Encephalitis in Children
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Direct answer
A febrile child who becomes drowsy, irritable or comatose with or without seizures has acute encephalitis syndrome — the Indian surveillance definition — until proven otherwise. Japanese encephalitis, carried by Culex mosquitoes breeding in rice paddies with pigs as amplifying hosts, remains the commonest identified cause of viral encephalitis in India, marked by sudden high fever, altered sensorium, dystonia, mask-like facies and poliomyelitis-like acute flaccid paralysis, with MRI showing thalamic involvement. Herpes simplex encephalitis is the treatable killer: fever with focal seizures, temporal-lobe behaviour change and periodic discharges on EEG demand immediate intravenous aciclovir 20 mg/kg per dose every eight hours for 21 days, started on suspicion without waiting for confirmation. Scrub typhus is a repeatedly forgotten, fully treatable mimic accounting for a large share of acute encephalitis syndrome in several North Indian series — hence empirical doxycycline alongside aciclovir.
What you must remember
- Meningoencephalitis versus encephalitis: meningism may be minimal; the defining feature is altered behaviour or consciousness with or without seizures, with CSF showing mild lymphocytic pleocytosis, near-normal glucose and mildly raised protein.
- Japanese encephalitis specifics: Culex tritaeniorhynchus vector, rice-paddy-pig ecology, July-to-November seasonality, thalamic and basal ganglia changes on MRI, dull expressionless facies with dystonic postures, and acute flaccid paralysis from anterior horn involvement; IgM in CSF or serum confirms, and roughly half of severe survivors retain sequelae.
- Herpes simplex encephalitis: temporal and frontal predilection, focal onset seizures, hyponatraemia, red cells or xanthochromia in CSF, periodic lateralised epileptiform discharges on EEG; aciclovir 20 mg/kg/dose (600 mg per square metre) eight-hourly for 21 days, with CSF polymerase chain reaction the confirmatory test.
- Treatable bacterial mimics: scrub typhus (eschar, doxycycline), leptospirosis, enteric fever and mycoplasma — the first step in many Indian units is empirical doxycycline plus aciclovir while results return.
- Post-infectious demyelination (acute disseminated encephalomyelitis): encephalopathy days to weeks after infection or vaccination, often with optic neuritis or transverse myelitis, MRI showing white-matter lesions; treat with methylprednisolone pulses.
- Anti-NMDA-receptor encephalitis in children: psychiatric onset, dyskinesias, autonomic instability, seizures, ovarian teratoma association; CSF antibody testing and immunotherapy.
- Prevention anchor: Japanese encephalitis vaccine (SA-14-14-2 live attenuated or inactivated) in endemic-district campaigns under the universal immunisation programme.
Working through an acute encephalitis admission
Imagine an August admission in eastern Uttar Pradesh: a six-year-old with three days of high fever, one seizure, and a Glasgow coma scale of 11, neck soft, a curiously frozen face with intermittent dystonic wrist postures. First, stabilise — airway, glucose, treat the seizure. Second, exclude the fatal and the treatable: lumbar puncture after imaging (CSF for cells, glucose, protein, Japanese encephalitis IgM, HSV polymerase chain reaction), blood for scrub typhus IgM and malaria, and contrast MRI. The dull facies with dystonia points to thalamic and basal ganglia involvement — Japanese encephalitis territory; thalamic signal change on MRI settles it. Management of Japanese encephalitis is meticulous supportive care — airway protection, fluid discipline, nasogastric feeding, anticipation of autonomic storms; no antiviral is proven, and steroid and interferon trials disappointed. Meanwhile aciclovir covers herpes simplex until the PCR returns, and doxycycline covers scrub typhus where the region demands it. Rehabilitation begins in the ward, with expectations set honestly. A different child with fever, bizarre behaviour and focal temporal discharges on EEG should have aciclovir flowing within the hour of suspicion — delay is the strongest modifiable predictor of poor outcome in herpes encephalitis.
Where students slip
Two frames recur in viva examinations. First, students await confirmation before treating herpes — the standard is empirical aciclovir on suspicion, since the polymerase chain reaction result days later cannot buy back neurons; the 21-day duration (not 14) is the companion mark. Second, "all acute encephalitis syndrome is Japanese encephalitis" — it is merely the commonest identified agent, with a substantial share attributed to scrub typhus and other treatable causes. A third trap is mislabelling acute disseminated encephalomyelitis as viral encephalitis: the post-infectious interval, multifocal white-matter lesions and steroid responsiveness separate it.
Frequently asked questions
What is the vector and reservoir cycle of Japanese encephalitis?
Culex tritaeniorhynchus transmits the virus among pigs (amplifying hosts) and wading birds, humans being dead-end hosts; rice-paddy ecology drives endemicity in eastern and southern India.
When should aciclovir be started in suspected herpes simplex encephalitis?
Immediately on clinical suspicion, before confirmation — 20 mg/kg per dose intravenously every eight hours for 21 days, with CSF polymerase chain reaction used to confirm or stop treatment later.
Which imaging and EEG features suggest herpes simplex encephalitis?
Temporal and inferior frontal signal change on MRI (often asymmetric, sometimes with haemorrhage) and periodic lateralised epileptiform discharges over the temporal region on EEG.
Why is scrub typhus considered in acute encephalitis syndrome?
Orientia tsutsugamushi infection is a common, rapidly fatal if untreated, yet fully treatable cause of acute febrile encephalopathy in several Indian regions; look for an eschar and start doxycycline early.
What distinguishes acute disseminated encephalomyelitis from viral encephalitis?
Post-infectious temporal separation from a febrile illness, multifocal demyelinating white-matter lesions on MRI, frequent optic neuritis or myelopathy, and response to high-dose corticosteroids.