How is encephalitis different from meningitis?

Meningitis primarily causes meningism — severe headache, neck stiffness, photophobia, and fever — with relatively preserved consciousness in the early phase. Encephalitis causes altered mental state (confusion, agitation, behavioural change, drowsiness) and focal neurological signs such as seizures, weakness, or speech disturbance as the dominant features; meningeal signs may also be present in meningoencephalitis. Any adult with unexplained altered consciousness, new seizure, or sudden personality change warrants urgent hospital transfer. Start empirical IV aciclovir alongside ceftriaxone before lumbar puncture results return — treatment delay is the primary determinant of neurological outcome.

What is anti-NMDA receptor encephalitis and who is most affected?

Anti-NMDA receptor encephalitis is the most commonly identified autoimmune encephalitis. Autoantibodies against the NR1 subunit of the NMDA receptor produce a characteristic four-phase illness: a viral-like prodrome, followed by psychiatric symptoms (psychosis, hallucinations, agitation, catatonia), then a movement disorder phase (orofacial dyskinesias, choreoathetoid movements), and finally autonomic instability and coma. About half of affected women have an ovarian teratoma driving antibody production — tumour removal markedly improves outcome. First-line treatment is methylprednisolone plus IVIG or plasma exchange; rituximab is used for refractory disease. Both blood and CSF antibody testing are needed for diagnosis.

Why is Japanese encephalitis now relevant in Australia?

Japanese encephalitis virus (JEV) emerged in south-eastern and inland Australia in 2022 and was declared a National Significant Communicable Disease Incident. Flooding events extended the Culex mosquito vector into New South Wales, Victoria, South Australia, Queensland, and the Northern Territory. Most infections cause mild febrile illness, but roughly 1 in 200 infected individuals develops severe encephalitis with up to 30% mortality and high rates of lasting neurological deficit. An NIP-funded JEV vaccine (Imojev or IXIARO) is available for people at elevated risk in affected areas. Notification to the state public health unit is mandatory.

How long does recovery from encephalitis take?

Recovery is measured in months to years, not weeks. Around 40% of survivors have lasting cognitive difficulties — impaired memory, attention, and processing speed — or behavioural changes including irritability, impulsivity, or depression. Anti-NMDA receptor encephalitis treated promptly with immunotherapy and tumour removal has better long-term outcomes, with approximately 80% achieving good functional recovery over 12 to 24 months. HSV encephalitis treated early carries approximately 20 to 30% mortality; survivors commonly need multidisciplinary rehabilitation including physiotherapy, occupational therapy, speech pathology, and neuropsychology. NDIS support may be available for Australians under 65 with persistent disability.

What should I do if I suspect encephalitis in my consulting room?

Call 000 immediately and state 'possible encephalitis' to activate a Category 1 paramedic response. While awaiting transfer, establish IV access, check blood glucose, and begin empirical IV aciclovir 10 mg/kg if available in a procedural setting — the interval between HSV encephalitis onset and starting aciclovir is the strongest predictor of neurological outcome. Do not delay transfer for lumbar puncture, CT, or bloodwork. Pre-notify the receiving emergency department so the team prepares. If bacterial meningitis cannot be excluded, add ceftriaxone 2 g IV empirically. Oral medication has no role in the acute phase.

Encephalitis (viral, autoimmune, paraneoplastic)

Encephalitis: start IV aciclovir immediately, then transfer

By Dr HB Lo, FACRRM Reviewed 16 September 2026 9 min read

Encephalitis is brain tissue inflammation producing altered consciousness, seizures, and focal neurological deficits. Untreated herpes simplex encephalitis carries ~70% mortality; empirical IV aciclovir reduces this to ~20%. Start IV aciclovir immediately and transfer as a Category 1 emergency — do not wait for investigation results. Australian causes include HSV, anti-NMDA receptor encephalitis (young women, often with ovarian teratoma), mosquito-borne flaviviruses (Murray Valley encephalitis; Japanese encephalitis emerged in south-eastern Australia in 2022), and paraneoplastic syndromes. Approximately 40% of survivors have lasting cognitive or behavioural sequelae.

