Integrating physiological and behavioral responses to stressors into an epidemiological framework


Meeting Abstract

P2.166  Thursday, Jan. 5  Integrating physiological and behavioral responses to stressors into an epidemiological framework WARNE, Robin*; REEVES, Brooke; CRESPI, Erica; BRUNNER, Jesse; Southern Illinois University; State University of New York; Washington State University; Washington State University rwarne@siu.edu

Environmental stressors as agents in disease emergence and epidemics have garnered much attention during the past decade. However, stressors are not all alike. Glucocorticoid (GC) stress hormone activation can vary in magnitude, while some stressors such as predation actually suppress GC activity. Furthermore, GC are also important regulatory hormones, with roles that vary across taxa and life stages. For GC profiles to serve as general biomarkers of stress, concerted research endeavors are clearly needed to provide greater resolution. Such endeavors could also shed light on how stressors influence disease outbreaks through understanding of how altered GC activity influence not only immune function but also animal behavior. For example, while food shortage induction of GC translates into increased foraging activity, exposure to predators suppresses GC expression and behavioral activity. Both interactions must influence pathogen transmission rates through GC immunomodulatory effects on host susceptibility, and behavioral effects on contact rates with infective agents. Here we argue that integration of these interactions into the susceptible-infectious-recovered (SIR) epidemiological framework is crucial to understanding disease transmission and persistence. Neuroendocrine and behavioral focused research could increase understanding of: (i) How differing environmental stressors alter host immunity and thus susceptibility and infectivity? (ii) What traits determine if recovered animals are susceptible or resistant to future pathogens? (iii) What are the conditions, costs and traits that underlie patterns of host tolerance to sublethal infections; and does tolerance contribute to disease persistence and epidemic outbreaks?

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