Meningitis and Encephalitis

Meet the patient

A 19-year-old university student is brought to the emergency department at 4am with a 12-hour fever, a thumping headache, and a stiff neck. She is confused, her heart rate is 130, and when you roll her over there are pinprick petechiae on her conjunctiva and palate that do not blanch when you press a glass against them.[1][4]

Meningococcal meningitis with septicaemia until proven otherwise. The two questions that decide her next hour are the two that decide every case on this page: what do you push in the next ten minutes? (antibiotics and dexamethasone, now) and when is it safe to do the lumbar puncture? (only after you have treated her). Treat first, investigate second.[1][4]

Two syndromes, one non-negotiable rule

Meningitis is the meninges; encephalitis is the parenchyma. The meninges are the three protective membranes — dura, arachnoid, pia — around the brain and cord; the parenchyma is the brain substance itself. When both are inflamed together, as often happens in severe viral disease, the syndrome is meningoencephalitis and the features of meningism and encephalopathy overlap at the bedside.[1][4]

These two diagnoses dominate emergency neurology because 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 deficit — hearing loss, epilepsy, cognitive impairment, motor weakness.[1][4]

Timing of antibiotics drives outcome. In a population-based Danish cohort, the median door-to-antibiotic time was 2 hours, delays beyond 6 hours carried an adjusted risk ratio of 1.5 for unfavourable outcome, and every hour of delay within the first 6 hours carried an adjusted risk ratio of 1.1. That is why the whole discipline of this topic reduces to one line, repeated until it is reflex.[20]

Viral meningitis, in contrast, is usually a self-limiting aseptic illness — enteroviruses cause over 80 percent — and needs supportive care only. Viral encephalitis is the dangerous one: HSV-1 accounts for about 10 to 15 percent of all encephalitis and is the single most important treatable cause.[3][6]

Untreated HSV encephalitis has a mortality of about 70 percent; with aciclovir it falls to about 20 percent, though roughly half of survivors report permanent sequelae at one year. A high pre-treatment death rate, a cheap effective drug, and a closing window — that combination is why every patient with suspected encephalitis gets empirical aciclovir until HSV PCR returns negative.[25][3]

[1]

Classification — two axes, one decision

CNS infections are read along two axes: the compartment (meninges versus parenchyma) and the bug (bacterial, viral, fungal, parasitic, non-infectious). The anatomical axis decides the syndrome you see at the bedside; the aetiological axis decides the drug you draw up.[1]

[1] [1]

Epidemiology and risk — who, and why now

Bacterial meningitis runs at roughly 1 to 5 per 100,000 per year in high-income countries and far higher where vaccination is incomplete. After conjugate Hib, PCV13, and meningococcal vaccines entered childhood schedules, the picture shifted: Hib meningitis nearly vanished in children, the median age of bacterial meningitis climbed, and S. pneumoniae became the dominant adult pathogen.[4][5]

Meningococcal disease peaks in adolescents and young adults (15 to 24 years) and across the meningococcal belt in the dry season (December to June). Viral meningitis is far commoner than bacterial and carries an excellent prognosis; viral encephalitis runs at roughly 5 to 10 per 100,000 per year, with HSV the most frequently identified cause in adults year-round. Autoimmune encephalitis, particularly anti-NMDA receptor, is increasingly recognised and in young people may exceed any single viral cause.[6][10]

[11] [25] [16]

The risk factors cluster into three groups that mirror the empirical antibiotic choice — host susceptibility (which decides whether you add ampicillin), anatomical breach (which points to the organism), and exposure (which sets the differential).[1]

[1]

Pathophysiology — why the brain swells, and why timing is everything

Bacteria reach the subarachnoid space by three routes, and the route predicts the organism. The dominant pathway is haematogenous spread — colonisation of the nasopharynx, invasion across the mucosa, bacteraemia, and crossing the blood-brain barrier at the choroid plexus or cerebral capillaries. The others are direct contiguous extension from sinusitis, otitis, mastoiditis, or a dental focus, and direct inoculation from skull fracture, neurosurgery, lumbar puncture, or a CSF shunt.[1][4]

