Meningitis and Encephalitis for NEET PG — Complete Guide 2026

Version 1.0 — Published February 2026

Meningitis and encephalitis vignettes are NEET PG bread-and-butter — the child with fever, headache, and purpuric rash; the HIV patient with slowly worsening headache and papilloedema; the elderly diabetic with subacute confusion and cranial nerve palsy; the young adult with fever, seizure, and temporal lobe hyperintensity on MRI. Getting the CSF analysis pattern, empirical antibiotic, and adjunctive dexamethasone or aciclovir decision right separates marks. This guide covers classification, clinical features, CSF comparison, age-based empirical therapy, TB meningitis, HSV encephalitis, cryptococcal disease, and vaccination. Pair with the medicine subject hub, the microbiology high-yield topics, and the tuberculosis diagnosis and treatment guide for integrated revision.

Classification and clinical features

Meningitis is inflammation of the pia and arachnoid meninges with pleocytosis in the CSF — its aetiological classification (bacterial, viral, TB, fungal, parasitic, non-infectious) directs diagnostic workflow and empirical therapy.

Aetiological categories:

Clinical features of meningitis:

Encephalitis clinical features:

• Altered sensorium (hallmark — distinguishes from meningitis)
• Personality / behaviour change, speech/language disturbance
• Focal or generalised seizures (30–60%)
• Focal neurological signs (aphasia, hemiparesis, cranial nerve palsies)
• Autonomic dysfunction (anti-NMDAR)
• Movement disorders (chorea, myoclonus)

Infant / neonatal presentation (non-specific):

• Fever or hypothermia, poor feeding, lethargy, irritability, high-pitched cry, paradoxical irritability (cries more when held), bulging anterior fontanelle, seizures, apnoea
• Kernig/Brudzinski unreliable in infants

Red flags on first contact: altered GCS, focal neurological signs, purpuric rash, new seizure, haemodynamic instability, immunocompromised host, post-neurosurgical, infant — all mandate urgent empirical antibiotics (and aciclovir in encephalitis) without waiting for LP.

CSF analysis — comparison table

Cerebrospinal fluid analysis from lumbar puncture remains the cornerstone investigation — and the characteristic pattern across bacterial, viral, TB, and fungal meningitis is a recurring NEET PG table.

Lumbar puncture pre-requisites:

• No contraindications — focal signs, GCS <=8, new seizure, papilloedema, immunocompromised with focal signs → CT head first to exclude mass/raised ICP
• No coagulopathy — platelets >50 × 10⁹/L, INR <1.5; stop anticoagulants as indicated
• No overlying skin infection
• Do not delay antibiotics for LP — if LP delayed >30–60 min, give antibiotics first after cultures (blood and urine) are drawn

Normal CSF:

• Opening pressure 8–20 cm H₂O
• Cells: <5 lymphocytes/μL (adults); <30 in neonates
• Protein: 15–45 mg/dL (higher in neonates)
• Glucose: 50–80 mg/dL; CSF-to-serum glucose ratio 0.6
• Clear and colourless

CSF comparison — classic pattern:

Pitfalls:

• Partially treated bacterial — may mimic viral (lymphocytosis, higher glucose, lower protein); clinical correlation and lactate help
• Early bacterial or enteroviral — may have neutrophilic pleocytosis initially; repeat LP in 24 h often clarifies viral shift to lymphocytes
• Traumatic tap — adjust WBCs (subtract 1 WBC per 700 RBC if peripheral blood counts normal); xanthochromia suggests true SAH/subarachnoid pathology
• HSV encephalitis — red cells in CSF are clue (haemorrhagic necrosis); protein raised, glucose normal
• Neutrophilic fungal meningitis — rare but seen in aspergillosis
• Pleocytosis absent in severe immunosuppression and overwhelming pneumococcal disease — still give antibiotics on clinical suspicion

Additional CSF tests:

• Latex agglutination / PCR for S. pneumoniae, N. meningitidis, H. influenzae, GBS, E. coli
• Multiplex PCR panel (BioFire ME — 14 pathogens including HSV, VZV, CMV, enterovirus, parechovirus, cryptococcus, commonest bacteria) — rapid, but not replacing culture
• HSV PCR — sensitivity ~95%; may be negative in first 72 h (repeat if clinically encephalitic)
• Cryptococcal antigen (CrAg) — lateral flow assay on serum and CSF — very sensitive/specific
• VDRL on CSF for neurosyphilis
• Cytology and flow cytometry for neoplastic meningitis

Empirical antibiotic therapy by age

Empirical antibiotic therapy in acute bacterial meningitis is age-adjusted because the likely organisms change with age and host factors — and delay in the first dose raises mortality measurably with every hour.

