Epidemiology

VEEV was first isolated in 1938 from the brain of a horse that had died of encephalitis.[6] The virus was first reported as a cause of human disease in Colombia in 1950.[6] Six subtypes of VEEV have been identified (classified I-VI). In subtype I, five antigenic varieties exist (IAB, IC, ID, IE, and IF). Varieties IAB and IC are epizootic and have been responsible for the majority of large outbreaks in humans.[5] Varieties ID, IE, and IF are enzootic viruses found in Central and South America. Subtypes II to VI are also enzootic viruses. Subtype II (Everglades virus) circulates in Florida. Subtypes III to VI (also known as Mucambo/Tonate, Pixuna, Cabassou, and Rio Negro, respectively) circulate in Central and South America.[7] The enzootic subtypes are transmitted between rodents and Culex mosquito species of the subgenus Melanoconion, while the epizootic strains are amplified in horses and transmitted by a variety of mosquito species, one of the most important of which is the Aedes (Ochlerotatus) taeniorhynchus mosquito.[7] There have also been reports of transmission of VEEV via aerosol, leading to laboratory-acquired infections. There is no evidence, however, for human-to-human transmission.[8]

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