Once in the subarachnoid space, bacteria multiply fast, because CSF carries low complement and immunoglobulin and has no effective cellular immune surveillance — a privileged niche that becomes their growth medium. The damage that follows is driven less by the bacteria than by the host inflammatory response.[1][4]

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 microglia. The cytokine cascade that follows — TNF-alpha, IL-1, IL-6, IL-8 — recruits neutrophils, opens the blood-brain barrier, and increases vascular permeability.[1]

The downstream end-organ damage (the reason patients herniate and stroke)

The cascade produces neutrophilic exudate in the subarachnoid space, cerebral oedema (vasogenic and cytotoxic), raised intracranial pressure, vasculitis of the penetrating vessels with cerebral infarction, communicating or obstructive hydrocephalus, and direct neuronal injury. Each of these is a reason a patient can die or be left permanently disabled — and each is the target of the dexamethasone you give up front.[1]

HSV-1 reaches the brain by a different and elegant route, and the neuroanatomy is itself the diagnosis. After primary orolabial infection, the virus sits latent in the trigeminal ganglion. Reactivation sends it by retrograde axonal transport along the trigeminal and olfactory nerves to their cortical terminations — the frontotemporal cortices and limbic structures.[3]

This neuroanatomy explains the temporal lobe. The striking temporal lobe predilection of HSV encephalitis, the haemorrhagic necrosis that is its pathology, and the bedside features — aphasia, behaviour change, complex partial seizures, memory disturbance — all flow from where the virus lands. Untreated, it destroys the temporal cortices bilaterally and is uniformly fatal; aciclovir halts viral DNA polymerase and rescues tissue.[3]

TB and cryptococcal meningitis run a subacute tempo because their pathogens replicate slowly and elicit a lymphocytic, low-grade, basilar inflammation. TB lodges in the basal meninges, forming a thick gelatinous exudate that encases cranial nerves, obstructs CSF at the basal cisterns (communicating hydrocephalus, cranial nerve palsies), and causes a vasculitis of the lenticulostriate and thalamoperforating vessels with basal ganglia infarcts.[1]

Cryptococcus crosses the choroid plexus inside its capsule and accumulates in the Virchow-Robin spaces as soap-bubble gelatinous pseudocysts, secreting capsular polysaccharide that impairs phagocytosis and producing a strikingly high CSF opening pressure. That high pressure is why cryptococcal meningitis needs serial therapeutic lumbar punctures, not just antifungals.[9]

Clinical presentation — the syndrome, then the exceptions

The one feature that separates meningitis from encephalitis is the level of consciousness. Meningitis preserves higher function until late; encephalitis disturbs it early. A patient with pure viral meningitis is uncomfortable but lucid; a patient with encephalitis is confused, obtunded, or comatose.[1][3]

Bacterial meningitis

The classic triad is often incomplete. In a contemporary review, headache was present in 84 percent, fever in 74 percent, stiff neck in 74 percent, nausea or vomiting in 62 percent, and altered mental status was common (median GCS 11) — so absence of one element never excludes the diagnosis.[11]

• Fever — present in most but not all cases; may be absent in the elderly, immunocompromised, or after self-administered antibiotics.
• Headache — the commonest individual symptom.
• Neck stiffness — resistance to passive flexion; meningism builds over hours. Kernig and Brudzinski signs may not be useful, with widely variable sensitivity and specificity.[19]
• 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.
• Focal deficits — cranial nerve palsies (III, IV, VI, VII, VIII), hemiparesis from vasculitic infarction.
• Rash — petechial or purpuric, non-blanching, in 50 to 75 percent of meningococcal cases; a sign that mandates immediate treatment. [1]

