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
Introduction
- Eastern equine encephalomyelitis/encephalitis (EEE) Eastern equine encephalomyelitis virus Eastern equine encephalomyelitis .
- Western equine encephalomyelitis/encephalitis (WEE) Western equine encephalomyelitis virus Western equine encephalomyelitis .
- Venezuelan equine encephalomyelitis/encephalitis (VEE) Venezuelan equine encephaloyelitis virus Venezuelan equine encephalomyelitis.
- West Nile Virus encephalitis West Nile fever virus .
- Cause: togavirus genera alphavirus; reservoir in wild animal population transmitted to the horse by insect vectors; considerable hazard to public health.
- Incidence: restricted to the Western hemisphere.
- Signs: various:
- Inapparent infections with viremia and pyrexia.
- Generalized febrile illness.
- Clinical encephalitis.
- Diagnosis: confirmed using serology.
- Treatment: non-specific, mainly supportive.
- Prevention: control insect vector concentration; vaccination.
- Prognosis: poor for complete recovery if neurologic deficits.
Presenting signs
- Animals in endemic areas, particularly unvaccinated or those recently brought into the area.
- Summer and autumn months.
- Inapparent infections with low-grade viremia, pyrexia, stiffness.
- Generalized febrile illness.
- Clinical encephalitis.
- Variable mortality rates.
Geographic incidence
- Western hemisphere, eg North, Central and South America.
- Temperate to desert climates.
- Each equine disease has a characteristic distribution which is smaller than the range of positive serology:
- WEE: west and central parts of USA and South America; Central America.
- EEE: east and central USA; Central America; central South America.
- VEE: south-western USA; Central America; northern South America.
- Philippines (EEE).
- ? Europe.
Cost considerations
- Loss of animal(s).
- Treatment.
Pathogenesis
Pathophysiology
- All 3 types of disease are caused by Togavirus genera Alphavirus.
- The 3 disease entities are:
- Eastern equine encephalomyelitis/encephalitis (EEE) Eastern Equine Encephalomyelitis virus .
- Western equine encephalomyelitis/encephalitis (WEE) Western Equine Encephalomyelitis virus .
- Venezuelan equine encephalomyelitis/encephalitis (VEE).
- 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.