Tetanus

• Tetanus is an acute, vaccine-preventable disease caused by tetanospasmin, the neurotoxin of the anaerobic, spore-forming bacterium Clostridium tetani.^[3][7]
• The toxin blocks inhibitory neurotransmitter release in the central nervous system, so muscles contract without opposing control: rigidity, painful spasms and autonomic instability follow.^[7]
• Infection does not produce immunity: everyone who recovers needs vaccination, and people who have recovered can be infected again.^[3][4][6]
• It is never spread from person to person; spores live in soil and animal faeces and enter through wounds, including tiny, forgotten ones.^[3][4][7]
• Treatment is supportive and time-critical: remove every source of toxin, neutralise unbound toxin with antitoxin, control the airway and spasms, and nurse in a quiet, dark environment for weeks.^[1][6][7]

By the end of this page you should be able to:

1. Explain how C. tetani spores germinate in a wound and how tetanospasmin produces rigidity, spasms and autonomic instability.^[3][7]
2. Recognise generalised, localised, cephalic and neonatal tetanus, and grade severity using the clinical features.^[3][6]
3. Investigate a suspected case without waiting for laboratory results, and state what supports the diagnosis.^[3][6][7]
4. Manage tetanus acutely: debridement, antibiotics, antitoxin, airway, spasms, dysautonomia and intensive nursing.^[1][6][7]
5. Apply wound-management rules for tetanus prophylaxis to a real wound and vaccination history.^[2][3][6]
6. State the childhood, adult, and neonatal tetanus immunisation schedules, and what prolonged protection requires.^[3][4][6][8]
7. Discuss prevention, surveillance and special groups, including maternal and neonatal tetanus elimination.^[4][5]

Four clinical forms are recognised.^[3][6][7]

• Generalised tetanus (more than 80% of cases). Descending illness: trismus (lockjaw) first, then neck stiffness, dysphagia and rigid abdominal wall, then generalised spasms with autonomic instability. ^[3]
• Localised tetanus. Rigidity and spasms confined to muscles around the inoculation site; more common in partially immune people; may stay local for weeks or become generalised. ^[3][7]
• Cephalic tetanus. Localised disease after a head or neck wound, producing cranial nerve palsies, trismus and dysphagia; diagnosis is often delayed and outcome poorer. ^[6][7]
• Neonatal tetanus. Generalised tetanus of the newborn, usually from infection of the umbilical stump with an unsterile instrument or contaminated cord-care material in a mother who was not adequately immunised. ^[3][4][5]

Tetanus is caused by Clostridium tetani: an anaerobic, spore-forming, gram-positive rod.^[3] Water, heat and oxygen kill the bacillus, but the spore is among the toughest infective particles known: it survives boiling, freezing, many antiseptics and autoclaving at 121 °C for 10 to 15 minutes, and can persist in soil for years.^[3][7] Spores are found in soil and in the intestinal tracts and faeces of horses, sheep, cattle, dogs, cats, rats, guinea pigs and chickens; manure-treated soil may contain large numbers.^[3] They are also found on human skin surfaces, in contaminated heroin and in some traditional remedies.^[3][7]

Spores reach human tissue through contaminated wounds, apparent or unnoticed: farming and gardening injuries, puncture wounds, crush and burn wounds, animal bites, dental infection, otitis media, elective surgery, injections and unclean traditional procedures such as male circumcision.^[3][6][7] Inapparent, healed or trivial wounds are an important route, and up to 30% of patients have no identifiable wound on admission.^[6][7] Injecting drug use, especially intramuscular or subcutaneous, carries a specifically increased risk, including tetanus-prone adulterants and paraphernalia.^[6][7]

Risk factors for disease include incomplete or absent tetanus immunisation, advanced age (born before routine immunisation, or waning antibody), diabetes, immunocompromise, HIV and male sex, the last combining with WHO's historically maternal immunisation focus and unsafe circumcision practice in some regions.^[6][7] Anyone can get tetanus, and because there is no herd immunity, protection is entirely individual.^[4][6]