Start antibiotics within 30–60 minutes of presentation — do not wait for CT or LP beyond this window.

Age-based empirical regimens:

Targeted therapy once organism confirmed:

Adjunctive dexamethasone (adults):

• 0.15 mg/kg (or 10 mg) IV every 6 h × 4 days
• Start with or before first antibiotic dose — stops TNF/IL-1 surge triggered by bacteriolysis
• Continue if S. pneumoniae confirmed; stop if alternative confirmed
• Reduces mortality and hearing loss in adult pneumococcal meningitis (de Gans and van de Beek NEJM 2002)
• In children — reduces hearing loss in Hib meningitis (Odio NEJM 1991); guidelines suggest continuing for all suspected bacterial meningitis in paediatrics, stopping if pathogen found not to benefit

Chemoprophylaxis for close contacts:

• N. meningitidis — ciprofloxacin 500 mg single dose; rifampicin 600 mg BD × 2 days; ceftriaxone 250 mg IM single dose; vaccinate if capsular match
• H. influenzae type b — rifampicin 20 mg/kg/day × 4 days for unvaccinated household children <4 y
• S. pneumoniae — no routine prophylaxis

Tuberculous meningitis

Tuberculous meningitis (TBM) is a subacute meningitis caused by M. tuberculosis — common in India given the national TB burden — and it is the deadliest form of tuberculosis with mortality 15–40% even with treatment.

Pathogenesis:

• Rich focus — subependymal caseous focus seeded during primary TB bacillaemia ruptures into subarachnoid space → thick basal gelatinous exudate → cranial nerve entrapment (VI, III, VII, II), vasculitis (infarcts in basal ganglia and thalamus), hydrocephalus (communicating, from exudate blocking basal cisterns)

Clinical features (MRC staging):

Prognosis worsens sharply with stage — earlier treatment is critical.

Clinical clues:

• Subacute tempo 2–4 weeks of headache, fever, weight loss
• Cranial nerve palsies — VI (abducens, most common from exudate stretching), III, VII; visual loss if optic nerve / chiasm
• Raised ICP — papilloedema, vomiting
• Focal signs from vasculitic infarcts (hemiparesis, aphasia)
• Hydrocephalus on imaging (~80%)
• Basal meningeal enhancement on contrast MRI/CT (pathognomonic)
• Tuberculoma (ring-enhancing) in 10–30%
• Hyponatraemia (SIADH or cerebral salt wasting)
• Evidence of TB elsewhere (pulmonary, abdominal, lymphadenitis) in 30–50%

Diagnosis:

• CSF — lymphocytic pleocytosis 100–500, very high protein 100–500 mg/dL, low glucose <40 — classic triad
• Cobweb / pellicle on standing CSF (from high protein)
• AFB smear sensitivity 10–20% (yield improves with repeated large-volume LPs)
• CSF MTB culture — gold standard but slow
• Xpert MTB/RIF Ultra — WHO-endorsed, sensitivity 70–90%, detects rifampicin resistance
• ADA >10 U/L supportive (not specific — also in bacterial, fungal, lymphoma)
• CSF lactate raised
• Imaging — contrast MRI: basal meningeal enhancement, hydrocephalus, infarcts (basal ganglia / thalamus), tuberculomas
• Chest X-ray / chest CT — co-existing pulmonary TB in 30–50%
• HIV testing mandatory in endemic settings

Treatment (WHO 2022 TB meningitis guidelines):