What encephalitis is

Encephalitis means inflammation of brain parenchyma — distinct from meningitis, which involves the surrounding membranes. This distinction matters because encephalitis causes altered consciousness, focal neurological deficits, and seizures, rather than headache and neck stiffness alone, and the empirical treatment (IV aciclovir) is different.

The International Encephalitis Consortium 2013 criteria define encephalitis as altered mental status lasting more than 24 hours with at least two of: fever above 38°C, new seizures, focal neurological signs, CSF pleocytosis, neuroimaging abnormality consistent with encephalitis, or an EEG pattern consistent with encephalitis. In general practice, the clinical threshold for emergency transfer is lower than this: any adult with unexplained altered consciousness, new focal neurology, or fever plus personality change should be transferred immediately.

Australia has a distinctive epidemiological profile. Herpes simplex virus (HSV) remains the most common identified viral cause in adults. Autoimmune encephalitis — especially anti-NMDA receptor encephalitis — is now recognised as more common than previously understood. And since 2022, Japanese encephalitis virus (JEV) has established transmission in south-eastern and inland Australia, joining Murray Valley encephalitis and Kunjin virus as endemic mosquito-borne threats.

A. Core clinical — the AU general-practice framework

Clinical patterns to recognise

HSV encephalitis evolves over days with fever, headache, and — crucially — behavioural or personality change that typically precedes more obvious confusion. It preferentially affects the medial temporal lobes, which explains the characteristic amnesia, olfactory hallucinations, aphasia, and temporal lobe seizures. Patients are often initially thought to have a psychiatric illness or a vascular event.

Anti-NMDA receptor encephalitis follows a recognisable sequence: a viral-like prodromal illness, then a prominent psychiatric phase with psychosis, hallucinations, agitation, or catatonia, then orofacial dyskinesias and choreoathetoid movements, and finally autonomic instability with labile blood pressure, tachycardia, hyperthermia, and central hypoventilation. Many patients are seen by psychiatry before the neurological progression makes the diagnosis clear. The Graus Lancet Neurol 2016 criteria formalise the diagnostic approach.

Mosquito-borne flaviviral encephalitis presents after outdoor exposure in endemic or epidemic regions during summer. JEV, Murray Valley encephalitis, and Kunjin all cause a febrile illness that in a minority of cases progresses to meningoencephalitis with altered consciousness, focal signs, and seizures.

History focused on red flags

Duration and evolution of altered mental state, especially over days to weeks
Fever, headache, nausea, vomiting
Behavioural or personality change (a relative’s account is invaluable)
New seizures: type, duration, recovery interval
Mosquito exposure, outdoor activity, geographic location (Top End, inland areas, flood-affected regions in summer months)
Travel to JEV-endemic regions of Asia
Known cancer, immunosuppression, or HIV — broadens the differential to opportunistic organisms
Oral or genital herpes history (though most HSV encephalitis is not obviously related to recurrent herpes)
Tick bite or animal contact (Australian Bat Lyssavirus — rare but transmissible via bat bites or scratches)

Examination

Systematic assessment should cover:

Full GCS and detailed mental status: orientation, memory, language, behaviour
Vital signs including temperature and autonomic parameters (HR, BP lability)
Cranial nerves — eye movement abnormalities, facial dyskinesias, tongue movements
Motor, sensory, cerebellar examination and reflexes
Neck stiffness (meningeal irritation in meningoencephalitis)
Skin: rash, vesicles (VZV), haemorrhagic lesions (meningococcal)
In young women with psychiatric features and movement disorder: pelvic assessment, given the teratoma association with anti-NMDA receptor encephalitis

GP bedside management before transfer

The GP’s role in suspected encephalitis is recognition plus immediate action — not outpatient workup:

Call 000. State “suspected encephalitis” to trigger Category 1 response and pre-notify the receiving emergency department.
Establish IV access if feasible.
Check blood glucose. If hypoglycaemia is present, treat with 50 mL of 50% glucose IV.
Begin empirical IV aciclovir 10 mg/kg if available — the time to aciclovir is the dominant predictor of outcome in HSV encephalitis. Adult dose is 10 mg/kg every 8 hours; paediatric dose under 12 years is 20 mg/kg every 8 hours.
If bacterial meningitis cannot be excluded, add ceftriaxone 2 g IV.
If Listeria is possible (age over 50, immunocompromised, pregnant), add ampicillin 2 g IV.