[1] [13] [11]

Encephalitis

Encephalitis is fever plus altered consciousness plus seizures plus focal deficit. The altered mental status is the cardinal feature distinguishing it from meningitis, and seizures are commoner than in meningitis. The focal signs reflect which bit of parenchyma is involved.[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 from the temporal lobe, and a Korsakoff-like memory disturbance in survivors.[3]

Anti-NMDA receptor encephalitis (commoner in young women, often with an ovarian teratoma) follows a sequence worth memorising: 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 needing prolonged ICU care.[10]

Atypical presentations — the ones examiners deliberately test

[1] [11]

Differential diagnosis — the mimics that kill

Fever plus headache plus altered mental status has a wide differential, and several mimics demand a specific, different treatment. The high-yield split is infectious CNS disease versus non-infectious causes.[1]

[1]

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

Bedside assessment — four aims in three minutes

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

Named meningeal signs such as Kernig and Brudzinski may not be useful for differentiating bacterial from aseptic meningitis, because their sensitivity and specificity are widely variable — their absence does not exclude meningitis.[19]

[1]

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

A full examination covers vital signs (fever, tachycardia, hypotension, tachypnoea, oxygenation, capillary refill — septic shock), GCS, pupils, fundoscopy for papilloedema (a red flag — do not LP), cranial nerves, motor and sensory exam, coordination, skin (rash, bite, chancre, erythema migrans, Janeway lesions), ears, nose, throat (otitis, mastoid and sinus tenderness, parotid), neck stiffness, chest (pneumonia, a murmur of endocarditis), abdomen (hepatosplenomegaly; the absent spleen), lymph nodes, joints, and signs of immunocompromise.[1][4]

In suspected meningococcal disease, repeat the skin examination every 15 minutes — the rash can evolve from a few petechiae to purpura fulminans within the hour.[1][4]

Investigations — LP is the test, but only when it is safe

Bedside and bloods

Bloods frame the organism and the severity. Take two sets of blood cultures before antibiotics if you can — but never at the cost of delaying therapy. Add FBC (leucocytosis in bacterial, lymphopenia in viral), CRP and procalcitonin (a high procalcitonin supports a bacterial cause and guides de-escalation), U and Es (hyponatraemia — SIADH or cerebral salt wasting), glucose alongside the CSF glucose (to calculate the ratio), LFTs, coagulation, arterial blood gas (lactate, acid-base), HIV serology, and a malaria film in the traveller.[1][3]

In viral syndromes, send throat and rectal swabs for enterovirus PCR. A chest X-ray hunts for pneumonia, TB, or a focus; echocardiography is added if endocarditis is suspected.[1][3]

Lumbar puncture — the key investigation, but only if safe

The LP is the cornerstone of diagnosis. Perform it at the L3-L4 or L4-L5 interspace (the adult cord ends at L1-L2; Tuffier's line through the iliac crests crosses L4). Position the patient lateral decubitus, knees to chest, fully flexed. Measure opening pressure with a manometer — normal is 8 to 20 cm CSF in adults; it is raised in bacterial, TB, and cryptococcal meningitis.[1][2]

Collect CSF into four numbered tubes: (1) cell count and differential, (2) glucose and protein, (3) Gram stain, culture and sensitivity, (4) cell count to compare with tube 1 (a 'traumatic tap') and reserve. A fifth tube goes for viral PCR (HSV-1 and -2, VZV, enterovirus) and, where indicated, TB PCR/GeneXpert, cryptococcal antigen, and autoimmune antibody panels.[1][2]

When to CT before LP — the red flags

A mass lesion with raised intracranial pressure can herniate when CSF is drained from below. CT comes before LP if any high-risk feature is present.[11][12]

[11] [12] [13]

The CSF face-off — the table that decides the bug

CSF parameters are among the most heavily examined facts in clinical medicine. Each pattern reflects the 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]

