Clostridium is a Gram-positive, spore-forming, obligatory anaerobic bacillus. Some species, such as C. botulinum and C. tetani, produce potent neurotoxins, whereas C. perfringens produces numerous enzymes and only occasionally an enterotoxin (see Table 1.19). All clostridia that are pathogenic to humans produce exotoxins and require a low redox potential for growth. They are normal commensals of human and animal gastrointestinal tracts, and are widely distributed in soil, where, as spores, they may survive for many years in adverse conditions.


Tetanus occurs when a wound is contaminated by C. tetani in unimmunized individuals. The wound may be trivial and disregarded by the patient. The clinical manifestations of the disease are due to the potent neurotoxin, tetanospasmin. Tetanospasmin acts on both the a and ‘Y 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. The organism is not invasive.


The incubation period varies from a few days to several weeks. Four clinical varieties are recognized.

GENERALIZED TETANUS is the commonest form. Initially the patient complains of feeling unwell. This is 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. Theinterval 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. The frequency of spasms usually increases and respiration becomes impaired due to laryngeal spasm. Oesophageal and urethral spasm lead to dysphagia and urinary retention, respectively. Arching of the neck and back muscles (opisthotonus) occurs.
Autonomic dysfunction is evidenced by 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 are:
• Short incubation period
• Short onset time
• Cephalic tetanus
• Extremes of age
• ‘Skin poppers’ (narcotic addicts who inject drugs subcutaneously)

LOCALIZED TETANUS. Pain and stiffness is confined to the site of the wound. The tone of the surrounding muscles is increased. Recovery usually occurs.

CEPHALIC TETANUS is an uncommon form and 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 mayor may not develop.

TETANUS NEONATORUM occurs in neonates owing to infection of the umbilical stump. Failure to thrive, poor sucking, grimacing and irritability are followed by rapid development of intense rigidity and spasms. Mortality approaches 100%.


Few diseases resemble tetanus in its fully developed form. The diagnosis is therefore a clinical one. Rarely, C. tetani may be isolated from wounds. Phenothiazine overdosage, strychnine poisoning, meningitisand tetany can mimic tetanus.


NURSING CARE. Improvement in nursing-care techniques 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, wellventilated, darkened room. Intragastric feeds may be ecessary; bladder and bowel care are also important.

WOUND DEBRIDEMENT should be carried out where indicated.

ANTIBIOTICS AND ANTITOXIN. Both antibiotics and antitoxin should be administered, even in the absence of an obvious wound (Information box 1.3). Intravenous penicillin is the drug of choice. Human antitetanus immunoglobulin 2000-3000 units i.m. should be given toneutralize any circulating toxin; it has no effect on fixed toxin. If human anti tetanus immunoglobulin is not available, immune equine tetanus immunoglobulin 10 000- 20000 units i.m. should be given, after excluding allergy to this product. Most antitoxins are heterologous and therefore dangerous Hypersensitivity reactions are common.
Prior to treatment:
Question patient about:
(a) Allergic conditions, e.g. asthma, hayfever
(b) Previous antitoxin administration Read instructions on antitoxin package carefully Always give a subcutaneous test dose.

CONTROL OF SPASMS. Diazepam is the drug of choice. Up to 120 mg per 24 hours may be required to control spasm and rigidity in adults. f3-Blocking drugs may be useful to control autonomic dysfunction.
The role of corticosteroids is controversial. Curarization and artificial respiratory support is best left to specialist units. The judicious use of a tracheostomy may be helpful in averting death.

ACTIVE IMMUNIZATION. Once recovery has occurred, active immunization should be instituted, as immunity following tetanus is incomplete.


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. Active immunization with either plain toxoid or the alum-adsorbed toxoid can be given. Of these, the latter is superior. Initially two doses of 0.5 ml of the toxoid are given intramuscularly at S-week intervals. The third dose is given 6–12 months later as a booster. Subsequent boosters are required at 5-year intervals. Infant immunization schedules in the UK include tetanus.
Protection by passive immunization with either the equine or human antitetanus toxin is short-lived, lasting only about 2 weeks.


Botulism is caused by C. botulinum. This organism is found in the soil and food is easily contaminated with the spores, which can survive heating to 100°C. The organisms proliferate in preserved canned foods and produce toxins. Only three types of neurotoxin – A, B and E-have been shown consistently to produce disease in humans. The toxins, which are the most potent known to man, result in marked neuromuscular blockade. Theyare heat-labile and are inactivated by heating at SO°C for 30 min or at 100°C for 10 min.
Three clinical forms are recognized:
1 Food-borne: ingestion of preformed toxin usually in home canned or bottled food
2 Infant botulism: toxin production in vivo
3 Wound botulism


Nausea, vomiting and diarrhoea are early symptoms and usually occur 1S-20 hours after ingesting contaminated food. Neurological symptoms dominate the clinical picture and include blurred vision and diplopia. Laryngeal and pharyngeal paralysis occur, and later generalized paralysis; consciousness is not altered. Respiratory insufficiency may occur. The marked cholinergic blockade results in urinary retention and constipation. Fever is unusual. A strabismus occurs due to lateral rectus weakness and the pupil is fixed mid position or dilated and unresponsiveto light or accommodation.


The presence of toxin in faeces, serum or suspected food items is demonstrated by injecting the material into mice. The differential diagnosis includes the Guillain-Barre syndrome and myasthenia gravis.


Treatment is supportive and should be directed at maintaining adequate respiration, with assisted ventilation if necessary. Intravenous administration of 20 ml of antitoxin is followed by 10 ml 2-4 hours later and then every 12-24 hours as necessary. The role of antibiotics has not been adequately evaluated. Guanidine hydrochloride in doses of 15-40 mg kg-l improves botulism-induced paralysis by reversing the intramuscular blockage.


The overall mortality rate for botulism is high (50-70%) but patients who survive the acute paralysis can recover completely.

Gas gangrene

Gas gangrene (clostridial myonecrosis) is commonly caused by C. perfringens; C. novyi and C. septicum are less frequently implicated. Gas gangrene occurs in lacerated wounds associated with fractures or retained foreign bodies. It is characterized by the onset of inordinately severe pain, with thickened induration and oedema at the injury site. When gas gangrene occurs in a limb, the part distal to the injury becomes cold and pulseless. Blebs occur and discharge a watery fluid, which later becomes haem orrhagic.
The involved muscles at first appear pale and oedematous, but later they become beefy-red in colour and then brownish-black and frankly gangrenous. The characteristic crepitus of gas gangrene is a late feature. Systemic signs of toxicity are prominent. The patient isfebrile, tachypnoeic and has a marked tachycardia. Hypotension, renal failure and hepatic failure develop as terminal events. Consciousness remains unaltered.


Treatment consists of adequate surgical debridement, with parenteral penicillin or chloramphenicol combined with another antibiotic to cover aerobic and anaerobic organisms that are frequent wound contaminants. The role of anti-gas gangrene toxin and hyperbaric oxygen is controversial.

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