Toxin-mediated neuromuscular disease caused by Clostridium tetani — prevention is vaccination; treatment is wound care, antitoxin, and supportive ICU care.
Also known as: tetanus, lockjaw, Clostridium tetani
Overview
Acute, often fatal disease caused by the neurotoxin tetanospasmin produced by Clostridium tetani, a gram-positive spore-forming obligate anaerobe. Characterized by rigidity and reflex spasms of skeletal muscle and autonomic instability.
Epidemiology
Rare in the US (<50 cases/year) due to widespread vaccination. Worldwide ~25,000-50,000 deaths annually, predominantly neonatal tetanus in low-income countries. US cases concentrate in unvaccinated or under-vaccinated adults and IV drug users.
Try two board-style Tetanus questions
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Question 1Infectious DiseaseEasy
A 35-year-old male sustained a deep puncture wound from a rusty nail 6 hours ago. He completed the primary tetanus series as a child, and his last tetanus booster was about 7 years ago. Which of the following is the most appropriate tetanus prophylaxis?
ABoth Tdap booster and tetanus immune globulin
BTdap booster vaccination
CNo tetanus prophylaxis
DTetanus immune globulin alone
Reveal answer & full explanation
Correct answer: B — Tdap booster vaccination
ABoth Tdap booster and tetanus immune globulin
BTdap booster vaccination✓
CNo tetanus prophylaxis
DTetanus immune globulin alone
Why Tdap booster vaccination is correct
Tetanus prophylaxis depends on (1) wound type — clean minor vs. all other wounds (dirty, deep, puncture) — and (2) vaccination status
For clean minor wounds: vaccinate if <3 prior doses or last dose >10 years ago
For all other wounds (this case — deep, dirty puncture): vaccinate if <3 prior doses or last dose >5 years ago
This patient completed the primary series and his last booster was 7 years ago with a dirty wound, so a Td/Tdap booster is indicated and tetanus immune globulin (TIG) is not
Why the others are wrong
Both Tdap booster and tetanus immune globulin — TIG is added only when the wound is dirty AND the primary series is incomplete or unknown (<3 doses); this patient completed the series, so TIG is unnecessary
Tetanus immune globulin alone — never appropriate alone; the vaccine is still required, and TIG is reserved for an incomplete/unknown series with a dirty wound
No tetanus prophylaxis — incorrect for a dirty, deep puncture when the last booster was >5 years ago; a booster is required
Question 2Infectious DiseaseMedium
A 58-year-old unvaccinated gardener presents 8 days after sustaining a deep puncture wound to the sole of his foot. He reports difficulty opening his mouth and a stiff neck, and his wife notes a fixed grimacing expression. On exam he is afebrile and fully alert, with masseter rigidity, generalized increased muscle tone, and episodes of painful whole-body muscle spasms triggered by a slamming door. Vital signs show labile blood pressure and tachycardia. Which of the following best explains the findings?
ABlocked release of inhibitory transmitters from spinal interneurons
BAutoantibodies against postsynaptic acetylcholine receptor proteins
CAutoantibodies against presynaptic voltage-gated calcium channels
DBlocked acetylcholine release at the neuromuscular junction terminal
Reveal answer & full explanation
Correct answer: A — Blocked release of inhibitory transmitters from spinal interneurons
ABlocked release of inhibitory transmitters from spinal interneurons✓
BAutoantibodies against postsynaptic acetylcholine receptor proteins
CAutoantibodies against presynaptic voltage-gated calcium channels
DBlocked acetylcholine release at the neuromuscular junction terminal
Why Blocked release of inhibitory transmitters from spinal interneurons is correct
The vignette is classic generalized tetanus from Clostridium tetani: trismus and masseter rigidity, risus sardonicus (fixed grimace), generalized rigidity, stimulus-triggered reflex spasms, and autonomic instability (labile BP, tachycardia) in an unvaccinated patient 8 days after a deep puncture wound, with fever absent and consciousness preserved.
Tetanospasmin is taken up by motor neurons and transported retrograde to the spinal cord, where it cleaves synaptobrevin and blocks release of the inhibitory neurotransmitters glycine and GABA from inhibitory interneurons (Renshaw cells).
Loss of inhibition leaves motor neurons firing unopposed, producing sustained rigidity and reflex spasms, while loss of sympathetic inhibition drives the autonomic storm; sensory and cortical function stay intact, so the patient remains alert.
Why the others are wrong
Blocked acetylcholine release at the neuromuscular junction terminal is the mechanism of botulinum toxin, which causes descending flaccid paralysis and hypotonia, the opposite of tetanic rigidity.
Autoantibodies against presynaptic voltage-gated calcium channels describe Lambert-Eaton myasthenic syndrome, which reduces ACh release and causes proximal weakness that improves with repeated effort, not trismus or painful spasms.
Autoantibodies against postsynaptic acetylcholine receptor proteins describe myasthenia gravis, which produces fatigable weakness (ptosis, diplopia), not sustained rigidity or opisthotonus.
