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About the Authors:
Kaci K. VanDalen
* E-mail: [email protected]
Affiliation: United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, Fort Collins, Colorado, United States of America
Jeffrey S. Hall
Current address: United States Department of the Interior, United States Geological Survey, National Wildlife Health Center, Madison, Wisconsin, United States of America
Affiliation: United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, Fort Collins, Colorado, United States of America
Larry Clark
Affiliation: United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, Fort Collins, Colorado, United States of America
Robert G. McLean
Affiliation: United States Department of Agriculture, Animal and Plant Health Inspection Service, Wildlife Services, National Wildlife Research Center, Fort Collins, Colorado, United States of America
Cynthia Smeraski
Affiliation: Colorado State University, Department of Biomedical Sciences, Fort Collins, Colorado, United States of America
Introduction
West Nile virus (WNV) was introduced into the United States at New York City in 1999 and spread rapidly across the continental United States and into Canada, Latin America, and the Caribbean within six years [1]. The natural transmission cycle of WNV involves mosquito vectors and avian hosts [2] and the Centers for Disease Control and Prevention have identified 326 avian species positive for WNV in their avian mortality database [3]. Avian hosts vary in their susceptibility to WNV infection. American crows (Corvus brachyrhynchos), blue jays (Cyanocitta cristata) and greater sage-grouse (Centrocercus urophasianus) experience near 100% mortality from experimental WNV infection [4-7], while disease severity in other avian species covers a broad spectrum [5,8,9].
Mosquitoes also vary in competency as vectors of WNV according to species and local populations as determined by their ability to become infected and in the quantity of virus that amplifies in their tissues [10,11]. The efficiency of mosquito infection increases with higher viremia titers in vertebrate hosts on which they feed [12]. Variation also exists in the amount of virus delivered by individual mosquitoes during feeding. For example, some Culex sp. expectorated anywhere from 100.78-103.58 plaque forming units (PFU) of virus during experimental feeding studies [12]. In another study, Culex pipiens quinquefasciatus transmitted an average of 104.3 PFU of WNV but the amounts...