Do not withhold aciclovir while waiting for CT, lumbar puncture, or MRI results.

B. Cause-specific management — what the evidence supports

HSV: empirical aciclovir is non-negotiable

Therapeutic Guidelines (eTG) and the Australian Medicines Handbook are unambiguous: IV aciclovir must be started empirically in any suspected encephalitis. Untreated HSV encephalitis carries approximately 70% mortality; prompt treatment reduces this to around 20%. Duration is at least 14 days (21 days for severe disease or immunocompromise), continuing until HSV PCR is negative and an alternative diagnosis is confirmed. The principal adverse effect is nephrotoxicity; maintain adequate hydration during infusion.

Anti-NMDA receptor encephalitis: immunotherapy and teratoma removal

The Titulaer Lancet Neurol 2013 cohort of 577 patients established that early immunotherapy combined with teratoma removal produces substantially better outcomes. First-line treatment is methylprednisolone 1 g IV daily for 5 days plus IVIG 0.4 g/kg/day for 5 days, or plasma exchange over 5 to 7 sessions. In women, ovarian teratoma must be actively sought — pelvic ultrasound, then MRI or CT if ultrasound is negative — and removed if found, even small teratomas. Second-line therapy for refractory disease is rituximab plus cyclophosphamide. Maintenance immunosuppression with mycophenolate or azathioprine reduces relapse.

Mosquito-borne flaviviruses: notification, vaccination, and supportive care

No antiviral therapy is effective for JEV, Murray Valley encephalitis, or Kunjin. Hospital management is supportive with ICU involvement for severe disease. Following the 2022 JEV emergence in Australia, NIP-funded JEV vaccination is available for residents, workers, and travellers in high-risk areas of New South Wales, Victoria, South Australia, Queensland, and the Northern Territory. ATAGI eligibility criteria are updated periodically. Both encephalitis and the underlying causative organism are notifiable conditions in most Australian jurisdictions — notify the state or territory public health unit promptly.

C. Hospital workup — what follows transfer

Hospital-phase investigations (not in scope for the GP consultation, but useful to discuss with patients) include:

MRI brain with gadolinium — the gold-standard imaging modality. HSV encephalitis produces bilateral asymmetric FLAIR and DWI hyperintensity in the medial temporal lobes, insular cortex, and orbital frontal lobe. Anti-NMDA receptor encephalitis often has a normal or non-specific MRI in the early phase.

EEG — periodic lateralised epileptiform discharges (PLEDS) over the temporal lobes are characteristic of HSV encephalitis. “Extreme delta brush” pattern is associated with anti-NMDA receptor encephalitis.

CSF analysis — lymphocytic pleocytosis with elevated protein and normal glucose in viral and autoimmune encephalitis. HSV PCR, VZV PCR, enterovirus PCR, and an autoimmune antibody panel (anti-NMDA, LGI1, CASPR2, GAD65, GABA-B) should be sent from both CSF and serum.

Paraneoplastic and cancer workup — anti-Hu, anti-Yo, anti-Ma2 antibodies and CT chest, abdomen, and pelvis (or PET-CT) if a paraneoplastic cause is suspected. Pelvic ultrasound in all women for anti-NMDA receptor encephalitis regardless of age.

Flavivirus serology — JEV, Murray Valley encephalitis, and Kunjin serology (IgM + IgG plus PCR) when exposure is plausible.

