Abstract: Intense and persistent use of DDT for malaria control has increased resistance and induced exophilic behavior of Anopheles pseudopunctipennis. An evaluation of bendiocarb and DDT to control this species in Sinaloa, Mexico, showed that, in spite of DDT-resistance, both insecticides produced similar effects. Feeding patterns were analyzed to explain these results. Resting mosquitoes were collected over the dry and wet seasons. Anophelines were tested in an ELISA to determine the source of the meals. The human blood index (HBI) ranged from 3.3 to 6.8% in DDT- and from 12.7 to 26.9% in bendiocarb-sprayed houses. Irritability and repellency in DDT-sprayed houses could explain the reduced HBI. In contrast, bendiocarb produced higher mortality. These effects could have affected different components of the vectorial capacity and similarly reduced malaria.

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.

Abstract: This is the introductory paper to a series on the ecology of arboviruses in Argentina. Epizootics of equine encephalitis have occurred since at least 1908, principally in the Pampa and Espinal biogeographic zones, with significant economic losses; human cases of encephalitis have been rare or absent. Both western equine and eastern equine encephalitis viruses have been isolated from horses during these epizootics, but the mosquitoes responsible for transmission have not been identified. A number of isolations of Venezuelan equine encephalitis (VEE) virus were reported between 1936 and 1958 in Argentina, but the validity of these findings has been seriously questioned. Nevertheless, serological evidence exists for human infections with a member of the VEE virus complex. Serological surveys conducted in the 1960s indicate a high prevalence of infection of humans and domestic animals with St. Louis encephalitis (SLE), and 2 SLE virus strains have been isolated from rodents. Human disease, however, has rarely been associated with SLE infection. Only 7 isolations of other arboviruses have been described (3 of Maguari, 1 of Aura, 2 of Una, and 1 of an untyped Bunyamwera group virus). In 1977, we began longitudinal field studies in Santa Fe Province, the epicenter of previous equine epizootics, and in 1980 we extended these studies to Chaco and Corrientes provinces. The study sites are described in this paper.

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.