Epidemiology

VEEV was first isolated in 1938 from the brain of a horse that had died of encephalitis.[5] The virus was first reported as a cause of human disease in Colombia in 1950.[5] 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 most large outbreaks in humans.[4] Varieties ID, IE, and IF are enzootic viruses 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.[6] The enzootic subtypes are transmitted between rodents and Culex mosquito species of the subgenus Melanoconion. At the same time, 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.[6] 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.[7]

VEEV is widely distributed throughout Central and Southern America, with human and horse outbreaks reported in at least 13 countries, including Venezuela, Colombia, Peru, Ecuador, Costa Rica, Nicaragua, Honduras, El Salvador, Guatemala, Panama, Trinidad, and Mexico.[5][8] ​​There have also been outbreaks reported in the US. In 1969, a widespread and long-lasting outbreak began in El Salvador and Guatemala and spread through most of Central America and Mexico, reaching southern Texas in the US in 1971.[5] During this outbreak, hundreds of thousands of cases of infection in humans were reported. The outbreak was contained when a large vaccination programme was initiated. 

Venezuelan equine encephalitis resulting from VEEV infection occurs throughout much of Latin America and the Caribbean and is likely responsible for 10% of the cases attributed to dengue and could account for as many as 50,000 cases of acute febrile illness per year throughout Latin America.[5] One of the largest epizootic outbreaks recorded resulted in 75,000 to 100,000 cases of human infection in Colombia and Venezuela in 1995, with around 3000 neurological complications and 300 deaths reported.[9]

In one large study involving febrile patients in South America, males were more often infected with enzootic VEEV than females, but all age groups were equally represented.[10] In an outbreak of epizootic VEEV in Texas (US) the infection rate was highest among males aged 20 to 39 years, but neurological symptoms and encephalitis were most common in children.[11]

Although VEEV infection is more common in rural areas, transmission can also occur within urban areas. Through a clinic-based febrile surveillance programme, an outbreak of VEEV infections was detected in Iquitos, Peru, in 2006.[12]

An epidemic of VEEV occurred in Colombia between February and March 2008. Approximately 13% (250/2000) of the area’s inhabitants had a febrile illness compatible with VEEV, with two fatalities.[13]​​

Outbreaks of VEEV occur alongside other alphaviruses. In 2010, an outbreak of Madariaga virus and VEEV occurred in the eastern province of Darién, Panama. Among hospitalised patients, there were 7 confirmed cases of Madariaga virus, 3 confirmed cases of VEE, and 1 confirmed case of co-infection with these viruses.[14]

‌VEEV is clinically indistinguishable from other arboviruses and can only be confirmed with consultant laboratory testing, which has limited availability in resource-limited countries, therefore endemic disease incidence rates in these countries are uncertain.[13]​ Expansion and development of disease surveillance networks is required in these countries to improve case and outbreak detection.

Overall mortality during outbreaks of VEEV does not typically exceed 1% of cases.[1]​ Mortality occurs mainly in children and is generally attributable to consequences of neurological involvement.​​[2]

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