Variation in immune responsiveness and tolerance of Mycoplasma infection between house finch populations


Meeting Abstract

9.1  Wednesday, Jan. 4  Variation in immune responsiveness and tolerance of Mycoplasma infection between house finch populations ADELMAN, JS*; HAWLEY, DM; Virginia Tech; Virginia Tech adelmanj@vt.edu

Revealing how population differences in immune defenses impact pathogen load and shedding will greatly improve predictive models of disease spread. However, such links remain poorly understood in natural systems. Here, we present population differences in host immune responses, disease pathology, and pathogen load in a naturally occurring host-pathogen system, house finches (Carpodacus mexicanus) infected with Mycoplasma gallisepticum (MG). This bacterial pathogen causes severe conjunctivitis and, since emerging in 1993, has spread rapidly across North America. In this study, wild-caught birds from two populations with different histories of pathogen co-evolution were experimentally infected in the same captive environment. MG arrived in the exposed population (Alabama) in the mid-1990s, but, as of capture, had not been detected in the naïve population (Arizona). While the Red Queen Hypothesis predicts that an exposed population should evolve increased resistance (the ability to reduce pathogen load more rapidly/completely), the populations displayed similar pathogen loads. However, early disease pathology (mass loss and conjunctival lesions) was less pronounced in the exposed population. This result suggests that tolerance of infection (reduced pathology per unit parasite), rather than resistance, may have evolved in the exposed population. Immunologically, the initial, inflammatory response (fever) began later in the exposed population, while subsequent, MG-specific antibody levels tended to be higher in that population. These data suggest that prioritization of different types of immune defense may help drive population differences in tolerance. We will discuss potential consequences of such differences in tolerance, rather than resistance, for disease spread and the evolution of virulence.

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