Meningitis and Encephalitis

Overview & Definition

Meningitis is inflammation of the meninges — the three protective membranes (dura mater, arachnoid mater, pia mater) that envelop the brain and spinal cord — most often caused by infection but occasionally by malignancy, drugs, or autoimmunity. Encephalitis is inflammation of the brain parenchyma itself, again usually infective (predominantly viral) or autoimmune. When both the meninges and the parenchyma are inflamed together — common in severe viral disease — the syndrome is termed meningoencephalitis, and the clinical features of meningism and encephalopathy overlap.[1][4]

The reason these two diagnoses dominate emergency neurology is that they are common, lethal, and treatable. Acute bacterial meningitis kills 10 to 30 percent of adults within days and leaves another 30 to 50 percent of survivors with permanent neurological sequelae — sensorineural hearing loss, epilepsy, cognitive impairment, and motor deficit. The single most important determinant of survival is the time to antibiotics: every hour of delay in the first few hours after presentation measurably increases mortality. For this reason the discipline of practice is to treat first and investigate second. The classical phrase "meningitis until proven otherwise" exists to make clinicians act before the cerebrospinal fluid (CSF) is back.[1][4][7]

Viral meningitis, in contrast, is usually a self-limiting, aseptic illness (enteroviruses cause over 80 percent) that needs supportive care only. Viral encephalitis, however, is dangerous: herpes simplex virus type 1 (HSV-1) accounts for about 10 to 15 percent of all encephalitis and is the single most important treatable cause. Untreated HSV encephalitis kills over 70 percent of patients; with prompt aciclovir, mortality falls to under 30 percent. The combination of a high pre-treatment mortality, a cheap and effective drug, and a treatable window makes HSV the central fact of the encephalitis workup — every patient with suspected encephalitis receives empirical aciclovir until HSV PCR returns negative.[3][6]

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Classification

Central nervous system (CNS) infections are classified along two axes — the anatomical compartment involved (meninges versus parenchyma) and the aetiological agent (bacterial, viral, fungal, parasitic, or non-infectious). The anatomical axis determines the clinical syndrome; the aetiological axis determines the drug. [1]

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Epidemiology & Risk Factors

Bacterial meningitis has an annual incidence of roughly 1 to 5 per 100,000 in high-income countries and far higher where vaccination is incomplete. After the introduction of conjugate Haemophilus influenzae type b (Hib), pneumococcal conjugate (PCV13) and meningococcal vaccines into childhood immunisation schedules, the epidemiology has shifted: Hib meningitis has nearly disappeared in children, the median age of bacterial meningitis has risen, and S. pneumoniae has become the dominant adult pathogen. Meningococcal disease peaks in adolescents and young adults (15 to 24 years) and in the meningococcal belt during the dry season (December to June).[4][5]

Viral meningitis is far commoner than bacterial (tens of thousands of cases per year), is dominated by enteroviruses in summer and autumn, and carries an excellent prognosis. Viral encephalitis has an annual incidence of roughly 5 to 10 per 100,000; HSV is the most frequently identified cause in adults year-round, while arboviruses are seasonal and geographically delimited. Autoimmune encephalitis, particularly anti-NMDA receptor, is increasingly recognised and in young people may exceed any single viral cause.[6][10]

The modifiable and host risk factors cluster into groups that mirror the empirical antibiotic choice: [1]

Pathophysiology

Bacteria reach the subarachnoid space by three principal routes: haematogenous spread (the dominant pathway — colonisation of the nasopharynx followed by invasion across the mucosa, bacteraemia, and crossing the blood–brain barrier at the choroid plexus or cerebral capillaries); direct contiguous extension from sinusitis, otitis media, mastoiditis, or a dental focus; and direct inoculation from skull fracture, neurosurgery, lumbar puncture, or a CSF shunt. Once in the subarachnoid space, bacteria multiply rapidly because the CSF has low concentrations of complement and immunoglobulin and no effective cellular immune surveillance — a privileged niche that becomes their growth medium.[1][4]