[11] [18] [19] [22] [23] [16]

The one discriminator examiners want: CSF lactate. In a meta-analysis of 25 studies, CSF lactate was the best single indicator distinguishing bacterial from aseptic meningitis, outperforming CSF glucose, the CSF-to-plasma glucose quotient, CSF protein and the leukocyte count. The bacterial pattern is granulocytic pleocytosis with protein over 2.2 g/L and glucose under 34 mg/dL (about 1.9 mmol/L).[18][11]

Imaging

CT brain (non-contrast) is performed before LP in patients with red flags, to exclude a mass lesion, hydrocephalus, or cerebral oedema; in bacterial meningitis it is often normal or shows only meningeal enhancement after contrast, and may reveal sinusitis, mastoiditis, or a focus.[1]

MRI brain with contrast is the modality of choice for encephalitis and subacute meningitis. HSV encephalitis shows T2 and FLAIR hyperintensity and restricted diffusion in the temporal lobes (often bilateral and asymmetric). TB meningitis shows basal meningeal enhancement, hydrocephalus, and basal ganglia infarcts; cryptococcosis shows gelatinous pseudocysts; autoimmune encephalitis often shows medial temporal lobe T2 hyperintensity (limbic encephalitis).[3][6]

The 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 — the one-hour bundle is the spine

Suspected bacterial meningitis is a time-critical emergency, and the first-hour bundle is the spine of management. The discipline is fixed: assess, take blood cultures, give empirical antibiotics and dexamethasone without delay, then perform LP if safe and image if needed. Treatment is never delayed for LP or imaging.[13][19]

[11] [13] [19]

The empirical bundle (adult, community-acquired)

The empirical regimen covers the three dominant adult pathogens — pneumococcus, meningococcus, Listeria. Third-generation cephalosporins are the backbone; vancomycin is added where ceftriaxone-resistant pneumococcus is a concern; ampicillin is added in neonates, older and immunocompromised patients to cover Listeria.[11][13]

[11] [13] [7] [16]

Adjunctive and supportive care

Resuscitation runs in parallel with the bundle. Protect the airway if consciousness is severely depressed, avoid hypoxia and hypotension (secondary brain injury), and resuscitate septic shock with isotonic crystalloid.[1]

[1]

Definitive therapy by organism — narrow and finish the course

Once the organism and sensitivities are known, narrow the antibiotic and follow guideline-directed total duration. Dexamethasone is stopped if Listeria is confirmed; the Cochrane meta-analysis found corticosteroids prevented hearing loss and neurological sequelae with the clearest benefit in high-income settings and reduced mortality in pneumococcal meningitis (RR 0.84), without significant overall mortality reduction.[11][14]

[1] [11] [14]

HSV encephalitis — the temporal lobe emergency

HSV encephalitis is treated with aciclovir 10 mg/kg every 8 hours for 10 to 21 days — the treatment of choice, started empirically in every patient with suspected encephalitis and continued until HSV PCR returns negative; foscarnet is the alternative when resistance is suspected.[16][25]

Never stop aciclovir on a single early negative PCR. PCR can be negative during the first 3 days of illness. With aciclovir, mortality falls from about 70 percent untreated to about 20 percent, though roughly half of survivors report permanent sequelae at one year.[16][25]

Why HSV PCR can be falsely negative early — and what to do

HSV-1 PCR is over 95 percent sensitive and specific, but it can be negative during the first 3 days of illness, so an early negative does not exclude HSV. Keep the aciclovir running and re-test if suspicion persists. Stopping on a single early negative is one of the classic, preventable errors on this topic.[16]

Tuberculous meningitis

TB meningitis is treated with standard antituberculous chemotherapy. Adjunctive dexamethasone improves survival — in the landmark Thwaites trial (NEJM 2004) in 545 Vietnamese patients over 14 years of age, adjunctive dexamethasone reduced the risk of death (RR 0.69), though it did not significantly reduce severe disability.[8]

