Encephalitis

DR. M. S. PRASAD 1

EncephalitisEncephalitis

DR. M. S. PRASADRetired Consultant & Head

Dept. of PaediatricsSafdarjung Hospital

New Delhi

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DefinitionsDefinitions

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DefinitionDefinition• The Encephalitis is an acute inflammatory

process involving brain tissue.

• Meningoencephalitis is an acute inflammatory process involving the meninges and, to a variable degree, brain tissue.

• They are often found associated together.

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EncephalitisEncephalitis

Two Components:

1. Inflammation of brain, and

2. Dysfunction of brain.

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EncephalopathyEncephalopathy

• Dysfunction of brain

• Encephalopathy describes a clinical syndrome of altered mental status, manifesting as reduced consciousness or altered behaviour. (Indian Pediat, vol 49, Nov 16, 2012 page 899)

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Causes of EncephalopathyCauses of Encephalopathy

• Systemic infection,• Metabolic derangement (e.g. DKA),• Toxins,• Drugs & Poisoning,• Hypoxia,• Trauma,• Vasculitis,• CNS infection.

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Acute Encephalitis Syndrome Acute Encephalitis Syndrome (AES)

Clinically, a case of acute encephalitis syndrome is defined as a person of any age, at any time of year with the acute onset of fever and a change in mental status (including symptoms such as confusion, disorientation, coma or inability to talk) AND/OR new onset of seizures (excluding simple febrile seizures)(Indian Pediatrics, volume 49, November 16, 2012 page 899)

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Conditions included in AES

• Viral Encephalitis,

• All causes of fever with altered sensorium:– Bacterial Meningitis (Acute Pyogenic Meningitis),– TBM,– Cerebral Malaria,– ADEM.

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Causes of AESCauses of AES

• Viral encephalitis,

• Acute Pyogenic Meningitis,

• TBM,

• Cerebral Malaria,

• Acute Disseminated Encephalomyelitis (ADE).

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Non-infective causes of epidemic AESNon-infective causes of epidemic AES

• Plant toxins (Cassia occidentalis),

• Heat stroke,

• Reye’s syndrome.

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Causes of Encephalitis

• Infectious causes:– Viral– Bacterial (TBM)– Ricketssial,– Fungal,

– Parasites (pl falciparum)

• Non-infectious causes.

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VIRAL CAUSESVIRAL CAUSES

• Enteroviruses: More than 80% of all cases.

• Arboviruses: e.g. Japanese-B Encephalitis which is more common during summer months.

• Herpesvirus.

• CMV.

• EBV.

• Mumps.

• RSV, Rubeola, Rubella or Rabies (Occasionally).

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Viral Causes Viral Causes (continued)(continued)

• Dengue Virus,

• Measles virus,

• Chandipura virus:– Outbreak: AP 2003, GJ 2004, Nagpur 2005 & 2007.

– Sporadic: AP 2005-2006.

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Viral EncephalitisViral Encephalitis

• Direct viral infection:– Primary Viral Encephalitis.

• Indirect immune mediated mechanism:– Post-infectious viral encephalitis.

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Viral EncephalitisViral Encephalitis• Epidemic:

– Japanese Encephalitis,– Dengue virus.

• Sporadic:– Herpes simplex Encephalitis,– Enterovirus (EV71),– Chandipura virus,– Nipah virus,– Chikangunya virus.

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Other virus causing sporadic encephalitisOther virus causing sporadic encephalitis

• Varicella zoster virus,

• Mumps,

• Human herpesvirus 6 & 7,

• EB virus,

• Herpes simplex virus.

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Emerging viral agentsEmerging viral agents• Human parvovirus 4,

• West Nile virus,

• Bagaza virus,

• Coxsackie virus.

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Non-Infectious Causes1.Acute Disseminated Encephalomyelitis

(ADEM),

2.Antibody-associated encephalitis,

3.Allergy: Post Vaccine.

4.Heat Hyperpyrexia.

Non-infectious causes Non-infectious causes (continued)

1.Electrolyte Imbalance.

2.Chemical:Lead, Organophosphorus, Carbon Monoxide, Cannabis indica (Bhang).

3.Malignancies.

4.Metabolic: Hepatic Coma.

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Signs & Symptoms of EncephalitisSigns & Symptoms of Encephalitis

• Fever,

• Headache,

• Lethargy,

• Vomiting,

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Clinical Features Clinical Features (continued)

• Behavioural changes,

• Impairment of consciousness,

• Focal neurological signs,

• Seizures.

