Equis ISSN 2398-2977

Equine viral encephalitides

Synonym(s): Togaviral encephalitis, Eastern equine encephalomyelitis/encephalitis (EEE, Western equine encephalomyelitis/encephalitis (WEE, Venezuelan equine encephalomyelitis/encephalitis (VEE, flaviviral encephalitis, West Nile fever virus

Contributor(s): Frank Andrews, Vetstream Ltd

Introduction

Print off the Owner factsheet on West nile virus - what owners should know to give to your clients.

Pathogenesis

Pathophysiology

  • All 3 types of disease are caused by Togavirus genera Alphavirus.
  • The 3 disease entities are:
  • Various antigenic variants occur.
  • The virus is inoculated into muscle by insect vectors   →   replicates in lymph nodes and endothelial cells   →   spreads to infect CNS in 3-5 days.
  • The viruses persist in reservoir populations, eg birds, from where they are transmitted to the horse via specific vectors, eg mosquitoes, biting flies.
  • The highest incidence of the disease is associated with the vector seasons.
  • After viral inoculation multiplication occurs in muscle before entry into the lymphatic circulation and localization into lymph nodes.
  • Viruses replicate in macrophages/neutrophils   →   shed in small numbers.
  • Many viral particles are cleared and often no clinical signs are noted.
  • Viral neutralizing antibodies are produced.
  • If viruses are not eliminated, infection of endothelial cells occurs   →   concentration in highly vascular organs, eg liver, spleen   →   virus replication here   →   increased circulating levels of virus   →   secondary viremia associated with clinical signs.
  • Infection of the CNS occurs within 3-5 days.

Timecourse

  • Experimental studies show that there is a 1-3 week incubation period for EEE and WEE (EEE<WEE).

Epidemiology

Reservoirs
  • Togaviridaegenerally persist by asymptomatically infecting wild animals, eg birds, small mammals and reptiles, by unknown mechanisms.
  • The viruses persist in thesereservoirsduring the winter and when no vectors are present.
  • Each virus has a specificvectorand the vector's distribution determines to a greater degree the virus's distribution.

Vectors

  • The vectors for EEE includeCuliseta melanuraandAedesspp: the former appears to act as a vector for the enzootic cycle in the reservoir hosts; the latter appears to be important in epizootic cycles and epidemics.
  • The vectors for WEE may beCuliseta melanurafor the enzootic cycle, but others, egCulex tarsalisare involved in epizootics.
  • The vectors for VEE include a number of species, egCulex melanoconium,Aedesspp andPhosporaspp.
  • Some insects appear to carry more than one virus and it is not known why some cause disease and others do not: virulence induction, specific to certain viruses, is thought to occur within the vector.
  • Although vector transmission is the major way of spreading the infection, contact with nasal secretions in WEE and VEE may also allow transmission, but to a lesser degree.
  • Vectors obtain the viruses by taking a blood meal from the reservoir hosts.
  • The virus may replicate in the vector or, if the blood meal is heavily infected, direct transmission may occur.
  • The highest incidence of cases occurs during the vector season, ie in temperate climates: June-November (prolonged in warmer climates).
  • Mules, burros, calves and pigs can all be infected with milder clinical signs in the non-equine cases.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • van Galen Get al(2013)Can horses be clinically screened for West Nile fever?Vet Rec172(4), 101PubMed.
  • Raleigh P Let al(2012)Suveillance for antibodies to West Nile virus in Ireland.Vet Rec170(7), 180PubMed.
  • Herholz C, Fussel A-E, Timoney P, Schwermer H, Bruckner L & Leadon D (2008)Equine travellers to the Olympic Games in Hong Kong 2008: A review of worldwide challenges to equine health, with particular reference to vector-borne diseases.Equine Vet J40(1), 87-95PubMed.
  • Traub-Dargatz J L, Cordes T & Evans M B (2007)The evolving means of protecting horses against West Nile infection through immunization.Equine Vet J39(6), 484-485PubMed.
  • Long M Tet al(2007)Safety of an attenuated West Nile virus vaccine, liveFlaviviruschimera in horses.Equine Vet J39(6), 486-490PubMed.
  • Lont M Tet al(2007)Efficacy, duration and onset of immunogenicity of a West Nile virus vaccine, liveFlaviviruschimera, in horses with a clinical disease challenge model.Equine Vet J39(6), 491-497PubMed.
  • Epp T, Waldner C & Townsend H G G (2007)A case-control study of factors associated with development of clinical disease due to West Nile virus, Saskatchewan 2003.Equine Vet J39(6), 498-503PubMed.
  • Tanner J Met al(2006)Evaluation of factors associated with positive IgM capture ELISA results in equids with clinical signs compatible with West Nile virus infection: 1017 cases (2003).JAVMA228(3), 414-421PubMed.
  • Durand Bet al(2005)Serosurvey for West Nile virus in horses in sounthern France.Vet Rec157(22), 711-713PubMed.
  • Guthrie A J, Howell P Get al(2003)West Nile virus infection of Thoroughbred horses in South Africa (2000-2001).Equine Vet J35(6), 601-605PubMed.
  • Centers for Disease Control and Prevention (CDC) (2003)West Nile virus activity--United States, October 30-November 5, 2003.MMWR Morb Mortal Wkly Rep52(44), 1080PubMed CDC Full Text Report.


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