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Mellor, P. S. (1993). African horse sickness: transmission and epidemiology. Vet Res, 24(2), 199–212.
Abstract: African horse sickness (AHS) virus causes a non-contagious, infectious, arthropod-borne disease of equines and occasionally of dogs. The virus is widely distributed across sub-Saharan African where it is transmitted between susceptible vertebrate hosts by the vectors. These are usually considered to be species of Culicoides biting midges but mosquitoes and/or ticks may also be involved to a greater or lesser extent. Periodically the virus makes excursions beyond its sub-Saharan enzootic zones but until recently does not appear to have been able to maintain itself outside these areas for more than 2-3 consecutive years at most. This is probably due to a number of factors including the apparent absence of a long term vertebrate reservoir, the prevalence and seasonal incidence of the vectors and the efficiency of control measures (vaccination and vector abatement). The recent AHS epizootics in Iberia and N Africa spanning as they do, 5 or more yr, seem to have established a new pattern in AHS virus persistence. This is probably linked to the continuous presence of adult C imicola in the area. Culicoides imicola is basically an Afro-Asiatic insect and prefers warm climates. Therefore its continuous adult presence in parts of Iberia and N Africa may be due to some recent moderations of the climate in these areas.
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Scherer, W. F., Madalengoitia, J., Flores, W., & Acosta, M. (1975). Ecologic studies of Venezuelan encephalitis virus in Peru during 1970-1971. Am J Epidemiol, 101(4), 347–355.
Abstract: Venezuelan encephalitis (VE) virus has intermittently produced epidemics and equine epizootics on the dry Pacific coastal plain of Peru since at least the 1930's. However, evidence that the virus exists in the Amazon region of Peru to the east of the Andes mountains was not obtained until antibodies were found in human sera collected in 1965, and 10 strains of the virus were isolated in a forest near the city of Iquitos, Peru during February and March 1971. Eight strains came from mosquitoes and two from dead sentinel hamsters. Three hamsters exposed in forests near Iquitos developed VE virus antibodies suggesting that hamster-benign strains also exist there. Antibody tests of equine sera revealed no evidence that VE virus was actively cycling during the late 1950's or 1960's in southern coastal Peru, where equine epizootics had occurred in the 1930's and 1940's. In northern coastal Peru bordering Ecuador, antibodies were present in equine sera, presumably residual from the 1969 outbreak caused by subtype I virus, since neutralizing antibody titers were higher to subtype I virus than to subtypes III or IV. No VE virus was detected in this northern region during the dry season of 1970 by use of sentinel hamsters. The possibility is considered that VE epidemics and equine epizootics on the Pacific coast of Peru are caused by movements of virus in infected vertebrates traversing Andean passes or in infected vertebrates or mosquitoes carried in airplanes from the Amazon region.
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Sudia, W. D., Fernandez, L., Newhouse, V. F., Sanz, R., & Calisher, C. H. (1975). Arbovirus vector ecology studies in Mexico during the 1972 Venezuelan equine encephalitis outbreak. Am J Epidemiol, 101(1), 51–58.
Abstract: Virus vector studies were conducted in the States of Durango, Chihuahua, and Tamaulipas, Mexico, in June and July 1972. Apparently only a low level of Venzuelan equine encephalitis (VEE) virus transmission to equines occured at the time of the study, and the infection was restricted to areas which had not experienced overt activity during the preceding year. The low level of infection was associated with a scarcity of mosquitoes. The IB (epidemic) strain of VEE virus was isolated from two pools of Anopheles pseudopunctipennis (Theo.) and the blood of one symptomatic equine. The low mosquito population, the relatively few equine cases observed, and the absence of reports of VEE human disease from the outbreak area suggested VEE virus persistence through a low-level mosquito-equine transmission cycle. Other studies have already indicated that wild vertebrates play no more than a minor role in outbreaks of epidemic VEE. Mosquito collections made in areas of the states of Durango, Chihuahua, and Tamaulipas, where considerable epidemic activity of VEE had occurred in 1971, failed to reveal evidence of VEE virus persistence. Twenty-nine ioslations of other arboviruses were also made in these studies: including 22 of St. Louis encephalitis virus (SLE), 2 of Flanders virus, 1 of Turlock virus, 1 of Trivittatus virus of the California Group, 1 of western equine encephalitis virus (VEE), and 2 (from Santa Rose) which possibly represent a hitherto unknown virus in the Bunyamwera Group. These are the first reports of SLE virus isolations from mosquitoes in Mexico, and the first demonstration of Trivittatus, VEE Turlock and Flanders viruses in Mexico from any source.
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