Pathogen safety data sheets: Infectious substances, Venezuelan equine encephalitis virus
On this page
- Section I - Infectious agent
- Section II - Hazard identification
- Section III - Dissemination
- Section IV - Stability and viability
- Section V - First aid and medical
- Section VI - Laboratory hazards
- Section VII - Exposure controls and personal protection
- Section VIII - Handling and storage
- Section IX - Regulatory and other information
Section I - Infectious agent
Name: Venezuelan equine encephalitis virus
Synonym or cross reference: Venezuelan equine encephalomyelitis, VEEV, VEE, Venezuelan equine fever, arbovirus
Characteristics: This spherical arbovirus belongs to the Togaviridae family and is an alphavirusFootnote 1. It is 70 nm in diameter and has an enveloped single stranded RNA genomeFootnote 2,Footnote 3. There are six subtypes of VEE viruses, although only varieties AB and C of subtype 1 are epizootic, while the other subtypes and varieties are enzooticFootnote 3.
Section II - Hazard identification
Pathogenicity/toxicity: In humans, this virus usually causes mild to severe influenza-like symptoms, however 4-14% of cases develop neurological complicationsFootnote 2. Children and young adults are more likely to develop encephalitis caused as a result of infection; however, fatalities in humans are rare at about 1% of all reported casesFootnote 4. Usually, flu-like symptoms such as headache, myalgia, fatigue, vomiting, nausea, diarrhoea, pharyngitis and fever appear abruptly, 2 to 5 days after exposure to the virusFootnote 3. The VEE virus can also cause retro-orbital and occipital headaches as well as leucopenia and tachycardiaFootnote 3. Symptoms of encephalitis, only appearing in a minority of cases, occur 4-10 days after exposure and include somnolence, convulsions, confusion, photophobia, and coma. Lethal human cases are usually caused by encephalitis as well as brain, lung and gastrointestinal bleedingFootnote 3. Long-term neurological damage can be caused by this virus and it can infect the foetus in pregnant women causing birth defects and stillbirthsFootnote 4. Generally, the symptoms last between 3 and 8 days and can be biphasic, recurring 4 to 8 days after the initial symptomsFootnote 5.
Epidemiology: The epizootic and enzootic strains of the VEE virus range from northern Argentina to Florida and parts of the Rocky Mountains; however, it is most prevalent in northern South AmericaFootnote 3,Footnote 4. The virus was first observed in horses in 1935 after outbreaks in Columbia, Venezuela and Trinidad, and was isolated in 1938Footnote 3,Footnote 6. In the 1960's, over 200,000 human cases and 100,000 equine deaths were reported in Colombia and smaller epidemics occurred in Venezuela and MexicoFootnote 3. Between 75,000 and 100,000 infections were reported in Venezuela and Colombia in 1995Footnote 3. The outbreaks usually occur after a season of heavy rains, due to increases in the mosquito populationFootnote 3,Footnote 7. Vaccinations of equines with the TC-83 vaccine and protection against mosquitoes (protective clothing, insecticides) are some of the proposed ways to reduce VEE outbreaksFootnote 3.
Host range: Horses and humans are the most common hosts; however, a variety of other animals have been shown to be susceptible to infectionFootnote 8. These include mammals such as cats, dogs, cattle, goats, pigs, rodents, and birdsFootnote 8.
Infectious dose: 1 viral infectious particle injected subcutaneously is enough to infect an individual with the VEE virusFootnote 9.
Mode of transmission: The VEE virus is most often transmitted by infected mosquito bites, although, it is also very contagious through aerosolsFootnote 6,Footnote 8. Subcutaneous injection, nasal instillation, and contact with broken skin or contaminated animal bedding are other ways to spread the virus, particularly in a laboratory settingFootnote 5.
Incubation period: The incubation period is usually about 2 to 6 days after exposure to the virus, but can be as short as 24 hoursFootnote 8,Footnote 10.
Communicability: Instances of person-to-person transmission have not been reported for the VEE virus, although an infected individual can transmit the virus to mosquitoesFootnote 8. Generally, humans and equines become infected by mosquitoes of the Psorophora and Ochlerotatus genuses. Equines can spread the virus to each other through aerosols and to mosquitoes via bitesFootnote 11.
Section III - Dissemination
Reservoir : There are two types of cycles involved in the VEE virusFootnote 1. The enzootic cycle is maintained by rodents and mosquitoesFootnote 11. The epizootic cycle implicates horses, mosquitoes and humans, although there is the potential for the virus to affect many other animal speciesFootnote 11. Horses are the amplifying host in the cycle and are necessary for a larger outbreak of VEEFootnote 4.
Zoonosis: Capable of zoonosis. This virus is spread between horses and humans via mosquitoesFootnote 11.
