Impacts of host biology on the urban eco-epidemiology of West Nile virus

Disease transmission is inherently ecological, requiring ecological interactions among vectors, hosts and pathogens. Disease ecology as a field, however, has only emerged within the past several decades. Despite significant advances in the study of ecology of infectious diseases in the past twenty years, many questions remain about how host and vector ecology shape patterns of disease outbreaks. For my dissertation, I used radio telemetry, mosquito trapping, and field experiments to study how aspects of host and vector ecology impact disease transmission in a model vector-borne disease system, West Nile virus, in the greater Chicago area. First, I found that social behavior of an important host species, the American robin (Turdus migratorius, hereafter robins), and results in decreased individual risk of West Nile virus exposure for social individuals compared to non-social birds. Using sentinel birds, I determined that birds which did not participate in communal roosts had higher risk of exposure to West Nile virus than birds within communal roosts. Decreased exposure to West Nile virus was mediated by a 40 fold decrease in encounters with infected mosquitoes for birds inside communal roosts, despite no significant differences between vector infection rates or abundances inside and outside of communal roosts. Second, I found significant correlations between habitats used by robins early in the summer and habitats associated with elevated vector West Nile virus infection rates several weeks later. Previous work has found evidence supporting the importance of robins to the transmission of West Nile virus, but also found that vector infection rates peak during periods when vectors are not actively feeding on robins. My findings support the importance of robins to the transmission cycle of West Nile virus, and also indicate interactions between vectors and hosts vary throughout the transmission cycle of West Nile virus. Furthermore, my results indicate vector-host interactions resulting in transmission of West Nile virus occur early in the season before outbreaks of West Nile virus are observed in wildlife or humans. Third, I observed no relationship between exposure to internal parasites and immune function in nestling robins. Infection by helminth parasites can over activate the T-helper cell 2 (Th2) immune response, leaving hosts more susceptible to infection by viruses or bacteria. Since juvenile robins are implicated in the West Nile virus transmission cycle due to lack of previous exposure to the virus, I hypothesized the high prevalence of internal parasites may suppress immune function in young birds resulting in elevated susceptibility to other infections. I found no evidence for this mechanism acting in nestling robins, suggesting the role of juvenile robins in the transmission cycle of West Nile virus may be mediated more by behavioral differences between juveniles and adults such as habitat selection, defensive anti-mosquito behaviors, or utilization of communal roosts than by physiological differences in immune function. In summary, I found evidence for decreased West Nile virus transmission associated with social behavior in robins, and support for vector-host interactions early in the transmission cycle of West Nile virus resulting in elevated vector infection rates late in the season. These results suggest a selective advantage to social behavior in hosts infected by vector-borne diseases, which runs contrary to historical theory on the selective pressure of disease on social behavior. Furthermore, my findings highlight the importance of fine-scale studies of the ecology of vectors and hosts for understanding spatio-temporal heterogeneity in disease transmission, as significant time-lags may occur between host or vector exposure and detectable infection