|
|
Milouchine, V. N. (1980). The role of WHO in international studies on the ecology of influenza in animals. Comp Immunol Microbiol Infect Dis, 3(1-2), 25–31.
|
|
|
|
Alexander, D. J. (1982). Ecological aspects of influenza A viruses in animals and their relationship to human influenza: a review. J R Soc Med, 75(10), 799–811.
|
|
|
|
Sabattini, M. S., Monath, T. P., Mitchell, C. J., Daffner, J. F., Bowen, G. S., Pauli, R., et al. (1985). Arbovirus investigations in Argentina, 1977-1980. I. Historical aspects and description of study sites. Am J Trop Med Hyg, 34(5), 937–944.
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.
|
|
|
|
Hardy, J. L. (1987). The ecology of western equine encephalomyelitis virus in the Central Valley of California, 1945-1985. Am J Trop Med Hyg, 37(3 Suppl), 18s–32s.
Abstract: Reeves' concept of the summer transmission cycle of western equine encephalomyelitis virus in 1945 was that the virus was amplified in a silent transmission cycle involving mosquitoes, domestic chickens, and possibly wild birds, from which it could be transmitted tangentially to and cause disease in human and equine populations. Extensive field and laboratory studies done since 1945 in the Central Valley of California have more clearly defined the specific invertebrate and vertebrate hosts involved in the basic virus transmission cycle, but the overall concept remains unchanged. The basic transmission cycle involves Culex tarsalis as the primary vector mosquito species and house finches and house sparrows as the primary amplifying hosts. Secondary amplifying hosts, upon which Cx. tarsalis frequently feeds, include other passerine species, chickens, and possibly pheasants in areas where they are abundant. Another transmission cycle that most likely is initiated from the Cx. tarsalis-wild bird cycle involves Aedes melanimon and the blacktail jackrabbit. Like humans and horses, California ground squirrels, western tree squirrels, and a few other wild mammal species become infected tangentially with the virus but do not contribute significantly to virus amplification.
|
|
|
|
Beveridge, W. I. (1993). Unravelling the ecology of influenza A virus. Hist Philos Life Sci, 15(1), 23–32.
Abstract: For 20 years after the influenza A virus was discovered in the early 1930s, it was believed to be almost exclusively a human virus. But in the 1950s closely related viruses were discovered in diseases of horses, pigs and birds. Subsequently influenza A viruses were found to occur frequently in many species of birds, particularly ducks, usually without causing disease. Researchers showed that human and animal strains can hybridise thus producing new strains. Such hybrids may be the cause of pandemics in man. Most pandemics have started in China or eastern Russia where many people are in intimate association with animals. This situation provides a breeding ground for new strains of influenza A virus.
|
|
|
|
Dierenfeld, E. S. (1994). Vitamin E in exotics: effects, evaluation and ecology. J Nutr, 124(12 Suppl), 2579s–2581s.
Abstract: The pathophysiology and lesions associated with vitamin E deficiency are similar between domestic and exotic species, and circulating plasma concentrations are also similar between comparable groups. However, many ecological variables must be considered for the most relevant comparisons. Tissue values of vitamin E, apart from plasma, are unknown for most exotics. Dietary vitamin E requirements of exotic species and domestics appear to differ; based on natural foodstuff analyses and clinical observations, between 50 and 200 mg vitamin E/kg DM are necessary to prevent vitamin E deficiency, 5- to 10-fold higher than current livestock recommendations.
|
|
|
|
Kida, H. (1997). [Ecology of influenza viruses in animals and the mechanism of emergence of new pandemic strains]. Nippon Rinsho, 55(10), 2521–2526.
Abstract: Ecological studies on influenza viruses revealed that the hemagglutinin genes are introduced into new pandemic strains from viruses circulating in migratory ducks through domestic ducks and pigs in southern China. Experimental infection of pigs with 38 avian influenza virus strains with H1-H13 hemagglutinins showed that at least one strain of each HA subtype replicated in the upper respiratory tract of pigs. Co-infection of pigs with a swine virus and with an avian virus generated reassortant viruses. The results indicate that avian viruses of any subtype can contribute genes in the generation of reassortants. Virological surveillance revealed that influenza viruses in waterfowl reservoir are perpetuated year-by-year in the frozen lake water while ducks are absent.
|
|
|
|
Marfin, A. A., Petersen, L. R., Eidson, M., Miller, J., Hadler, J., Farello, C., et al. (2001). Widespread West Nile virus activity, eastern United States, 2000. Emerg Infect Dis, 7(4), 730–735.
Abstract: In 1999, the U.S. West Nile (WN) virus epidemic was preceded by widespread reports of avian deaths. In 2000, ArboNET, a cooperative WN virus surveillance system, was implemented to monitor the sentinel epizootic that precedes human infection. This report summarizes 2000 surveillance data, documents widespread virus activity in 2000, and demonstrates the utility of monitoring virus activity in animals to identify human risk for infection.
|
|
|
|
Endy, T. P., & Nisalak, A. (2002). Japanese encephalitis virus: ecology and epidemiology. Curr Top Microbiol Immunol, 267, 11–48.
|
|
|
|
Komar, N. (2003). West Nile virus: epidemiology and ecology in North America. Adv Virus Res, 61, 185–234.
|
|
