Laura Schoenle, a Ph.D. candidate in Dr. Ignacio Moore‘s lab, recently presented a poster at the 2015 Annual Meeting of the Society for Integrative and Comparative Biology (SICB) in West Palm Beach, FL.
Laura won the Best Student Poster Award in the Ecoimmunology and Disease Ecology division for the poster, “The relationship between corticosterone and haemosporidian parasites: are stress hormones key to tolerating infection?” See the abstract below.
The relationship between corticosterone and haemosporidian parasites: are stress hormones key to tolerating infection?
SCHOENLE, L.A.*; GONG, S.; DUDEK, A.; ROCHELEAU, L.; VAN TOL, A.; WEINSTEIN, N.M.; MOORE, I.T.; BONIER, F.; Virginia Tech; Queen’s University; Virginia Tech; Queen’s University; Queen’s University; Virginia Tech; Virginia Tech; Queen’s University email@example.com
Individuals vary in their responses to parasite infection, yet we do not understand what drives these differences, nor the proximate mechanisms that underlie them. When confronted with a pathogen, an individual can respond in part by tolerating infection – attempting to minimize damage and maintain normal function. Glucocorticoids are highly conserved steroid hormones involved in regulating responses to energetic demands and environmental challenges, including infection. Thus, these hormones might influence individual variation in tolerance of infection. We investigated the relationship between corticosterone, the primary glucocorticoid in birds, and tolerance to avian haemosporidian parasites in free-living male red-winged blackbirds (Agelaius phoeniceus). More than 90% of individuals in the study population experience infection with haemosporidian parasites, and individuals display substantial variation in a metric of disease tolerance (hematocrit for a given parasitemia). Males with higher corticosterone were more tolerant to haemosporidian infections than those with lower corticosterone. To establish whether or not the relationship between corticosterone and tolerance is causal, we experimentally elevated corticosterone in captive individuals and measured the resulting changes in tolerance and parasitemia. Our results provide support for a potentially adaptive role for corticosterone in mediating the response of a host to parasitic infection. When corticosterone is elevated in response to challenging environmental conditions, tolerance might be a strategy that reduces the costs of infection.