Can Chikungunya Virus Trigger Brain Infections in Infants, Adults?
Outbreaks of the mosquito-borne Chikungunya virus may trigger a deadly brain infection.
An outbreak of the mosquito-borne Chikungunya virus on La Réunion Island in the Indian Ocean that occurred between September, 2005 and June, 2006 resulted in 57 cases of associated central nervous system disease initiated by encephalitis. This was a highly significant outbreak of a modified strain with more serious outcomes than previous outbreaks of the virus, according to a study published in Neurology.
Of the 57 patients studied who had Chikungunya virus (CHIKV)- associated central nervous system (CNS) disease, 24 had altered mental status that corresponded to encephalitis according to International Encephalitis Consortium (IEC) criteria, for a regional incidence of 8.6 per 100,000. The burden of the La Réunion outbreak therefore, was greater than that reported from 1999 to 2007 with the West Nile virus in the U.S. or the worldwide spread of Japanese encephalitis.
The investigators found that the pattern of CHIKV-encephalitis showed a U-shaped distribution, favoring very old and very young people. Of the 57 patients who developed encephalitis, 21 were adults aged 33 to 88 years (mean age = 63.9) and 36 were infants aged 4 days to 5.4 months (mean age = 1.6 months).
Symptoms varied between the age groups: impaired consciousness, coma, focal neurological signs, seizures, and fatal events occurred more frequently among adults, while infants were more likely to display fever prior to hospitalization, skin rash, and behavioral changes.
Infants with CHIKV-associated encephalitis were more likely to survive than adults who were infected. The infants carried higher CHIKV loads than the adults, while protein, glucose, and chloride levels in cerebral spinal fluid (CSF) were higher in the adults. All of the infants survived, while six adults died during hospitalization from outcomes associated with CHIKV infection. Eight adults who were discharged continued to experience neurologic consequences, one of whom died 3 months after discharge. The overall death rate for CHIKV-encephalitis was 17%, while 35-45% of survivors experienced persistent disability.
More than half of the 36 infants who were infected were lost to later follow up. The remaining 17 infants were re-evaluated at approximately 38 months of age. Four of these children had showed impaired neurological development and one developed cerebral palsy and blindness. The number of children lost to follow up was attributed to a milder course of infection.
The investigators concluded that although infants seemed to be more susceptible to CHIKV-encephalitis than older persons, 3-year outcomes were far more likely to be poor among adults infected with the virus (52.6% vs. 18%, p = 0.020).