Meningitis / Encephalitis

Meningitis

Inflammation of the meninges and CSF — viral, bacterial, or fungal.

• Bacterial: Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis (meningococcus), other less common organisms.
• Viral: enteroviruses, mumps, HSV, varicella-zoster, EBV, primary HIV infection.
• Fungal: Cryptococcus neoformans, Histoplasma capsulatum.

Classic triad: headache, photophobia, neck stiffness — also malaise, vomiting, fever, drowsiness.

Bacterial meningitis

Demographics: most common in childhood, typically age 6–12 months.

Presentation:

• Infancy — fever, pallor, vomiting, altered consciousness, irritability/ drowsiness, neck stiffness (an unreliable sign at this age), bulging fontanelle; a diffuse purpuric rash on the trunk/limbs suggests meningococcaemia.
• >3 years — meningeal irritation is more obvious: headache, fever, vomiting, neck stiffness, followed by delirium and altered consciousness.
• Kernig sign — with the hip flexed 90°, inability to straighten the knee (hamstring pain).
• Brudzinski sign — neck flexion causes involuntary hip/knee flexion.
• Fulminant meningitis — dramatic, sudden-onset shock, purpura, ± coma.

Investigations: LP for CSF culture/PCR; blood culture; CT before LP in adults and those at risk of raised ICP. Only pursue hospital investigation if it won’t cause significant treatment delay — aim to start antibiotics within 60 minutes of hospital arrival.

Management: IV access; IV saline if hypoperfusion signs present. Early antibiotics (ceftriaxone or cefotaxime) — ideally after LP, but don’t withhold for delay. Dexamethasone 0.15mg/kg with the first antibiotic dose. If meningococcaemia with a purpuric rash is suspected and hospital transfer will be delayed, give antibiotics immediately (IV benzylpenicillin or ceftriaxone) before transfer.

Prevention: meningococcal B vaccine (Bexsero) was added to the Australian National Immunisation Program for infants from 2020, alongside the existing adolescent MenACWY program.

Encephalitis

Inflammation of the brain parenchyma itself (as opposed to the meninges) — presents with the meningitic triad plus features of brain dysfunction: altered mental status/behaviour change, seizures, focal neurological deficits. Classically infective (most often HSV, which needs urgent IV aciclovir pending confirmation — don’t wait for PCR results if clinical suspicion is high), but an important and increasingly recognised alternative cause is autoimmune (antibody-mediated) encephalitis.

Autoimmune encephalitis (anti-NMDA receptor encephalitis)

The best-characterised of a group of disorders caused by antibodies against neuronal cell-surface/synaptic proteins (rather than the intracellular/nuclear antigens seen in classic paraneoplastic syndromes) — clinically important because, unlike cytotoxic-T-cell-mediated paraneoplastic disorders, the neuronal dysfunction here is often reversible with immunotherapy rather than causing permanent neurodegeneration.

Presentation: prominent psychiatric symptoms (psychosis, agitation, paranoid ideation) alongside encephalopathy — memory disturbance, stereotyped/repetitive motor behaviours, seizures, autonomic instability, and (in severe cases) central hypoventilation requiring ventilatory support. The psychiatric-symptom-forward presentation means these patients are often initially misdiagnosed with a primary psychotic illness before the neurological features (movement disorder, seizures, autonomic instability) become apparent — consider autoimmune encephalitis in a young person with acute/subacute psychosis plus any neurological feature (seizures, abnormal movements, reduced consciousness), rather than assuming a primary psychiatric disorder.

Triggers:

• Ovarian teratoma — found in up to ~50–58% of young women (18–45) with NMDAR encephalitis; tumour screening is an important part of work-up in this group, since tumour removal is part of definitive treatment.
• Herpes simplex encephalitis (HSE) — around 20% of HSE patients (especially children) go on to develop NMDAR antibodies and a secondary autoimmune encephalitis phase, historically described as “post-HSE choreoathetosis.” A child with new behavioural change or choreoathetosis weeks after apparently treated HSV encephalitis warrants reassessment for this secondary autoimmune process, not just assumed post-infective sequelae.

Management: immunotherapy — first-line typically plasma exchange and/or IV immunoglobulin (± corticosteroids); rituximab is used for refractory cases. Tumour removal (where a teratoma is found) is an important adjunct to immunotherapy. Most patients show substantial clinical recovery with treatment, consistent with the underlying mechanism being reversible antibody-mediated neuronal dysfunction rather than irreversible degeneration — though recovery can take months to years, and some cases are refractory to first-line immunotherapy.

GP relevance: this is specialist (neurology/immunology)-managed care once suspected, but recognising the possibility — particularly the psychosis-plus- neurological-feature pattern, and the post-HSE relapse pattern in children — is what prompts the referral and antibody testing (serum and CSF) that leads to diagnosis.