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Encephalitis associated with GIT symptomsEncephalitis associated with GIT symptoms

• Enteroviruses,

• Rotavirus,

• Parechovirus.

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Encephalitis associated with respiratory illnessEncephalitis associated with respiratory illness

• Influenza viruses:– Myositis may also be associated.

• Paramyxoviruses,

• Bacteria.

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Clue on physical examinationClue on physical examination

• Pallor:– Cerebral Malaria,– Intracranial bleed.

• Icterus:– Leptospirosis,– Hepatic Encephalopathy,– Cerebral Malaria.

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Clues Clues (continued)(continued)

• Skin rash:Skin rash:– Meningococcemia,– Dengue,– Measles,– Varicella,– Rickettsial diseases,– Arboviral diseases,– Enteroviral encephalitis.

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• Petechiae:– Meningococcemia,– Dengue,– Viral Hemorrhagic Fever,

• Parotid swelling:– Mumps.

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• Orchitis:– Mumps

• Labial herpes in young children:– Herpes simplex virus encephalitis.

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CSF in viral encephalitis

• Pressure: normal or slightly raised,

• Sugar: normal,

• Cells: acellular (no cell) or mild leukocytosis (mostly lymphocytes)

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ImagingImaging• CT Scan:

– Normal.

• MRI:– Localized areas of inflammation,– Diffuse brain swelling.

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UK Regimen UK Regimen (till culture-report is available)

• Aciclovir:– to cover HSV,

• 3rd generation cephalosporin: – to cover bacterial cause,

• Erythromycin: – to cover mycoplasma.

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IndiaIndia

Add antimalarials to UK protocol,

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Japanese-B Japanese-B EncephalitisEncephalitis

Japanese Encephalitis (JE)Japanese Encephalitis (JE)

• One of the commonest cause of AES.

• Year 2014:– Cases: 1661– Deaths: 293 (17.6%)

• Assam, West Bengal, Uttar Pradesh and Jharkhand.

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Japanese Encephalitis (JE)Japanese Encephalitis (JE)• Leading viral cause of acute encephalitis syndrome

(AES) in Asia.

• Primarily affects children under age 15.

• Acute onset, fulminant course, and high mortality & morbidity.

• 70% of patients either die or survive with long term neurological disability.

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JEJE

• Group-B arbovirus (Flavivirus).

• Mosquito borne Encephalitis.

• Transmitted by Culicine (culex) mosquitoes.

• Zoonotic Disease.

• Rice or Pig Farming.

• Peak season: JUN – SEPJUN – SEP.

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VirusVirus

• Japanese Encephalitis Virus (JEV),

• Single stranded RNA virus,

• Genus: flaviviridae

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CULICINE MosquitoesCULICINE Mosquitoes• Culex tritaenorhyncus.

• Culex vishnui.

• Culex galidus.

They breed in rice-field.

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Japanese-B Encephalitis• 50000 cases p. a. globally.

• 15000 deaths.

• 9000 disabled.

• 85% among children less than 15 years of age.

• 1/4th of the cases in India.

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Emerging Problem inEmerging Problem in• West Bengal,

• Bihar,

• Assam,

• Madhya Pradesh,

• Maharastra,

• Manipur,

• Haryana,

• Odisha,

• Goa, and

• Puduchery.

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SpreadSpread

• Spreads by mosquito bite only,

• Man is an incidental dead end host,

• Man-to-man transmission not reported.

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Life-cycle of virusLife-cycle of virus

Pig Mosquito Pig

Bird Mosquito Bird

MAN IS AN INCIDENTAL “DEAD END”“DEAD END” HOST

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HOSTSHOSTS• Infected pigs do not manifest any overt

symptoms of illness.

• AMPLIFIER OF VIRUS.

• Others: – Cattle– Buffaloes– Horses– Birds.

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Japanese-B Japanese-B EncephalitisEncephalitis

• Incubation Period: 5-15 days.

• Ratio of overt disease to unapparent infection = 1:300 to 1: 1000.

• Cases represent tip of iceberg.

• Case Fatality Rate: 10 –70%.

• Incidence: 1- 10/10, 000 population.

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JE & DengueJE & Dengue

IN HUMANS, prior dengue virus infection provides partial protection from clinical Japanese Encephalitis.

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PathologyPathology

• Mosquito bite transmission to man JEV multiplies Neurologic invasion enters CNS JEV replicates in endoplasmic reticulum and Golgi apparatus and destroys them.

