MBBSPediaMBBSPedia
Gram-positiveBacilliSpore-forming

Clostridium tetani

Gram-positive, obligate anaerobic, spore-forming bacillus that produces tetanospasmin, causing tetanus characterized by sustained muscular spasms and autonomic dysfunction.

Organism Card

DomainMust know
Identity
  • G+ve, anaerobic, spore-forming bacillus
  • Terminal round spore → classic "drumstick" / "tennis racket" morphology
  • Obligate anaerobe; vegetative form is fragile, spores are extremely hardy
Lab discriminator
  • Drumstick-shaped spore (terminal, round) distinguishes from C. perfringens (no spores on Gram stain, stormy fermentation), C. botulinum (subterminal spore), C. difficile (subterminal spore)
  • Tetanus is a clinical diagnosis; lab culture is NOT relied upon [1]
  • Culture rarely positive; organism difficult to isolate from wound
Reservoir / transmission
  • Spores ubiquitous in soil, dust, animal faeces worldwide
  • Transmission via contaminated wound (puncture, crush, burn, umbilical stump)
  • Not transmitted person-to-person
  • HK-relevant: rare due to high vaccination uptake; consider in unvaccinated elderly or migrants; neonatal tetanus in developing countries via contaminated umbilical stump
Key virulence
  • Tetanospasmin (tetanus toxin) = A-B exotoxin, one of most potent toxins known
  • Encoded on plasmid; released on autolysis of vegetative cells
  • Mechanism: retrograde axonal transport → cleaves SNARE protein (synaptobrevin/VAMP) at inhibitory interneurons in spinal cord & brainstem [1]
  • Blocks release of inhibitory neurotransmitters (GABA, glycine) → unopposed excitatory activity → spastic paralysis
  • Key contrast: botulinum toxin → flaccid paralysis (blocks ACh at NMJ); tetanospasmin → spastic paralysis (blocks inhibitory NT centrally)
Clinical syndromes
  • Generalised tetanus (most common, ~80%): trismus (lockjaw) → risus sardonicus → opisthotonus → reflex spasms → respiratory failure
  • Incubation typically 3–21 days; shorter incubation = worse prognosis
  • Localised tetanus: rigidity confined to muscles near wound
  • Cephalic tetanus: follows head/ear wound; cranial nerve palsies
  • Neonatal tetanus: contaminated umbilical stump in unvaccinated mother; poor feeding, rigidity, spasms; high mortality
  • Autonomic dysfunction (sympathetic storms, labile BP, arrhythmia) is a major cause of death [1]
Diagnosis
  • Primarily a clinical diagnosis — classic triad: trismus + rigidity + reflex spasms after wound
  • Spatula test: touching posterior pharyngeal wall → jaw clamp (reflex masseter spasm) rather than gag = highly specific
  • Wound culture has low sensitivity; negative culture does NOT exclude diagnosis
  • No useful serological test for acute diagnosis (anti-tetanus Ab level only shows prior immunisation status, not acute disease)
Treatment
  • Neutralise unbound toxin: human tetanus immunoglobulin (HTIG) IM — does NOT reverse already-bound toxin
  • Eliminate source: wound debridement + antibiotics (metronidazole first-line; penicillin is alternative but may potentiate spasms via GABA-antagonism) [1]
  • Control spasms: benzodiazepines (diazepam); severe cases may need neuromuscular blockade + mechanical ventilation
  • Supportive: ICU care, manage autonomic instability (IV magnesium, labetalol)
  • Disease does NOT confer immunity → must give tetanus toxoid (active immunisation) during recovery [1]
Prevention
  • Tetanus toxoid vaccine (inactivated toxin) — included in childhood DPT/DTaP schedule; boosters every 10 years [1]
  • Wound management: clean wound + > 10 yr since booster → give toxoid; dirty/tetanus-prone wound + incomplete series or > 5 yr → give toxoid + HTIG
  • Neonatal tetanus prevention: maternal vaccination (at least 2 doses TT before delivery)
  • Notifiable disease in Hong Kong
  • No person-to-person spread → standard precautions only, no isolation needed
Classic traps
  • Tetanus = spastic paralysis (UMN-type, central) vs Botulism = flaccid paralysis (LMN-type, peripheral) — both are clostridial A-B toxins cleaving SNARE proteins but at different sites [1]
  • Trismus DDx: peritonsillar abscess, dental infection, TMJ pathology — but reflex spasms + opisthotonus are specific for tetanus
  • Strychnine poisoning mimics tetanus (also blocks glycine) — ask about exposure
  • Tetanus toxin is irreversible; recovery requires new synapse formation (weeks–months)
  • Past paper trap: C. tetani listed among outbreak pathogens — tetanus is NOT an outbreak/foodborne pathogen (unlike C. botulinum, C. perfringens) [2][3]

Exam Intelligence

  1. Tetanospasmin cleaves synaptobrevin (VAMP) at inhibitory interneurons → blocks GABA/glycine release → spastic paralysis. This is the single most examinable mechanism point. Contrast with botulinum toxin, which cleaves SNARE proteins at the peripheral NMJ → flaccid paralysis. Both are zinc-dependent metalloproteases encoded on bacteriophage/plasmid [1].

