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Venezuelan Equine Encephalitis (VEE) Infection in Horses

  • Authors: Thomas Walton 1, Erica Suchman 2
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Animal and Plant Health Inspection Service (Retired), United States Department of Agriculture, Fort Collins, CO, 80526-8117; 2: Colorado State University, Fort Collins, Colorado, 80523
  • Citation: Thomas Walton, Erica Suchman. 2007. Venezuelan equine encephalitis (vee) infection in horses.
  • Publication Date : January 2007
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Venezuelan equine encephalitis (VEE) is caused by a virus in the family Togaviridae genus Alphavirus.  It is an enveloped virus with an icosahedral capsid 60 to 70 nm in diameter with a linear, single-stranded positive-sense RNA nonsegmented genome of approximately 11.4 kilobases (4).  VEE periodically occurs in South and Central America and occurred in Texas in 1971 (6).   VEE viruses exist in two settings: (i) a continuous cycle maintained between Culex mosquito vectors and rodents (enzootic), and (ii) epidemics that involve several mosquito species that feed on mammals (epizootic).  Epizootic VEE virus varients occur in irregular epizootic cycles and cause clinical disease and deaths in equines only during those cycles.  Sylvatic or enzootic VEE viruses may be found at any time in enzootic cycles involving rodents; equine disease is rarely associated with infection by sylvatic VEE viruses.  Aedes taeniorhynchus is thought to be the main mosquito vector (1); however, other mosquitoes are thought to play a role, and during an epidemic in horses in 1969 to 1971 Aedes aegypti, Culex tarsalis, Deinocerites pseudes, and Psorophora confinnis mosquitoes were shown to be infected.  This epidemic began in 1969 in northern South America and by the time it ended in 1971, it had resulted in the deaths of hundreds of thousands of horses throughout Central America, Mexico, and Texas (3).   Female mosquitoes ingest the virus when bloodfeeding on infected rodents or horses to obtain protein for egg production and after a 7 to 20 day extrinsic incubation period can transmit the virus when feeding on a new host.  The mosquitoes remain infected for life. The principal mosquito vector for human infections is thought to be Culex pipiens although more than 30 other species have been implicated (5)           

Usually 0.5 to 5 days after being bitten by an infected mosquito, horses begin to show signs. Infections range from asymptomatic, to mild (anorexia, fever), or severe either with fatality or without.  Horses with a severe response show a distinctive lack of coordination that leads to a "leaning stance" and circling due to the swelling of the brain (Fig. 1–3).  Other signs include fever, lack of appetite with rapid weight loss, and depression, and may include seizures.  The sylvatic virus is endemic in northern South America, Trinidad, Central America, Mexico, and Florida. Epizootic virus appears sporadically in epizootics mostly in Mexico, Central and South America.  The photos shown here were taken in Gualaca, Panama.  Prognosis is poor for horses infected with epizootic viruses (50 to 90% mortality).  Horses often die from trauma induced during seizures.  Figure 4 shows a horse that has died, and shows lesions on the eyes and face incurred during seizures.  Also note the lack of vegetation around the head, which is caused as the horse's head swings back and forth during the seizures.  Similar defoliation is also often noted near the legs of horses that die of VEE as their legs will swing in a "paddling" motion.  Upon necropsy the brain shows signs of encephalitis (swelling of the brain) and hemorrhaging that is actually caused by head trauma during the seizures rather than viral damage (Fig. 5).  Horses are often euthanatized before they reach this point, as recovery in cases this severe is rare (3, 6).  There is a vaccine to control this disease that should be administered yearly and also contains western and eastern encephalitis viruses along with VEE viruses.                                                                                                 

Similar to western and eastern encephalitis, humans can become infected with VEE.  In humans, signs of VEE infection include fever, exhaustion, back pain, nausea, vomiting, and headache; children are at greatest risk for developing central nervous system infections. The overall mortality rate in epidemics is 0.5 to 1%. In patients who develop encephalitis, the mortality rate is about 20%, in the absence of adequate medical care this can approach 25 to 30%.  Encephalitis is clinically diagnosed in only 1 to 4% of adults and 3 to 5% of children.  There is no vaccination for humans (3). 

The virus is cultivated typically in cell culture and quantified using plaque assays; virus is serially diluted and plated on the African green monkey kidney cell line Vero V76 cells and cytopathic effect is quantified.  Diagnosis is usually attempted using paired serums (acute and convalescent; 2 weeks apart) assaying for a four-fold increase in serum neutralizing antibody titers.  This assay detects antibodies in the serum, if animals have had an immune response.   However, this is problematic as many animals die before the second, 2 week, convalescent sample can be obtained (6). 

See also:
Venezuelan Equine Encephalitis Virus
 
References. 



1.  Brault, A. C., A. M. Powers, and S. C. Weaver.  2002. Vector infection determinants of Venezuelan equine encephalitis virus reside within the E2 envelope glycoprotein. J. Virol. 76 :6387–6392.
 
2.  Committee on Foreign Animal Diseases of the United States Animal Health Association.  1998, revision date.  The Gray book of foreign animal diseases, 6th ed.  United States Animal Health Association, Richmond, Va.  [Online.] http://www.vet.uga.edu/VPP/gray_book/FAD/index.htm.
 
3.  Fenner, F., P. A. Bachmann, E. P. J. Gibbs, F. A. Murphy, M. J. Studdert, and D. O. White.  1987.  Veterinary virology, p. 460–462.  Academic Press, Inc., Orlando, Fla. 



4.  Griffin, D. E. 2001. Alphaviruses, p. 917–962. In D. M. Knipe and P. M. Howley (ed.), Fields virology.  Lippincott Williams and Wilkins, Philadelphia, Pa. 
 
5.  Nasci, R. S., and B. R. Miller. Culicine mosquitoes and the agents they transmit, p. 85–97. In B. J. Beaty and W. C.  Marquardt (ed.), The biology of disease vectors. University Press of Colorado, Niwot, Colo.



6.  Roberts, W. A., and G. A. Carter. 1976. Essentials of veterinary virology, p. 107. Michigan State University Press, East Lansing, Mich.

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