Tetanus occurs worldwide, most often in densely populated, hot, damp regions with organic soil; one recent Ugandan study estimated an incidence of 3.43 cases per 100 000 population per year, which probably typifies many countries with similar vaccination coverage.^[7] The burden has fallen dramatically: deaths from tetanus fell by almost 90% between 1990 and 2019, driven largely by maternal and neonatal tetanus elimination efforts, and tetanus was eliminated as a public-health problem in all but 14 countries by 2018.^[7] Infections and deaths nonetheless plateau in children and adults, and 21 830 cases were reported to WHO in 2023, a figure that most experts consider a substantial undercount, with global mortality estimated at 30 to 50 thousand deaths per year, mostly in South and South-East Asia and sub-Saharan Africa.^[7] Seasonality is seen in Europe, with peaks in July and October.^[7]

In high-income countries disease is now rare but not absent: 32 to 92 cases a year in the EU/EEA, 17 to 33 in the United States and 4 to 11 in the United Kingdom, with older adults predominating; in the UK the highest incidence is in people over 64 years, and only 17% of cases with known status were appropriately immunised for age.^[6][7] Disease under-reporting is also marked: an English hospital-record study from 2001 to 2014 suggested that cases were under-reported by 88%.^[7]

In the United States, 500 to 600 cases a year (about 0.4 per 100 000) were reported in the late 1940s; since the mid-1970s about 50 to 100 (about 0.05 per 100 000) have been reported annually, falling further to an average of 29 cases a year from 2009 to 2018, with 19 deaths (all in adults 55 years or older) among those 297 cases, and none among 23 cases in 2018.^[3] Vaccine coverage is high in the young: 93.3% of US children born in 2016 to 2017 had received at least 3 doses of DTaP by 24 months, 80.6% had received 4 doses, and 90.2% of adolescents 13 to 17 years had Tdap coverage in 2019, but only 63.4% of adults had received any tetanus-toxoid-containing dose in 2017.^[3] Globally in 2025, 85% of infants received 3 doses of a diphtheria-tetanus-pertussis (DTP)-containing vaccine, while just over 7 700 newborns died of neonatal tetanus in 2021, an 84% reduction since 2000.^{[4] [6]}

Maternal and neonatal tetanus is the dominant problem where routine immunisation is weak. It is defined as maternal tetanus (tetanus during pregnancy, or within 6 weeks after pregnancy ends) and neonatal tetanus (within the first 28 days of life).^[3][4][5] Nonsterile cord-cutting, contaminated cord-care material and deliveries on contaminated surfaces drive neonatal cases, and in 2025 8 countries had still not achieved maternal and neonatal tetanus elimination (MNTE), which requires fewer than one case per 1 000 live births in every district.^[4][5]

All clinical features of tetanus follow from three facts about the toxin: it is among the most potent poisons known, with an estimated lethal dose of 2.5 nanograms per kilogram of body weight (about 175 nanograms for a 70 kg adult); it reaches the nervous system; and it silences inhibition.^[3][7]

Tetanospasmin (tetanus neurotoxin, TeNT) is a 150 kDa zinc-dependent metalloproteinase composed of a heavy and a light chain linked by a disulfide bond.^[7] Once spores germinate in anaerobic, necrotic tissue, two toxins are produced: tetanolysin, whose role is uncertain, and tetanospasmin, the cause of disease.^[3][7] Tetanospasmin binds to presynaptic motor neurons at the neuromuscular junction, travels by retrograde axonal transport and transcytosis to the spinal cord and brainstem, enters inhibitory glycine- and GABA-releasing interneurons, and cleaves synaptobrevin-2 (VAMP2).^[7] By disrupting the SNARE complex it blocks inhibitory neurotransmitter release while excitatory drive continues, giving rigidity, spasms, hyperreflexia and dysautonomia.^[7] It resembles but is distinct from botulinum neurotoxin type B, which acts peripherally and produces flaccid paralysis with a short incubation.^[7]

TeNT may spread by lymphatics, blood and trans-synaptic routes within the central nervous system, and autonomic dysfunction probably reflects disinhibition of autonomic neurons with dysregulated catecholamine release.^[7] In generalised disease, 4 to 6 weeks are needed for inhibitory transmission to recover, which is why supportive care is prolonged.^[7]

The further the injury from the central nervous system, the longer incubation tends to be; a shorter incubation, especially 7 days or fewer, predicts more severe disease and death.^[3][7] The four forms share one toxin mechanism, and how wide the illness becomes depends on how much toxin spreads.^[7]