The clinical damage is driven less by the bacteria themselves than by the host inflammatory response. Bacterial cell-wall components — pneumococcal lipoteichoic acid and pneumolysin, meningococcal and Gram-negative lipopolysaccharide (endotoxin) — activate Toll-like receptors (TLR-2, TLR-4) on meningeal macrophages and brain microglia. This releases a cytokine cascade — tumour necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-8 (IL-8) — that recruits neutrophils, upregulates adhesion molecules, opens the blood–brain barrier, and increases vascular permeability. The consequences are neutrophilic exudate in the subarachnoid space, cerebral oedema (vasogenic and cytotoxic), raised intracranial pressure, vasculitis of perforating vessels producing cerebral infarction, impairment of CSF reabsorption at the arachnoid granulations producing hydrocephalus, and direct neuronal injury. This single cascade is why dexamethasone (which dampens the cytokine response) works — and works only if given before or with the first antibiotic dose, before the inflammatory cascade is fully triggered.[1][4][7]

HSV-1 reaches the brain by a different and elegant route. After primary infection (usually orolabial), the virus establishes latency in the trigeminal ganglion. Reactivation periodically sends virus in a retrograde axonal transport along the trigeminal and olfactory nerves to their cortical terminations — the frontotemporal cortices and limbic structures. This neuroanatomy explains the striking temporal lobe predilection of HSV encephalitis, the haemorrhagic necrosis that is its pathology, and the clinical features (aphasia, behaviour change, complex partial seizures, memory disturbance) that result. Untreated, the virus destroys the temporal cortices bilaterally and is uniformly fatal; aciclovir halts viral DNA polymerase and rescues tissue that has not yet necrosed.[3]

Tuberculous and cryptococcal meningitis follow a subacute tempo because their pathogens replicate slowly and elicit a lymphocytic, low-grade, basilar inflammation. TB organisms lodge in the basal meninges and form a thick gelatinous exudate that encases the cranial nerves and obstructs CSF flow at the basal cisterns, producing cranial nerve palsies and communicating hydrocephalus, and causing a vasculitis of the lenticulostriate and thalamoperforating vessels with basal ganglia infarcts. Cryptococcus reaches the brain via the capsule of yeasts crossing the choroid plexus and accumulates in the Virchow–Robin spaces as "soap-bubble" lesions; it secretes capsular polysaccharide that impairs phagocytosis and produces a strikingly high CSF opening pressure.[4][9]

Clinical Presentation

The clinical syndromes of meningitis and encephalitis differ in one decisive feature: the level of consciousness and the presence of parenchymal signs. Meningitis (especially bacterial) preserves higher function until late; encephalitis disturbs it early. [1]

Bacterial meningitis

The classic triad of fever, neck stiffness and altered mental status is present in only about 40 to 50 percent of adults at presentation; adding headache raises sensitivity to roughly 95 percent, so that almost every patient has at least two of fever, headache, neck stiffness or confusion. The full syndrome comprises:[1][4]

• Fever — present in 80 to 95 percent (may be absent in the elderly, immunocompromised, or after self-administered antibiotics).
• Headache — severe, often holocranial, the most sensitive individual symptom (over 90 percent).
• Neck stiffness — resistance to passive flexion; meningism appears over hours.
• Photophobia and phonophobia.
• Altered mental status — drowsiness, confusion, agitation; at the severe end, coma.
• Nausea and vomiting — from raised intracranial pressure or meningeal irritation.
• Seizures — focal or generalised, in 15 to 30 percent, commoner with S. pneumoniae.
• Focal neurological deficits — cranial nerve palsies (especially III, IV, VI, VII, VIII), hemiparesis from vasculitic infarction.
• Rash — petechial or purpuric, non-blanching, in 50 to 75 percent of meningococcal cases; a vital sign that mandates immediate treatment. [1]

