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Weapons of Mass Destruction (WMD)

Venezuelan Equine Encephalitis Virus

Common Name(s) Venezuelan Equine Encephalitis Virus (VEEV)
Scientific Name(s) Alphavirus belonging to the family Togaviridae
Physical Attributes Positive-sense, single stranded RNA
Geography North, Central, and South America
Mode(s) of Transmission Mosquitoes that bite an infected animal and then bite and feed on another animal or human
Likely BW Form(s) Aerosol
  • Signs range from mild flu-like fever, chills, headache, nausea, vomitting to depression, weakness, EEE (inflammation of the brain), coma and death
  • Severe cases: muscle and back pain, headache, sensitivity to light, impaired vision, vomiting, weakness, exhaustion, and confusion
  • Rarely: seizures, paralysis, tremors, coma, and severe encephalitis
  • May cause severe permanent neurologic damage
  • Host(s) Human, horses, birds, donkeys
    Vector/Dormant Form Mosquitos, esp. Culiseta melanura, Aedes, Coquillettidia, and Culexfound species
    Incubation Period ~5 days (2-6 days)
    Fatality Less than 1%; up to 20% in children
    Vaccine Vaccine is available to protect equines; experimental vaccines but no commercially licensed human VEEV vaccine is available (as of 2007)
    Treatment None, only supportive care

    Venezuelan Equine Encephalitis Virus (VEEV) is a mosquito-borne viral disease, an Alphavirus belonging to the family Togaviridae. VEE has a single, positive strand of RNA. VEE has affected equine and humans in South, Central, and North American for the past century.

    A BW attack with virus disseminated as an aerosol would cause human disease as a primary event. If Equidae were present, disease in these animals would occur simultaneously with human disease. Secondary spread by person-to-person contact occurs at a negligible rate. However, a BW attack in a region populated by Equidae and appropriate mosquito vectors could initiate an epizootic epidemic.

    Nearly 100% of those infected suffer an overt illness. After an incubation period of 1-5 days, onset of illness is extremely sudden, with generalized malaise, spiking fever, rigors, severe headache, photophobia, myalgia in the legs and lumbosacral area. Nausea, vomiting, cough, sore throat, and diarrhea may follow. This acute phase lasts 24-72 hours. A prolonged period of aesthenia and lethargy may follow, with full health and activity regained only after 1-2 weeks. Approximately 4% of patients during natural epidemics develop signs of central nervous system infection, with meningismus, convulsions, coma, and paralysis. These necrologic cases are seen almost exclusively in children. The overall case-fatality rate is <1%, but in children with encephalitis, it may reach 20%.

    An outbreak of VEE may be difficult to distinguish from influenza on clinical grounds. Clues to the diagnosis are the appearance of a small proportion of neurological cases or disease in Equidae, but these might be absent in a BW attack.

    There is no specific therapy. Patients who develop encephalitis may require anticonvulsant and intensive supportive care to maintain fluid and electrolyte balance, adequate ventilation, and to avoid complicating secondary bacterial infections.

    An experimental vaccine, designated TC-83 is a live, attenuated cellculture-propagated vaccine which has been used in several thousand persons to prevent laboratory infections. Approximately 10% of vaccinees fail to develop detectable neutralizing antibodies, but it is unknown whether they are susceptible to clinical infection if challenged. A second investigational product that has been tested in humans is the C-84 vaccine, prepared by formalin-inactivation of the TC-83 strain. The vaccine is presently not recommended for primary immunization, on the basis of animal studies indicating that it may not protect against aerosol infection.

    In experimental animals, alpha-interferon and the interferon-inducer poly-ICLC (lysine-polyadenosine) have proven highly effective for post-exposure prophylaxis of VEE. There are no clinical data on which to assess efficacy in humans.

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    Page last modified: 24-07-2011 03:44:58 ZULU