Changes

====Epidemiology====

====Epidemiology====

Disease associated with EEE, WEE and VEE is largely restricted to the Western Hemisphere, ranging from temperate to desert climates.  EEE in the United States is mainly seen in the Southeastern United States but has been detected in all states east of the Mississippi River and some Western states.  Large outbreaks of WEE have been described in California and other Western states but the incidence of clinical disease in these areas has experienced a dramatic decrease. The reason for this unknown but may be due to geographical variation in virulence.  Equine disease associated with WEE is rare on the Eastern seaboard ofthe United States. VEE  virus is a very important human andveterinary pathogen in the Western Hemipshoere that can cause large outbreaks of disease in humans and horses over large geopgrahic areas. VEE has spread into Central America, causing devastating epidemics as far north as Texas. The disease distribution is determined by climatic conditions as well as agricultural practices, such as irrigation, which favour the life cycle and spread of mosquitoes.  Transfer is via '''vector''': mostly through '''[[Culicidae|mosquito salivary transfer]]'''.  WEE and VEE may also be transmitted via nasal secretions but this is less likely.  Disease amplification occurs during the viraemic phase which lasts until nervous signs develop.  Amplification from horses is unlikely with EEE and WEE but occurs with VEE in association with a relatively high viraemia.  Ocular and nasal discharges from infected horses cotnain high concentrations of VEE.  Zoonotic spread has been noted with VEE but is unlikely for the other two serotypes.  Horse to horse spread of EEE is possible.  Humans and horses are terminal hosts for WEE.  Horses with WEE are sentinels for humans in a given area.

Disease associated with EEE, WEE and VEE is largely restricted to the Western Hemisphere, ranging from temperate to desert climates.  EEE in the United States is mainly seen in the Southeastern United States but has been detected in all states east of the Mississippi River and some Western states.  Large outbreaks of WEE have been described in California and other Western states but the incidence of clinical disease in these areas has experienced a dramatic decrease. The reason for this unknown but may be due to geographical variation in virulence.  Equine disease associated with WEE is rare on the Eastern seaboard ofthe United States. VEE  virus is a very important human andveterinary pathogen in the Western Hemipshoere that can cause large outbreaks of disease in humans and horses over large geopgrahic areas. VEE has spread into Central America, causing devastating epidemics as far north as Texas. The disease distribution is determined by climatic conditions as well as agricultural practices, such as irrigation, which favour the life cycle and spread of mosquitoes.   

Highlands J virus, antigenically related to WEE virus, has been isolated in eastern USA. Although it is generally believed not to cause disease in mammals, it has been isolated from the brain of a horse dying of encephalitis in Florida (4).WEE virus infection in horses is often observed over a wide geographical area, e.g. sporadic cases over 1000 square miles. EEE virus infections are usually observed in limited geographical areas.  

Transfer is via '''vector''': mostly through '''[[Culicidae|mosquito salivary transfer]]'''.  WEE and VEE may also be transmitted via nasal secretions but this is less likely.  Disease amplification occurs during the viraemic phase which lasts until nervous signs develop. Amplification from horses is unlikely with EEE and WEE but occurs with VEE in association with a relatively high viraemia.  Ocular and nasal discharges from infected horses cotnain high concentrations of VEE.  Zoonotic spread has been noted with VEE but is unlikely for the other two serotypes.  Horse to horse spread of EEE is possible.  Humans and horses are terminal hosts for WEE.  Horses with WEE are sentinels for humans in a given area.WEE virus infection in horses is often observed over a wide geographical area, e.g. sporadic cases over 1000 square miles. EEE virus infections are usually observed in limited geographical areas. Highlands J virus, antigenically related to WEE virus, has been isolated from the brain of a horse dying of encephalitis in Florida (4).

=====Seasonal Incidence=====

=====Seasonal Incidence=====

The disease is not directly contagious between horses and humans but occurs sporadically in both species from mid-summer to late autumn - during the height of the vector season.  In temperate climates, case numbers peak in June to November.  In warm climates, where the vector season is longer, the disease period is prolonged.  Global warming may promote more cold climate outbreaks.

The disease is not directly contagious between horses and humans but occurs sporadically in both species from mid-summer to late autumn - during the height of the vector season.  Case numbers peak in June to November in temperate climates.  The vector season is longer in warmer climates, where the disease period is prolonged.  Global warming may promote more outbreaks in historically colder climates.

 

=====Epidemics=====

=====Epidemics=====

Prerequisites for epidemics to occur include adequate and adjacent numbers of reservoir animals, sufficient quantities of virulent virus, infected intermediate hosts, insect vectors and susceptiple horse and human populations.  Outbeak prediction has been inaccurate, implyingf that other, unidentified factors may be important.

Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation.  However, there are some epidemic requirements are beyond question.  Adequate amounts of infective virus, sufficent vectors, infected sylvatic hosts and susceptible terminal hosts, and finally, appropriate reservoirs, are all crucial.

====Pathogenesis====

====Pathogenesis====