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Published on: July 24, 2016
Chandipura virus encephalitis outbreak among children in Nagpur division, Maharashtra, 2007
Yogesh K Gurav1, Babasaheb V Tandale, Ramesh S Jadi
1National Institute of Virology (ICMR), Pune, India.
Insights
Chandipura virus caused a severe acute encephalitis outbreak in children in Maharashtra, leading to a high fatality rate. This investigation confirmed the virus and identified its clinical features and potential transmission vectors.
Area of Science:
- Virology
- Epidemiology
- Pediatrics
Background:
- An outbreak of acute encephalitis syndrome (AES) occurred in children in the Nagpur division of Maharashtra.
- The investigation aimed to determine the cause and clinical characteristics of the AES outbreak.
Purpose of the Study:
- To identify the etiological agent responsible for the acute encephalitis syndrome outbreak.
- To describe the clinical and epidemiological features of AES cases in children.
Main Methods:
- Investigated AES cases in children under 15 hospitalized between June-September 2007.
- Tested serum and cerebrospinal fluid (CSF) for IgM antibodies against Chandipura virus (CHPV) and Japanese encephalitis virus (JEV) using RT-PCR.
- Conducted phylogenetic analysis of CHPV N gene sequences and tested sandflies for CHPV RNA.
Main Results:
- 78 AES cases were recorded, with a case fatality ratio of 43.6%.
- Chandipura virus (CHPV) was confirmed in 39 cases; CHPV RNA was detected in CSF and serum.
- Clinical manifestations included fever, convulsions, altered sensorium, headache, vomiting, and diarrhea; CHPV RNA was found in sandflies.
Conclusions:
- Chandipura virus was confirmed as the cause of the acute encephalitis outbreak.
- The outbreak was characterized by high case-fatality rates among affected children.
Background & Objectives:
An outbreak of acute encephalitis syndrome (AES) among children from Nagpur division, Maharashtra was investigated to confirm the aetiology and to describe clinico-epidemiological features.
Methods:
AES cases among children<15 yr, from Nagpur division, hospitalized between June-September 2007, were investigated. Serum and cerebrospinal fluid (CSF) were tested for IgM antibodies against Chandipura virus (CHPV) and Japanese encephalitis virus (JEV) and for CHPV RNA by RT-PCR. Partial N gene sequences were used for phylogenetic analysis. Virus isolations were attempted in rhabdomyosarcoma (RD) cell line. Sandflies were collected, pooled and tested for CHPV RNA by RT-PCR.
Results:
A total of 78 AES cases were recorded in children<15 yr of age. Case fatality ratio was 43.6 per cent. Male to female ratio was 1:1.2. Chandipura (CHP) was confirmed in 39 cases. CHPV RNA was detected in both CSF and serum specimens of 2 cases and in serum of 22 cases. Phylogenetic analysis showed 99.98-100 per cent nucleotide identity in the sequences studied. Anti-CHPV IgM antibodies were detected in CSF of 2 cases and in serum of 8 cases. Seroconversion to anti-CHPV IgM antibodies was observed in 5 cases. Clinical manifestations of CHP cases (n=38) were fever (100%), convulsion (76.3%), altered sensorium (34.2%), headache (23.7%), vomiting (44.7%) and diarrhoea (23.7%). CHPV RNA was detected in one of two pools of sandflies from affected locality.
Interpretation & Conclusions:
Chandipura virus was confirmed as the aetiological agent of this acute encephalitis outbreak with high case-fatality among children.
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