Viral meningitis

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Viral meningitis is inflammation confined predominantly to the meninges, in contrast to encephalitis where brain dysfunction is central. In practice the boundary can blur, and the initial priority is not to miss bacterial infection. Headache, photophobia and meningism with alert, coherent cognition favour meningitis; confusion beyond that expected from fever or pain, focal deficit and seizures suggest parenchymal involvement. Immunosuppressed, very young, pregnant and older patients may have atypical or more severe disease and warrant a lower threshold for senior infection and neurological review.

The label aseptic meningitis describes cerebrospinal-fluid inflammation without routine bacterial growth and is not synonymous with benign viral disease. Tuberculosis, fungi, spirochaetes, partially treated bacteria, medicines, malignancy and inflammatory disease can produce similar fluid. Exposure history should cover sick contacts, sexual risk and acute HIV symptoms, shingles or genital herpes, vaccination, travel, mosquitoes or ticks, rodent exposure, immunosuppression and medicines associated with drug-induced meningitis.

Management becomes narrower only after sufficient evidence. A clinically stable person with supportive cerebrospinal-fluid findings and a recognised virus may not need antibiotics once bacterial disease is excluded with microbiology input. Discharge requires adequate oral intake, controlled symptoms, reliable review and explicit instructions to return for confusion, seizure, weakness, rash, persistent vomiting or worsening headache. Exact antiviral decisions, isolation and follow-up depend on the organism, host and local microbiology policy.

Key points

Viral meningitis presents with fever, headache, photophobia, neck stiffness, nausea and malaise, usually with preserved or only mildly altered cognition; substantial encephalopathy suggests encephalitis or severe systemic disease.
Enteroviruses are frequent causes, while herpes simplex virus type 2, varicella-zoster virus, acute HIV, mumps and travel-related arboviruses become relevant in the right exposure context.
Clinical appearance and cerebrospinal-fluid lymphocytes do not immediately exclude bacterial meningitis, because early viral infection may be neutrophilic and partially treated bacterial disease may become lymphocytic.
Take blood cultures and give empirical antibacterial treatment first when indicated; lumbar puncture should follow promptly when it is safe and does not create treatment delay.
Typical cerebrospinal fluid has a lymphocytic pleocytosis, normal glucose ratio and moderately raised protein, but interpretation must integrate timing, immune status and prior antimicrobials.
Request targeted cerebrospinal-fluid PCR according to the syndrome and season rather than an indiscriminate panel whose low-prevalence positives may mislead.
Marked confusion, personality change, aphasia, focal seizures or temporal-lobe abnormalities should trigger an encephalitis pathway and immediate intravenous aciclovir, not reassurance about viral meningitis.
Antiviral treatment is not routine for uncomplicated enteroviral meningitis; HSV, VZV or immunocompromised disease requires infection-specialist advice on intravenous or oral therapy.
Most immunocompetent adults recover with fluids, antiemetics, analgesia and graded activity, although headache, fatigue, poor concentration and sleep disturbance can persist for weeks.
Explain hand hygiene and pathogen-specific precautions and offer HIV testing when appropriate. In England, every suspected acute meningitis case is notifiable urgently by telephone within 24 hours and online within 3 days; report on suspicion rather than waiting to identify a pathogen, using equivalent devolved-nation routes elsewhere.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Enterovirus infection

Enteroviruses are frequent causes and commonly spread through faecal–oral or respiratory routes, with seasonal and outbreak variation.

Herpes-family viruses

HSV type two and VZV can cause meningitis, sometimes with genital lesions, radicular symptoms or rash but occasionally without visible skin disease.

Acute HIV and other viruses

Primary HIV, mumps and selected respiratory viruses become relevant according to vaccination, exposure and systemic phenotype.

Travel and immune-status pathogens

Arboviruses and unusual viral infections require geographical, vector and immunosuppression history and may cause meningoencephalitis rather than isolated meningitis.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Viral entry
Virus reaches the meninges through bloodstream, neural spread or local reactivation after systemic or mucocutaneous infection.
2
Meningeal immune response
Lymphocytes and cytokines inflame pia and arachnoid, activating pain-sensitive structures and producing headache, photophobia and neck stiffness.
3
Cerebrospinal-fluid disturbance
Inflammation raises protein and cells and can modestly alter pressure while usually preserving glucose in uncomplicated disease.
4
Resolution
Immune clearance commonly restores meningeal function, though inflammatory symptoms and fatigue can persist after active replication falls.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Meningitic syndrome

Fever, diffuse headache, photophobia and painful neck flexion occur while orientation and coherent behaviour are largely preserved between painful episodes.

Enteroviral context

Summer or autumn illness, household or childcare exposure, sore throat, gastrointestinal symptoms or a hand-foot-and-mouth eruption can accompany enterovirus infection.

