Chandipura Virus Encephalitis

The Ministry of Health and Family Welfare, Government of India, reported 245 cases of acute encephalitis syndrome (AES) between early June and mid-August 2024. Among these, 82 (33%) cases resulted in death. Among the cases of AES, 64 were confirmed as Chandipura virus (CHPV) encephalitis.¹

Unusual strains of hitherto unrecognized arboviruses were isolated from serum samples of two febrile patients that were collected during an outbreak of febrile illness in Nagpur, Maharashtra in 1965. These samples exhibited cytopathic effects. The agent proved to be a new filterable virus. The condition was recognized in Chandipura, a village near Nagpur, and thus the virus was named after this place.² Similar virus was isolated from sandflies during a routine entomological study in Aurangabad, Maharashtra in 1967.³ A subsequent study made on serum sample collected from a child with features of encephalopathy in Jabalpur, Madhya Pradesh, revealed the presence of Chandipur virus.⁴ CHPV an arthropod borne virus, is transmitted to humans and other vertebrates through the bite of an infected female sandfly.

CHPV is endemic to India, with outbreaks previously occurring at regular intervals of every four to five years. The current outbreak has been labeled as the largest in the past two decades.

Global attention was drawn to the causative agent as an emerging neurotropic pathogen, known for causing high mortality in affected children.⁵ The epicenter of activity of CHPV is predominantly in Central India in Maharashtra, Madhya Pradesh, Andhra Pradesh, Telangana, Gujarat and Rajasthan.

Seroprevalence studies carried out on CHPV using human serum samples collected between 1955-1966 have shown the prevalence of neutralizing antibodies in humans to be high in Lucknow, Uttar Pradesh (89.3%), Banni, Gujarat (83.8%), Nagpur, Maharashtra (78.3%),Visakhapatnam, Andhra Pradesh (69.7%), and Madras (now Chennai), Tamil Nadu (64.4%). The seroprevalence was (15.1%) in Bengaluru.⁶

CHPV belongs to the genus Vesiculovirus. It is part of the Rhabdoviridae (GK. rod-shaped) family and is responsible for sporadic cases of the disease, with a potential to cause outbreaks. It is a single-stranded RNA virus. It consists of bullet shaped virions possessing five structural proteins. Outbreaks of the infection have been noted in a few selected areas in western, central and southern India during the monsoon season. The virus had been found in the neighboring countries such as Bhutan, Nepal, Sri Lanka, and Nigeria and Senegal in Africa.⁷

In Gujarat, children presenting with a febrile illness showed the presence of anti-CHPV IgM antibodies in 2011. It is noteworthy that similar antibodies were detected in 2012 in the outbreaks in Maharashtra and Gujarat.⁸

A noticeable association of CHPV with sporadic encephalitis has been observed in children, as well as in several outbreaks that occurred in Andhra Pradesh (2003, 2004, 2005, 2007 and 2008), Gujarat (2005, 2009-12) and the Vidarbha region of Maharashtra (2007, 2009-12).

Around 322 children succumbed to the outbreaks that occurred in 2003 in Andhra Pradesh (AP) (183 deaths), Maharashtra (115 deaths) and Gujarat (24 deaths). The case fatality rates (CFRs) during the outbreaks in AP and Gujarat were 56 to 75 percent, respectively.^9-11

CHPV encephalitis was found in a tribal population of Odisha in Eastern India in 2015.12 In recent years, a greater number of cases have been reported, predominantly from Gujarat state (61 cases) and three cases from the state of Rajasthan. The virus spreads through sandflies, Phlebotomus papatasi and even the mosquitoes and ticks may transmit the infection. There is no human-to-human transmission.

CHPV replication takes place in neuronal cells, leading to rapid cell destruction through the process of apoptosis.

The disease predominantly affects younger children below 15 years of age. They demonstrate features of acute encephalitis syndrome which include, high grade fever, headache, vomiting, diarrhoea, altered sensations, convulsions, decerebrate posture, coma and death within a few hours to 48 hours of hospitalization (killer brain disease).

The presence of infection is confirmed by utilizing immunoglobulin M enzyme-linked immunosorbent assay (IgM ELISA) or reverse transcription polymerase chain reaction (RT-PCR).⁷

CHPV infection is associated with a high mortality (56-75%) rate. No specific treatment is available for the condition. The treatment is predominantly supportive, including intensive care. There is no available vaccine to prevent the condition. Two candidate vaccines, viz a recombinant vaccine and a killed vaccine with siRNAs targeting P and M proteins have been developed and the results look promising.¹³

Preventive measures include vector control and protection against the bites of sandflies, mosquitoes and ticks. Improper disposal of waste, poor sanitary conditions and poor housing offer breeding grounds to sandflies. Comprehensive insecticidal spraying and fumigation are to be undertaken to control vectors. The control of vectors is challenging in endemic regions, as they breed in damp areas that are difficult to reach with insecticide sprays. Traditional practice of smearing cow dung on the floors of the houses and storing cow dung cakes outside the houses for cooking, should be avoided as they serve as feed for the sandfly larvae.¹⁴

As currently there is no specific treatment available, preventive measures and early detection become crucial. Vector control, hygienic surroundings and public awareness play a significant role in combating the spread of infection in the community, especially among children. Timely referral and symptomatic management of cases of acute encephalomyelitis syndrome are essential to improve the outcomes.