IM26.12-13 | Central Nervous System and Clostridial Infections — Summary & Reflection

KEY TAKEAWAYS

CNS infections:
- Bacterial meningitis: fever + headache + neck stiffness (triad present in only 44%); non-blanching rash = meningococcaemia emergency; organism varies by age — add ampicillin for Listeria in >50 years or immunocompromised; CSF: turbid, neutrophilic pleocytosis (1000–10,000 WBC), glucose ratio <0.4, protein >100 mg/dL; management: blood cultures → dexamethasone → ceftriaxone (± ampicillin); LP before CT if no papilloedema or focal signs.
- HSV encephalitis: temporal lobe involvement; MRI FLAIR hyperintensity; CSF HSV PCR; aciclovir 10 mg/kg 8-hourly × 14–21 days empirically — do not wait for PCR results; 70% mortality untreated.
- CSF interpretation: bacterial (PMNs, low glucose, high protein, turbid) vs viral (lymphocytes, normal glucose, mildly elevated protein) vs TB (lymphocytes, very low glucose, high protein, cobweb clot) vs cryptococcal (India ink positive, CrAg positive).

Clostridial infections:
- Tetanus: tetanospasmin cleaves synaptobrevin (VAMP) at spinal inhibitory interneurons → ascending spastic paralysis; trismus, risus sardonicus, opisthotonus, stimulus-triggered spasms; treat: HTIG + wound debridement + metronidazole (NOT penicillin) + IV diazepam + tracheostomy/ventilation; Grade III–IV = ICU.
- Botulism: botulinum toxin cleaves SNARE at NMJ → descending flaccid paralysis; diplopia/dysphagia → limb weakness → respiratory failure; no fever, no sensory loss; treat: antitoxin + ventilatory support.
- Gas gangrene: C. perfringens alpha-toxin → rapid myonecrosis, crepitus, haemolysis, systemic toxaemia; surgical emergency — radical debridement/amputation + IV penicillin + clindamycin.

REFLECT

Return to the two patients in the opening hook. The student with meningococcaemia: the non-blanching rash told you the diagnosis before any investigation returned. How quickly would you have administered antibiotics? The answer should be: within 5 minutes of identifying the rash — before blood cultures, before blood pressure monitoring if access is delayed. The farm worker with tetanus: his wound had apparently healed, yet the toxin was already bound to his spinal cord. HTIG now can only limit further binding by neutralising circulating toxin — everything else is managing the consequence of toxin already bound. Reflect on this asymmetry — in bacterial meningitis, early antibiotics remove the cause and the inflammatory response subsides; in tetanus, early HTIG limits the toxin burden but the damage already done must be managed symptomatically for weeks as the presynaptic terminals regenerate. This mechanistic asymmetry should shape your expectation of treatment response: dramatic improvement within 24–48 hours in meningitis vs slow resolution over days to weeks in tetanus. How does this change your communication with the patient's family in each case?