Vectors: The VEE virus is typically spread by mosquitoes, although certain types of ticks and mites can spread the virus as wellFootnote 3. The Culex (Melanoconion) mosquito is normally responsible for the dispersal of the enzootic strain of the VEE virusFootnote 3,Footnote 6. Ochlerotatus taeniorhynchus, Psorophora confinnis, Psorophora columbiae, Ochleratus sollicitans, Mansonia titillans and Anophilis aquasalis are some of the species of mosquitoes known to carry the epizootic varieties of the VEE virusFootnote 3,Footnote 5,Footnote 7.
Section IV - Stability and viability
Drug susceptibility: No drug susceptibilities have been determined to dateFootnote 5.
Susceptibility to disinfectants: Like other enveloped viruses, the VEE virus is susceptible to disinfectants such as 1% sodium hypochlorite, 4% formaldehyde, 2% gluteraldehyde, 70% ethanol, 3-6% hydrogen peroxide, and 2% peracetic acidFootnote 9.
Physical inactiviation: Microbial inactivation is possible using moist or dry heatFootnote 12. Toga viruses can be inactivated by heating for 15 minutes at 65°CFootnote 13.
Survival outside host: The virus is stable in blood and exudates as well as in freeze-dried materials (aerosols)Footnote 9,Footnote 14.
Section V - First aid and medical
Surveillance: Monitor for symptoms. Confirm infection by isolating the virus from the CSF of infected individuals with CNS complications and determine the antibody titre by serology tests such as serum neutralizing (SN), complement fixation (CF), and hemagglutination inhibition (HI) testsFootnote 5,Footnote 15,Footnote 16. Many laboratory techniques can be used to confirm arbovirus infections, including PCR, ELISA and serology, as well as immunohistochemical (IHC) staining of tissue sections Footnote 15.
Note: The availability of diagnostic methods may vary by country.
First aid/treatment: No specific treatment available. Supportive treatment may be given to alleviate symptomsFootnote 8.
Immunization: An investigational live-attenuated TC-83 vaccine is recommended for laboratory workers in some countries Footnote 7,Footnote 14. This vaccine is quite effective in preventing infection by the epizootic strains of the VEE virus. A formalin-inactivated vaccine (C-84) has been formulated for use in individuals who do not mount effective immune responses to the TC-83 vaccineFootnote 3. However, although the TC-83 and C-84 vaccines are available for use in laboratory workers in some countries, there is no licensed vaccine available for the general populationFootnote 3. Furthermore, there are no VEE virus vaccines available for use in Canada.
Prophylaxis: None apart from avoidance of mosquito bites.
Section VI - Laboratory hazards
Laboratory-acquired infections: Several laboratory-acquired cases of the VEE virus have been reported. As of 2006, a total of 186 cases and 2 deaths have been documentedFootnote 16. Most of these incidents were related to egg culture techniques, suckling mice and aerosol exposureFootnote 9. A physical exam and a careful medical check-up are recommended after a laboratory accident involving VEE in order to avoid laboratory-acquired infectionsFootnote 16.
Sources/specimens: Arboviruses may be present in blood, cerebrospinal fluid, urine and exudatesFootnote 14.The virus may be found in nasal, eye and mouth secretions of infected animals, and in contaminated animal beddingFootnote 5,Footnote 14.
Primary hazards: The greatest risks when working with the VEE virus are exposure to infected aerosols, accidental subcutaneous inoculation, and contact with broken skin or contaminated animal beddingFootnote 14.
Special hazards: The VEE virus is fairly stable in dried blood and exudatesFootnote 14.
Section VII - Exposure controls/personal protection
Risk group classification: Risk group 3Footnote 17.
Containment requirements: Containment Level 3 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.
Protective clothing: Personnel entering the laboratory should remove street clothing and jewellery, and change into dedicated laboratory clothing and shoes, or don full coverage protective clothing (i.e., completely covering all street clothing). Additional protection may be worn over laboratory clothing when infectious materials are directly handled, such as solid-front gowns with tight fitting wrists, gloves, and respiratory protection. Eye protection must be used where there is a known or potential risk of exposure to splashesFootnote 18.
Other precautions: All activities with infectious material should be conducted in a biological safety cabinet (BSC) or other appropriate primary containment device in combination with personal protective equipment. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are loaded or unloaded in a biological safety cabinet. The use of needles, syringes, and other sharp objects should be strictly limited. Open wounds, cuts, scratches, and grazes should be covered with waterproof dressings. Additional precautions should be considered when working with animals or performing large scale activitiesFootnote 18.
Section VIII - Handling and storage
Spills: Allow aerosols to settle and while wearing protective clothing, gently cover spill with paper towels and apply appropriate disinfectants, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean upFootnote 18.
