Venezuelan equine encephalitis is an acute viral disease characterized by fever, chills, headache, nausea, vomiting, lumbosacral pain, and myalgia, which may progress to encephalitis. It is caused by the Venezuelan equine encephalitis virus and is a significant disease in the Americas. Epidemics of Venezuelan equine encephalitis involving tens of thousands of humans and hundreds of thousands of equines have been reported. Although predominantly a disease found in South and Central America, Venezuelan equine encephalitis has spread to the United States. (See Etiology, History, and Physical Examination.) 
Venezuelan equine encephalitis was first recognized in Venezuela in 1938. In 1943, the first descriptions of Venezuelan equine encephalitis in humans were reported from laboratories where equine isolates were being characterized. Researchers determined that these infections were acquired from aerosolized virus. (Venezuelan equine encephalitis virus is highly infectious by the aerosol route, and numerous laboratory infections have occurred.) In 1952, the first naturally acquired human case of Venezuelan equine encephalitis was reported from Colombia, while the first reported natural human infection in the United States was not documented until 1968. (See Etiology.)
A 1995 outbreak of Venezuelan equine encephalitis in Colombia and Venezuela affected an estimated 75,000 humans; 3000 people developed neurologic complications, and 300 fatalities occurred. Of the estimated 50,000 equines infected, 8% died of the disease. This was the first major epidemic of Venezuelan equine encephalitis in 22 years. The extensive transmission of the virus was probably due to a combination of unvaccinated horses and a record high level of rainfall leading to an increase in the mosquito population. (See Etiology and Epidemiology.)
Studies have begun to document a geographic spread of Venezuelan equine encephalitis. As new communications are created between countries, vector spread of the virus has been documented. Over the past few years, Venezuelan equine encephalitis has been found in Brazil and the northern countries of South America. This can be attributed to new trade routes being established and maintained. (See Epidemiology.) 
Major outbreaks involving humans have been associated with Venezuelan equine encephalitis subtype I, varieties AB and C. The IA and IB strains are considered genetically indistinguishable and are thus classified as IAB. While these epizootic strains are virulent in equines and humans, the enzootic Venezuelan equine encephalitis virus serotypes ID, IE, and IIIA can cause illness in humans but not in equines. All transmission of Venezuelan equine encephalitis is via mosquitoes. (See Etiology.)
Recognition of signs and symptoms of illness by those living and working in endemic areas is essential to limit the spread of Venezuelan equine encephalitis.
Venezuelan equine encephalitis virus is a positive-strand, unsegmented ribonucleic acid (RNA) virus. A lipid membrane encapsulates the icosahedral nucleocapsid. Two outwardly projecting glycoproteins, E1 and E2, are inserted in the lipid membrane surrounding the nucleocapsid. E2 appears to be primarily responsible for attachment of the viruses to cell surfaces. Antibodies to E2 can neutralize virus infectivity. 
Venezuelan equine encephalitis virus is a member of the genus Alphavirus of the family Togaviridae.  These viruses were known formally as group A arboviruses. Epizootic viral strains IAB and IC are virulent in humans and equines. Enzootic Venezuelan equine encephalitis serotypes ID, IE, and IIIA are avirulent in equines but can cause illness in humans.
Venezuelan equine encephalitis is an arthropod-borne virus, with the mosquito serving as the most common vector. The virus incubates in the mosquito for 1 week after the mosquito bites an infected equine or rodent host. The virus is then transmitted when the mosquito feeds on an uninfected host.
Venezuelan equine encephalitis has a zoonotic reservoir in bats, birds, rodents, equines (horses, donkeys, mules), and certain tropical jungle mammals. Rodents and other small animals are the most important amplifiers in endemic preservation of the virus in tropical forests, swamps, and marshlands. Horses are the most important amplifier hosts in large epidemic outbreaks. [4, 5]
Alphaviruses are limited in their geographic spread primarily by the presence of an appropriate competent arthropod vector. At least 10 mosquito species, including Aedes, Culex, Psorophora, Mansonia, and Deinocerites species, have been identified as probable epidemic vectors for the Venezuelan equine encephalitis virus, with different mosquito vectors possessing varying levels of efficiency. The principal vector for humans is A aegypti.
The mosquito vector becomes infected after biting a viremic equine host. Humans can develop a viremia significant enough to infect mosquitos, but humans never have been directly implicated in epidemic transmission.
For approximately 1 week, the virus replicates in the midgut epithelium of the mosquito. The virus then is disseminated to other organs, including the hemolymph and salivary glands. Spread to humans occurs when the infected mosquito deposits the virus in the skin of a naïve host while feeding. Viremia and a febrile response mark the initial phase of infection, during which the virus replicates in extraneural tissues. Sites of human replication remain unclear, but, in equines and laboratory rodents, the sites include skeletal muscle, lymphoid, and hematopoietic tissues. This may lead to relative lymphopenia, neutropenia, and thrombocytopenia.
Circulating virus gains access to the central nervous system (CNS) via the bloodstream or perhaps via the olfactory apparatus. Neuronal infection with Venezuelan equine encephalitis is associated with the onset of acute encephalitis and cell death by apoptosis. 
Although Venezuelan equine encephalitis virus can be demonstrated in human throat swabs, human-to-human transmission never has been conclusively demonstrated. However, the Centers for Disease Control and Prevention (CDC) extensively analyzed the 1995 Venezuelan equine encephalitis outbreak in northwest Colombia and reported a 5% secondary household attack rate.  Whether these secondary attacks were from bites by mosquitoes infected from animals or humans was unclear. At the present time, direct human-to-human transmission is not scientifically proven but is suspected.
Outbreaks of Venezuelan equine encephalitis in the United States have been rare. From 1969-1972, a major outbreak of Venezuelan equine encephalitis involving much of Central America spread to Texas. Approximately 1500 horses died of Venezuelan equine encephalitis in Texas, and several hundred humans were infected.
Western equine encephalitis and eastern equine encephalitis alphaviruses are those most associated with a similar infection in the United States. Strains nonvirulent to equines (subtypes 1D and 1E) have caused sporadic infection in Central America and Florida. The mosquito vector and the rodents that live in tropical swamps and forests maintain these strains of Venezuelan equine encephalitis viruses.
Changing climatic patterns may favor establishment of the virus in wild rodents in warmer areas of the United States.
Venezuelan equine encephalitis continues to occur most commonly in Central and South America.  Tens of thousands of humans and hundreds of thousands of equine infections have resulted from periodic epidemics in these areas. Spread tends to occur to areas contiguous to the site of the outbreak.
Human seroprevelance in rural areas of Mexico has been reported to be more than 60% in older age groups. Thus, mild or asymptomic infections may be more common than previously believed. 
Data from epidemics demonstrate that children have the highest risk of acquiring moderate or severe forms of the infection.
Nonneurologic infections are self-limited, and complete recovery generally occurs within several weeks of onset. The overall fatality rate is less than 1%. Neurologic manifestations occur at a rate of 4-14% in infected children (< 1% in adults), with a case fatality rate of 20%.
The fatality rate is approximately 20% in older children and young adults who develop acute encephalitis, but it is as high as 35% in persons aged 0-5 years.
Chronic neurologic deficits, such as dysarthria, motor disorders, abnormal reflexes, and affective disorders, may occur in patients who survive an episode of acute encephalitis. An increased risk for spontaneous abortions has been noted during Venezuelan equine encephalitis epidemics.
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