Abstract
Emergent infectious diseases can have a devastating impact on host populations. The high selective pressures on both the hosts and the pathogens frequently lead to rapid adaptations not only in pathogen virulence but also host resistance following an initial outbreak. However, it is often unclear whether hosts will evolve to avoid infection-associated fitness costs by preventing the establishment of infection (here referred to as qualitative resistance) or by limiting its deleterious effects through immune functioning (here referred to as quantitative resistance). Equally, the evolutionary repercussions these different resistance mechanisms have for the pathogen are often unknown. Here, we investigate the co-evolutionary dynamics of pathogen virulence and host resistance following the epizootic outbreak of the highly pathogenic bacterium Mycoplasma gallisepticum in North American house finches (Haemorhous mexicanus). Using an evolutionary modelling approach and with a specific emphasis on the evolved resistance trait, we demonstrate that the rapid increase in the frequency of resistant birds following the outbreak is indicative of strong selection pressure to reduce infection-associated mortality. This, in turn, created the ecological conditions that selected for increased bacterial virulence. Our results thus suggest that quantitative host resistance was the key factor underlying the evolutionary interactions in this natural host-pathogen system.
Highlights
Antagonistic interactions between hosts and pathogens can give rise to intense selection pressures and trigger rapid evolutionary changes in both (Buckling & Rainey, 2002; Paterson et al, 2010)
Our results suggest that the observed spread of host resistance was the result of strong selection pressure to reduce M. gallisepticum induced mortality, which in turn provided the competitive advantage for more virulent bacteria to take hold in the population
In order to investigate the evolutionary dynamics of host resistance and pathogen virulence, we developed a two-strain, two-phenotype SIRS model with seasonal forcing
Summary
Antagonistic interactions between hosts and pathogens can give rise to intense selection pressures and trigger rapid evolutionary changes in both (Buckling & Rainey, 2002; Paterson et al, 2010) This is true in the context of novel disease outbreaks, in which potentially devastating impacts on the host population are expected to feed back to the pathogen through a rapidly changing host environment (Lively, 1989; Best & Kerr, 2000; Paterson et al, 2010). Evolution of different resistance strategies has been observed in many species, the distinction between qualitative and quantitative resistance in animal populations is rarely made Understanding such mechanisms is important, in particular for predicting the likely direction of virulence evolution. Our results suggest that the observed spread of host resistance was the result of strong selection pressure to reduce M. gallisepticum induced mortality, which in turn provided the competitive advantage for more virulent bacteria to take hold in the population
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