Chikungunya virus (CHIKV) is a single-stranded RNA alphavirus that has now become prevalent throughout the world. Originally described from Sub-Saharan Africa, this mosquito-borne infection derives its name from the Makonde language, where it implies “bone breaking fever,” where the person experiencing the illness stoops over with severe arthralgias, a characteristic for the disease.1 The conventional vector was Aedes egyptii, but currently, Aedes albopictus has also been identified as a vector in Asia, including India.
Chikungunya virus infection has an incubation period of approximately 3 days and is manifested by abrupt-onset fever, myalgias, arthralgias, headache, and a rash.2 The fevers last about a week, the severity corresponding to the degree of viremia, and is followed by the severe arthralgias and a rash. Severe infection can present with encephalopathy or encephalitis, among other manifestations.
In the study by Gohel et al in this issue,3 the authors conducted a retrospective, observational cohort study of CHIKV infection at a single center in India. Specifically, they were looking for the proportion of patients that developed CHIKV encephalitis (CHIKVE). Patients with higher likelihood for development of CHIKVE were younger than 30 years or older than 60 years. Overall mortality in this study, for those with CHIKVE, was 18.75%, which does not seem to be controlled for other comorbidities.
Although this study seems to validate concerns that CHIKVE does occur even in Asian patients and that CHIKVE was associated with an almost 20% mortality, at least in this single-center study, this study poses some limitations to its results.
First, this is a retrospective cohort study from a single center and provides mainly descriptive statistics for the protean neurological manifestations of patients with CHIKV infection. What cannot be inferred with any certainty is what predisposing factors put patients at higher risk for acquisition of CHIKVE.
Furthermore, in this cohort, extremes of age seemed to demonstrate a higher predilection for CHIKVE, but the sample size was not large enough to achieve statistical significance.
Although most patients were treated with supportive care, 2 patients with transverse myelitis were treated with intravenous immune globulin with reported improvement. Given the absence of a structured intervention or randomization, it is unclear whether the response to intravenous immune globulin was random or there was a true “cause and effect” relationship.
Lastly, the multiple nonspecific clinical syndromes and neuroimaging findings suggest the absence of a defined syndrome or anatomic localization of lesions in CHIKVE, at least in this study.
In summary, this study suggests that CHIKV infection is more than a debilitating viral infection with severe arthralgias and other constitutional symptoms and that approximately 1 in 5 individuals may develop CHIKVE with risk for long-term neurologic deficits and even death.
With global migration and travel, CHIKV has become a universal infection, even in the Western Hemisphere; therefore, the need for awareness of potential neurological complications after acquisition of disease has become all the more prescient.
1. Ross RW. The Newala epidemic. III. The virus: isolation, pathogenic properties and relationship to the epidemic. J Hyg (Lond)
2. Rudolph KE, Lessler J, Moloney RM, et al. Incubation periods of mosquito-borne viral infections: a systematic review. Am J Trop Med Hyg
3. Gohel S, Modi R, Patel KK, et al. Prevalence, risk factors, and outcome of chikungunya encephalitis in hospitalized patients at tertiary care center in Gujarat, India, during the 2016 outbreak. Inf Dis Clin Pract