Encephalitis

Encephalitis presents with fever plus altered consciousness plus seizures plus focal neurological deficit. The altered mental status is the cardinal feature distinguishing encephalitis from meningitis — a patient with pure viral meningitis is uncomfortable but lucid; a patient with encephalitis is confused, obtunded, or comatose. Seizures are commoner than in meningitis. The focal signs reflect the site of parenchymal involvement.[3][6]

HSV encephalitis classically produces a temporal lobe syndrome: aphasia (dominant hemisphere), behaviour and personality change, anosmia, complex visual or olfactory hallucinations, focal seizures arising from the temporal lobe, and memory disturbance (Korsakoff-like state in survivors). Anti-NMDA receptor encephalitis (more common in young women, often with an ovarian teratoma) follows a characteristic sequence: a viral-like prodrome, then psychiatric symptoms (psychosis, agitation, paranoia), then seizures, dyskinesias (orofacial, choreoathetoid), autonomic instability (hyperthermia, tachycardia, hypertension, hypoventilation) and decreased consciousness, often progressing to require prolonged ICU care.[10]

Atypical presentations (examiners deliberately test these)

Differential Diagnosis

The differential of fever plus headache plus altered mental status is broad and contains several mimics that demand specific treatment. The high-yield framework separates infectious CNS disease from non-infectious causes. [1]

The decisive can't-miss mimics in the acute setting are subarachnoid haemorrhage (CT), brain abscess (CT/MRI — never LP if a mass lesion is present), cerebral malaria (blood film in the traveller), and autoimmune encephalitis (CSF antibody panels, MRI). All patients with suspected encephalitis should also receive empirical antibiotics until bacterial meningitis is excluded, and all patients with suspected HSV encephalitis should receive aciclovir until PCR returns negative.[3][6]

Clinical & Bedside Assessment

The focused examination in suspected CNS infection has four aims: to confirm the syndrome (meningism, encephalopathy, rash), to search for a focus (ear, sinus, skin, heart), to identify red flags mandating CT before LP, and to stage severity (GCS, sepsis) for disposition. [1]

Named meningeal signs (low sensitivity 5 to 30 percent, but high specificity when present): [1]

• Kernig sign — with the patient supine and the hip and knee flexed to 90 degrees, attempted extension of the knee meets resistance or produces pain in the back/hamstrings (stretch on inflamed meninges/nerve roots).
• Brudzinski sign (nape of the neck) — passive flexion of the neck produces involuntary flexion of the hips and knees.
• Brudzinski sign (contralateral / cheek) — flexion of one hip causes flexion of the contralateral leg; pressure on the cheek produces forearm flexion.
• Jolt accentuation — exacerbation of an existing headache on horizontal rotation of the head twice per second; more sensitive than Kernig/Brudzinski for meningitis. [1]

A full examination must include: vital signs (fever, tachycardia, hypotension, tachypnoea, oxygenation, capillary refill — septic shock), GCS, pupils, fundoscopy for papilloedema (a red flag for raised ICP — do not LP), cranial nerves, motor and sensory exam, coordination, skin (rash, bite, chancre, erythema migrans, Janeway lesions), ears/nose/throat (otitis, mastoid tenderness, sinus tenderness, parotid), neck stiffness, chest (pneumonia, murmur of endocarditis), abdomen (hepatosplenomegaly, splenomegaly of asplenia absent), lymph nodes, joints, and signs of immunocompromise (oral candidiasis, Kaposi sarcoma, wasting, needle marks). In suspected meningococcal disease, repeat the skin examination every 15 minutes — the rash can evolve rapidly.[1][4]

Investigations

Bedside and bloods

Bloods: full blood count (leucocytosis in bacterial; lymphopenia in viral), C-reactive protein and procalcitonin (high procalcitonin supports a bacterial cause and helps guide empiric de-escalation), urea and electrolytes (hyponatraemia from SIADH or cerebral salt wasting), glucose (must be measured alongside CSF glucose to calculate the ratio), liver function, coagulation, arterial blood gas (lactate, acid–base), blood cultures (two sets, before antibiotics if possible but never delaying therapy), HIV serology, malaria film in the traveller, and (in viral syndromes) throat and rectal swabs for enterovirus PCR. Chest X-ray looks for pneumonia, TB, or a focus; echocardiography if endocarditis is suspected.[1][3]