Monitor for hepatotoxicity, optic neuritis (ethambutol), and peripheral neuropathy (isoniazid). Communicating hydrocephalus may need a shunt; thalidomide and infliximab are reserved for refractory cases.[8]

Cryptococcal meningitis

Cryptococcal meningitis induction uses fungicidal combination therapy — a polyene plus flucytosine. A randomised trial showed amphotericin B 1 mg/kg/day plus flucytosine 100 mg/kg/day for 2 weeks improved survival compared with amphotericin alone (HR for death by day 70 0.61) with faster CSF yeast clearance; consolidation and maintenance use fluconazole. The 2010 IDSA guideline frames management across three risk groups — HIV-infected, transplant recipients, and non-HIV non-transplant hosts.[15][9]

Early recognition and treatment of increased intracranial pressure is a key management principle in cryptococcal meningoencephalitis, alongside immune reconstitution inflammatory syndrome and drug resistance; lipid formulations of amphotericin B are used in patients with renal impairment.[9]

Autoimmune encephalitis

Anti-NMDA receptor encephalitis and its cousins are treated with immunotherapy. First-line therapy is corticosteroids, intravenous immunoglobulin or plasmapheresis; second-line therapy (rituximab or cyclophosphamide) is used when first-line fails; tumour removal is part of first-line management. In a 577-patient cohort study, 94 percent received first-line immunotherapy or tumour removal; most patients respond, second-line therapy is usually effective when first-line fails, relapse occurs in about 12 percent within 2 years, and recovery can continue for up to 18 months.[26]

A teratoma search is mandatory in young women with anti-NMDAR — tumour removal is part of first-line therapy. Recovery is slow (months), and prolonged ICU support for autonomic instability is often needed.[26]

Specific subtypes and scenarios

[11] [21] [17] [16] [26] [7]

Complications — how patients die (the preventable-harm list)

Most meningitis mortality and disability is preventable by getting the first hour right. The complications cluster into acute neurological, systemic, and long-term sequelae — and each has a preventable cause attached.[1]

[1] [11] [14]

The preventable-harm list — every item is an avoidable error that examiners (and coroners) test:[1]

• Delaying antibiotics for LP or CT — the single biggest error.
• Missing Listeria by omitting ampicillin in the over-50, pregnant, or immunocompromised patient.
• Giving dexamethasone after the antibiotic — no benefit once the cascade is firing.
• Performing LP with papilloedema or a mass lesion present — herniation.
• Stopping aciclovir on a single early negative HSV PCR — HSV missed, brain lost.
• Fluid-restricting hyponatraemia that is cerebral salt wasting — cerebral infarction.
• Forgetting chemoprophylaxis for meningococcal contacts — a second case.[1][3]

Prognosis and disposition

Bacterial meningitis carries substantial mortality — up to 54 percent in low-income settings — rising with age, immunocompromise, septicaemic shock, altered mental status, delayed antibiotics, and pneumococcal aetiology. Among survivors, up to 24 percent develop chronic neurological sequelae, most often hearing loss or focal neurological deficits.[11][20]

HSV encephalitis, even with aciclovir, has a mortality of about 20 percent, and roughly half of survivors report permanent sequelae at one year. Anti-NMDA receptor encephalitis has a good prognosis with early immunotherapy and tumour removal, and recovery can continue for up to 18 months; relapse occurs in about 12 percent within 2 years.[25][26]

[1]

Special populations — the doses change, and so does the bug

[1] [11] [17]

What examiners expect in special groups. Neonates: ampicillin is part of empirical cover (group B strep and E. coli cause about 35 percent of early-onset neonatal meningitis, plus Listeria) alongside a third-generation cephalosporin. Adults with Listeria risk factors: an anti-Listeria agent such as ampicillin or benzylpenicillin is added to the empirical regimen.[11][13]