• Changes mainly in gray matter.

• Growth of the virus across vascular endothelium mainly thalamus, basal ganglia, brain-stem, cerebellum, hippocampus and cerebral cortex.

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Pathology outside CNSPathology outside CNS• Hyperplasia of germinal centers of lymph-nodes,

• Enlargement of malpigian bodies in spleen.

• Interstitial myocarditis, swelling and hyaline changes in Kuffer’s cells of liver, pulmonary interalviolitis, and focal hemorrhages in kidneys.

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Clinical Features.Clinical Features.

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Japanese-B EncephalitisJapanese-B Encephalitis• Abortive.

• Aseptic Meningitis.

• Severe Encephalomyelitis.– With Radiculitis.– Without Radiculitis.

• Sudden onset with high fever, headache, vomiting, Mental Confusion, Irritability, Loss of consciousness.

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3 Stages

1. Prodromal Illness [2 - 3 days]

2. Encephalitis stage• Acute Stage [3 - 4 days]• Sub-acute Stage [7 - 10 days]

3. Convalescence [4 - 7 weeks]

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Prodromal StageProdromal Stage• High grade fever +/- rigor,

• Headache,

• General malaise,

• Nausea and Vomiting.

• During this stage, a definitive clinical diagnosis is not possible.

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Encephalitic StageEncephalitic Stage• Altered mental status:

– Confusion, agitation, coma

• Generalized weakness,

• Hypertonia & Hyper-reflexia,

• Seizures,

• Papilloedema and/or Cr. N. involvement,

• GIT bleed & Pulmonary Hemorrhage.

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Late StageLate Stage• Stage of convalescence,

• Recovery,

• Persistence of signs of CNS injury:– Residual neurological impairments

• Secondary infections are frequent in this stage.

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Residual neurological impairmentsResidual neurological impairments

• Involuntary movements:– Choreoathetosis or extrapyramidal symptoms,

• Paralysis & Paresis,

• Speech disorders.

• Decorticate or Decerebrate Posturing.

• Post-Encephalitis Cerebral Palsy.

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Clinical Manifestations

• Altered sensorium.• Headache.• Convulsions.• Fever.• Vomiting/Nausea.• Photophobia.• Abnormal movements.• Signs of raised ICT.• Altered Tone and Reflexes

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DiagnosisDiagnosis

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DIAGNOSIS• Clinical Manifestations.

• Epidemiology.

• CSF:– Pleocytosis: Initially Polymorphs then Lymphocytes.– Increased protein.– Normal sugar.

• EEG: Diffuse slow-wave activity.

• CT or MRI: Swelling of the brain parenchyma.

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Diagnosis (Contd)

• Virus isolation

• Detection of viral component (antigen detection)

• Viral serology

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Virus Isolation

• CSF

• Nasopharynx

• Faeces

• Urine

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Detection of antigen and specific Detection of antigen and specific antibodyantibody

• Nucleic Acid ProbeNucleic Acid Probe

• PCRPCR

• RIARIA

• ELISAELISA

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Viral Serology

IgM & IgG:IgM & IgG:

IgM appears early within 2 weeks of infection

IgG appears later, peaking around 8 weeks.

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Two Samples1. Acute Serum (at admission).

2. Convalescent Serum (after at least four weeks).

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Differential DiagnosisDifferential Diagnosis

• Encephalitic form of PolioEncephalitic form of Polio– Convulsion is not seen in polio.

• Cerebral MalariaCerebral Malaria– Splenomegaly.

• Encephalitic form of TBM.Encephalitic form of TBM.– TBM has insidious onset, usually more than 15 days.– Encephalitis has acute onset; less than a week.

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Cerebral Malaria (CM)Cerebral Malaria (CM)

• The closest differential diagnosis.

• CM also characterized by fever with altered state of sensorium and gradually deepening coma.

• CM also occurs in same geographical areas and in the same climatic conditions.

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Causes of impaired consciousness in a child with malariaCauses of impaired consciousness in a child with malaria

• Hypoglycaemia,

• Seizures,

• Postictal state.

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Other features of CM; not seen in encephalitisOther features of CM; not seen in encephalitis

• Hidden dehydration,

• Fast Breathing,

• Laboured Breathing,

• Jaundice (5% of cases),

• Hepatosplenomegaly/splenomegaly,

• Pallor (Anaemia),

• Malarial Retinopathy.

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DD with CM

• P/S positive for pl. falciparum,

• Positive RDT for malaria,

• Raised lactate levels in plasma and CSF.