Lumbar puncture — the key investigation, but only if safe

The lumbar puncture (LP) is the cornerstone of diagnosis. It is performed at the L3–L4 or L4–L5 interspace (adult spinal cord ends at L1–L2; Tuffier's line through the iliac crests crosses L4). The patient is positioned lateral decubitus, knees to chest, fully flexed. Opening pressure is measured with a manometer attached to the needle (normal 8 to 20 cm CSF in adults; elevated in bacterial, TB, and cryptococcal meningitis). CSF is collected into four numbered tubes sent for: (1) cell count and differential, (2) glucose and protein, (3) Gram stain, culture and sensitivity, (4) cell count (to compare with tube 1 and detect a 'traumatic tap') and reserve for special tests (PCR, antigen, cytology). A fifth tube is sent for viral PCR (HSV-1/2, VZV, enterovirus) and, where indicated, TB PCR/GeneXpert, cryptococcal antigen, and autoimmune antibody panels.[1][2]

When to perform CT before LP — the red flags

A mass lesion with raised intracranial pressure can herniate when CSF is drained from below. CT must be performed before LP if any of the following are present (the IDSA criteria): [1]

CSF interpretation — the patterns

The CSF parameters are among the most heavily examined facts in clinical medicine. Each pattern reflects the underlying pathophysiology (neutrophils for bacteria; lymphocytes for viruses, TB, and fungi; low glucose when organisms consume it or infiltrate the meninges; high protein when the blood–CSF barrier is breached). [1]

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Imaging

CT brain (non-contrast) is performed before LP in patients with red flags (above), to exclude a mass lesion, hydrocephalus, or cerebral oedema. In bacterial meningitis the CT is often normal or shows only meningeal enhancement after contrast; it may show sinusitis, mastoiditis, or a focus. MRI brain with contrast is more sensitive and is the modality of choice for encephalitis and subacute meningitis: HSV encephalitis shows T2/FLAIR hyperintensity and restricted diffusion in the temporal lobes (often bilateral, asymmetric), TB meningitis shows basal meningeal enhancement, hydrocephalus, and basal ganglia infarcts, cryptococcosis shows gelatinous pseudocysts, and autoimmune encephalitis often shows medial temporal lobe T2 hyperintensity (limbic encephalitis). Electroencephalogram (EEG) is highly characteristic in HSV encephalitis — periodic lateralising epileptiform discharges (PLEDs) over a temporal lobe — though MRI and PCR have largely supplanted its diagnostic role.[3][6]

Management — Resuscitation

Suspected bacterial meningitis is a time-critical emergency. The discipline of practice is: assess, take blood cultures, give empirical antibiotics and dexamethasone within one hour, then perform LP if safe and image if needed. Treatment is never delayed for LP or imaging. [1]

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Empirical antibiotic bundle (adult, community-acquired)

The empirical regimen is chosen to cover the three dominant adult pathogens (pneumococcus, meningococcus, Listeria) and to penetrate the CSF at meningeal doses. Third-generation cephalosporins achieve excellent CSF penetration in inflamed meninges; vancomycin covers penicillin-resistant pneumococci; ampicillin covers Listeria, which is intrinsically resistant to all cephalosporins.[1][2][4]

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Adjunctive and supportive care

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Management — Definitive & Stepwise

Once the organism and sensitivities are known, antibiotics are narrowed and continued for the appropriate total duration. Dexamethasone is continued for four days in confirmed pneumococcal disease; in meningococcal or Hib disease it is given if started empirically but offers little additional benefit. In suspected or confirmed Listeria, dexamethasone is not continued (no benefit, possible harm).[1][2]