D. Australian operations

MBS items

Standard GP consultation items (23, 36, 44) apply. CT brain (item 56001) is GP-initiable for urgent exclusion of space-occupying lesion. MRI brain (item 63007) requires specialist referral for the full Medicare rebate. EEG (item 11221 and adjacent range, to be confirmed at request time) is specialist-billed. After discharge, GPCCMP items 965 and 967 apply to post-encephalitis chronic management. Mental Health Care Plan items 2715 and 2717 are relevant given the high rates of depression, anxiety, and PTSD in survivors.

PBS medications

IV aciclovir and IV methylprednisolone are hospital-supplied. Oral valaciclovir is PBS General Schedule. IVIG requires PBS S100 BloodSafe Authority for confirmed autoimmune encephalitis indications. Rituximab requires PBS Authority (specialist-initiated, off-label for autoimmune encephalitis). Levetiracetam is PBS General Schedule for seizure management. JEV vaccines (Imojev, IXIARO) are NIP-funded for eligible groups — check the current ATAGI schedule.

Mandatory notification

Japanese encephalitis virus and Murray Valley encephalitis virus are mandatorily notifiable in all Australian states and territories. Other organisms associated with encephalitis (measles, mumps, Hendra, Australian Bat Lyssavirus) are also notifiable. Contact the state or territory public health unit — phone numbers on the health department website.

NDIS and long-term support

Persistent encephalitis-related disability qualifies for NDIS support in Australians under 65. NDIS supports rehabilitation, assistive technology, and supported living arrangements. Apply early — assessment does not require recovery to be finalised. DVA pathways support eligible veterans. My Aged Care (phone 1800 200 422) for those over 65.

E. Special populations

Immunocompromised patients — HIV infection, organ transplant, and haematological malignancy expand the differential substantially to include cryptococcal meningoencephalitis (India ink and cryptococcal antigen on CSF), CMV encephalitis (CMV PCR), toxoplasma encephalitis (ring-enhancing lesions on CT/MRI, serology), and progressive multifocal leukoencephalopathy. Empirical cover must be broader; early infectious disease specialist involvement is essential. Cryptococcal meningoencephalitis requires amphotericin plus flucytosine induction before fluconazole consolidation.

Aboriginal and Torres Strait Islander communities in endemic regions of the Northern Territory and north-western Australia carry higher rates of Murray Valley encephalitis. Mosquito bite prevention — DEET-containing repellents, long-sleeved clothing, window screens, and treated sleeping nets — is the primary prevention strategy. Coordinate prevention messaging with Aboriginal Community Controlled Health Organisations.

Children and adolescents — ADEM (acute disseminated encephalomyelitis) is a post-viral autoimmune demyelinating encephalitis that predominantly affects children aged 5 to 14. It typically begins 1 to 3 weeks after a viral illness with encephalopathy, focal deficits, and large bilateral white matter lesions on MRI. Corticosteroids are first-line treatment and the prognosis is generally good. Anti-NMDA receptor encephalitis also occurs in children, often without a teratoma but with the same multi-phase presentation.

Pregnant patients — HSV encephalitis in pregnancy carries high maternal and fetal mortality. IV aciclovir at standard doses is the appropriate treatment; it is not contraindicated in pregnancy. JEV in pregnancy is associated with fetal loss and preterm birth. Gestational encephalitis management requires obstetric co-management and consideration of fetal wellbeing alongside maternal treatment.

When to escalate

Transfer immediately (000) for any patient with:

Altered mental state with no immediately obvious reversible cause
New seizure with incomplete recovery within 30 minutes
Fever plus focal neurological signs or personality change
Clinical suspicion of bacterial meningitis, encephalitis, or meningoencephalitis

After hospital discharge, refer to neurology within 1 to 2 weeks. Refer to neuropsychology when cognitive sequelae are apparent. Initiate NDIS planning early for persistent disability. Return to neurology or infectious diseases for any symptom relapse, new seizure, or concern about disease recurrence — anti-NMDA receptor encephalitis has a relapse rate of roughly 15 to 25% without maintenance immunosuppression.