Generalised disease usually begins after an incubation of about 8 days, with a usual range of 1 to 21 days (reported extremes 1 to 60, with onset after 21 days uncommon).^[3][7] It descends: first trismus (painful masseter and neck contraction producing facial spasms, "risus sardonicus"), then neck stiffness, dysphagia and a board-like rigid abdomen, then generalised spasms and autonomic instability.^[3][6][7] Spasms are triggered by noise, touch or light, which makes nursing in a quiet, darkened room important; they continue for 3 to 4 weeks and complete recovery may take months.^[3][7] Other features are fever, profuse sweating, hypertension and paroxysmal tachycardia; patients remain fully conscious.^[3][6] Jaw and abdominal rigidity can mimic a peritonitic acute abdomen, and premature laparotomy has been reported.^[7]

Localised tetanus causes persistent contraction of muscles around the injury for weeks; it may precede generalised disease and is more common in partially immune people.^[3][7] Cephalic tetanus, after head or neck wounds, produces trismus and cranial nerve palsies with sometimes stroke-like, fluctuating findings; facial weakness may be flaccid, spastic or mixed.^[6][7] Neonatal tetanus usually appears 4 to 14 days after birth, averaging about 7, and the inability to suck or breastfeed with excessive crying often precedes spasms.^[3][4]

Autonomic nervous system dysfunction is now the most feared complication: painful urinary retention, faecal incontinence, profuse sweating, and labile cardiovascular signs with paroxysms of tachycardia and hypertension alternating with bradycardia and hypotension in 10 to 30% of patients.^[7] Fever above 38.4 °C is unusual at first presentation and should suggest superinfection or another diagnosis.^[7] Trismus (93 to 98%) and dysphagia (83%) are almost always present at hospital admission in generalised disease, while dyspnoea is rare initially but signals impending airway compromise.^[7] Severe spasms can cause rhabdomyolysis, fractures, airway obstruction and asphyxia.^[3][7]

Examination is clinical. The mouth may be almost impossible to open; there is risus sardonicus, rigid masseters and neck, and abdominal rigidity with superimposed painful spasms of agonist and antagonist muscles; reflexes are brisk, power reduced, sensation and cerebellar findings typically normal, and patients are alert.^[7] Common inoculation sites are the foot and any recent injury; look for track marks from injecting drug use.^[7]

Tetanus is never spread from person to person; infection does not produce immunity, so survivors must be vaccinated.^[3][4][6]

Tetanus is a clinical diagnosis. Its most dangerous mimic is strychnine poisoning, which is virtually indistinguishable: strychnine is a competitive glycine-receptor antagonist sold as rodenticide in many countries, with onset within minutes to hours and diagnosis by assay.^[7] Other differentials for generalised tetanus include hypocalcaemic tetany, neuroleptic malignant syndrome (antipsychotic exposure, gradual onset, altered mental state, very high creatine kinase), drug-induced dystonia (recent antidopaminergic drugs, reversible with procyclidine), stiff-person syndrome and progressive encephalomyelitis with rigidity and myoclonus (subacute, brainstem signs, absent trismus), cerebral malaria, and severe dental infection with trismus but normal tone and no spasms.^[7] Cephalic tetanus mimics brainstem stroke, Bell's palsy, myasthenia gravis and botulism.^[7]

A compact comparison:

Tetanus is a clinical diagnosis; laboratory tests support but never exclude it.^[3][6][7] Case definitions help early recognition: in the UK it is an acute illness with muscle spasms or hypertonia and a diagnosis of tetanus by a health-care provider; another widely used clinical formulation requires trismus, dysphagia and continuous generalised muscle rigidity or spasms with normal consciousness and no fever at onset.^[7] Antibiotic and immunoglobulin treatment must not be delayed for results.^[6]

Where available, the best microbiological modalities are real-time PCR for the C. tetani neurotoxin gene and anaerobic culture, preferably from tissue obtained by surgical debridement and transported in cooked meat broth.^[6][7] PCR is usually favoured for speed; culture can identify coincident pathogens.^[7] Positive results support the diagnosis only in a compatible clinical picture, and negative results do not exclude it, because C. tetani is recovered from the wound in only about 30% of cases and can be isolated from healthy people.^[3][7] The traditional mouse bioassay for tetanus neurotoxin is constrained by ethics and practicality and little used.^[7]