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D/D with Febrile SeizureD/D with Febrile Seizure• Age:

– Febrile seizures limited to age group from 6 months to 6 years.

– Encephalitis and CM occur at any age.

• Recovery from unconsciousness:– Patients with febrile seizures become fully

conscious and alert after control of seizure.– Patients with CM or Encephalitis do not gain

consciousness even after control of seizures.

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Suspected JESuspected JE

• All cases of Acute Encephalitis Syndrome, i.e.

• Any presenting with acute onset of fever, and altered state of consciousness with or without seizures.

• Please remember, patient regains consciousness after control of seizures in simple febrile seizure but continues to have altered state of consciousness in JE.

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Probable JEProbable JE

A suspected case that occurs in close geographic and temporal relationship to a laboratory-confirmed case of JE, in the context of an outbreak.

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Confirmed JEConfirmed JE

A probable case that has been confirmed by laboratory tests.

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ManagementManagement

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Problems encountered in managemntProblems encountered in managemnt

• Paucity of data about the regional epidemiology and etiology of viral encephalitis.

• Lack of easily available, low-cost microbiological testing for agents of viral encephalitis.

• Lack of specific treatment for majority of etiological agents.

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Problems Problems (continued)

• High incidence of mimickers:– Pyogenic meningitis,– Cerebral malaria,– TBM,– Acute Disseminated Encephalomyelitis (ADE).

• Lack of facility for intensive care in periphery.

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• Lack of facility for neuroimaging in periphery.

• Patient delay in seeking health care.

• Delay/not performing lumbar puncture.

• Inappropriate supportive care.

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Inappropriate response during epidemic:

• What samples to take?

• How to store?

• Whom to inform?

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Documents recommended for managementDocuments recommended for management

• PATH: Japanese Encephalitis Clinical Care Guidelines, 2005.

• UNICEF & GOI: Facility Based IMNCI (F-IMNCI) Participants’ Manual

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Principles of ManagementPrinciples of Management• Hospitalization.

• Line-listing with correct address.

• Save Life.

• Prevent neurological residues.

• Relieve symptoms.

• Provide specific treatment.

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Steps of evaluation Steps of evaluation and managementand management

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6 steps6 steps• Step 1: Rapid assessment and

stabilization.• Step 2:Step 2: Clinical evaluation:

– History & Physical Examination.• Step 3:Step 3: Investigations.• Step 4:Step 4: Empirical Treatment• Step 5:Step 5: Supportive care and treatment.• Step 6:Step 6: Complications and Rehabilitation.

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Step 1: Rapid Assessment & StabilizationStep 1: Rapid Assessment & Stabilization

• Maintain ABC.

• Intubate SOS (children with GCS < 8).

• Oxygen.

• Ventilation.

• Establish IV line and take samples.

• Fluid bolus (RL/NS 20 ml/kg) SOS.

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Step 1Step 1 (continued)(continued)

• Fluid bolus (RL/NS 20 ml/kg) SOS.

• Treat/Prevent hypoglycemia.

• Identify signs of cerebral herniation and raised ICP.

• Manage fever.

• Control seizure.

• Correct acid-base and electrolyte imbalance, if any.

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Step 2Step 2

• Clinical evaluation:

– History including environmental details and

– Thorough Physical Examination.

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HistoryHistory• Onset & duration,

• Fever, headache, vomiting, diarrhoea, irritability, seizures, and rash.

• Contact with TB, Chicken Pox, Mumps,

• Place of residence– Endemic for JE?– Near rice-field?– Cattle, Pigs?

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Physical ExaminationPhysical Examination

• Vitals, GPE, and Systemic,

• Thorough CNS evaluation,

• GCS,GCS,

• Pupil: – size, shape, symmetry, and response to light.

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Clue!Clue!

Unilateral pupillary dilatation in the comatose patient should be considered as evidence of 3rd Nerve compression from ipsilateral uncal herniation, unless proved otherwise.

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Bickerstaff Brain-Stem EncephalitisBickerstaff Brain-Stem Encephalitis

Symptoms of progressive symmetrical external ophthalmoplegia suggest Bickerstaff brainstem encephalitis in association with M. pneumoniae, and can serve as a clue to the diagnosis, especially when associated with ataxia.

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Herpes simplex encephalitis (HSE)Herpes simplex encephalitis (HSE)

• Personality changes, confusion, and disorientation.