• Intensive phase — 2 months: HRZE (isoniazid, rifampicin, pyrazinamide, ethambutol)
• Continuation phase — 10 months: HR (isoniazid, rifampicin)
• Total duration — 12 months
• Dosing — weight-based per WHO fixed-dose combinations; NTEP regimens in India
• Adjunctive dexamethasone — 0.3–0.4 mg/kg/day IV tapered over 6–8 weeks (Thwaites NEJM 2004) — reduces mortality; unclear effect on disability
• Pyridoxine 50 mg/day to prevent isoniazid-induced neuropathy
• Drug-resistant TBM (MDR/XDR) — individualised regimen based on DST; linezolid and bedaquiline penetration; prolonged therapy

Complications and surveillance:

• Hydrocephalus — VP shunt or ETV (endoscopic third ventriculostomy) for obstructive
• Raised ICP — mannitol, dexamethasone, ventriculostomy
• Seizures — antiepileptics (avoid enzyme inducers that interact with rifampicin)
• Paradoxical worsening (especially on ART re-initiation in HIV) — continue TB drugs, add/continue steroids

HSV encephalitis and other viral CNS infections

Herpes simplex virus encephalitis is the commonest sporadic viral encephalitis in adults — HSV-1 in 90% of adult cases — with a devastating natural history (untreated mortality ~70%) that is transformed by early empirical aciclovir.

Pathogenesis:

• HSV reactivation ascending along olfactory/trigeminal tracts → haemorrhagic necrotising encephalitis of temporal and orbitofrontal lobes — often asymmetric and bilateral
• HSV-2 in neonates (birth-acquired), recurrent Mollaret meningitis

Clinical features:

• Fever, headache (~90%)
• Altered sensorium — confusion, drowsiness, coma
• Personality and behaviour change — psychiatric features (mistaken for functional)
• Focal temporal-lobe signs — aphasia (dominant), memory impairment, olfactory hallucinations, complex partial seizures
• Generalised or focal seizures (30–60%)
• Rare: non-dominant temporal involvement → Klüver-Bucy features (hyperoral, hypersexual)

Investigations:

• MRI — asymmetric T2/FLAIR hyperintensity in temporal lobes, insula, and cingulate; restricted diffusion early; haemorrhage on SWI/GRE; pre-contrast images more specific than CT
• CT — often normal early; late temporal hypodensity and mass effect
• EEG — PLEDs (periodic lateralised epileptiform discharges) over temporal leads — ~80%
• CSF — lymphocytic pleocytosis 10–500 cells/μL, raised protein 60–200 mg/dL, normal glucose, raised RBCs (haemorrhagic)
• HSV PCR on CSF — sensitivity ~95%, specificity >99%; may be negative in first 72 h — repeat if clinical suspicion high
• Autoimmune panel — post-HSV anti-NMDAR encephalitis (secondary autoimmune) relapse

Management:

• IV aciclovir 10 mg/kg every 8 h (adjust for renal function) — start empirically on first suspicion, before PCR confirmation
• Duration 14–21 days (14 for immunocompetent confirmed, 21 in immunocompromised or severe)
• Adequate hydration during aciclovir (crystal nephropathy risk)
• Supportive — airway, seizure control (levetiracetam preferred), ICP management
• Monitor — repeat PCR at end of therapy; relapse or incomplete response may need re-treatment
• Corticosteroids — role under study (GACHE trial); often used in severe cerebral oedema

Prognosis: without treatment 70% mortality, survivors severely disabled; with treatment mortality 15–20%, but up to 50% have long-term deficits (memory loss, epilepsy, dysphasia).

Other viral encephalitis entities:

Cryptococcal meningitis and other fungal CNS infections

Cryptococcal meningitis is the most common fungal meningitis globally and the commonest cause of meningitis in advanced HIV (CD4 <100) in India — a chronic lymphocytic meningitis needing a distinct induction-consolidation-maintenance regimen.