Serology for anti-tetanospasmin antibodies was once common, but cases occur in immunised people with antibody titres above the assumed "protective" level of 0.1 IU/mL, so the test is falling out of favour and can never exclude the disease.^[6][7] If performed, the serum sample must be drawn before immunoglobulin is given.^[6] Point-of-care antibody kits are not WHO-recommended.^[6]

Basic tests exclude differentials and complications: urinalysis for haematuria as a proxy for myoglobinuria and rhabdomyolysis, serum creatine kinase (CK), full blood count (mild leukocytosis is common; neutrophilia carries a worse prognosis), CRP (moderately raised; a marked rise suggests bacterial superinfection), renal and liver function, bone profile (to exclude hypocalcaemia), magnesium and blood gases, wound imaging (CT to find foreign bodies or gas locules), and swabs for coincident infection.^[7] Neuroimaging and lumbar puncture are usually unnecessary; CT brain may show gas locules in cephalic tetanus.^[7]

Tetanus is confirmed microbiologically only when a clinically diagnosed case has viable C. tetani on culture or the neurotoxin gene on PCR from debrided tissue or pus.^[6] In practice, treatment precedes proof.

Severity is graded clinically. One widely used scheme divides generalised disease into four grades.^[6]

Many centres track severity with the modified Ablett score; mechanical ventilation is generally recommended for Ablett grade III or IV disease.^[7] Practical decision points are airway vulnerability, frequency and duration of spasms, severity of dysphagia, and presence of dysautonomia rather than the label alone.

Tetanus is a medical emergency that requires hospitalisation; complete recovery can take months.^[1][3] Management has several parallel streams: removing the source of toxin and stopping its production; neutralising unbound toxin; protecting and supporting the airway; controlling muscle spasms and dysautonomia; meticulous intensive nursing; and vaccinating for the future, because infection does not immunise.^{[1][3][4][6][7]}

Appropriate antibiotic therapy is recommended to reduce the number of tetanus bacteria, but antibiotics alone are not the treatment.^[1][3]

Clean, debride and remove foreign material from all wounds; this removes anaerobic foci and provides samples.^[1][3][7] Nurse the patient in a quiet, darkened room with minimal stimulation (noise, touch, light) because these trigger spasms.^[7] Start venous access, check glucose (hypoglycaemia risk from poor intake), fluid resuscitate if dehydrated, and establish a urinary catheter for fluid balance and urinary retention.^[7] Ensure immediate senior and, where available, intensive-care review.

Surgical debridement is required to eradicate necrotic tissue that may harbour C. tetani, even for wounds that appear innocuous, and provides samples.^[7] For inoperable wounds, scrupulous wound care is key. Enteral or IV antibiotics are given for 7 to 10 days. Metronidazole is widely used (excellent anaerobic coverage, inexpensive), benzylpenicillin (and co-amoxiclav) are alternatives; a 1985 open-label trial found lower mortality with metronidazole, but three later studies found no difference in mortality, length of stay or need for ventilation; one found lower muscle-relaxant requirement with metronidazole, perhaps reflecting penicillin's effects on GABAergic transmission. The evidence marginally favours metronidazole, but penicillin remains an effective, well-tolerated alternative. Choose with the microbiology team.^[6][7]

Antitoxin, given intramuscularly or intravenously, improves mortality. It comes from horses (equine antitoxin) or from pooled plasma of fully vaccinated human donors (human tetanus immune globulin, TIG). Historically TIG was preferred because of adverse-reaction concerns with equine antitoxin, but cost and global shortages have made equine antitoxin standard in many high-burden, resource-constrained settings. A recent Vietnamese trial found no difference in mortality, ventilation duration or ICU stay between equine and human antitoxin, and adverse events were rare in both groups, although the full equine dose should follow a negative intramuscular test dose. Most experts give a single 500 IU intramuscular dose of TIG for treatment of clinical tetanus in adults and children, with part of the dose infiltrated around the wound if it can be identified, although benefit of local infiltration has not been proven; higher doses (3 000 to 6 000 IU) appear no more effective and are less comfortable. TIG only removes unbound toxin and has no effect on toxin already fixed to nerve endings.^[1][3][7]

