Experimental Infection of Potential Reservoir Hosts with Venezuelan Equine Encephalitis Virus, Mexico

Eleanor R Deardorff,Jose G Estrada-Franco,Scott C Weaver,Roberto Navarro-Lopez,Naomi L Forrester,Robert B Tesh,Amelia P Travassos Da Rosa

doi:10.3201/eid1504.081008

Abstract

In 1993, an outbreak of encephalitis among 125 affected equids in coastal Chiapas, Mexico, resulted in a 50% case-fatality rate. The outbreak was attributed to Venezuelan equine encephalitis virus (VEEV) subtype IE, not previously associated with equine disease and death. To better understand the ecology of this VEEV strain in Chiapas, we experimentally infected 5 species of wild rodents and evaluated their competence as reservoir and amplifying hosts. Rodents from 1 species (Baiomys musculus) showed signs of disease and died by day 8 postinoculation. Rodents from the 4 other species (Liomys salvini, Oligoryzomys fulvescens, Oryzomys couesi, and Sigmodon hispidus) became viremic but survived and developed neutralizing antibodies, indicating that multiple species may contribute to VEEV maintenance. By infecting numerous rodent species and producing adequate viremia, VEEV may increase its chances of long-term persistence in nature and could increase risk for establishment in disease-endemic areas and amplification outside the disease-endemic range.

Highlights

In 1993, an outbreak of encephalitis among 125 affected equids in coastal Chiapas, Mexico, resulted in a 50% case-fatality rate
Animals During October 2007, wild rodents of 5 species were collected from coastal Chiapas, Mexico: Baiomys musculus, Liomys salvini (Salvins spiny pocket mouse), Oligoryzomys fulvescens, Oryzomys couesi (Coues’ rice rat) and Sigmodon hispidus
S. hispidus rodents have been included in previous experimental Venezuelan equine encephalitis virus (VEEV) infection studies

Summary

Introduction

In 1993, an outbreak of encephalitis among 125 affected equids in coastal Chiapas, Mexico, resulted in a 50% case-fatality rate. The outbreak was attributed to Venezuelan equine encephalitis virus (VEEV) subtype IE, not previously associated with equine disease and death. During the mid-1990s, 2 epizootic equine outbreaks occurred in coastal Oaxaca and Chiapas states in Mexico; the causative agent was determined to be VEEV subtype IE (VEEV-IE), which was previously considered to be not virulent for equids [1]. Enzootic strains of VEEV are maintained naturally by transmission between mosquitoes of the subgenus Culex (Melanoconion) and wild rodents [4]. These viruses are thought to circulate continuously among mosquitoes and their principal vertebrate amplifying hosts, whereas horses and humans are considered spillover, dead-end hosts not required for maintenance of the natural cycle.

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