Doctor of Philosophy, The Ohio State University, 2006, Evolution, Ecology, and Organismal Biology
West Nile virus (WNV) is a single-stranded RNA virus in the family Flaviviridae that first appeared in North America in 1999, and in Ohio in 2001. From 2002 to 2005, I examined the patterns of WNV antibody seroprevalence in Northern Cardinals (Cardinalis cardinalis), the ability of female cardinals to pass WNV antibodies to their offspring, the fitness consequences of a previous WNV infection, and the role of innate immunity in response to infection. Over the three years of the study, WNV antibody seroprevalence was 36% in female cardinals, and 21% in male cardinals. Most females lost antibodies after one year. In three summers, 44 female cardinals produced 59 nests with fledglings. Thirty of the females were seronegative, 13 were seropositive, and one was seropositive in the last of three years. None of these birds raised a seropositive nestling, and none of 23 other nestlings tested positive for WNV IgM antibodies. Although survival measures for female cardinals were slightly higher for seronegative than seropositive birds, there was no significant effect of seroprevalence on cardinal survival. Previous WNV infection also did not significantly influence the percentage of females fledging at least one nestling. Seropositive females, however, had half as many nestlings as seronegative females (0.90 ± 0.26 vs. 1.71 ± 0.24), and fledged half as many young as seronegative birds (0.84 ± 0.18 vs. 1.64 ± 0.23). These results suggest that female cardinals who survive WNV infection trade their survival for some reproductive success. In a related study of Downy Woodpeckers (Picoides pubescens), I found that wintering birds provided with supplemental food had greater ability to kill bacteria than unsupplemented birds. The ability to kill bacteria significantly decreased through the winter. Because innate immunity is crucial in the immune response to WNV, the results suggest that birds under greater energy stress may have a reduced immune response to WNV infection. The results (open full item for complete abstract)
Committee: Thomas Grubb, Jr. (Advisor)
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