Herpes-associated clues

Recent genital lesions, sacral radicular pain, urinary retention or recurrent lymphocytic meningitis can suggest HSV-2; a dermatomal rash raises VZV.

Acute HIV possibility

Fever, rash, lymphadenopathy, pharyngitis, diarrhoea and recent sexual or blood exposure alongside aseptic meningitis should prompt an appropriate antigen-antibody and RNA pathway.

Encephalitic transitionRed flag

Sustained altered behaviour, new focal deficit, dysphasia or seizure signifies brain involvement and requires urgent aciclovir and encephalitis investigation.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Blood cultures and acute blood profileFirst step
Why
Preserve evidence of bacterial disease and identify organ dysfunction before treatment.
Interpretation and limitations
Take cultures, blood count, CRP, renal, liver, glucose and clotting tests promptly; normal early values do not certify a viral cause.
02
Lumbar puncture with paired glucose
Why
Characterise meningeal inflammation and obtain microbiological samples.
Interpretation and limitations
Lymphocytes, moderately raised protein and preserved glucose support viral disease, but early enterovirus can be neutrophilic and partially treated bacteria can resemble this pattern.
03
Cerebrospinal-fluid PCR
Why
Identify enterovirus, HSV, VZV or another pathogen selected from the clinical context.
Interpretation and limitations
Timing and assay performance matter; discuss unexpected positives, negatives after antivirals and broader testing with microbiology or virology.
04
HIV antigen-antibody test and viral load
Why
Detect acute or established HIV when exposure or an unexplained aseptic syndrome makes it relevant.
Interpretation and limitations
Very early infection can precede a reactive routine test, so specialist advice and HIV RNA testing may be needed with informed consent and a follow-up plan.
05
MRI brain and electroencephalography
Why
Investigate suspected encephalitis, focal signs, seizures or persistent altered cognition.
Interpretation and limitations
These are not routine in uncomplicated meningitis; temporal abnormalities, focal swelling or epileptiform activity redirect care to parenchymal disease.
06
Targeted second-line microbiology
Why
Evaluate tuberculosis, fungi, spirochaetes or travel-associated infections in a non-resolving or high-risk case.
Interpretation and limitations
Select tests with infection specialists because sample volume, prolonged culture, serology timing and pre-test probability determine value.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Bacterial meningitis

Neutrophils, low glucose, shock and rapid severe illness favour bacteria, but early viral and partially treated bacterial patterns overlap substantially.

Encephalitis

Marked confusion, personality change, aphasia, focal seizure or temporal imaging indicates brain involvement requiring immediate antiviral assessment.

Subarachnoid haemorrhage

Thunderclap onset, collapse and subarachnoid blood on imaging support haemorrhage, although meningism can develop in either condition.

Drug or autoimmune meningitis

Recent medicine exposure, systemic autoimmunity and recurrent sterile inflammation may mimic viral disease after infection is investigated.

Additional chapter-specific clues

Non-viral mimic

Prolonged course, low cerebrospinal-fluid glucose, cranial neuropathies, weight loss or marked immunosuppression should broaden assessment to tuberculosis, fungal disease, malignancy or inflammation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Acute presentationTreat uncertainty as potentially bacterialFirst stepA patient presents with fever, headache and meningism.

1Assess ABCDE, consciousness, rash, focal neurology and seizures, taking blood cultures and urgent blood samples while initiating sepsis support where required.
2Give empirical antibacterial treatment and dexamethasone according to the bacterial-meningitis pathway whenever that diagnosis remains plausible; do not wait for a viral PCR.
3Perform lumbar puncture promptly if safe, sending cells, paired glucose, protein, culture and syndrome-directed PCR with enough retained sample for additional tests.
4At first clinical suspicion, report acute meningitis through the statutory health-protection route without waiting for cerebrospinal-fluid PCR, culture or serology.

02Viral evidenceNarrow treatment after reviewThe patient is stable and cerebrospinal fluid or PCR supports a viral cause.

1Reconcile the fluid pattern, blood cultures, illness trajectory and pretreatment with microbiology before concluding bacterial infection is sufficiently excluded.
2Stop antibacterial therapy only through senior clinical and microbiology review, and decide whether HSV, VZV, HIV or host immunosuppression creates a targeted antiviral indication.
3Provide oral hydration, antiemetic and simple analgesic support, avoiding unnecessary opioids and repeated lumbar puncture for a resolving uncomplicated illness.

03Brain involvementConvert immediately to an encephalitis pathwayConfusion, focal deficit, behavioural change or seizure persists beyond a simple meningitic illness.

