Equis ISSN 2398-2977

Venezuelan equine encephalomyelitis

Synonym(s): VEE

Contributor(s): Sarah Binns, Jennifer L Davis


  • Cause: VEE virus   Venezuelan equine encephalomyelitis virus  ; can be isolated from single cases, sporadic outbreaks or epidemics of encephalitis in equids (horses, donkeys and mules).
  • The proportional mortality rate in affected equids can be 20-85%.
  • The disease is transmitted by mosquitoes, and hence is an arbovirus (arthropod-borne).
  • VEE is an important zoonosis and human infection usually follows equine infection by about 2 weeks. Clinical signs in humans range from mild flu-like symptoms to neurologic disease (4-14%) and death (1%), and surviving patients generally show residual neurological deficits.
  • Signs: pyrexia, anorexia, depression   →   neurological disease.
  • Diagnosis: hematology, serology.
  • Treatment: fluid therapy, anticonvulsants, anti-inflammatory drugs.
  • Prognosis: poor.



Predisposing factors

  • Disease occurs in epidemics related to vector-borne transmission; therefore areas in which mosquitoes breed are at increased risk.
  • Transmission from mosquitoes to horses tends to occur during the rainy season.


  • Variants I-AB and I-C cause high mortality in horses, and high morbidity in humans during equine epidemics.
  • After inoculation in the saliva of the mosquito, the virus travels in the lymphatics to the lymph nodes. There it replicates in macrophages and neutrophils.
  • This results in leukopenia, lymphopenia and pyrexia.
  • Viremia associated with these variants can be at a very high level (up to 10¹º virions/ml blood). Animals are pyrexic during the viremic period.
  • The disease may be partly immune-mediated, and antibodies do not lead to elimination of the virus from the brain or other tissues.
  • Neurological signs may be referable to cortical, thalamic and/or brain stem lesions.


  • Incubation period 16 days.
  • Two distinct phases of disease in horses and humans.
  • Viremia and replication in the viscera occur 25 days post-infection and are associated with pyrexia, depression and anorexia. Recovery may occur following this stage.
  • Neurological signs develop 68 days following infection.
  • Duration of clinical signs 49 days if recovery occurs.


  • VEE virus variants I-AB and I-C are associated with epidemics in all equine species.
  • Ancillary hosts can be any non-immune vertebrates.
  • Non-pathogenic subtypes exist endemically in sylvatic cycles focused on areas containing mangrove swamps and brackish water with rodent reservoirs and mosquitoes ofCulexspecies to act as vectors.
  • Variants I-AB and I-C have not been isolated from natural hosts between epidemics, and the reservoirs have not been identified. It is likely that the virus may persist in mosquitoes during the dry season and then be spread to the mammalian hosts during the rainy season.
  • Variants I-AB and I-C can be transmitted by any competent mosquito vector.


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login


This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Smith D R, Aguilar P V, Coffey L L, Gromowski G D, Wang E & Waever S C (2006)Venezuelan equine encephalitis virus transmission and effect on pathogenesis.Emerg Inf Dis12(8), 11901196PubMed.
  • Carrara A-S, Gonzales M, Ferro C, Tamayo M, Aronson J, Paessler S, Anishchenko M, Boshell J & Weaver S C (2005)Venezuelan equine encephalitis virus infection of spiny rats.Emerg Inf Dis11(5), 663669PubMed.
  • Navarro J-C, Medina G, Vasquez C, Coffey L L, Wang E, Suarez A, Biord H, Salas M & Weaver S C (2005)Postepizootic persistence of Venezuelan equine encephalitis virus, Venezuela.Emerg Inf Dis11(12), 19071915PubMed.
  • Weaver S C (2005)Host range, amplification and arboviral disease emergence.Arch Virol Suppl(19), 3344PubMed.
  • Aguilar P V, Greene I Pet al(2004)Endemic Venezuelan equine encephalitis in northern Peru.Emerg Inf Dis10(5), 880888PubMed.
  • Estrada-Franco J G, Navarro-Lopez Ret al(2004)Venezuelan equine encephalitis virus, southern Mexico.Emerg Inf Dis10(12), 21132121PubMed.
  • Weaver S C, Ferro C, Barrera R, Boshell J & Navarro J C (2004)Venezuelan equine encephalitis.Annu Rev Entomol49, 141174PubMed
  • Rico-Hesse R (2000)Venezuelan equine encephalomyelitis.Vet Clin North Am Equine Pract16(3), 553563PubMed.
  • Weaver S C, Power A M, Brault A C & Barrett A D (1999)Molecular epidemiological studies of veterinary arboviral encephalitides.Vet J157(2), 123138PubMed.
  • Walton T E, Holbrook F R, Bolivar-Raya R, Ferrer-Romero J & Ortega M D (1992)Venezuelan equine encephalomyelitis and African horse sickness. Current status and review.Ann N Y Acad Sci653, 217227PubMed.
  • Walton T E (1992)Arboviral encephalomyelitides of livestock in the western hemisphere.JAVMA200(9), 13851389PubMed.