Tetanus

Introduction

Tetanus is caused by Clostridium tetani, an anaerobic, spore-forming Gram-positive bacillus found widely in soil, dust and animal faeces. Spores enter the body through a wound - classically a puncture wound, but also burns, contaminated surgical or obstetric wounds, and injection sites in people who inject drugs - and germinate in the anaerobic environment of devitalised tissue, releasing the potent neurotoxin tetanospasmin.

It is now rare in the UK because of high vaccine coverage, but it remains an important topic because it tests a distinct and elegant piece of neurophysiology - loss of inhibitory control rather than direct excitation - and because it is a genuine emergency that can still be missed in an unvaccinated or under-vaccinated patient with an unassuming wound.

Pathophysiology

Tetanospasmin travels retrogradely along motor neurone axons from the wound to the spinal cord and brainstem. There, it blocks the release of the inhibitory neurotransmitters GABA and glycine from inhibitory interneurons (Renshaw cells), which normally dampen motor neurone activity once a movement has been made. With this inhibition removed, motor neurones fire unopposed, producing sustained, generalised muscle rigidity and spasm rather than a picture of true excitation from the toxin itself.

In more severe disease, the toxin also disrupts the autonomic nervous system, producing labile blood pressure, tachycardia, arrhythmias and profuse sweating - autonomic instability is a major cause of death in severe cases.

The incubation period is typically 3-21 days (commonly around 10 days on average); a shorter incubation period, generally reflecting a wound closer to the CNS, is associated with more severe disease and a worse prognosis.

Clinical features

• Trismus ("lockjaw") - spasm of the masseter muscles, often the earliest sign
• Risus sardonicus - a fixed, grinning facial expression from sustained facial muscle spasm
• Opisthotonus - severe arching of the back from spasm of the spinal extensor muscles
• Generalised, painful muscle spasms, which can be triggered by minor external stimuli such as light, noise or touch - patients are typically nursed in a quiet, dimly lit environment to minimise this
• Autonomic instability in severe disease - labile blood pressure and heart rate, arrhythmias, sweating
• Laryngospasm and respiratory muscle spasm, which can cause life-threatening respiratory failure

Less common presentations include localised tetanus (rigidity confined to the area around the wound), cephalic tetanus (following a head or neck wound, with cranial nerve palsies), and neonatal tetanus (via the umbilical stump, still a significant cause of mortality globally, though now very rare in the UK).

Differential diagnosis

• Strychnine poisoning - closely mimics tetanus by directly antagonising glycine receptors, but the history (ingestion rather than a wound) usually distinguishes it
• Acute dystonic drug reaction (for example from antipsychotics) - typically more asymmetric, and lacks the classic trismus/risus sardonicus pattern with an identifiable wound
• Hypocalcaemic tetany - a different mechanism entirely (neuromuscular excitability from low ionised calcium), with carpopedal spasm and positive Chvostek's and Trousseau's signs rather than trismus
• Meningitis or encephalitis - neck stiffness can be present, but the characteristic trismus, risus sardonicus and preserved consciousness of tetanus are absent
• Rabies - hydrophobia and agitation, but a very different clinical course and typically an animal bite exposure history

Investigations

Tetanus is a clinical diagnosis - there is no reliable blood test, and wound culture for C. tetani is insensitive and rarely helpful (a substantial proportion of confirmed cases have negative wound cultures). Diagnosis rests on the combination of a compatible clinical picture, a plausible wound (which may be trivial or even unnoticed), and the patient's vaccination history.

Management

Management combines neutralising circulating toxin, removing the source of ongoing toxin production, and supportive care through what can be a prolonged and severe illness.

• Human tetanus immunoglobulin (HTIG), given as soon as possible - it neutralises toxin that has not yet bound to neural tissue, but has no effect on toxin already bound, which is why early administration matters
• Wound debridement - removing necrotic tissue and any foreign material to eliminate the anaerobic environment C. tetani needs to keep producing toxin
• Metronidazole - the preferred antibiotic to eliminate the organism and stop further toxin production; historically penicillin was used, but it has theoretical GABA-antagonist properties that could worsen spasms, and metronidazole is now generally preferred
• Benzodiazepines to control muscle spasm and provide sedation
• Magnesium sulfate infusion - can help control both spasms and autonomic instability
• Intensive/critical care support for severe disease - a quiet, dimly lit environment to reduce stimulus-triggered spasm, and escalation to neuromuscular blockade and mechanical ventilation if respiratory or laryngeal spasm threatens the airway
• Management of autonomic instability, for example with labetalol for episodes of severe hypertension

Prevention and wound management

Primary prevention is through the routine UK immunisation schedule - tetanus toxoid is given as part of combined vaccines at 8, 12 and 16 weeks, with further reinforcing doses in the pre-school and teenage booster programmes, giving five doses in total and long-lasting immunity.

Every wound presenting for medical attention should prompt a tetanus risk assessment, combining the patient's vaccination history with whether the wound itself is "tetanus-prone" (features include heavy contamination, puncture wounds, devitalised tissue, delayed presentation beyond 6 hours, or clinical signs of sepsis).¹

The exact detail is set out in UKHSA guidance and updated periodically, but the underlying principle - a heavily contaminated or high-risk wound needs immunoglobulin regardless of how confident the vaccination history seems - is the point most often tested.

Complications

• Laryngospasm and respiratory failure
• Autonomic dysfunction and cardiac arrhythmias, a major cause of death in severe disease
• Vertebral compression fractures and other injuries from the force of severe spasms
• Aspiration pneumonia
• Rhabdomyolysis
• Death - mortality is highest with a short incubation period, autonomic involvement, and in neonatal tetanus

Red flags

Prognosis

With modern intensive supportive care, most patients with tetanus survive, though recovery from severe disease can take weeks and requires prolonged ventilatory and autonomic support. Mortality remains significant in severe cases, particularly with a short incubation period, marked autonomic instability, or where treatment is delayed - and remains substantial in neonatal tetanus in settings without access to modern critical care, which is why this largely UK-eradicated disease remains a major global health concern.