• Herpes labialis,• Focal seizures,• Unilateral neurological findings,• Normal CT in first 4-6 days.• MRI and FLAIR more reliable.• Positive CSF PCR.

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FundusFundus

• Papilloedema,

• Haemorrhage (Clue for CM)

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Look for!Look for!• Hepato-splenomegaly,

• Pneumonia,

• Pleural Effusion,

• Myocarditis– (An important complication of EV 71 encephalitis)

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Step 3: InvestigationsStep 3: Investigations• CSF,

• Blood/Serum, Urine,

• Throat Swab, Nasopharyngeal Swab,

• MRI (if available), avoid sedation.

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Basic InvestigationsBasic Investigations• CBC including platelet count,

• Blood Glucose,

• Serum Electrolytes,

• Liver & Kidney Function Test,

• Blood C/S,

• ABG,

• P/S for MP.

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CSFCSF• Gross appearance: colour, transparency

• Chemistry including CSF: Blood Sugar,

• Cytology,

• C/S,

• Latex Agglutination,

• PCR for HSV 1 & 2,

• IgM antibodies for JE & Dengue.

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Step 4: Empirical TreatmentStep 4: Empirical Treatment

• Do not wait for report, start treatment immediately.

• Ceftriaxone + Acyclovir + Artesunate (stop artesunate if P/S and RDT are negative).

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Step 5: Supportive Care & TreatmentStep 5: Supportive Care & Treatment1. Maintain airway, breathing and circulation.2. Control of seizures.3. Treatment of raised ICT.4. Manage fever ((Never give aspirin)Never give aspirin)..5. Maintain fluid & electrolyte balance.6. Maintain blood-sugar level.7. Feeding: NPO initially then NG Tube Feeding.8. Specific Treatment.9. Methylprednisolone or dexamethasone must be

given to children with suspected ADEM.


Step 6: Prevention/Treatment of Step 6: Prevention/Treatment of complications and rehabilitationcomplications and rehabilitation

• Physiotherapy, posture change, prevent bed-sore and exposure keratitis.

• Prevent complications: aspiration pneumonia, nosocomial infection, coagulation disturbances.

• Nutrition: early feeding.

• Psychological support to patient and family.


Features of raised ICPFeatures of raised ICP

• Asymmetric pupil,

• Tonic posturing,

• Papilloedema


Treatment of raised ICT

• Proper positioning: Head elevated 15-300.

• Fluid Restriction: 2/3rd of maintenance.

• 20% Mannitol 5 ml/kg over 10 – 15 min followed by 3 ml/kg every 6 hourly for 48 hrs then SOS, oror

• Acetazolamide: 50 – 75 mg/kg/day, oror

• Glycerin: 1 ml/kg/day through NG Tube.


Raised ICT Raised ICT (continued)

• Hyperventilation,

• Furosemide– Persistence of ICT after mannitol therapy.– 1-2 mg/kg/dose every 12 hourly.

• Paralysis & Ventilation

• While tracheal suctioning, boluses of i. v. lignocaine 0.5-1 mg/kg may be used to prevent rise of ICP.


Specific Treatment• Until a bacterial cause is excluded, parenteral antibiotics

therapy should be administered:– Age 0 to 3 months:

• Inj. Cefotaxime + Inj. Ampicillin.– Age 3 months to 12 years:

• Inj. Ceftriaxone/Inj. Cefotaxime/Inj. Ampicillin + Inj. Chloramphenicol.

• T/T for HSV: – Inj. Acyclovir 30 mg/kg/day for 14 to 21 days


Role of AntibioticsRole of Antibiotics• Under most situations, it may be

nearly impossible to rule out a bacterial infection.

• Incidence of super-added bacterial infection is high.

• Therefore, a good antibiotic shield is recommended.


DosageDosage• Inj. Chloramphenicol:

– 100 mg/kg/day in 4 divided doses for 10 days.• Inj. Ceftriaxone:

– 100 mg/kg/day in 2 divided doses for 10 days.• Inj. Cefotaxime:

– 200 mg/kg/day in 3-4 divided doses for 10-14 days..• Inj. Ampicillin:

– 300 mg/kg/day in 4 divided doses for 10 days.


PrognosisPrognosis• Mortality: 10 – 70%, 24 – 42%.

• Mortality highest in age 5 – 9 yrs.

• Sequelae: 5 - 70%.


PreventionPrevention


Control MeasuresControl Measures

a. Vector Control:1. Fogging.

ULV

2. Indoor mosquito spray

b. Vaccination.


