CBRNE - Venezuelan Equine Encephalitis 

Venezuelan equine encephalitis (VEE) is a viral disease caused by exposure to mosquitoes infected with VEE in endemic or epidemic areas or by intentional release of a VEE biological weapon. It is caused by an enveloped single-stranded RNA togavirus of the Alphavirus genus.^[1]

Some species of the Alphavirus genus have characteristics suitable for weaponization, a fact that was recognized in the 1930s and 1940s. Alphaviruses could potentially be produced in large quantities and delivered effectively via an aerosol route.^[2] Unlike many other pathogenic viruses, these viruses are relatively stable in the environment.

No specific treatment other than supportive care is available. VEE is caused by an RNA virus; therefore, antivirals that have been successful against DNA viruses are ineffective.

A live-attenuated VEE vaccine has been used in horses. A formalin-inactivated vaccine has been developed for use in humans, although further investigation of its protective effects is needed.^[3]

Go to Encephalitis and Viral Encephalitis for complete information on these topics.

Patient education

For patient education resources, see the Bioterrorism and Warfare Center and the Brain and Nervous System Center, as well as Biological Warfare, Personal Protective Equipment, and Encephalitis.

The potential for person-to-person transmission exists. Venezuelan equine encephalitis (VEE) virus has been isolated from the human pharynx.^[4] Furthermore, aerosol transmission of the virus has occurred as a result of laboratory accidents or lack of laboratory precautions. An analysis of laboratory incidents suggests the aerosol form of VEE virus is highly infectious and therefore is a potential biowarfare agent. This could be an especially worrisome possibility if strains are genetically altered to increase pathogenicity.^[5]

The VEE virus is potentially susceptible to genetic manipulation in advanced laboratories. This characteristic has proven useful for researchers aiming to develop more effective vaccines; however, it could also be exploited to produce more effective biological weapons.

The Centers for Disease Control and Prevention (CDC) extensively analyzed the 1995 VEE outbreak in northwest Colombia and reported a 5% secondary household attack rate.^[6] 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.

Venezuelan equine encephalitis (VEE) is a mosquito-borne viral disease characterized by fever and other symptoms that may include severe headache, back pain, myalgias, prostration, chills, nausea, vomiting, and weakness.^[7] The disease may progress from encephalitis to death.

These clinical symptoms are similar to those of many other zoonotic viral infections that cause fever and headache, including St. Louis encephalitis, Japanese virus encephalitis, West Nile encephalitis, and dengue fever. Unlike these infections, which are caused by flaviviruses, VEE is caused by an enveloped single-stranded RNA virus of the Alphavirus genus in the Togaviridae family.^[1] Alphaviruses also cause eastern equine encephalitis, western equine encephalitis, Chikungunya fever, Semliki Forest disease, Barmah Forest fever, and Ross River fever.

VEE virus remains a potentially potent biological weapon.^[8] If this virus were to be deployed efficiently, it could incapacitate thousands of people for a week or more and cause untold psychological stress to millions. Accordingly, suspect biological warfare or terrorism when large numbers of patients present with VEE from a nonendemic region.^[2] It is important to maintain a high index of suspicion for this diagnosis in such situations.

Aside from than supportive care, no specific treatment is available for Venezuelan equine encephalitis (VEE). Treatment is symptomatic; in the emergency department (ED), it most likely involves correcting fluid deficiencies.

Because VEE is caused by an RNA virus, antivirals that have been successful against DNA viruses are ineffective. No medications have been approved specifically for treatment of VEE. In vitro laboratory studies suggest that ribavirin and other nucleoside analogues may be appropriate, but these have not been used clinically in humans.

Contact an infectious disease specialist if VEE is suspected. In addition, involve the county and/or state health department. Admit patients with potential VEE who have moderate-to-severe symptoms and observe for progression to encephalitis.

In areas where VEE virus is endemic, protection from mosquito bites is important. Visitors to endemic areas should take appropriate precautions to avoid mosquito bites, including proper clothing, insect repellant, and mosquito nets.

Areas where the virus is epidemic should be avoided by everyone other than persons on approved medical response teams. It is advisable to check the Centers for Disease Control and prevention (CDC) Web site before traveling to specific countries to determine if an epidemic is occurring or if special warnings have been issued.

A live-attenuated virus is used to vaccinate equines. A formalin-inactivated virus has been used to vaccinate human laboratory workers at risk, but this vaccine is not available to the general public. Work is continuing on the development of a low-cost vaccine with minimal adverse effects.^{[3, 9]}