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HSV encephalitis

HSV encephalitis is treated with IV aciclovir 10 mg/kg every 8 hours (infused over one hour, renal-adjusted) for 14 to 21 days. Treatment is started empirically in every patient with suspected encephalitis and continued until HSV PCR returns negative; a single early negative PCR does not exclude HSV (sensitivity is low in the first 24 to 48 hours) and the LP should be repeated at 3 to 7 days. With aciclovir, mortality falls from over 70 percent to 20 to 30 percent; survivors often have residual cognitive and behavioural deficits. Repeat MRI at the end of therapy is reasonable; clinical relapse occurs in a minority and warrants re-treatment.[3][6]

Tuberculous meningitis

TB meningitis is treated with four-drug intensive therapy — isoniazid (with pyridoxine), rifampicin, pyrazinamide, ethambutol (HRZE) for two months, followed by isoniazid plus rifampicin (HR) for a total of 12 months (some authorities extend to 18 months). Adjunctive corticosteroids improve survival (dexamethasone or prednisolone, tapering over 6 to 8 weeks) — the landmark Thwaites trial in NEJM established this. Thalidomide and infliximab are reserved for refractory cases. Monitor for hepatotoxicity, optic neuritis (ethambutol), and peripheral neuropathy (isoniazid). Communicating hydrocephalus may need a shunt.[8]

Cryptococcal meningitis

Cryptococcal meningitis (HIV-related or not) follows the 2010 IDSA three-phase regimen: induction with amphotericin B deoxycholate 0.7 to 1 mg/kg/day IV PLUS flucytosine 100 mg/kg/day orally in four divided doses for at least two weeks; consolidation with fluconazole 400 mg (6 mg/kg) daily for eight weeks; and maintenance (in HIV) with fluconazole 200 mg daily until immune reconstitution (CD4 over 100 for at least 6 months on antiretroviral therapy). Manage raised intracranial pressure with serial therapeutic lumbar punctures daily until pressure normalises; a lumbar drain or shunt may be needed. Liposomal amphotericin is preferred where toxicity (renal, electrolyte, anaemia) is a concern.[9]

Autoimmune encephalitis

Anti-NMDA receptor encephalitis and other autoimmune encephalitides are treated with immunotherapy: first-line — methylprednisolone 1 g IV daily for 3 to 5 days, intravenous immunoglobulin 0.4 g/kg/day for 5 days, and/or plasma exchange (5 sessions); second-line for non-response — rituximab and/or cyclophosphamide. A teratoma search (CT chest/abdomen/pelvis, transvaginal ultrasound, MRI pelvis) is mandatory in young women with anti-NMDAR — resection of the tumour is the most effective single intervention. Recovery is slow (months), and prolonged ICU support for autonomic instability is often required. Anti-LGI1 encephalitis responds well to first-line immunotherapy and classically presents with faciobrachial dystonic seizures.[10]

Specific Subtypes & Scenarios

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Complications & Pitfalls

The classic pitfalls that examiners test — and that cause avoidable harm — are: delaying antibiotics for LP or CT (the single biggest error); omitting ampicillin in the over-50 or immunocompromised patient, missing Listeria; giving dexamethasone after the antibiotic (no benefit); performing LP in the presence of papilloedema or a mass lesion (herniation); stopping aciclovir on a single early negative HSV PCR (HSV may be missed); fluid-restricting hyponatraemic patients with cerebral salt wasting (worsens cerebral perfusion); and failing to arrange chemoprophylaxis for meningococcal contacts.[1][3]

Prognosis & Disposition

Bacterial meningitis carries a case-fatality of 10 to 30 percent, rising with age (over 60), immunocompromise, septicaemic shock, low GCS, seizures, focal deficit, delayed antibiotics, and pneumococcal aetiology. Among survivors, 30 to 50 percent have some neurological sequelae, most often sensorineural hearing loss (about 10 percent), cognitive impairment, epilepsy, or motor deficit. HSV encephalitis, even with aciclovir, kills 20 to 30 percent and leaves half of survivors with cognitive and behavioural deficits that may only become fully apparent months later. TB meningitis mortality is 20 to 60 percent and is heavily stage-dependent (Medical Research Council grade I vs III). Cryptococcal meningitis mortality in HIV depends on immune reconstitution and intracranial pressure control. Autoimmune encephalitis has a good prognosis with early immunotherapy and tumour removal, but a poor prognosis with delay.[1][3][4]

