension. Rarely, the only manifestation of the disease may be ‘local tetanus’ -stiffness or spasm of the muscles near the infected wound-and the prognosis is good if treatment is commenced at this stage.
The diagnosis is made on clinical grounds. It is rarely possible to isolate the infecting organism from the original locus of entry. Spasm of the masseters due to dental abscess, septic throat or other causes is painful, in contradistinction to tetanus. Conditions which can mimic tetanus include hysteria and phenothiazine over dosage.
This should be begun as soon as possible.
Active immunization must be given. Contaminated injuries are treated by debridement. The immediate danger of tetanus can be greatly reduced by the injection of 1200 mg of penicillin followed by a 7-day course of oral penicillin. For those who are allergic to penicillin, erythromycin should be used. When the risk of tetanus is judged to be no evidence of infection. Seizures, raised intracranial pressure and focal hemisphere signs occur alone or in combination and distinction from a cerebral tumor may be impossible on clinical grounds.