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Wilhelm, W. E., & Anderson, J. H. (1971). Vahlkampfia lobospinosa (Craig. 1912) Craig. 1913: rediscovery of a coprozoic ameba. J Parasitol, 57(6), 1378–1379.
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Scherer, W. F., & Dickerman, R. W. (1972). Ecologic studies of Venezuelan encephalitis virus in southeastern Mexico. 8. Correlations and conclusions. Am J Trop Med Hyg, 21(2), 86–89.
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Valova, G. P., & Mefod'ev, V. V. (1972). [Specific features of an epidemic process in leptospiroses in northern conditions in Western Siberia]. Zh Mikrobiol Epidemiol Immunobiol, 49(11), 138–145.
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Bast, T. F., Whitney, E., & Benach, J. L. (1973). Considerations on the ecology of several arboviruses in eastern Long Island. Am J Trop Med Hyg, 22(1), 109–115.
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Pitchford, R. J., Visser, P. S., du Toit, J. F., de Pienaar, U. V., & Young, E. (1973). Observations on the ecology of Schistosoma mattheei Veglia & Le Roux, 1929, in portion of the Kruger National Park and surrounding area using a new quantitative technique for egg output. J S Afr Vet Assoc, 44(4), 405–420.
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Bourdin, P., & Laurent, A. (1974). [Ecology of African horsesickness]. Rev Elev Med Vet Pays Trop, 27(2), 163–168.
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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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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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Dowdle, W. R., & Schild, G. C. (1976). Influenza: its antigenic variation and ecology. Bull Pan Am Health Organ, 10(3), 193–195.
Abstract: Influenza viruses have two surface antigens, the glycoprotein structures hemagglutinin (HA) and neuraminidase (NA). Antibodies to each of these are associated with immunity, but the structures themselves are antigenically variable. When an antigenic change is gradual over time it is referred to as a drift, while a sudden complete or major change in either or both antigens is termed a shift. The mechanism of antigenic drift is usually attributed to selection of preexisting mutants by pressure from increasing immunity in the human population. The mechanism of antigenic shift is less clear, but one tentative hypothesis is that shifts arise from mammalian or avian reservoirs, or through genetic recombination of human and animal influenza strains.
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Grafner, G., Zimmermann, H., Karge, E., Munch, J., Ribbeck, R., & Hiepe, T. (1976). [Incidence and damages inflicted by simuliid flies in the GDR district of Schwerin]. Angew Parasitol, 17(1), 2–6.
Abstract: Systematic faunal studies in the district Schwerin showed at the present time there are 3 more or less damage-biotopes existing in the districts of Perleberg, Ludwigslust and Parchim; 5 river sources can be considered as potential sources, 5 are temporary and 2 are ephemeral whilst in 3 further areas environmental influences such as effluent impairs the flow of the river and the developmental stages of Simuliidae were not observed.--The following species were found: Boophthora erythrocephala, Wilhelmia salopiensis, Wilhelmia equina, Odagmia ornata, Eusimulium aureum and Eusimulium lundstroemi.--The damage statistics covering the period 1966--1971 showed in the district of Schwerin, due to Simuliid attacks, 38 cattle died, 170 were seriously ill; in 1967 5 horses were seriously ill; in 1971, 3 pigs died and 27 were seriously ill.--The symptoms were manifested by pathological petechiae, scabs and oedema, also by insufficiency of the heart and circulatory system, diminished performance and growth disturbance. In severe cases heart and circulation failure occurred, paresis, coma and death followed.--The real economic significance of the Simuliid attacks rest with its strong and prolonged distrubance in young animals, as well as in pronounced irreparable diminished performance in diseased dairy cattle.
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