Viral meningitis

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

Viral meningitis is inflammation of meninges without predominant brain-parenchymal dysfunction. Enteroviruses dominate many community cases, while HSV-2 and VZV are important adult causes; acute HIV, mumps, lymphocytic choriomeningitis and arboviruses arise from specific exposures. Immunosuppression broadens the differential and can blunt CSF inflammation.

CSF leukocytes are often lymphocytic after an early neutrophilic phase, glucose is usually preserved and protein modestly raised. These patterns overlap bacterial and chronic infection, so safe de-escalation requires physiology, examination, CSF, blood results and treatment history together. Encephalopathy or focal signs reclassifies the emergency toward encephalitis.

Key points

Viral meningitis usually causes fever, headache, neck stiffness, photophobia and nausea while cognition remains relatively preserved.
Enteroviruses are common; HSV-2, varicella zoster, acute HIV, mumps and other viruses are selected by lesions, vaccination, season, exposure and immune status.
Perform lumbar puncture promptly when safe, sending cells, paired glucose, protein, bacterial studies and exposure-directed viral PCR.
Lymphocytic pleocytosis with preserved glucose supports viral meningitis but does not exclude early bacterial, TB, fungal or partially treated infection.
Treat bacterial meningitis empirically until clinical and microbiological evidence supports stopping; stewardship is an active reassessment, not a timetable.
Give intravenous aciclovir for suspected HSV or VZV encephalitis and for severe or high-risk HSV or VZV meningeal disease under specialist guidance.
An isolated positive PCR can represent persistence or contamination; integrate viral target, quantity if available, timing, host and CSF inflammation.
Provide hydration, antiemesis, simple analgesia and return advice, and investigate recurrent aseptic meningitis or persistent neurological symptoms.

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

Enterovirus infection

Coxsackie and echoviruses spread faecal-orally or through respiratory secretions and commonly cause seasonal community aseptic meningitis.

Herpesvirus and exposure causes

HSV-2, VZV, acute HIV, mumps and travel-related viruses arise according to sexual, rash, immune, vaccine and vector context.

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

1
Haematogenous meningeal seeding
Systemic viral replication crosses choroid plexus or vascular barriers and recruits lymphocytes into CSF and leptomeninges.
2
Sensory-ganglion reactivation
HSV and VZV reactivate from latency, travel along nerves and inflame meninges, roots or cerebral vessels.
3
Cytokine headache and pressure
Meningeal inflammation sensitises pain fibres and may raise pressure without the destructive purulence typical of bacterial disease.

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

Uncomplicated meningeal syndrome

Headache, photophobia, neck stiffness and fever with alert cognition and stable physiology supports meningitis without proving a viral cause.

HSV-2 meningitisRed flag

Genital lesions, sacral symptoms or recurrent episodes can accompany HSV-2 lymphocytic meningitis, but lesions may be absent.

VZV meningitisRed flag

Dermatomal rash, cranial neuropathy or vasculitic features raises VZV, while zoster sine herpete can occur.

Encephalitic conversionRed flag

Confusion, personality change, focal seizure or deficit signifies parenchymal involvement and requires urgent aciclovir and MRI or EEG.

Red flags requiring action

Altered behaviour, focal seizure or focal deficit suggests encephalitis rather than isolated meningitis and needs intravenous aciclovir.
Purpura, shock, high lactate or neutrophilic low-glucose CSF requires bacterial treatment despite a plausible viral exposure.
Low CSF glucose, cranial neuropathy or a subacute course raises TB, cryptococcus, malignancy and other chronic meningitis.
Pregnancy, transplantation, advanced HIV or antibody deficiency changes viral spectrum, persistence and treatment threshold.

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
Lumbar puncture with broad CSF panelFirst step
Why
Separate bacterial, viral and chronic meningeal patterns and identify a viral target.
Interpretation and limitations
Send opening pressure, cells, glucose, protein, culture and bacterial PCR plus targeted viral PCR; early timing and prior treatment alter patterns.
02
Blood cultures and paired glucose
Why
Preserve bacterial evidence and interpret CSF glucose accurately.
Interpretation and limitations
Take before antibiotics when safe. A low CSF-to-blood glucose ratio is atypical for simple enterovirus and reopens bacterial, TB and fungal causes.
03
Targeted viral PCR
Why
Confirm enterovirus, HSV, VZV or another selected pathogen.
Interpretation and limitations
A positive result supports causality when host, syndrome and CSF inflammation align; negative early HSV testing may require repeat if encephalitis probability remains high.
04
HIV and exposure testing
Why
Identify acute HIV and immune states that change the viral and chronic differential.
Interpretation and limitations
Use fourth-generation plus RNA when acute seroconversion is plausible and assess travel, vector, animal and vaccination history for targeted testing.

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

Bacterial meningitis

Shock, purpura, neutrophilic low-glucose CSF or rapid decline requires immediate ceftriaxone until bacterial disease is confidently excluded.

