Difference between revisions of "Equine Encephalitis Virus"
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Vectors transmit viral particles between sylvatic hosts when takin ga blood meal. If the virus can peentrate the gut of the vector, then it may pass throhg the haemolymph to the oral glands, multiply and subsequntrly be shed in the saliva and other oral secretions. If th eblood meal octnains adequate numbers of viral particles, multiplication may not be rrequired for transmission. It is likely tha the mosquito remians infected for life. | Vectors transmit viral particles between sylvatic hosts when takin ga blood meal. If the virus can peentrate the gut of the vector, then it may pass throhg the haemolymph to the oral glands, multiply and subsequntrly be shed in the saliva and other oral secretions. If th eblood meal octnains adequate numbers of viral particles, multiplication may not be rrequired for transmission. It is likely tha the mosquito remians infected for life. | ||
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=====Zoonology===== | =====Zoonology===== | ||
Revision as of 23:11, 6 July 2010
This article is still under construction. |
Viral Family
Members of the Togaviridae are small, lipid- and protein-enveloped RNA viruses. Within this family are disease-causing arboviruses (insect-borne virsuses) of the Alphavirus genus.
Viral Genus
Alphaviruses are single-stranded, linear, positive-sense RNA viruses, 60-70nm in diameter.
Important Serotypes
During equine and human epidemics of encephalitis in the Western Hemisphere, the most frequently isolated alphaviruses have included:
EEE and WEE are specific and discrete species. There are North and South American antigenic variants of EEE. WEE is a recombinant between an EEE-like virus and a Sindbis-like virus. There are two antigenic subtypes of WEE virus: WEE and Highlands J viruses. Extensive geographical overlap occurs between the various strains which have equivocal differences in antigenic properties and biological behaviour. There are 6 distinct subtypes of VEE virus. Over the last 20 years, large outbreaks of equine encephalitis in the Western Hemisphere have been caused by subtypes IAB, IC and IE. ID and IF variants from Central America and Brazil respectively, type II (Everglades) virus in Florida and types II, IV, V ad VI viruses are considered endemic and are of low pathogenicity for horses under most circumstances.
Diseases
Epizootiology
Distribution
Virus distribution is largely dictated by vector distribution. EEE virus is found as far north as eastern Canada, south throughout the Caribbean and in parts of Central and South America. EEE has been identifed in the Philippines and it may have a presence in Europe. WEE virus is recognised in reservoir avian hosts in the western United States but clinical disease has been rare here in the last 20 years. As well as Mexico, Venezuela and colombia, VEE virus has been recently isolated in Trinidad, French Guiana, Peru and Brazil.
Epidemic
Reservoirs
Togaviridae generally persist by asymptomatically infecting wild animals (sylvatic hosts) such as birds, small mammals and reptiles. Viruses overwinter in sylvatic populations.
Vectors
The major disease vectors for each serotype of veterinary significance are:
- EEE: Aedes spp.
- WEE: Culex tarsalis
- VEE: Culex melanconium, Aedes spp., Phosphora spp.
Culiseta melanura is a vector for EEE. It is largely confined to freshwater swamps, feeds primarily on swamp birds and is rarely found in areas of increased horse density. This mosquito generally serves as a vector for the enzootic cycle involving swamp birds. Aedes spp. are more important in epizootics and epidemics. Culex tarsalis is the primary vector that maintains WEE virus in an enzootic cycle with passerine birds. Dermacentor andersoni ticks, Triatoma sanguisuga (assassin bug), and the cliff swallow bug (Oeciacus vicarius) may also be involved as vectors or overwintering reservoirs fro WEE. Several species of mosquitoes from at least 11 geerna have been determined ot be naturally infected with epidemic strains of VEE virus. Ticks may also be capable of viral trasnmission. Vectors transmit viral particles between sylvatic hosts when takin ga blood meal. If the virus can peentrate the gut of the vector, then it may pass throhg the haemolymph to the oral glands, multiply and subsequntrly be shed in the saliva and other oral secretions. If th eblood meal octnains adequate numbers of viral particles, multiplication may not be rrequired for transmission. It is likely tha the mosquito remians infected for life.