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IV drug use (subcutaneous heroin injection — 'skin popping')
Puncture wounds, burns, deep contaminated wounds with devitalized tissue
Neonatal tetanus (umbilical stump contamination in non-sterile delivery)
Diabetes mellitus
Pathophysiology
Tetanospasmin is taken up by motor neurons and transported retrograde to the spinal cord, where it blocks release of inhibitory neurotransmitters (glycine and GABA) from Renshaw cells. The resulting loss of inhibition causes uncontrolled motor neuron firing → sustained muscle rigidity and reflex spasms. Sympathetic autonomic dysregulation produces hypertension, tachycardia, arrhythmias.
Clinical presentation
Symptoms
Incubation 3-21 days (shorter incubation = worse prognosis)
Trismus ('lockjaw') — earliest sign, masseter rigidity (~75% of cases)
Risus sardonicus (sustained facial grin from facial muscle spasm)
Neonatal tetanus: poor sucking, generalized rigidity, opisthotonus in days 4-14 of life
Classic findings
Trismus, risus sardonicus, opisthotonus, and reflex spasms in a patient with an unattended wound and incomplete vaccination history — clinical diagnosis.
Differential diagnosis
Strychnine poisoning — Glycine receptor antagonism produces near-identical presentation; toxicology screen and history
Dystonic reaction (neuroleptic, metoclopramide) — Recent dopamine antagonist; resolves with diphenhydramine or benztropine
Clinical: trismus, generalized muscle rigidity, reflex spasms, autonomic dysfunction in a patient with consistent exposure (wound, IV drug use) and inadequate vaccination.
Labs
Clinical diagnosis — no specific lab confirms tetanus
Wound culture insensitive (positive in only ~30%) and not diagnostic
Routine CBC, CMP, CK (elevated from muscle activity)
Anti-tetanus antibodies — adequate level virtually excludes diagnosis but not always feasible acutely
Imaging
Imaging used to evaluate alternative diagnoses
CT/MRI brain to rule out central causes of trismus
Diagnostic algorithm
Wound Type
<3 doses or unknown
≥3 doses — booster due
≥3 doses — booster not due
Clean, minor
Td/Tdap; no TIG
Td/Tdap if last dose >10 yr
No vaccine, no TIG (last dose ≤10 yr)
Dirty, major, puncture, burn
Td/Tdap PLUS TIG 250 IU IM
Td/Tdap if last dose >5 yr
No vaccine, no TIG (last dose ≤5 yr)
Tetanus post-exposure prophylaxis based on wound type and vaccination history (CDC).
Treatment
First-line
ICU admission with quiet, dimly lit environment to minimize stimuli
Wound debridement to eliminate spore reservoir
Human tetanus immune globulin (HTIG) 500 units IM (some use 3,000-6,000 IU) — neutralizes circulating toxin; toxin already bound is not neutralized
Tetanus toxoid (Td or Tdap) at a different site — clinical disease does not produce protective immunity
Antibiotics: metronidazole 500 mg IV q6-8h (preferred) × 7-10 days; alternative penicillin G but GABA antagonism may worsen spasms
Benzodiazepines (diazepam, midazolam, lorazepam) for muscle spasms and sedation
Magnesium sulfate infusion for autonomic instability
Intubation and neuromuscular blockade (vecuronium) for severe spasms or respiratory failure
Baclofen (intrathecal in refractory cases)
Beta-blockers (labetalol) or alpha-blockers for autonomic storm
Second-line / adjunct
Dantrolene for refractory muscle rigidity
Tracheostomy for prolonged ventilation
Nutritional support, DVT prophylaxis
Complications
Respiratory failure from laryngospasm or sustained chest wall rigidity
Aspiration pneumonia
Autonomic storm with arrhythmias, cardiac arrest
Vertebral compression fractures and long-bone fractures from violent spasms
Rhabdomyolysis, AKI
Death (10-20% even with optimal care; >40% in elderly and neonates)
PANCE pearls
Wound management for tetanus prophylaxis: clean minor wound + ≥3 prior doses → Td if last dose >10 years ago. Dirty/major wound + ≥3 doses → Td if >5 years. Any wound + <3 doses or unknown → Td plus TIG (250 units IM) for dirty/major wounds.
Use Tdap rather than Td if the patient has not received Tdap previously (single Tdap, then Td boosters).
Tetanus disease does NOT produce immunity — always give toxoid even after recovery.
Metronidazole is preferred over penicillin (penicillin is itself a GABA antagonist and may worsen spasms).
Magnesium reduces both autonomic instability and spasm intensity; target serum Mg 2.5-4 mmol/L.
References
CDC — Pinkbook: Tetanus — Epidemiology and Prevention of Vaccine-Preventable Diseases (chapter)
ACIP — Updated Recommendations for Use of Tetanus Toxoid, Reduced Diphtheria Toxoid, and Acellular Pertussis Vaccine (MMWR)
WHO — Current recommendations for treatment of tetanus during humanitarian emergencies
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