Temperature-induced feeding increases do not augment pathogen deposition on bird feeders potential consequences for climate-disease relationships


Meeting Abstract

125.6  Monday, Jan. 7  Temperature-induced feeding increases do not augment pathogen deposition on bird feeders: potential consequences for climate-disease relationships ADELMAN, JS*; WILSON, AF; HOPKINS, WA; HAWLEY, DM; Virginia Tech; Virginia Tech; Virginia Tech; Virginia Tech adelmanj@vt.edu

Ambient temperature can play important roles in disease progression and transmission. However, unraveling how temperature influences the links among within- and between-host disease processes remains an important challenge, especially in the face of global climate change. Here, we address this issue in an emerging wildlife disease system: house finches (Haemorhous mexicanus) infected with the bacteria Mycoplasma gallisepticum (MG). Recent work suggests that bird feeders act as fomites in this system, transmitting MG deposited by one bird to another. We hypothesized that the amount of MG deposited on feeders should increase in response to two, non-exclusive factors: 1) increased MG load in the eye and 2) increased interaction with feeders. We tested how ambient temperature influences these links by housing experimentally infected finches under two thermal regimes: at thermoneutral (TN) and below thermoneutral (sub-TN). As in a prior study, MG load in the eye did not differ between temperature treatments. At the individual level, however, and regardless of temperature treatment, MG load in the eye predicted MG deposition onto feeders in an exponentially increasing manner. With regard to interaction with feeders, we predicted that sub-TN birds would compensate for thermoregulatory costs by increasing food intake, thus interacting with feeders more often and increasing MG deposition. While sub-TN birds consumed more food than TN birds, MG deposition on feeders did not differ between groups. We discuss how nonlinear relationships among feeding efficiency, pathogen load, and pathogen deposition may explain these patterns, contribute to heterogeneous transmission, and buffer the effects of climate on fomite-transmitted diseases.

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