HSV encephalitis: aciclovir 10 mg/kg every 8 hours for 10 to 21 days, continuing until PCR is negative or the full course is done. Cryptococcal meningitis in HIV: induction with amphotericin B plus flucytosine, then fluconazole consolidation, with early recognition and treatment of raised intracranial pressure. Contact prophylaxis after meningococcal disease: rifampicin, ciprofloxacin or ceftriaxone — household contacts carry the highest risk in the first week.[16][15][9][17]

Evidence, guidelines, and regional differences

The contemporary evidence base for bacterial meningitis rests on two landmark trials of adjunctive dexamethasone. The European Dexamethasone in Adulthood Bacterial Meningitis Study (de Gans and van de Beek, NEJM 2002) randomised 301 adults with acute bacterial meningitis to dexamethasone 10 mg (given 15 to 20 minutes before or with the first dose of antibiotic, then every 6 hours for four days) or placebo.[7]

Dexamethasone reduced the risk of an unfavourable outcome (RR 0.59, P=0.03) and of death (RR 0.48, P=0.04); in pneumococcal meningitis, unfavourable outcomes occurred in 26 percent of the dexamethasone group versus 52 percent of the placebo group. Later Cochrane meta-analysis confirmed prevention of hearing loss and neurological sequelae. The Thwaites trial (NEJM 2004) showed adjunctive dexamethasone improved survival in tuberculous meningitis (RR of death 0.69).[7][14][8]

[7] [8] [1] [3] [9] [10] [13] [3] [13] [11] [13] [11]

Prevention — vaccines and chemoprophylaxis

Prevention of bacterial meningitis rests on vaccination and chemoprophylaxis, and the conjugate vaccines have redrawn the epidemiology wherever they are routine.[1]

[1] [17]

Exam pearls and high-yield minutiae

[11] [16]

• Classic triad is often incomplete — headache 84 percent, fever 74 percent, stiff neck 74 percent in a contemporary review.
• Meningococcal rash — petechial or purpuric, non-blanching; check conjunctiva and palate; can evolve hourly.
• CSF bacterial: granulocytic pleocytosis; suspect bacterial if CSF granulocytes over 1,180 per microlitre, protein over 2.2 g/L or glucose under 34 mg/dL.
• CSF viral: lymphocytes, normal glucose, mildly raised protein.
• CSF TB: lymphocytes, low glucose, increased protein; ADA 84 percent sensitive, 95 percent specific against PCR.
• CSF HSV: lymphocytes, often with red cells; PCR over 95 percent sensitive and specific but can be negative in the first 3 days.
• Dexamethasone 10 mg every 6 hours for 4 days, before or with the first antibiotic.
• Aciclovir 10 mg/kg every 8 hours for 10 to 21 days for HSV encephalitis — do NOT wait for PCR.
• Vancomycin added where ceftriaxone-resistant pneumococcus exceeds 1 percent; ampicillin added in neonates, older and immunocompromised patients for Listeria.
• Kernig and Brudzinski signs may not be useful — widely variable sensitivity and specificity.
• CT before LP if altered mental status, new focal deficit, new seizures, papilloedema, or immunocompromised state.
• Prophylaxis — rifampicin, ciprofloxacin or ceftriaxone eradicate meningococcal carriage in close 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 and E. coli cause about 35 percent of early-onset meningitis, plus Listeria; ampicillin is part of empirical cover.
• Sequelae — up to 24 percent of survivors have chronic neurological sequelae such as hearing loss; corticosteroids reduce hearing loss. [11][18][22][16][19][17][14][7]

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

This is meningococcal meningitis or septicaemia until proven otherwise. Immediate management: airway, breathing, circulation; ceftriaxone IV immediately (do not wait for LP); blood cultures; fluid resuscitation for shock; ICU if shocked; notify public health; chemoprophylaxis for household and close contacts (rifampicin, ciprofloxacin or ceftriaxone — household contacts carry the highest risk in the first week). LP is performed once stable, with imaging first if any red flag.