Tuberculous or fungal meningitis

Subacute headache, low glucose, high opening pressure, cranial neuropathy or immune suppression requires targeted chronic-infection testing.

Autoimmune and drug aseptic meningitis

SLE, vasculitis, malignancy and medicines such as NSAIDs or immunoglobulin can produce sterile lymphocytic meningeal inflammation.

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

01ASSESSExclude dangerous mimicsFirst stepA patient presents with a possible aseptic meningitis syndrome.

1Stabilise physiology and examine cognition, focal neurology, skin, eyes and immune status before attributing symptoms to a benign virus.
2Take blood cultures and perform lumbar puncture promptly when safe; start bacterial treatment whenever danger or CSF uncertainty persists.
3Add aciclovir immediately for encephalitic features and request MRI, EEG and repeat HSV testing according to timing.
4Investigate low glucose, cranial neuropathy, prolonged course or high opening pressure for TB, cryptococcus, malignancy and inflammatory causes.

02TREATUse antivirals selectivelyHSV, VZV or encephalitic disease remains plausible after initial assessment.

1Use supportive fluids, antiemetics and analgesia while avoiding NSAIDs when renal, bleeding or pregnancy risk is material.
2Continue renal-adjusted intravenous aciclovir for HSV or VZV disease when neurological, immune or severity factors justify treatment.
3Do not use aciclovir for proven enterovirus meningitis; explain expected symptom course and infection-control measures.
4Involve HIV, infection or neurology teams for immune suppression, recurrent meningitis, vasculopathy or persistent deficit.

03REVIEWDe-escalate and follow recoveryEscalationBacterial cultures and PCR are negative and the clinical course supports viral disease.

1Stop empirical ceftriaxone only after blood, CSF, prior antibiotics and clinical trajectory make bacterial meningitis sufficiently unlikely.
2Reassess headache, hydration, cognition and focal findings before discharge and provide explicit return advice for deterioration.
3Review viral PCR in context and avoid declaring colonising or persistent nucleic acid the cause without concordant inflammation.
4Arrange follow-up for prolonged fatigue, recurrent episodes, hearing concerns or neurological deficit and notify relevant infections when required.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Relieves headache, fever and myalgia while the self-limiting infection resolves.

Supportive analgesia

Give paracetamol 500 mg to 1 g orally up to four times daily, at least 4 hours apart, maximum 4 g daily in a suitable adult.

Reduce maximum for low weight, liver disease, malnutrition or heavy alcohol use and avoid duplicate combination products.

Treats replicating HSV and VZV while PCR and neurological assessment proceed.

Intravenous aciclovir for severe HSV or VZV disease

Give aciclovir 10 mg/kg intravenously every 8 hours using protocol weight and renal adjustment when encephalitis or severe high-risk disease is suspected.

Hydrate, monitor creatinine and neurological toxicity and never delay treatment for MRI or lumbar puncture when encephalitis is credible.

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

Encephalitis and seizure

Parenchymal viral spread causes altered cognition, focal injury and epilepsy requiring longer antiviral and neurological care.

VZV vasculopathy

Viral arterial inflammation causes transient cerebral ischaemia or stroke, sometimes occurring without a current vesicular rash.

Persistent and recurrent symptoms

Headache, fatigue and HSV-associated recurrent lymphocytic meningitis can impair daily function long after the acute infection resolves.

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

Repeat cognition, focal neurology, headache severity, temperature and cardiorespiratory observations until dangerous progression is excluded.
Review CSF bacterial and viral PCR, culture and paired glucose with timing, immune status and prior treatment before stopping antibiotics.
Monitor renal function and fluid balance during aciclovir and investigate new myoclonus or confusion for drug accumulation as well as disease.
Provide follow-up for recurrent meningitis, persistent fatigue, hearing concern, cognitive symptoms or a newly identified immune disorder.

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

Lymphocytes are not a verdict

Early bacterial infection and partially treated disease can become lymphocytic, while enterovirus can initially be neutrophilic.

Positive PCR needs a host

Detection is strongest when the target, CSF inflammation and syndrome agree; nucleic acid alone does not replace clinical attribution.

Alertness separates syndromes imperfectly

Preserved cognition supports meningitis, but subtle behavioural or focal seizure changes should trigger encephalitis treatment.

Stopping antibiotics is a decision

De-escalation requires documented negative evidence and clinical improvement rather than an automatic number of hours.

11Common pitfallsFrequent interpretation and management errors.

01
Calling lymphocytic CSF viral without checking glucose, timing, immune status and prior antibiotics.
02
Withholding aciclovir from a patient with personality change or focal seizure because meningism is also present.
03
Continuing broad antibiotics after convincing viral confirmation without a documented bacterial reassessment.
04
Discharging persistent severe headache or new neurology without repeat examination and safety-netting.