Special Populations

Dose anchors examiners expect in special groups. Neonates: never default to adult ceftriaxone monotherapy — use ampicillin + gentamicin/cefotaxime with neonatal weight-based charts. Adults with Listeria risk (age >50, pregnancy, cell-mediated immunosuppression): ampicillin 2 g IV every 4 hours added to a third-generation cephalosporin. HSV encephalitis: aciclovir 10 mg/kg IV every 8 hours (adjust in renal impairment) until PCR negative or full course completed. Cryptococcal meningitis in HIV: induction with amphotericin B + flucytosine (guideline regimen), then fluconazole consolidation — LP for raised pressure is therapeutic as well as diagnostic. Contact prophylaxis after meningococcus: ciprofloxacin 500 mg PO once (adult) or ceftriaxone 250 mg IM once in pregnancy. [1]

Evidence, Guidelines & Regional Differences

The contemporary evidence base for bacterial meningitis rests on two landmark randomised trials of adjunctive dexamethasone. The European Dexamethasone in Adulthood Bacterial Meningitis Study (de Gans and van de Beek, NEJM 2002) randomised adults with suspected bacterial meningitis to dexamethasone 10 mg every six hours for four days versus placebo, given before or with the first antibiotic. Mortality fell from 25 to 15 percent overall, and from 30 to 14 percent in pneumococcal meningitis, with a striking reduction in sensorineural hearing loss. Benefit was confined to pneumococcal disease and only when dexamethasone was given before the antibiotic. The Thwaites trial (NEJM 2004) showed that dexamethasone similarly improved survival in tuberculous meningitis.[7][8]

[1] [1] [1] [1]

Prevention

Prevention of bacterial meningitis rests on vaccination and chemoprophylaxis. The conjugate vaccines have changed the epidemiology in countries with routine programmes. [1]

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Exam Pearls & High-Yield Minutiae

[1]

• Classic triad of bacterial meningitis — fever, neck stiffness, altered mental status — is present in only about 40 to 50 percent; the presence of two of fever, headache, neck stiffness, confusion is over 95 percent sensitive.
• Meningococcal rash — petechial or purpuric, non-blanching; check conjunctiva and palate; can evolve hourly.
• CSF bacterial: neutrophils, glucose under 2.2 mmol/L or CSF-to-serum ratio under 0.4, protein over 1 g/L.
• CSF viral: lymphocytes, normal glucose, mildly raised protein.
• CSF TB: lymphocytes, very low glucose, very high protein, cobweb, ADA elevated.
• CSF HSV: lymphocytes with red cells (haemorrhagic necrosis); PCR over 95 percent sensitive but may be negative in first 24 to 48 hours — repeat.
• Dexamethasone 10 mg IV q6h for 4 days, before or with the first antibiotic, for suspected pneumococcal meningitis.
• Aciclovir 10 mg/kg IV q8h for 14 to 21 days for HSV encephalitis — do NOT wait for PCR.
• Vancomycin added for penicillin-resistant pneumococcus; ampicillin for Listeria (cephalosporin-resistant).
• Kernig and Brudzinski signs — low sensitivity (under 30 percent) but high specificity.
• CT before LP if immunocompromised, new seizures, focal deficit, papilloedema, GCS under 12, or anticoagulated.
• Prophylaxis — rifampicin 600 mg BD x2 days or ciprofloxacin 500 mg single dose for meningococcal contacts.
• Listeria — food-borne (soft cheese, deli meats, unpasteurised milk); over 50, pregnant, immunocompromised.
• Waterhouse–Friderichsen — adrenal haemorrhage in meningococcaemia; adrenal crisis.
• Neonate — group B strep, E. coli, Listeria; treat with ampicillin plus gentamicin/cefotaxime.
• Hearing loss in about 10 percent — audiometry at discharge and 6 weeks. [1]