[11] [21] [17]

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

Consider HSV encephalitis and Listeria meningitis. Give empirical ceftriaxone plus vancomycin plus ampicillin (Listeria cover in the older patient) plus dexamethasone 10 mg plus aciclovir 10 mg/kg every 8 hours. Imaging before LP (new seizure and focal deficit are high-risk features), but treatment is not delayed for imaging. LP after imaging: send for cells, glucose, protein, Gram stain, culture, HSV PCR, and bacterial PCR or antigen. MRI the temporal lobes. Continue aciclovir until HSV PCR is negative; narrow antibiotics once the organism is identified.

[11] [12] [16] [7]

Ward-round test — four stems, thirty seconds each

Stem 1 — the petechial rash at 4am (answer)

The 19-year-old from the top of the topic: fever, headache, neck stiffness, confusion, petechiae on palate and conjunctiva that do not blanch. Diagnosis and first actions? Model: Meningococcal meningitis with septicaemia until proven otherwise. ABCDE; ceftriaxone IV immediately with dexamethasone; blood cultures first but never delay therapy; aggressive isotonic fluid resuscitation and ICU if shocked; notify public health; chemoprophylaxis for household and close contacts (rifampicin, ciprofloxacin or ceftriaxone); LP and imaging only once stable and safe.[11][21][17]

Stem 2 — the confused febrile elder (answer)

A 68-year-old with fever, confusion and a focal seizure arrives in the ED. The registrar wants to do an LP first. Your move? Model: New seizure and focal deficit are high-risk features — imaging before LP, but antibiotics and dexamethasone come first, without delay. Give ceftriaxone plus vancomycin plus ampicillin (age over 50, Listeria cover) plus dexamethasone 10 mg plus aciclovir 10 mg/kg every 8 hours (seizures and confusion raise HSV). Imaging, then LP for cells, glucose, protein, Gram stain, HSV PCR. The classic trap here is delaying antibiotics for the LP.[11][12][13][7][16]

Stem 3 — the early negative HSV PCR (answer)

A 30-year-old with fever, confusion and temporal lobe seizures is started on aciclovir. The first CSF HSV PCR at 12 hours is negative. The team plans to stop the aciclovir. Right call? Model: No. HSV PCR is over 95 percent sensitive and specific but can be negative during the first 3 days of illness. Continue aciclovir 10 mg/kg every 8 hours and re-test if suspicion persists. Stopping on a single early negative is one of the classic preventable errors — untreated HSV mortality is about 70 percent.[16][25]

Stem 4 — the hyponatraemic trap (answer)

A patient with pneumococcal meningitis has a sodium of 124 mmol/L on day 2. The nurse plans to fluid restrict for SIADH. What do you say? Model: Stop. Hyponatraemia in meningitis has several mechanisms — in a tuberculous meningitis cohort cerebral salt wasting was the commonest (36 of 79 patients versus 4 with SIADH). CSW and SIADH are managed differently, so reassess volume status before fluid-restricting. The classic trap is applying the SIADH reflex to a salt-wasting brain.[24]

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 plus vancomycin where ceftriaxone-resistant pneumococcus is prevalent, ampicillin added for neonates, older and immunocompromised patients, and dexamethasone 10 mg before or with the first antibiotic) must start without delay, 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 every 8 hours for 10 to 21 days, without waiting for PCR. CSF analysis (cell count, glucose, protein, Gram stain, culture, PCR) distinguishes bacterial, viral, tuberculous and fungal causes. [11][13][7][16]

Worked stems (answer without another resource)

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

Stem 2 — Unstable or 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, or theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition and classification
2. Pathophysiology chain
3. Bedside signs and 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 or 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 and 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, et al. Acute bacterial meningitis in adults Lancet, 2016.PMID 27265346
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