Organisms:

• Cryptococcus neoformans — worldwide; soil/pigeon droppings; immunocompromised hosts (HIV, transplant, lymphoma, steroids, sarcoidosis)
• Cryptococcus gattii — eucalyptus trees; immunocompetent hosts can be infected; Pacific Northwest, tropical/subtropical

Clinical features:

• Subacute — weeks of headache (most common), low-grade fever, malaise
• Visual loss (papilloedema, optic neuropathy from raised ICP)
• Cranial nerve palsies (VI, III, VII)
• Seizures, altered sensorium later
• Meningeal signs often mild or absent (~50%)

Diagnosis:

• India ink CSF microscopy — encapsulated yeasts with broad clear halo; sensitivity 60–80% in HIV (higher burden), <50% in non-HIV
• Cryptococcal antigen (CrAg) — lateral flow assay on serum and CSF: sensitivity/specificity >95%; preferred test
• Fungal culture on Sabouraud dextrose agar; colonies in 5–14 days
• CSF — lymphocytic pleocytosis (may be acellular in severe immunosuppression), raised protein, low glucose
• Very high opening pressure >25 cm H₂O in ~70% — prognostic and therapeutic target
• Imaging — basal meningeal enhancement, Virchow-Robin space dilatation (gelatinous pseudocysts), cryptococcomas; hydrocephalus
• Always test for HIV and CD4 count

Treatment (WHO 2022 HIV-associated cryptococcal meningitis):

Raised intracranial pressure management:

• Serial lumbar punctures (drain 20–30 mL until closing pressure <20 cm H₂O) — daily if symptomatic; continue until sustained normalisation
• Lumbar drain if frequent LPs required
• VP shunt for persistent hydrocephalus/IIH-like picture

Antiretroviral therapy timing:

• Defer ART by 4–6 weeks after starting antifungals in cryptococcal meningitis to reduce IRIS (immune reconstitution inflammatory syndrome)

Screening:

• Serum CrAg screening in newly diagnosed HIV with CD4 <100–200 — pre-emptive fluconazole for CrAg-positive asymptomatic patients prevents cryptococcal meningitis (WHO-recommended)

Other fungal CNS infections:

• Candida — premature neonates, long-term ICU with central lines; micro-abscesses
• Aspergillus — immunocompromised; angioinvasive, brain abscess, stroke
• Mucormycosis — rhino-orbito-cerebral in uncontrolled diabetes; post-COVID outbreak in India; amphotericin + surgical debridement
• Coccidioides, histoplasma, blastomyces — endemic regions

Complications, vaccines, and prevention

Meningitis and encephalitis carry high rates of acute and long-term complications — and vaccination has transformed the epidemiology in the last 30 years.

Acute complications:

Long-term sequelae:

• Sensorineural hearing loss (up to 30% pneumococcal; 5–10% Hib) — screen all survivors with audiometry
• Cognitive impairment, epilepsy, developmental delay (in children)
• Hydrocephalus, motor deficits (hemiparesis, quadriparesis)
• Cranial nerve palsies (VI, III, VII — TBM)
• Vision loss (optic neuropathy — TB, cryptococcal)
• Behaviour and memory problems (HSV)

Vaccines — prevention:

Special populations needing all three conjugate vaccines (PCV, Hib, MenACWY + MenB):

• Splenectomy / functional asplenia (sickle cell)
• Complement deficiency (late complement — C5–9 in particular)
• Cochlear implant recipients
• CSF leak
• Immunocompromised (HIV, transplant, long-term steroids)

Chemoprophylaxis (already detailed above): meningococcal contacts, Hib household contacts with unvaccinated children <4 y.

Sources and references

1. Harrison's Principles of Internal Medicine, 21st Edition (Loscalzo, Fauci, Kasper, Hauser, Longo, Jameson, Eds., 2022) — Chapters on acute bacterial meningitis, viral meningitis and encephalitis, and CNS infections in immunocompromised hosts.
2. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 9th Edition (Bennett, Dolin, Blaser, Eds., 2020) — Detailed chapters on every CNS infection covered here.
3. Tunkel AR et al. Practice Guidelines for the Management of Bacterial Meningitis. Clin Infect Dis 2004; 39:1267-1284 (IDSA); updates in subsequent society statements.
4. van de Beek D et al. ESCMID guideline: diagnosis and treatment of acute bacterial meningitis. Clin Microbiol Infect 2016; 22 Suppl 3:S37-S62.
5. Thwaites GE et al. Dexamethasone for the treatment of tuberculous meningitis in adolescents and adults. N Engl J Med 2004; 351:1741-1751.
6. World Health Organization. WHO consolidated guidelines on tuberculosis. Module 4: Treatment — Drug-susceptible tuberculosis treatment. 2022 update.
7. World Health Organization. Guidelines for diagnosing, preventing and managing cryptococcal disease among adults, adolescents and children living with HIV. 2022.
8. Indian Academy of Pediatrics. Consensus Guidelines on Evaluation and Management of Suspected Acute Viral Encephalitis in Children in India. Indian Pediatr 2012; 49:897-910.