Methods of spraying Commercial PesticidesMethods of spraying Commercial Pesticides

• Portable Spray Pump.

• Helicopter.

• Light Aircraft.


Personal Personal ProtectionProtection

•Avoid mosquito bites:– Use mosquito-net– House Screening– Mosquito Repellents.– Avoid evening outdoor exposure.– Cover body with clothing

•Vaccination


VaccinationVaccination

• Vaccination against JE is advised in endemic areas

• In such areas, it is given routinely to children above 1 year of age,


VaccinesVaccines

• Inactivated Mouse Brain Vaccine (JE-VAXJE-VAX),

• Inactivated Primary Hamster Kidney Cells-P3-China,

• Live Attenuated Primary Hamster Kidney (PHK) Cells-SA14-14-2SA14-14-2 strain – China: Marketed for both domestic use and for use in Nepal, S. Korea, Sri Lanka and India.

• Inactivated Vero Cell Culture Derived SA-14-14-2 JE vaccine (IC51)-(IXIARO)


Live Attenuated SA-14-14-2 VaccineLive Attenuated SA-14-14-2 Vaccine• Launched in India in 2006.

• Single Dose.

• Efficacy: 94.5% (95% CI, 81.5 to 98.9).

• JE Vaccine efficacy: – 60% in UP and 70% in Assam– Results better in Nepal.


Dosage (SA-14-14-2)Dosage (SA-14-14-2)• Amount: 0.5 ml

• Route: SQ

• Single dose between 1 and 15 years of age.

• UIP: 16 – 18 months with 1st booster of DPT.

• Store at 80 C

• Protect from sunlight

Dosage Dosage (continued)

• 2011:– Brought under the UIP.– Single dose at 16-18 months of age along

with 1st booster of DPT.

• 2013:– Another dose added at 9 months of age

along with Measles vaccine.



Inactivated Vero Cell culture-derived SA-14-14-2 JE Vaccine Inactivated Vero Cell culture-derived SA-14-14-2 JE Vaccine (JE-VC)(JE-VC)

• This is an inactivated vaccine (JE-VC) derived from the attenuated SA-14-14-2 JEV strain propagated in Vero Cells.

• Approved for use in children from age of 2 months onwards.

• Efficacy data not available yet.


JEEVJEEV – the Indian variant of IC51 – the Indian variant of IC51

• Licensed by Drug Controller General of India for use in prevention of JE virus infection in children and adult population on the basis of its ability to induce JEV neutralizing antibodies as a surrogate for protection.


Inactivated Vero Cell culture-derived Kolar Inactivated Vero Cell culture-derived Kolar strain, 821564XY, JE Vaccine strain, 821564XY, JE Vaccine (JENVAC)(JENVAC)

• JENVAC is a Vero Cell culture-derived, inactivated, adjuvanted and thiomersal containing vaccine.

• The original virus strain used in the vaccine was isolated from a patient in the endemic zone in Kolar, Karnataka, India.


IAP RecommendationIAP Recommendation

• JE vaccine not recommended for routine use.

• Needed only for individuals living in endemic area.


Live Attenuated SA-14-14-2 VaccineLive Attenuated SA-14-14-2 Vaccine

• The IAP thinks there is a need of a second dose of the vaccine to provide more complete and sustained protection.

• 1st dose at 9 months along with Measles vaccine.

• 2nd dose at 16 to 18 months at the time of 1st booster of DPT vaccine.


JEEVJEEV• Primary schedule of 2 doses,

• 0.25 ml for children ≥ ≥ 1 to ≤ ≤ 3 years,

• 0.5 ml for children >> 3 years, adolescents and adults,

• IM on day 0 and 28.


JENVAC (Kolar Strain)JENVAC (Kolar Strain)

• Lacks the experience of multinational trials,

• 2 doses of the vaccine, 0.5 ml IM at 4 weeks interval for the primary immunization for children ≥≥ 1 year of age.

• Need of booster dose at later stage (further study required for exact timing).


VaccinationVaccination

• Protective immunity develops in about a month’s time after the second dose.

• Revaccination after 3 yrs.Revaccination after 3 yrs.

• Best used in inter-epidemic period.

Adult JE Vaccination ProgramAdult JE Vaccination Program

• Adult JE outnumbered pediatric cases.

• The JE vaccine available for adults in 179 districts of 9 states.

• The NVBDCP has identified 20 high burden districts in Assam, Uttar Pradesh and West Bengal.



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Encephalitis

Health & Medicine

Transcript of Encephalitis