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 G et al (2013) Can horses be clinically screened for West Nile fever?Vet Rec 172 (4), 101 PubMed.
  • Raleigh P L et al (2012) Suveillance for antibodies to West Nile virus in Ireland. Vet Rec 170 (7), 180 PubMed.
  • 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 J 40 (1), 87-95 PubMed.
  • Traub-Dargatz J L, Cordes T & Evans M B (2007) The evolving means of protecting horses against West Nile infection through immunization. Equine Vet J 39 (6), 484-485 PubMed.
  • Long M T et al (2007) Safety of an attenuated West Nile virus vaccine, liveFlaviviruschimera in horses. Equine Vet J 39 (6), 486-490 PubMed.
  • Lont M T et al (2007) Efficacy, duration and onset of immunogenicity of a West Nile virus vaccine, live Flavivirus chimera, in horses with a clinical disease challenge model. Equine Vet J 39 (6), 491-497 PubMed.
  • 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 J 39 (6), 498-503 PubMed.
  • Tanner J M et 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). JAVMA 228 (3), 414-421 PubMed.
  • Durand B et al (2005) Serosurvey for West Nile virus in horses in sounthern France. Vet Rec 157 (22), 711-713 PubMed.
  • Guthrie A J, Howell P G et al (2003) West Nile virus infection of Thoroughbred horses in South Africa (2000-2001). Equine Vet J 35 (6), 601-605 PubMed.
  • Centers for Disease Control and Prevention (CDC) (2003) West Nile virus activity-United States, October 30-November 5, 2003. MMWR Morb Mortal Wkly Rep 52 (44), 1080 PubMed CDC Full Text Report.


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