If TIG is unavailable, clinicians can use intravenous immune globulin (IGIV) at 200 to 400 milligrams per kilogram, although it is not licensed for tetanus, and anti-tetanus antibody content varies by lot.^[1] In the UK, confirmed tetanus is treated with IVIG using weight-based dosing: 5 000 IU for patients under 50 kg and 10 000 IU for patients 50 kg or over, because no IV tetanus-specific immunoglobulin is available there. This equates to 200 to 800 mL of commercial product.^[6][7] Adult antitoxin doses in practice vary widely, from 500 to 10 000 IU. Intrathecal antitoxin is not recommended, because a robust 272-patient trial found no benefit in ventilation or 6-month mortality, and the procedure carries a theoretical risk of central nervous system infection and spasms.^[7]

Tetanus disease does not result in tetanus immunity; active immunisation with a tetanus toxoid vaccine should begin or continue as soon as the patient's condition is stable, providing protection while endogenous immunity develops.^[1][3][6]

About 50% of adults with generalised tetanus require mechanical ventilation.^[7] The primary indication is protecting the airway from fulminant obstruction caused by laryngeal spasm, although many patients have a small oxygen requirement and difficulty clearing secretions at first. Ventilation is generally recommended for Ablett grade III or IV disease. Where available, primary tracheostomy is preferred over prolonged intubation, which carries increased risks of subglottic stenosis and vocal-cord immobility; percutaneous tracheostomy may minimise spasms provoked by theatre transfer.^[7]

Benzodiazepines are the cornerstone: both diazepam and midazolam are used, and have never been compared head-to-head. Diazepam is cheaper and can be given by several routes, but its long-acting metabolites persist for days and increase the risk of respiratory depression, especially in renal impairment. High doses are usually required, often more than 1 milligram per kilogram per day of diazepam, escalated from intravenous boluses to continuous infusion, with a switch to midazolam when needed.^[7]

If benzodiazepines are inadequate, most guidelines use neuromuscular blockade, which is only safe in ventilated, sedated patients (vecuronium, pipecuronium and rocuronium are generally preferred where available); propofol may be used as an adjunct. Other drugs (barbiturates, phenothiazines, dantrolene) are rarely used unless first-line agents are unavailable, and intrathecal baclofen is occasionally used for refractory spasms.^[7]

Dysautonomia is treated principally with intravenous magnesium sulphate and short-acting opioids (fentanyl, morphine) for analgesia, sedation and autonomic control, although high opioid doses may be impractical where availability is low. A systematic review of 13 studies concluded that IV magnesium may improve control and shorten hospital stay; one double-blind trial in 195 Vietnamese adults randomised to 7 days of IV magnesium or placebo found reduced mean heart rate and reduced need for midazolam and pipecuronium, but no statistically significant difference in ventilation, hospital stay or in-hospital mortality. Magnesium is nonetheless widely used; give a bolus followed by continuous infusion for up to a week, targeting serum levels of 2 to 4 millimoles per litre, or titrate to the knee jerk at the bedside where laboratory monitoring is unavailable.^[7]

Tachycardia and hypertension often require adrenoceptor antagonists: labetalol (combined alpha and beta blockade, short half-life) is commonly preferred, with clonidine, dexmedetomidine and verapamil as alternatives where evidence is limited, plus inotropes for refractory shock and atropine for bradyarrhythmias.^[7]

Prolonged immobility carries risks of pressure sores and venous thromboembolism: use air mattresses where available, teach families to turn patients in low-resource settings, and use pharmacological venous thromboembolism prophylaxis rather than intermittent pneumatic compression (which can trigger spasms); give stress-ulcer prophylaxis to ventilated patients.^[7] At first presentation patients are often dehydrated from poor oral intake, worsening with hyperpyrexic losses, so fluid resuscitation and maintenance of euvolaemia are needed; most require a urinary catheter. Monitor blood glucose. Hyperpyrexia is treated with passive cooling and antipyretics. Nutritional requirements are high because spasms burn energy; feed early via nasogastric tube even if the airway is secure, to reduce aspiration risk. Start passive limb mobilisation early to prevent contractures, deferring active physiotherapy until spasms have abated, and avoid excess handling or physical contact at the bedside.^[7]

TIG can provide temporary protection against tetanus by directly binding and neutralising circulating toxin, but TIG cannot neutralise toxin that is already bound to nerve endings.^[1][2]