Frequently asked questions

How many meningitis and encephalitis questions appear in NEET PG?

Meningitis and encephalitis contribute 3-4 direct questions per NEET PG paper across medicine, microbiology, paediatrics, and infectious diseases. Recurring themes include the CSF analysis comparison table (bacterial vs viral vs TB vs fungal), empirical antibiotic regimens by age group (vancomycin plus ceftriaxone as the adult backbone; add ampicillin for Listeria in greater than 50 years or immunocompromised), dexamethasone in suspected pneumococcal meningitis, HSV encephalitis with temporal lobe involvement and aciclovir, and India-ink / cryptococcal antigen for cryptococcal meningitis.

What is the difference between meningitis and encephalitis?

Meningitis is inflammation of the meninges (pia and arachnoid), presenting with headache, fever, neck stiffness, photophobia, and Kernig/Brudzinski signs — the patient is typically conscious and oriented. Encephalitis is inflammation of the brain parenchyma, presenting with altered consciousness, seizures, focal neurological signs, and behaviour change. The two often overlap as meningoencephalitis (both present together), especially in viral and TB infections. HSV is the classic encephalitis with temporal lobe predilection; bacteria cause meningitis predominantly.

What is the CSF analysis in bacterial meningitis?

Typical bacterial meningitis CSF shows raised opening pressure (greater than 25 cm H2O), cloudy or turbid appearance, markedly raised total cells (usually greater than 1000 cells/microL) with polymorphonuclear predominance (neutrophils greater than 80 percent), raised protein (greater than 100 mg/dL, often 100-500), and low glucose (less than 40 mg/dL or CSF-to-serum ratio less than 0.4). Gram stain is positive in 60-80 percent of untreated cases; culture is positive in 70-85 percent. Lactate greater than 3.5 mmol/L and procalcitonin help distinguish from viral when mixed cellularity is present.

What is the empirical antibiotic therapy for community-acquired bacterial meningitis?

Empirical therapy depends on age and host factors. Neonates (less than 1 month) — ampicillin plus cefotaxime plus gentamicin (covers Group B strep, E. coli, Listeria). Infants and children (1 month to 50 years) — ceftriaxone 2 g IV every 12 h plus vancomycin (for resistant pneumococci). Adults greater than 50 years or immunocompromised — add ampicillin 2 g IV every 4 h for Listeria monocytogenes. In penicillin-allergic — meropenem plus vancomycin. Post-neurosurgical or penetrating head trauma — vancomycin plus cefepime or meropenem (gram-negative and staphylococcal cover). Start dexamethasone 10 mg IV with or before the first antibiotic dose in suspected pneumococcal meningitis.

How is tuberculous meningitis diagnosed and treated?

TB meningitis presents subacutely over 2-4 weeks with fever, headache, cranial nerve palsies (VI, III, VII), altered sensorium, and often basal meningitis features on imaging. CSF shows lymphocytic pleocytosis (100-500 cells/microL with early neutrophil phase), markedly raised protein (100-500 mg/dL with cobweb clot formation), and low glucose. Raised CSF ADA (greater than 10 U/L) supports the diagnosis. Xpert MTB/RIF Ultra is the NAAT of choice (WHO-endorsed). Treat with 2 months HRZE followed by 10 months HR (total 12 months per WHO 2022 update), plus adjunctive dexamethasone (tapered over 6-8 weeks) to reduce mortality and neurological sequelae. Evaluate for co-existing HIV.

What is HSV encephalitis?

