Abstract

Since the introduction of West Nile virus (WNV) to New York in 1999, the virus spread rapidly and became established in much of North America. This arbovirus is maintained in an urban enzootic cycle among Culex spp. mosquitoes and birds with occasional spillover to humans. The mechanisms for WNV amplification remain poorly understood and this dissertation investigates several hypotheses associated with transmission among vectors and hosts leading to rapid amplification.

Mosquitoes and birds were collected in southwest suburban Chicago from May to October in 2005-2007. WNV infection in Culex spp. mosquitoes, principally Culex pipiens and tested using quantitative polymerase chain reaction (PCR), peaked in early August in all three years. The proportion of hatch-year birds (juvenile) captured in mist-nets increased as the season progressed and hatch year bird seroprevalence of WNV antibodies, was 18.5% (100/540) in 2005 and 2.8% (14/493) in 2006. Virus was detected in 11 of 998 bird sera in 2005 and 3 of 1285 in 2006; 11 of the 14 virus positive birds were hatch-year. Significant cross-correlations among these factors indicate a key role for hatch-year birds in the amplification of epizootic transmission of WNV, and in increasing human infection risk by facilitating local viral amplification.

To further explore associations between the vector and host, I conducted a blood meal analysis using PCR and DNA sequencing techniques on bloodfed mosquitoes. Results showed that Cx. pipiens fed predominantly (83%) on birds with a high diversity of species utilized as hosts (25 species). Cx. pipiens also fed substantially on mammals (19%; 7 species; humans representing 16%). During a WNV epidemic in 2005, WNV RNA was detected in the head and thorax of a bloodfed Cx. pipiens and the blood meal was identified as human. These results fulfill a criterion for incrimination of Cx. pipiens as a bridge vector. American robins were marginally overutilized and common grackle (Quiscalus quiscula), house sparrow, and European starling (Sturnus vulgaris) were underutilized based upon relative abundance measures. West Nile virus transmission intensified in late-July, at times when American robins were heavily fed upon, and then declined when robin abundance declined, after which other birds species were selected as hosts. There was no shift in feeding from birds to mammals coincident with emergence of human cases. Predictions were that—ca. 66% of WNV-infectious Cx. pipiens became infected from feeding on just a few species of birds, including American robins (35%), blue jays (17%; Cyanocitta cristata), and house finches (15%; Carpodacus mexicanus).

Finally, I explored landscape-level patterns of WNV infection in Culex spp. mosquitoes for a 3-year database (2004-2006) in the state of Illinois to identify landscape features that predict mosquito infection. I observed variability in the associations among three years but the most parsimonious multivariate model explaining Culex spp. mosquito infection rate included elevation and precipitation in 2004, precipitation in 2005, and percent white people and vegetation in 2006. A negative relationship between precipitation and Culex infection emerged as the most consistent pattern explaining more variation than any other independent variable. Further multivariate tests reveal a 3-4 week time lag between a lack of rain and an increase in Culex infection.