  2. Metronidazole is preferred over penicillin for the antibiotic component of tetanus treatment, because penicillin is a GABA antagonist and may theoretically worsen spasms [1].

  3. Tetanus does NOT confer natural immunity — always give active immunisation (toxoid) during convalescence, as the amount of toxin causing disease is too small to generate an immune response [1].

  4. The spatula test is a bedside clinical test with reported sensitivity ~94% and specificity ~100% for tetanus — useful exam vignette clue.

  5. HTIG neutralises only unbound (circulating) toxin; once toxin is fixed to neurons, it cannot be reversed. This explains why early administration is critical and why recovery is prolonged.

  6. Neonatal tetanus from contaminated umbilical stump is a classic exam scenario for prevention by maternal vaccination — two doses of tetanus toxoid before delivery.

  • Tetanus vs botulism: Both are Clostridium toxin-mediated diseases; both involve SNARE protein cleavage. The critical discriminator is the site of action: tetanospasmin acts centrally (inhibitory interneurons → spastic paralysis, trismus, opisthotonus), while botulinum toxin acts peripherally (NMJ → descending flaccid paralysis starting with cranial nerves, diplopia, dysphagia, then respiratory failure).
  • Tetanus vs strychnine poisoning: Both present with reflex spasms and opisthotonus. Strychnine blocks glycine receptors directly. History of ingestion and rapid onset (minutes–hours) vs wound + longer incubation (days–weeks) differentiates.
  • C. tetani vs C. perfringens: Both are G+ve anaerobic clostridia, but C. perfringens causes gas gangrene (alpha-toxin/lecithinase), food poisoning, and is notable for double-zone haemolysis + Nagler reaction. C. perfringens is a common outbreak pathogen (food poisoning), whereas tetanus is NOT an outbreak pathogen.
  • Exam trap on outbreak EMQs: In past paper EMQ lists of "disease pathogens/agents with outbreak potential," C. perfringens and C. botulinum appear but C. tetani does not — tetanus is a sporadic, wound-associated disease, not a foodborne outbreak [2][3].
  • Wound management vignette trap: A common MCQ tests whether HTIG is indicated. The decision depends on vaccination status AND wound type (clean vs tetanus-prone). Fully vaccinated with booster < 10 years + clean wound → no HTIG needed.

The indexed past papers (2016–2025 Fourth Summative MCQ/SAQ/Minicases) do not contain a question stem that directly names or tests Clostridium tetani specifically. However, the following questions include C. tetani-adjacent organisms in their option lists, providing useful context:

  • 2018 Fourth Summative MCQ Q26–Q27 [2]: EMQ with options including Clostridium botulinum (B) and Clostridium perfringens (C) among outbreak pathogens. Q26 stem describes vomiting 1 hour after egg/ham sandwich → answer is Staphylococcus aureus (preformed enterotoxin). Q27 describes projectile vomiting, diarrhoea and fever in child care centre with person-to-person spread → answer is Norovirus. Note: C. tetani is NOT listed as an outbreak option — this reinforces that tetanus is sporadic, not outbreak-associated.

  • 2019 Fourth Summative MCQ Q19–Q20 [3]: Same EMQ template with identical option list including C. botulinum and C. perfringens but NOT C. tetani. Q19 (frozen cheesecake, diarrhoea in children/elderly over 2 months) → answer is Listeria monocytogenes. Q20 (reversed hot-cold sensation after fish) → answer is Ciguatoxin.

No other directly relevant past paper questions on C. tetani were identified in the indexed context.

[1] Lecture slides: GC 105. Medically important microbes what every doctor should know.pdf; GC 237. Musculoskeletal infection [Updated in 2025].pdf; Gen Clerk Anaes + Microbiology Summary.pdf [2] Past papers: 2018 Fourth Summative MCQ.pdf [3] Past papers: 2019 Fourth Summative MCQ.pdf

Clostridium perfringens

Gram-positive, spore-forming, anaerobic bacillus that produces potent exotoxins (notably alpha-toxin/lecithinase), causing gas gangrene (clostridial myonecrosis) and enterotoxin-mediated food poisoning.

Clostridium botulinum

Anaerobic, spore-forming, Gram-positive bacillus that produces a potent neurotoxin causing flaccid paralysis (botulism) by blocking acetylcholine release at the neuromuscular junction.

On this page

No Headings