Herpes simplex virus encephalitis is the commonest sporadic viral encephalitis in adults — HSV-1 classically, HSV-2 in neonates. Presents with fever, headache, altered mental state, seizures, behavioural change, and focal signs (aphasia if dominant temporal lobe involvement). MRI shows asymmetric temporal lobe hyperintensity on T2/FLAIR, often involving orbitofrontal cortex. EEG shows periodic lateralising epileptiform discharges (PLEDs) over temporal leads. CSF — lymphocytic pleocytosis, raised protein, normal glucose, raised RBCs (haemorrhagic); HSV PCR is diagnostic (sensitivity 95 percent, may be negative in first 72 h). Start IV aciclovir 10 mg/kg every 8 h empirically in any suspected encephalitis — do not wait for PCR. Treat 14-21 days; mortality without treatment approaches 70 percent, with treatment 15-20 percent.

How do you diagnose and treat cryptococcal meningitis?

Cryptococcal meningitis (Cryptococcus neoformans, rarely C. gattii) mostly affects immunocompromised patients (HIV with CD4 less than 100, organ transplant, long-term steroids). Classic presentation — subacute headache, fever, visual loss, cranial nerve palsies. Diagnosis — India ink shows encapsulated yeasts (sensitivity 60-80 percent; higher in HIV), cryptococcal antigen (CrAg) on serum and CSF by lateral flow assay (sensitivity and specificity greater than 95 percent), and culture on Sabouraud agar. Opening pressure is often very high (greater than 25 cm H2O) — serial LPs or lumbar drain for symptomatic pressure. Treatment — induction 2 weeks amphotericin B (liposomal) 3-4 mg/kg/day IV plus flucytosine 100 mg/kg/day (or single high-dose liposomal ampho B plus flucytosine plus fluconazole per WHO 2022); consolidation fluconazole 800 mg/day for 8 weeks; maintenance fluconazole 200 mg/day for at least 1 year and until CD4 greater than 100 on ART.

What is the role of dexamethasone in pneumococcal meningitis?

Adjunctive dexamethasone 0.15 mg/kg (or 10 mg in adults) IV every 6 h for 4 days, starting with or BEFORE the first antibiotic dose, reduces mortality and neurological sequelae (especially hearing loss) in adult pneumococcal meningitis — European Dexamethasone Study (de Gans and van de Beek NEJM 2002). Benefit is less clear in meningococcal and Haemophilus; continue if Streptococcus pneumoniae confirmed, stop if alternative pathogen confirmed. In children with Hib meningitis, dexamethasone reduces sensorineural hearing loss. Not routinely used in low-resource settings where TB meningitis and HIV-related cryptococcal disease predominate — case-by-case decision; adjunctive dexamethasone is still indicated in TB meningitis and clinically suspected pneumococcal disease.

Which vaccines prevent meningitis?

Key vaccines are conjugate pneumococcal vaccines (PCV13, PCV15, PCV20 — Streptococcus pneumoniae), Haemophilus influenzae type b conjugate (Hib — given as part of DPT-HepB-Hib pentavalent in the Indian Universal Immunisation Programme), and meningococcal vaccines (MenACWY conjugate, MenB recombinant). BCG provides some protection against disseminated TB and TB meningitis in children but not against pulmonary TB in adults. Rubella vaccination prevents congenital rubella syndrome; mumps vaccine (in MMR) prevents viral meningoencephalitis. Japanese encephalitis vaccine is used in endemic Indian states. Post-splenectomy, functional asplenia, and complement deficiency patients need all three conjugate capsular vaccines.

What is the difference between Kernig and Brudzinski signs?

Kernig sign — with the patient supine and hip flexed to 90 degrees, attempted extension of the knee causes pain and resistance in the hamstrings due to meningeal irritation. Brudzinski sign (neck sign) — passive flexion of the neck elicits involuntary flexion at the hips and knees. Both signs have high specificity but low sensitivity (present in only 5-30 percent of acute bacterial meningitis) — absence does not rule out meningitis. Classical jolt accentuation of headache (patient rotating head 2-3 times per second) and neck stiffness are more sensitive. In infants, the bulging anterior fontanelle and paradoxical irritability (worsens when picked up) replace Kernig/Brudzinski.

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Written by: NEETPGAI Editorial Team Reviewed by: Pending SME Review Last reviewed: February 2026

This article is reviewed by qualified medical professionals for clinical accuracy and exam relevance. For corrections or updates, contact the editorial team.