Host individuals and populations often vary in their responses to infection, with direct consequences for pathogen spread and evolution. While considerable work has focused on the mechanisms underlying differences in resistance-the ability to kill pathogens-we know little about the mechanisms underlying tolerance-the ability to minimize fitness losses per unit pathogen. Here, we examine patterns and mechanisms of tolerance between two populations of house finches (Haemorhous [formerly Carpodacus] mexicanus) with different histories with the bacterial pathogen Mycoplasma gallisepticum (MG). After infection in a common environment, we assessed two metrics of pathology, mass loss and eye lesion severity, as proxies for fitness. We calculated tolerance using two methods, one based on pathology and pathogen load at the peak of infection (point tolerance) and the other based on the integrals of these metrics over time (range tolerance). Alabama birds, which have a significantly longer history of exposure to MG, showed more pronounced point tolerance than Arizona birds, while range tolerance did not differ between populations. Alabama birds also displayed lower inflammatory cytokine signaling and lower fever early in infection. These results suggest that differences in inflammatory processes, which can significantly damage host tissues, may contribute to variation in tolerance among house finch individuals and populations. Such variation can affect pathogen spread and evolution in ways not predictable by resistance alone and sheds light on the costs and benefits of inflammation in wild animals.

A TaqMan† -based real-time, quantitative polymerase chain reaction (qPCR) assay utilizing the mgc2 gene was developed to detect Mycoplasma gallisepticum in conjunctival swabs of experimentally infected house finches. The assay was demonstrated to be quantitative by the standard curve method with reproducible results within runs and between runs. The detection limit of the mgc2 assay was examined using two standards. The test had a detection limit of less than 14 copies per reaction when tested with a plasmid standard and less than 10 copies per reaction when tested with M. gallisepticum genomic DNA. All M. gallisepticum-negative birds (10 specific pathogen free chickens and 10 house finches) were negative by mgc2 qPCR assay. Existing evidence suggests that an important part of M. gallisepticum pathogenesis includes both its attachment to and invasion of host cells. Thus, our test also made use of rag-1 as an internal control gene. The rag-1 qPCR results showed that host cell quantity varied greatly between conjunctival samples. After inoculation, M. gallisepticum levels in the house finch conjunctiva increased over the 7-day period post infection. The bird with the most pronounced clinical conjunctivitis harboured the highest level of M. gallisepticum and the bird that did not develop conjunctivitis had very low numbers of M. gallisepticum. Thus, it appears that development of conjunctivitis may correlate with M. gallisepticum load.

The ethical and logistical challenges inherent in experimental infections of wild-caught animals present a key limitation to the study of wildlife diseases. Here we characterize a potentially useful domestic model for a wildlife disease that has been of particular interest in recent decades; that is, infection of North American house finches (Carpodacus mexicanus) with Mycoplasma gallisepticum, more commonly known as a worldwide poultry pathogen. Seven domestic canaries (Serinus canaria domestica) were infected experimentally with M. gallisepticum alongside two wild-caught house finches (C. mexicanus) and the resulting clinical disease, pathogen load, serology and pathology were compared. Although rates of morbidity were higher in domestic canaries in response to M. gallisepticum infection, no significant differences were detected between the two species in the four measures of infection and disease studied. Our results support previous field and experimental studies that have documented universal susceptibility to M. gallisepticum infection in the avian family Fringillidae, which includes domestic canaries. Our results also indicate that domestic canaries may serve as a potentially useful model system for the experimental study of M. gallisepticum infection in songbirds.

Host genetic diversity can mediate pathogen resistance within and among populations. Here we test whether the lower prevalence of Mycoplasmal conjunctivitis in native North American house finch populations results from greater resistance to the causative agent, Mycoplasma gallisepticum (MG), than introduced, recently‐bottlenecked populations that lack genetic diversity. In a common garden experiment, we challenged wild‐caught western (native) and eastern (introduced) North American finches with a representative eastern or western MG isolate. Although introduced finches in our study had lower neutral genetic diversity than native finches, we found no support for a population‐level genetic diversity effect on host resistance. Instead we detected strong support for isolate differences: the MG isolate circulating in western house finch populations produced lower virulence, but higher pathogen loads, in both native and introduced hosts. Our results indicate that contemporary differences in host genetic diversity likely do not explain the lower conjunctivitis prevalence in native house finches, but isolate‐level differences in virulence may play an important role.