1Start intravenous aciclovir without awaiting PCR, adjust for renal function and ensure active hydration and renal monitoring.
2Arrange MRI and electroencephalography, repeat neurological examination and seek neurology, infection and critical-care input according to severity.
3Reconsider autoimmune encephalitis, abscess, tuberculosis and vascular or toxic causes if standard viral studies do not explain the syndrome.

04RecoveryDischarge with meaningful safety nettingDangerous bacterial and encephalitic causes have been excluded and symptoms are controlled.

1Confirm stable observations, normal or improving cognition, adequate oral intake, manageable pain and a reliable contact route for pending microbiology results.
2Explain that fatigue and concentration difficulty may outlast fever, advise graded return to work or driving, and avoid promising recovery by an exact date.
3Arrange review for persistent neurological or cognitive symptoms and advise immediate return for worsening headache, vomiting, rash, drowsiness, weakness or seizure.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Controls fever and headache as supportive treatment after emergency causes and hydration have been addressed.

Paracetamol

Use the current BNF adult oral regimen, reducing the maximum in low body weight, liver disease or other circumstances that increase toxicity risk.

Check cold remedies and combination analgesics to prevent duplicate dosing; symptom improvement does not exclude bacterial disease or encephalitis.

Provides time-critical antiviral therapy for suspected herpetic brain infection and selected severe herpes meningitis presentations.

Intravenous aciclovir

When HSV or VZV encephalitis is possible, use the current BNF weight-based intravenous regimen, commonly 10 mg/kg every 8 hours, with renal adjustment and specialist oversight.

Ensure hydration, infuse correctly and monitor creatinine because crystal nephropathy and neurotoxicity can occur; uncomplicated enterovirus meningitis does not benefit.

Supports oral hydration and reduces vomiting during a self-limiting meningitic illness.

Antiemetic selected locally

Choose an oral or parenteral agent and adult dose from the current BNF according to vomiting severity, cardiac risk and interacting medicines.

Review QT prolongation, dystonia, sedation and pregnancy, and reassess raised intracranial pressure or deterioration rather than repeatedly suppressing unexplained vomiting.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Encephalitic progression

Some viral infections extend into brain tissue, causing seizures, focal deficits, reduced consciousness and permanent cognitive injury.

Persistent headache and fatigue

Concentration, sleep, headache and exercise tolerance may remain impaired for several weeks despite otherwise uncomplicated virological recovery.

Encephalitic involvement

New confusion, focal deficit or seizure suggests parenchymal involvement or an alternative infection and changes the diagnosis, treatment and monitoring needs.

Transmission and public-health impact

Enteroviral, mumps, HIV and travel-related diagnoses may require contact assessment, hygiene advice, testing, notification or outbreak measures.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Repeat mental-state and neurological observations because emergence of encephalopathy, seizure or focal findings changes diagnosis and treatment immediately.
Monitor temperature, perfusion, oral intake, vomiting and urine output, giving intravenous fluids when dehydration prevents safe oral management.
Track renal function daily during intravenous aciclovir and more often if kidney injury, older age or nephrotoxic co-medication increases risk.
Review pending blood and cerebrospinal-fluid cultures and PCR results through an accountable system after discharge, contacting the patient when management changes.
Assess headache, fatigue, sleep, cognition and return to study, work or caring at follow-up rather than assuming virological recovery equals functional recovery.
Escalate persistent fever, falling sodium, new rash or neurological deterioration for renewed investigation of bacterial, inflammatory or opportunistic disease.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Aseptic is not benign

The laboratory description includes tuberculosis, drug reactions and malignancy as well as viruses, so it should open a differential rather than close it.

Early cells can mislead

Enterovirus may initially produce cerebrospinal-fluid neutrophils, while pretreated bacteria may produce lymphocytes; timing is integral to interpretation.

Cognition marks the boundary

Drowsiness from pain is possible, but sustained disorientation, behavioural change or language dysfunction points toward encephalitis and demands treatment.

PCR needs context

A multiplex result has different meaning in an immunocompetent improving adult and an immunosuppressed deteriorating patient; microbiology review prevents both neglect and overtreatment.

Recovery often lags

Post-infectious fatigue, headache and cognitive slowing can remain after uncomplicated viral meningitis, warranting validation and graded rehabilitation.

11Common pitfallsFrequent interpretation and management errors.

01
Calling the illness viral before lumbar-puncture and microbiology evidence.
02
Withholding empirical antibiotics because the patient has no rash.
03
Assuming lymphocytic cerebrospinal fluid excludes partially treated bacteria.
04
Missing acute HIV or VZV when exposure clues are present.
05
Treating encephalopathy as an expected feature of simple meningitis.
06
Giving aciclovir without hydration, renal adjustment or creatinine monitoring.
07
Discharging without ownership of pending culture and PCR results.