COS 103-3
Do host stress hormones mediate individual variation in resistance and tolerance?

Thursday, August 13, 2015: 8:40 AM
323, Baltimore Convention Center
Laura A. Schoenle, Biological Sciences, Virginia Tech
Alana M. Dudek, Biological Sciences, Virginia Tech
Sophie Gong, Biology, Queen's University
Allyshia Van Tol, Biology, Queen's University
Nicole M. Weinstein, Biomedical Sciences & Pathobiology, Virginia Tech
Ignacio T. Moore, Biological Sciences, Virginia Tech
Fran Bonier, Biology, Queen's University

When faced with a parasitic infection, individuals can either resist by reducing their parasite burden and/or tolerate by minimizing the fitness costs of infection. The optimal investment in each strategy might change across life history stages or with an individual’s physiological condition. Therefore, understanding host-parasite interactions requires assessing both among and within individual variation in resistance and tolerance. Glucocorticoids are steroid hormones that mediate responses to environmental challenges, life history trade-offs, and immune responsiveness in all vertebrates. Thus, glucocorticoids might also facilitate changes in resistance and tolerance that align with shifts in life history stage or condition. To test this hypothesis, we (1) measured resistance and tolerance to avian malaria parasites (Plasmodium and Haemoproteus spp.) and glucocorticoid levels in free-living red-winged blackbirds (Agelaius phoeniceus), and (2) conducted a pilot study in which we experimentally increased glucocorticoid levels in captive red-winged blackbirds and assessed changes in resistance and tolerance.


Free-living red-winged blackbirds with higher levels of glucocorticoids were more tolerant of avian malaria than individuals with lower glucocorticoids. However, we found no evidence for a relationship between glucocorticoid levels and resistance. Preliminary results suggest that experimental elevation of glucocorticoid levels in captive red-winged blackbirds might change both resistance and tolerance to avian malaria. Long-term elevation of glucocorticoids frequently suppresses the inflammatory actions of the immune response. Across multiple host species, many of the pathologies associated with malaria infection are attributed to immunopathology, rather than directly to the parasites. Thus, we would expect the immunosuppressive actions of glucocorticoids to decrease resistance but increase tolerance to parasite infection. Our results suggest that this may indeed be the case.