Venezuelan equine encephalitis

Venezuelan equine encephalitis

The agent is a member of the genus Alphavirus of the family Togaviridae. The virion is about 70 nm in diameter, consisting of a positive single stranded RNA enclosed in an icosahedral capsid, surrounded by a lipid bilayer membrane in which surface glycoproteins are embedded. Subtypes IAB and IC are pathogenic for equines and are responsible for major outbreaks in humans. Other variants do not normally cause encephalitis in equids and, although sometimes encountered in humans, have not been isolated from major outbreaks.


Epidemics were first registered in the 1930s in the northern part of South America and then spread to Central America. Sizeable epidemics were registered in Mexico in 1969, in Texas in 1971, and in Venezuela in 1995. The disease is endemic in central and northern parts of South America. Enzootic Venezuelan equine encephalitis (VEE) virus is endemic in Mexico and Florida. The Florida virus is Everglades virus, a distinct species.


The virus is maintained in a rodent–mosquito–rodent cycle. Dur ing major outbreaks affecting humans, the disease is transmitted in a cycle involving mosquito vectors and horses or other equines as hosts. For this reason, natural outbreaks are normally preceded by equine epizootics. Humans also may develop sufficient viraemia to serve as hosts in human–mosquito–human cycles. Epidemic and non-epidemic strains may be distinguished antigenically.


Mode of transmission

Humans become infected from the bite of infected mosquitoes. The major species of mosquito that transmit epidemic VEE are Psorophora confinnis, Aedes sollicitans, Aedes taeniorhynchus (recently revised to Ochlerotatus taeniorhynchus) and Deinocerites pseudes. There is no evidence of direct person-to-person transmission or of direct transmission from horses to humans. Although natural aerogenic transmission is not documented in humans, primary aerosol infection in laboratories is well known and inhalation of only a few infective organisms is sufficient to cause a significant likelihood of infection.

The VEE virus can initiate infection via the nasal mucosa and the olfactory epithelium of the upper respiratory tract. Virus-containing airborne droplets too large to penetrate more deeply into the respiratory system can therefore constitute a hazard.
Incubation period

The incubation period in natural or aerogenic infection is usually 1–6 days.

Clinical features

Clinical manifestations of the naturally occurring disease are influenza like, with abrupt onset of severe headache, high fever, chills, myalgia in the legs and lumbosacral area and retroorbital pain. There may also be photophobia, sore throat, nausea, diarrhoea and vomiting. Conjunctival and pharyngeal congestion are the only external signs. Most infections are fairly mild, with symptoms usually lasting 3–5 days. 

The overall casefatality rate in the 1962–1963 epidemic in Venezuela, among some 30 000 cases, was approximately 0.6%. In some patients there is a second wave of fever and, particularly in children, CNS involvement ranging from somnolence and disorientation to personality change, convulsions, paralysis and death. The initial symptoms of respiratory infection are like those of insectborne infection but CNS involvement appears to be more frequent.

Laboratory diagnosis

The disease exhibits leukopenia during a period usually limited to 1–3 days after onset. During this time, the virus may be sampled from serum or nasopharyngeal swabs and propagated in cell culture or in newborn mice. A variety of serological tests are applicable, including specific IgM ELISA, haemagglutination inhibition, immuno- fluorescence and complement fixation.

PCR has been successfully used to distinguish strains. It may be applied to serum and cerebrospinal fluid without prior propagation of the pathogen. Neutralizing antibodies first appear in convalescent sera from the fifth day up to 2 weeks after onset of symptoms. Biosafety Level 3 practices, equipment and facilities are recommended for activities using infective clinical materials.

Medical management and public health measures

Persons caring for infected patients should wear gloves, caps, gowns and surgical masks. Infective virus may be present in fresh or dried blood, exudates, cerebrospinal fluid and urine. Such materials should be decontaminated by autoclaving or by chemical disinfection, as with hypochlorite or chloramine. If mosquito vectors are present, patients should be kept in screened or insecticide-treated rooms to prevent mosquito transmission to healthy persons and general mosquito control measures should be instituted.

Prophylaxis and treatment
Attenuated cell-culture propagated live vaccine TC-83, produced but not licensed in the USA, is moderately effective against both natural infection and aerosol challenge but is somewhat reactogenic and fails to induce a minimum neutralizing antibody response in approximately one-fifth of persons receiving it, presumably leaving them unprotected.


Two other attenuated live virus vaccines, strains 15 and 230, reported to offer good protection against aerosol challenge, were developed in the Russian Federation. An inactivated vaccine designated C-84, prepared by formalin-inactivation of the TC-83 strain, is currently used to immunize TC-83 non-responders and as a booster for individuals who have declining titres after TC-83 vaccination.



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