What this article is and is not

This is general health information drawn from current Australian general practice guidelines including Therapeutic Guidelines (eTG), the Australian Medicines Handbook, and the Australian Encephalitis Consortium, alongside peer-reviewed literature. It is not personal medical advice and does not create a doctor–patient relationship. Diagnosis, treatment selection, and duration of antiviral or immunosuppressive therapy are determined in partnership with hospital neurologists, infectious disease specialists, and treating teams.

For patient-facing information: HealthDirect — Encephalitis, Better Health Channel, Brain Foundation Australia.

For acute emergencies: call 000.

Sources cited

Frequently asked questions

How is encephalitis different from meningitis?

Meningitis primarily causes meningism — severe headache, neck stiffness, photophobia, and fever — with relatively preserved consciousness in the early phase. Encephalitis causes altered mental state (confusion, agitation, behavioural change, drowsiness) and focal neurological signs such as seizures, weakness, or speech disturbance as the dominant features; meningeal signs may also be present in meningoencephalitis. Any adult with unexplained altered consciousness, new seizure, or sudden personality change warrants urgent hospital transfer. Start empirical IV aciclovir alongside ceftriaxone before lumbar puncture results return — treatment delay is the primary determinant of neurological outcome.
What is anti-NMDA receptor encephalitis and who is most affected?

Anti-NMDA receptor encephalitis is the most commonly identified autoimmune encephalitis. Autoantibodies against the NR1 subunit of the NMDA receptor produce a characteristic four-phase illness: a viral-like prodrome, followed by psychiatric symptoms (psychosis, hallucinations, agitation, catatonia), then a movement disorder phase (orofacial dyskinesias, choreoathetoid movements), and finally autonomic instability and coma. About half of affected women have an ovarian teratoma driving antibody production — tumour removal markedly improves outcome. First-line treatment is methylprednisolone plus IVIG or plasma exchange; rituximab is used for refractory disease. Both blood and CSF antibody testing are needed for diagnosis.
Why is Japanese encephalitis now relevant in Australia?

Japanese encephalitis virus (JEV) emerged in south-eastern and inland Australia in 2022 and was declared a National Significant Communicable Disease Incident. Flooding events extended the Culex mosquito vector into New South Wales, Victoria, South Australia, Queensland, and the Northern Territory. Most infections cause mild febrile illness, but roughly 1 in 200 infected individuals develops severe encephalitis with up to 30% mortality and high rates of lasting neurological deficit. An NIP-funded JEV vaccine (Imojev or IXIARO) is available for people at elevated risk in affected areas. Notification to the state public health unit is mandatory.
How long does recovery from encephalitis take?

Recovery is measured in months to years, not weeks. Around 40% of survivors have lasting cognitive difficulties — impaired memory, attention, and processing speed — or behavioural changes including irritability, impulsivity, or depression. Anti-NMDA receptor encephalitis treated promptly with immunotherapy and tumour removal has better long-term outcomes, with approximately 80% achieving good functional recovery over 12 to 24 months. HSV encephalitis treated early carries approximately 20 to 30% mortality; survivors commonly need multidisciplinary rehabilitation including physiotherapy, occupational therapy, speech pathology, and neuropsychology. NDIS support may be available for Australians under 65 with persistent disability.
What should I do if I suspect encephalitis in my consulting room?

Call 000 immediately and state 'possible encephalitis' to activate a Category 1 paramedic response. While awaiting transfer, establish IV access, check blood glucose, and begin empirical IV aciclovir 10 mg/kg if available in a procedural setting — the interval between HSV encephalitis onset and starting aciclovir is the strongest predictor of neurological outcome. Do not delay transfer for lumbar puncture, CT, or bloodwork. Pre-notify the receiving emergency department so the team prepares. If bacterial meningitis cannot be excluded, add ceftriaxone 2 g IV empirically. Oral medication has no role in the acute phase.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.