Local complications include laryngospasm, airway obstruction, asphyxia, fractures from sustained contractions and convulsions, and hyperactivity of the autonomic nervous system leading to hypertension and arrhythmia.^[3] Systemic and nosocomial complications include aspiration pneumonia (found in 50 to 70% of autopsied cases), sepsis from catheters, hospital-acquired pneumonia, decubitus ulcers, pulmonary embolism (particularly in people who inject drugs and older patients), and rhabdomyolysis with acute kidney injury.^[3][7] ICU complications dominate late morbidity and mortality: nosocomial infection, stress ulcer, venous thromboembolism, pressure sores and critical-care neuromyopathy.^[7] Recent US data report tetanus fatal in approximately 11% of cases, mostly in people 60 years or older and unvaccinated people; in about 20% of deaths no obvious pathology is found and death is attributed to the direct effects of the toxin.^[3]

Adult tetanus case-fatality rates range from 5 to 50%, reflecting disparities in care access. Where mechanical ventilation is readily available, the lowest reported rate is 2.4%, with a median ventilation duration of 16 days in one higher-prevalence Vietnamese setting. Historically, respiratory failure from laryngeal spasm was the leading cause of death; in well-resourced settings, cardiovascular events, most commonly arrhythmias from dysautonomia, are now the prevailing cause, particularly in older patients.^[7]

Negative prognostic indicators include extremes of age, immunocompromise, generalised disease, an incubation period of fewer than 7 days, a short symptom-to-first-spasm interval, short time from first symptom to hospitalisation, a high Ablett score, autonomic dysfunction and need for mechanical ventilation.^[7] Most late mortality and morbidity is indirect, from ICU complications. Long-term outcomes are encouraging: 61% of ICU survivors in an older French cohort had no lasting disability after a median follow-up of almost 4 years, and a Japanese series discharged 35% of survivors to non-home settings. Prolonged intensive care can, however, be financially ruinous.^[7]

In the UK, case-fatality fell from 29% (1984 to 2000) to 11% (the following 14 years), then was estimated at 27% for 2015 to 2025, although surveillance-completion and case-ascertainment changes make these later figures harder to compare.^[6]

Tetanus is prevented by tetanus-toxoid-containing vaccines (TTCV). WHO recommends 6 doses over a lifetime for full protection: 3 primary doses starting as early as 6 weeks of age with at least 4 weeks between doses, then 3 boosters in the second year of life (12 to 23 months), at 4 to 7 years, and at 9 to 15 years, with at least 4 years between boosters.^[4][5] Countries have shifted from single-antigen tetanus toxoid to combinations containing diphtheria toxoid (Td), and almost all had made that shift by December 2023.^[5] A primary series of 3 doses gives near-total protection lasting at least 5 years; 5 doses are probably sufficient for lifelong immunity, though WHO recommends 6.^{[7] [2]}

CDC's schedule: DTaP (for children under 7 years) at 2, 4 and 6 months, boosters at 15 to 18 months and 4 to 6 years; Tdap for preteens at 11 to 12 years; thereafter Td or Tdap every 10 years. Tdap is recommended during the early part of the third trimester of every pregnancy; Tdap can be given as the first catch-up dose for people without documentation of a full series of 3 doses. Adults who have not previously received Tdap should receive a single dose.^[3][8] UK schedule: DTaP/IPV/Hib/HepB at 2, 3 and 4 months, DTaP/IPV at 18 months and at 3 years 4 months, and Td/IPV at 13 to 18 years, with a routine 5-dose total increased to 6 doses from July 2025. Boosters every 10 years may not be needed for lifelong immunity once 5 properly spaced doses are given, and immunity typically persists for 10 years after the preschool dose and at least 20 years after the adolescent booster.^[6]

Vaccine safety and handling: local reactions and low-grade fever are common and self-limiting; moderate or severe systemic reactions to DTaP occur in fewer than 1 in 10 000 doses; contraindications are severe allergy or encephalopathy within 7 days of a previous dose, with precautions for acute illness and certain neurologic conditions. Vaccines should be stored at 2 to 8 °C (36 to 46 °F).^[3]

