Research Article: Venezuelan Equine Encephalitis Virus in Iquitos, Peru: Urban Transmission of a Sylvatic Strain

Date Published: December 16, 2008

Publisher: Public Library of Science

Author(s): Amy C. Morrison, Brett M. Forshey, Desiree Notyce, Helvio Astete, Victor Lopez, Claudio Rocha, Rebecca Carrion, Cristhiam Carey, Dominique Eza, Joel M. Montgomery, Tadeusz J. Kochel, Jeffrey M. Bethony

Abstract: Enzootic strains of Venezuelan equine encephalitis virus (VEEV) have been isolated from febrile patients in the Peruvian Amazon Basin at low but consistent levels since the early 1990s. Through a clinic-based febrile surveillance program, we detected an outbreak of VEEV infections in Iquitos, Peru, in the first half of 2006. The majority of these patients resided within urban areas of Iquitos, with no report of recent travel outside the city. To characterize the risk factors for VEEV infection within the city, an antibody prevalence study was carried out in a geographically stratified sample of urban areas of Iquitos. Additionally, entomological surveys were conducted to determine if previously incriminated vectors of enzootic VEEV were present within the city. We found that greater than 23% of Iquitos residents carried neutralizing antibodies against VEEV, with significant associations between increased antibody prevalence and age, occupation, mosquito net use, and overnight travel. Furthermore, potential vector mosquitoes were widely distributed across the city. Our results suggest that while VEEV infection is more common in rural areas, transmission also occurs within urban areas of Iquitos, and that further studies are warranted to identify the precise vectors and reservoirs involved in urban VEEV transmission.

Partial Text: Members of the Venezuelan equine encephalitis virus (VEEV) complex are arboviruses belonging to the Alphavirus genus of the Togaviridae family. First identified among equines in the 1930s [1], VEEV-associated human disease was not recognized until 1943 [2],[3] , although epidemiological data suggest that outbreaks may date back to the 1920s [4]. VEEV subtypes cause a wide clinical spectrum of disease ranging from undifferentiated fever to severe neurological symptoms, with a case fatality rate of 1–4% [5]. Two transmission cycles have been identified: an enzootic cycle, maintained among rodent reservoirs in forest habitats, and an epizootic cycle that causes high rates of mortality in horses as well as epidemics among human populations [4]. These cycles are typically associated with distinct subtypes of the VEE virus complex: subtypes IAB and IC with equine epizootics, subtypes ID, IF, and II–VI with the equine avirulent enzootic cycle [4],[6], and subtype IE with both enzootic and equine-virulent transmission cycles [7],[8],[9]. Despite disparate serological and clinical phenotypes some enzootic and epizootic subtypes are highly genetically conserved. In particular, strains of the enzootic subtype ID (Columbia/Venezuela genotype) show less than 0.5% divergence from epizootic IAB and IC subtypes at the amino acid level [10],[11],[12]. Based on this genetic conservation, epizootic strains have been proposed to emerge periodically from progenitor strains continuously maintained in an enzootic forest cycle. Accordingly, a single amino acid change within the E2 envelope gene has been shown to confer an epizootic phenotype on an enzootic VEEV strain [10],[11],[12],[13].

Based on data from a clinic-based febrile illness surveillance program, transmission of enzootic VEEV subtypes has been well documented in the Iquitos area of northeastern Peru at consistent but low levels since the early 1990s [6],[19],[42]. In this study we report an outbreak of human VEEV infections during the first half 2006 detected through the NMRCD surveillance program, with the majority of patients residing within city limits. In response to this outbreak, we conducted an antibody prevalence study and mosquito collections within urban areas of Iquitos, targeting neighborhoods with large numbers of cases during the 2006 outbreak. The prevalence of VEEV antibody exceeded 18% in all areas, and known vectors of the disease were identified across the city. To our knowledge, this is the first antibody survey for enzootic VEEV in an urban population.



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