tetano
Editor, Senior Moderator
Citation: Hawley DM, Osnas EE, Dobson AP, Hochachka WM, Ley DH, et al. (2013) Parallel Patterns of Increased Virulence in a Recently Emerged Wildlife Pathogen. PLoS Biol 11(5): e1001570. doi:10.1371/journal.pbio.1001570
Abstract
The evolution of higher virulence during disease emergence has been predicted by theoretical models, but empirical studies of short-term virulence evolution following pathogen emergence remain rare. Here we examine patterns of short-term virulence evolution using archived isolates of the bacterium Mycoplasma gallisepticum collected during sequential emergence events in two geographically distinct populations of the host, the North American house finch (Haemorhous [formerly Carpodacus] mexicanus). We present results from two complementary experiments, one that examines the trend in pathogen virulence in eastern North American isolates over the course of the eastern epidemic (1994?2008), and the other a parallel experiment on Pacific coast isolates of the pathogen collected after M. gallisepticum established itself in western North American house finch populations (2006?2010). Consistent with theoretical expectations regarding short-term or dynamic evolution of virulence, we show rapid increases in pathogen virulence on both coasts following the pathogen's establishment in each host population. We also find evidence for positive genetic covariation between virulence and pathogen load, a proxy for transmission potential, among isolates of M. gallisepticum. As predicted by theory, indirect selection for increased transmission likely drove the evolutionary increase in virulence in both geographic locations. Our results provide one of the first empirical examples of rapid changes in virulence following pathogen emergence, and both the detected pattern and mechanism of positive genetic covariation between virulence and pathogen load are consistent with theoretical expectations. Our study provides unique empirical insight into the dynamics of short-term virulence evolution that are likely to operate in other emerging pathogens of wildlife and humans.
Author Summary
A 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.
http://www.plosbiology.org/article/...0;jsessionid=0D99CBCAABF9FD67458D9450F86398D8
Abstract
The evolution of higher virulence during disease emergence has been predicted by theoretical models, but empirical studies of short-term virulence evolution following pathogen emergence remain rare. Here we examine patterns of short-term virulence evolution using archived isolates of the bacterium Mycoplasma gallisepticum collected during sequential emergence events in two geographically distinct populations of the host, the North American house finch (Haemorhous [formerly Carpodacus] mexicanus). We present results from two complementary experiments, one that examines the trend in pathogen virulence in eastern North American isolates over the course of the eastern epidemic (1994?2008), and the other a parallel experiment on Pacific coast isolates of the pathogen collected after M. gallisepticum established itself in western North American house finch populations (2006?2010). Consistent with theoretical expectations regarding short-term or dynamic evolution of virulence, we show rapid increases in pathogen virulence on both coasts following the pathogen's establishment in each host population. We also find evidence for positive genetic covariation between virulence and pathogen load, a proxy for transmission potential, among isolates of M. gallisepticum. As predicted by theory, indirect selection for increased transmission likely drove the evolutionary increase in virulence in both geographic locations. Our results provide one of the first empirical examples of rapid changes in virulence following pathogen emergence, and both the detected pattern and mechanism of positive genetic covariation between virulence and pathogen load are consistent with theoretical expectations. Our study provides unique empirical insight into the dynamics of short-term virulence evolution that are likely to operate in other emerging pathogens of wildlife and humans.
Author Summary
A 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.
http://www.plosbiology.org/article/...0;jsessionid=0D99CBCAABF9FD67458D9450F86398D8