Meeting Abstract
Tolerance of infection, or minimizing the fitness losses for a given pathogen load, should have dramatic impacts on the dynamics of wildlife diseases. However, empirical studies of the mechanisms underlying tolerance and its consequences for pathogen transmission remain limited. Among animals, tolerance manifests in two principle ways, behavioral vs. tissue-specific tolerance, with the potential to either enhance or impede transmission. Behavioral tolerance maintains fitness-enhancing behaviors during infection, likely leading to increased contact rates and enhanced spread of directly transmitted pathogens. On the other hand, tissue-specific tolerance reduces damage to tissues (pathology), which could hinder transmission of certain pathogens by limiting dissemination routes (e.g. diarrhea, coughing). This presentation outlines recent and ongoing research into the mechanistic causes and transmission consequences of tolerance in an ecologically relevant wildlife disease system: house finches infected with Mycoplasma gallisepticum. This bacterial pathogen jumped into finches from poultry in the mid-1990s, causing pronounced conjunctivitis and reduced survival in the new host. Using the severity of conjunctivitis as a proxy for fitness during experimental infections, we have found that lower pro-inflammatory immune signaling predicts enhanced tissue-specific tolerance. These results are consistent with reduced inflammatory responses as proximate drivers of tolerance in this system. In addition, recent experimental epidemics in captivity suggest that tissue-specific tolerance may have a larger impact on transmission than behavioral tolerance, although prior work has highlighted a key role for behavior in the transmission of this pathogen. I discuss the implications of these findings on host-pathogen interactions at the ecological and evolutionary time scales.
