Meeting Abstract
Hosts have two main ways to combat parasitic infections: resistance, which lowers pathogen load directly, and tolerance, which decreases the fitness costs of infections at a given pathogen load. Among animals, the mechanisms underlying variation in tolerance are not well understood. Early immune defenses against infection often include the release of free-radicals, which help kill pathogens, but also result in oxidative damage to host cells and tissues, potentially reducing host fitness. As such, minimizing this oxidative damage may be an important mechanism of tolerance in animals. We tested this hypothesis in house finches (Haemorhous mexicanus) infected with an emerging bacterial pathogen, Mycoplasma gallisepticum (MG). MG spilled over to house finches in the early 1990’s in the eastern United States and has since spread to most house finch populations. Previous work in this system suggests that tolerance may be evolving to MG in populations with the longest history of MG endemism, and that more tolerant populations have dampened inflammatory responses. As inflammation and free radical production are intricately linked, oxidative damage may play an important role in producing tolerant phenotypes in this system. In this study, we compared levels of oxidative damage both before and during experimental MG infections among house finches from populations that differ in their tolerance to MG. These populations span the temporal scale of MG endemism, including a population near the original spill-over and a population still naïve to MG. We predicted that individuals from populations that are more tolerant to MG would have a lower amount of oxidative damage than individuals from less tolerant populations following experimental infection with MG. This work represents one of the first investigations into the mechanisms of tolerance in a wild animal host.