Self-test: a 22-year-old university student with fever, headache and a petechial rash

This is meningococcal meningitis/septicaemia until proven otherwise. Immediate management: airway, breathing, circulation; ceftriaxone 2 g IV immediately (do not wait for LP); blood cultures; fluid resuscitation for shock; ICU if shocked; notify public health; chemoprophylaxis for household and kissing contacts (rifampicin 600 mg BD x2 days or ciprofloxacin 500 mg stat). LP is performed once stable, with CT first if any red flag. Droplet precautions for the first 24 hours.

[1]

Self-test: a 65-year-old with fever, confusion and a focal seizure

Consider HSV encephalitis and Listeria meningitis. Give empirical ceftriaxone 2 g IV plus vancomycin plus ampicillin (Listeria cover, age over 50) plus dexamethasone 10 mg IV plus aciclovir 10 mg/kg IV. CT first (new seizure, focal deficit = red flag). LP after CT: send for cells, glucose, protein, Gram stain, culture, HSV PCR, and bacterial PCR/antigen. MRI temporal lobes. Continue aciclovir until HSV PCR negative; narrow antibiotics once the organism is identified.

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Exam application bank (NEET-PG / INICET)

One-line answer

Meningitis is inflammation of the meninges, most often infective; encephalitis is inflammation of the brain parenchyma, and meningoencephalitis is both together. Bacterial meningitis is a time-critical emergency — fever plus headache plus neck stiffness plus altered mental status is bacterial meningitis until proven otherwise, and empirical therapy (ceftriaxone 2 g IV q12h plus vancomycin plus dexamethasone 10 mg IV q6h, add ampicillin if over 50 or immunocompromised) must start within one hour, before lumbar puncture or imaging. Herpes simplex encephalitis is the treatable encephalitis not to miss — fever plus altered mental status plus seizures needs empirical IV aciclovir 10 mg/kg q8h for 14 to 21 days, without waiting for PCR. CSF analysis (cell count, glucose, protein, Gram stain, culture, PCR) distinguishes bacterial, viral, tuberculous and fungal causes. [1]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Meningitis and Encephalitis.

References

1. [1]van de Beek D, Cabellos C, Dzupova O, et al. ESCMID guideline: diagnosis and treatment of acute bacterial meningitis Clin Microbiol Infect, 2016.PMID 27062097
2. [2]Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis Clin Infect Dis, 2004.PMID 15494903
3. [3]Solomon T, Michael BD, Smith PE, et al. Management of suspected viral encephalitis in adults--Association of British Neurologists and British Infection Association National Guidelines J Infect, 2012.PMID 22120595
4. [4]McGill F, Heyderman RS, Panagiotou S, Tunkel AR, van de Beek D. Acute bacterial meningitis in adults Lancet, 2016.PMID 27265346
5. [5]Brouwer MC, Tunkel AR, van de Beek D. Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis Clin Microbiol Rev, 2010.PMID 20610819
6. [6]Venkatesan A, Tunkel AR, Bloch KC, et al. Case definitions, diagnostic algorithms, and priorities in encephalitis: consensus statement of the international encephalitis consortium Clin Infect Dis, 2013.PMID 23861361
7. [7]de Gans J, van de Beek D, European Dexamethasone in Adulthood Bacterial Meningitis Study Investigators. Dexamethasone in adults with bacterial meningitis N Engl J Med, 2002.PMID 12432041
8. [8]Thwaites GE, Nguyen DB, Nguyen HD, et al. Dexamethasone for the treatment of tuberculous meningitis in adolescents and adults N Engl J Med, 2004.PMID 15496623
9. [9]Perfect JR, Dismukes WE, Dromer F, et al. Clinical practice guidelines for the management of cryptococcal disease: 2010 update by the infectious diseases society of america Clin Infect Dis, 2010.PMID 20047480
10. [10]Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis Lancet Neurol, 2011.PMID 21163445