Clostridium tetani

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.