Wound management is the other key preventive intervention. Beyond vaccination, prevention depends on clean delivery and clean cord care for neonates, safe circumcision, and clean wound care for all injuries.^[4][5]

Wound management prevents disease and reinfection. Appropriate care means assessing the wound, observing for infection and treating infected wounds; systemic or topical antibiotics should not be used to try to prevent tetanus after a wound, although antibiotics may be given when infection is present.^[2][3] Wounds divide into clean and minor (no major tetanus risk) and dirty or major (puncture, contaminated with dirt, soil, faeces or saliva, or containing devitalised tissue such as burns, compound fractures, crush injuries, frostbite or necrosis).^[2][3]

Vaccination and TIG for wound prophylaxis depend on history, grouped as unknown or incomplete series, a completed primary series with 3 or more doses, or completed series.^[2][3][6] The practical scheme:

• A primary tetanus series is 3 doses. Anyone with unknown or incomplete status is treated as unprotected. UK guidance uses "adequate priming" as at least 3 tetanus doses at appropriate intervals, but emphasises that this narrower definition applies only to wound risk assessment; full protection still means completing the full national schedule.^[2][3][6]
• Unknown or incomplete series with any wound: give a vaccine dose now; if the wound is dirty or major, also give TIG at a different site.^[2][3][6]
• Completed series: no vaccine and no TIG for a clean, minor wound if the last dose was within 10 years; for a dirty or major wound the same applies if it was within 5 years.^[2][3]
• Completed series with the last dose more than 10 years ago: booster for a tetanus-prone wound, and TIG as well if it is high-risk. People within 10 years of the last dose need a booster only if the wound is tetanus-prone.^[2][3][6]
• TIG prophylaxis is never indicated for clean, minor wounds. For dirty or major wounds it is indicated for an unknown history, never-vaccinated people, incomplete series, and people with HIV or severe immunodeficiency, regardless of their history.^[2]
• TIG is 250 IU intramuscularly for most wounds, rising to 500 IU if more than 24 hours have elapsed, or if there is heavy contamination or a burn; the same dose applies to adults and children. In the UK, if intramuscular TIG cannot be sourced, intramuscular human normal immunoglobulin (HNIG) is an alternative, with the corresponding volumes.^[2][6]
• Newborn infants follow separate rules depending on maternal vaccination in pregnancy: an infant under 8 weeks born to a mother who received a pertussis-containing vaccine at least 2 weeks before delivery generally needs no TIG for a tetanus-prone wound, while an infant born to an unvaccinated mother needs both vaccine and TIG.^[6]

TIG does not neutralise toxin already bound to nerve endings, so timely administration matters; once toxin is irreversibly fixed, antitoxin no longer helps.^[1][2][3]

Once a course is started, give further doses at the scheduled intervals to ensure future immunity; any individual who is not completely immunised should be brought up to the full schedule.

Pregnancy. Tetanus in a woman during pregnancy, or within 6 weeks after pregnancy ends, is maternal tetanus and usually signals incomplete immunisation. CDC recommends Tdap during the early part of the third trimester of every pregnancy; a single Tdap dose, preferably in pregnancy, is part of catch-up series and protects the newborn. The risk of neonatal tetanus is minimal if a previously unvaccinated woman has received at least 2 properly spaced doses during pregnancy, at least 1 of which is Tdap. WHO recommends 5 properly spaced doses for women without documentation, with 2 doses one month apart in the first pregnancy, a third at least 6 months later and one in each subsequent pregnancy or every year, to 5, with antenatal screening and coverage above 80% in high-burden settings.^[3][5][8]

Children. Children under 7 years receive DTaP; preschool and school doses close the primary series. Encephalopathy without another cause within 7 days of a previous dose is a contraindication; moderate or severe acute illness, unstable neurologic disorder and Guillain-Barre syndrome within 6 weeks are precautions. Systemic reactions are uncommon. Teens who missed Tdap should receive it at the next visit.^[3]

Neonates. Tetanus within the first 28 days is neonatal tetanus; WHO defines a confirmed case as an infant who sucks and cries normally in the first 2 days, then loses that ability between days 3 and 28 and becomes rigid or has spasms. The MNTE goal is fewer than 1 case per 1 000 live births in every district; strategies include routine immunisation of pregnant women, tetanus toxoid SIAs in high-risk districts (3 doses for women of reproductive age), clean delivery and cord care, and reliable surveillance. Cases are massively under-reported (less than 10% of cases and deaths). Treatment follows the same principles as adult tetanus, with antitoxin and intensive supportive care; mortality remains high.^{[4][5][7] [6]}