Disposal: Decontaminate all used material before disposal via incineration, steam sterilization, or chemical disinfectantsFootnote 18.
Storage: Store in sealed containers that are appropriately labelled inside the locked containment level 3 laboratoryFootnote 18.
Section IX - Regulatory and other information
Regulatory information: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, the Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.
Updated: August 2021
Prepared by: Centre for Biosecurity, Public Health Agency of Canada.
Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.
Public Health Agency of Canada, 2021
- Footnote 1
Atasheva, S., Fish, A., Fornerod, M., & Frolova, E. I. (2010). Venezuelan equine Encephalitis virus capsid protein forms a tetrameric complex with CRM1 and importin alpha/beta that obstructs nuclear pore complex function. Journal of Virology, 84(9), 4158-4171. doi:10.1128/JVI.02554-09
- Footnote 2
Gardner, C. L., Burke, C. W., Tesfay, M. Z., Glass, P. J., Klimstra, W. B., & Ryman, K. D. (2008). Eastern and Venezuelan equine encephalitis viruses differ in their ability to infect dendritic cells and macrophages: impact of altered cell tropism on pathogenesis. Journal of Virology, 82(21), 10634-10646. doi:10.1128/JVI.01323-08
- Footnote 3
Weaver, S. C., Ferro, C., Barrera, R., Boshell, J., & Navarro, J. C. (2004). Venezuelan equine encephalitis. Annual Review of Entomology, 49, 141-174. doi:10.1146/annurev.ento.49.061802.123422
- Footnote 4
De la Monte, S., Castro, F., Bonilla, N. J., Gaskin de Urdaneta, A., & Hutchins, G. M. (1985). The systemic pathology of Venezuelan equine encephalitis virus infection in humans. The American Journal of Tropical Medicine and Hygiene, 34(1), 194-202.
- Footnote 5
Sidwell, R. W., Gebhardt, L. P., & Thorpe, B. D. (1967). Epidemiological Aspects of Venezuelan Equine Encephalitis Virus Infections. Bacteriological Reviews, 31(1), 65-81.
- Footnote 6
Zacks, M. A., & Paessler, S. (2010). Encephalitic alphaviruses. Veterinary Microbiology, 140(3-4), 281-286. doi:10.1016/j.vetmic.2009.08.023
- Footnote 7
Knipe, D. M., & Howley, P. M. (Eds.). (2001). Fields Virology (4th ed.). Philidelphia: Lippincot Williams & Wilkins.
- Footnote 8
Krauss, H., Weber, A., Appel, M., Enders, B., Isenberg, H. D., Schiefer, H. G., Slenczka, W., von Graevenitz, A., & Zahner, H. (Eds.). (2003). Zoonoses Infectious Diseases Transmissible from Animals to Humans (3rd ed.). Washington: ASM press.
- Footnote 9
Collins, C. H., & Kennedy, D. A. (Eds.). (1983). Laboratory-acquired Infections (4th ed.). Oxford: Butterworth-Heinermann.
- Footnote 10
Heymann, D. L. (2008). Control of Communicable Diseases Manual (19th Edition ed.). Washington, D.C.: American Public Health Association.
- Footnote 11
Pfeffer, M., & Dobler, G. (2010). Emergence of zoonotic arboviruses by animal trade and migration. Parasites and Vectors, 3(1), 35.
- Footnote 12
Block, S. S. (Ed.). (2001). Disinfection, Sterilization, and Preservation (5th ed.). Philidelphia: Lippincott Williams & Wilkins.
- Footnote 13
Lelie, P. N., Reesink, H. W., & Lucas, C. J. (1987). Inactivation of 12 viruses by heating steps applied during manufacture of a hepatitis B vaccine. Journal of Medical Virology, 23(3), 297-301.
- Footnote 14
Richmond, J. Y., & McKinney, R. W. (Eds.). (1999). Biosafety in Microbiological and Biomedical Laboratories (4th ed.). Washington: CDC-NIH.
- Footnote 15
Murray, P. R., Baron, E. J., Jorgensen, J. H., Landry, M. L., & Pfaller, M. A. (Eds.). (2007). Manual of Clinical Microbiology (9th ed.). Washington: ASM Press.
- Footnote 16
Fleming D & Hunt D (Ed.). (2006). Biological Safety Principles and Practices (4th ed.). Washington: ASM Press.
- Footnote 17
Human pathogens and toxins act. S.C. 2009, c. 24, Second Session, Fortieth Parliament, 57-58 Elizabeth II, 2009. (2009).
- Footnote 18
Public Health Agency of Canada. (2004). In Best M., Graham M. L., Leitner R., Ouellette M. and Ugwu K. (Eds.), Laboratory Biosafety Guidelines (3rd ed.). Canada: Public Health Agency of Canada.
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