Abstract
Author SummaryA long-standing paradox in the study of infectious diseases is why pathogens evolve to cause harm to the very hosts they depend on to survive and reproduce. Research over several decades suggests that this harm, or virulence, is an inevitable by-product of the pathogen replication needed to maximize the chance that a given pathogen will be transmitted to another host. Here we demonstrate that a recently emerged bacterial pathogen of a North American songbird species has gradually become more virulent during each of two emergence events in different regions of the host range. This evolution of higher virulence appears to have been driven by selection for high rates of pathogen replication, because bacterial isolates that are more virulent in finches also attain the highest loads in infected host tissues. Overall, our results indicate that emerging pathogens can evolve to become more virulent in their hosts, at least in the short term, when an increase in the pathogen's ability to replicate is linked with higher virulence. Our findings have important implications for understanding and predicting the severity of disease caused by emerging pathogens in wildlife, domestic animals, and humans.
Highlights
The extensive variation in the amount of harm that pathogens cause their hosts has intrigued biologists for centuries and has generated several decades of theoretical work to explain the evolution of pathogen virulence (e.g., [1,2,3,4])
Consistent with theoretical assumptions, we describe positive correlations between indices of transmission and virulence among isolates of Mycoplasma gallisepticum (MG) circulating in North American house finches
We present results from two complementary experiments, one that examines the trend in pathogen virulence in eastern North American MG isolates collected from a limited geographic region over the course of the epidemic (1994–2008), and the other a parallel experiment using Pacific coast isolates of the pathogen collected after MG established itself in western house finch populations (2006–2010)
Summary
The extensive variation in the amount of harm that pathogens cause their hosts has intrigued biologists for centuries and has generated several decades of theoretical work to explain the evolution of pathogen virulence (e.g., [1,2,3,4]). Despite this broad and long-standing interest, empirical studies of virulence evolution in non-laboratory systems remain rare (but see [5,6,7,8,9,10]). If increased virulence and transmission to a new host are both associated with higher pathogen load, under certain conditions virulence is expected to evolve toward an intermediate value that is evolutionarily stable [1,2,4,11,18,19,20,21]
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