Older adults. Many older people were vaccinated before routine programmes began, or have waning antibodies; vaccination coverage is lower and case-fatality higher than in younger adults. Catch-up with Tdap and boosters, and careful wound assessment, are important.^[3][6][7]

Immunocompromised patients. People with HIV or severe immunodeficiency need TIG for dirty or major wounds regardless of their tetanus immunisation history, and may not be adequately protected despite completed series, so additional booster doses may be required.^[2][6]

People who inject drugs. Cases in this group are well described; consider tetanus in unexplained rigidity or spasms, and give meticulous wound care and vaccination.^[6][7]

• Tetanus is a clinical diagnosis: treat on clinical grounds and do not wait for laboratory proof. Point-of-care antibody tests are not WHO-recommended.^[6]
• Where intensive care is unavailable, mortality is high. The low-cost essentials are: quiet, darkened nursing; early benzodiazepine and (where needed) opioid sedation; intravenous magnesium sulphate titrated to knee jerk; debridement and wound care; early nasogastric feeding; fluid resuscitation; passive cooling; and systematic turning.^[7]
• Tetanus-specific immunoglobulin and IVIG may be unaffordable (IVIG runs to thousands of pounds per patient), and equine antitoxin is often the available option. IVIG itself is prescribed by weight in settings that use it.^[6][7]
• Prevention rests on routine immunisation, school-based boosters, antenatal vaccination, clean delivery, safe cord care and clean wound care. More than 80% of pregnant women should be protected in MNTE-maintaining countries, and post-validation assessments are recommended at least every 5 years. Keep vaccines at 2 to 8 °C.^[3][4][5]

• Tetanus is caused by tetanospasmin of Clostridium tetani, an anaerobic, spore-forming bacterium whose spores survive heat, antiseptics and years in soil.^[3][7]
• It blocks inhibitory (GABA and glycine) neurotransmission, producing rigidity, painful spasms and dysautonomia; recovery of inhibition takes 4 to 6 weeks.^[7]
• It is never person-to-person; infection does not produce immunity, so vaccination is always needed after disease.^[3][4][6]
• Spores often enter through tiny, forgotten wounds; up to 30% of patients have no identifiable wound on admission.^[6][7]
• Forms: generalised (more than 80% of cases), localised, cephalic and neonatal (within 28 days of birth).^[3][7]
• Incubation is about 8 days (range 1 to 21); shorter incubation predicts worse disease and death.^[3][7]
• Diagnosis is clinical; PCR and culture support it but cannot exclude it; serology above 0.1 IU/mL also cannot exclude it.^[3][6][7]
• Acute management: debridement, antibiotics 7 to 10 days, antitoxin (500 IU intramuscular TIG standard), airway and ventilation, benzodiazepines, magnesium for dysautonomia, meticulous intensive nursing, early vaccination.^[1][6][7]
• TIG does not neutralise toxin already fixed to nerve endings.^[1][2]
• Vaccine prevention is multi-dose: 6 doses over life (WHO), DTaP primary at 2, 4, 6 months with boosters, Tdap in adolescence and in every pregnancy, and Td or Tdap every 10 years for adults; boosters may be needed after wounds by elapsed time (10 years for clean wounds, 5 for dirty).^{[3][4][5][6][8]}
• Maternal and neonatal tetanus remains a global problem; 8 countries had not eliminated it by 2025; clean delivery and cord care are as important as vaccination.^[4][5]
• A primary 3-dose series gives near-total protection for at least 5 years; 5 doses probably give lifelong immunity, although WHO recommends 6.^[7]

Plain-text follow-ons (not yet linked): diphtheria and pertussis immunisation, rabies post-exposure prophylaxis, wound management and surgical site infection, sepsis and intensive care supportive care, adverse drug reactions, normal immunoglobulin use, paediatric emergency care.

Related topics: generalised tetanus, localised tetanus, cephalic tetanus, neonatal tetanus, wound management, vaccines and immunisation schedule, maternal and neonatal tetanus elimination, pharmacology of benzodiazepines and magnesium.