Clostridium tetani - Tetanus

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When tetanus spores enter a suitable low-oxygen environment (soil-contaminated wounds, devitalised tissue), Clostridium tetani germinates and releases tetanospasmin — a lethal neurotoxin causing spastic paralysis. 🦠 Recovery does not confer immunity, so vaccination is always required after infection.

📖 About

• Clostridium tetani is a Gram-positive, spore-forming anaerobe found in soil, dust, and animal waste.
• Disease results from tetanospasmin toxin → blocks inhibitory neurotransmitters (GABA, glycine) → sustained muscle contraction.
• Fatality rate: 20–60% (highest in neonates and elderly, often due to respiratory failure or autonomic instability).
• High-risk in areas with poor wound hygiene or inadequate immunisation programmes.
• No natural immunity: Even survivors must complete full tetanus toxoid vaccination. 💉

🔬 Microscopy

🧫 Characteristics

• Gram-positive, motile, obligate anaerobe.
• Spore-forming bacillus with a "drumstick" appearance (terminal spores).
• Produces:
  • Tetanospasmin – neurotoxin (clinical tetanus).
  • Tetanylisin – haemolysin, minor role in disease.

⚙️ Aetiology & Pathophysiology

• Transmission: Spores enter via puncture wounds, deep lacerations, burns, animal bites, or contaminated surgical wounds. Neonatal tetanus: via infected umbilical stump.
• Toxin action: Retrograde axonal transport → spinal cord → blocks inhibitory neurotransmitters (GABA, glycine) → unchecked motor neuron activity → spasms/rigidity.
• Incubation: 3–21 days (shorter = worse prognosis).

🩺 Clinical Presentation

• Trismus (lockjaw) 😬 – often first sign.
• Risus sardonicus – characteristic “sardonic smile.”
• Opisthotonus – severe arching of the back from spasm.
• Generalised rigidity, painful spasms triggered by minor stimuli (light, touch, noise).
• Autonomic features: tachycardia, labile hypertension, sweating, salivation, fever.
• Respiratory muscle involvement → hypoxia, arrest.
• Forms: Generalised, localised, cephalic, neonatal.

📊 Grading of Severity

• I (Mild): Trismus + rigidity, no spasms or respiratory compromise.
• II (Moderate): Rigidity + spasms, mild respiratory distress.
• III–IV (Severe): Frequent prolonged spasms, airway compromise, autonomic dysfunction.

🧾 Differential Diagnosis

• Strychnine poisoning: Glycine antagonist; mimics tetanus.
• Acute dystonia: Can cause trismus; resolves with anticholinergics (benztropine).

🔎 Investigations

• Primarily clinical diagnosis – lab confirmation is rare.
• Blood agar culture: poor, indistinct growth.
• Toxin assays confirm but not widely available.
• Check wound cultures – but often negative.

💉 Prevention

• Vaccination: Tetanus toxoid (part of UK DTaP schedule: 2, 3, 4 months + boosters at 3 yrs, 14 yrs).
• Wound prophylaxis: TIG for contaminated wounds if vaccination incomplete/uncertain.
• Neonatal tetanus: Prevented via maternal immunisation + clean delivery practices.

💊 Management

• Supportive Care: ABC support, ITU, tracheostomy/ventilation if needed.
• Sedation/Spasm control: Diazepam or midazolam IV; may require neuromuscular blockade + ventilation.
• Antitoxin: Human TIG 150 U/kg IM across multiple sites. (Equine TIG possible where human unavailable, but risk of anaphylaxis.)
• Antibiotics: IV metronidazole preferred. (Older studies showed penicillin may worsen spasms.)
• Wound Care: Debridement after TIG to remove necrotic tissue/spores.
• VTE prophylaxis in immobilised patients.
• Autonomic dysfunction: Morphine (sympathetic overdrive), labetalol (hypertension), inotropes (hypotension).

⚠️ Complications

• Respiratory failure from spasm.
• Autonomic dysregulation → labile BP, arrhythmias.
• Secondary infections (VAP, sepsis) in ITU.
• Fractures/dislocations from violent spasms.