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→Epidemiology
====Epidemiology====
====Epidemiology====
=====Distribution=====
=====(1) Distribution=====
Togaviral encephalitis in equids is largely confined to the Western Hemisphere. Venezuelan EEV can cause large outbreaks of disease over extensive geographical areas in both humans and horses. Spread of this virus into Central America has had disasterous consequences with epidemics as far north as Texas. Climatic conditions and interventions that support vector populations, such as irrigation, greatly influence the geographical spread of the disease. EEE has been recorded across the United States, but mostly in the Southeastern States. As its names suggests, WEE has a predilection for the Western states which have been subject to significant outbreaks in the past. A regional alteration in virulence has been proposed for the steep decline in clinical case numbers observed in this area. A lag phase of 2-5weeks is commonly observed between horse and human cases of WEE in a given locus. Both are dead-end hosts for the virus. A subtype of Western EEV, Highlands J virus, was isolated from the brain of a horse with encephalitis in Florida (Karabatsos ''et.al'', 1988).
Togaviral encephalitis in equids is largely confined to the Western Hemisphere. Venezuelan EEV can cause large outbreaks of disease over extensive geographical areas in both humans and horses. Spread of this virus into Central America has had disasterous consequences with epidemics as far north as Texas. Climatic conditions and interventions that support vector populations, such as irrigation, greatly influence the geographical spread of the disease. EEE has been recorded across the United States, but mostly in the Southeastern States. As its names suggests, WEE has a predilection for the Western states which have been subject to significant outbreaks in the past. A regional alteration in virulence has been proposed for the steep decline in clinical case numbers observed in this area. A lag phase of 2-5weeks is commonly observed between horse and human cases of WEE in a given locus. Both are dead-end hosts for the virus. A subtype of Western EEV, Highlands J virus, was isolated from the brain of a horse with encephalitis in Florida (Karabatsos ''et.al'', 1988).
=====Transmission=====
=====(2) Transmission=====
Transfer is '''vector'''-mediated, primarily via '''[[Culicidae|mosquito salivary transfer]]'''. WEE and VEE may also be transmitted horse to horse through nasal secretions. This mode of transmission is less likely, despite the fact that high concentrations of VEE virus are found in ocular and nasal discharges from infected horses. The viraemic phase ends when nervous signs develop and is important for disease amplification. Amplification from horses is likely only with VEE virus, in association with a relatively high and potentially persistent viraemia. Similarly, zoonotic spread is unlikely for Eastern and Western equine encephalitis, but has been noted with VEE.
Transfer is '''vector'''-mediated, primarily via '''[[Culicidae|mosquito salivary transfer]]'''. WEE and VEE may also be transmitted horse to horse through nasal secretions. This mode of transmission is less likely, despite the fact that high concentrations of VEE virus are found in ocular and nasal discharges from infected horses. The viraemic phase ends when nervous signs develop and is important for disease amplification. Amplification from horses is likely only with VEE virus, in association with a relatively high and potentially persistent viraemia. Similarly, zoonotic spread is unlikely for Eastern and Western equine encephalitis, but has been noted with VEE.
=====Seasonal Incidence=====
=====(3) 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. 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.
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=====
=====(4) Epidemics=====
Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation. However, 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.
Outbeak prediction to date has been inaccurate, implying that other, unidentified factors may be in operation. However, 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.