2018 ESA Annual Meeting (August 5 -- 10)

COS 26-6 - Genetic diversity is linked to epidemic severity in a wild pathogen metapopulation

Tuesday, August 7, 2018: 9:50 AM
335-336, New Orleans Ernest N. Morial Convention Center
Jenalle L. Eck, Organismal and Evolutionary Biology, University of Helsinki, Helsinki, Finland, Benoit Barrès, USC CASPER, Université de Lyon, ANSES, Lyon, France, Samuel Soubeyrand, BioSP, INRA, Avignon, France and Anna-Liisa Laine, Research Centre for Ecological Change, University of Helsinki, Helsinki, Finland
Background/Question/Methods

Epidemic severity can vary greatly among connected host populations due to local variation in host resistance, pathogen genetic composition, or environment. To examine how pathogen genetic diversity affects epidemic severity in a wild plant species, we collected epidemiological and genetic data on 15 populations of powdery mildew (Podosphaera plantaginis), an obligate fungal pathogen of the perennial herb, Plantago lanceolata, in the Åland Islands (Finland). In each population, we measured the connectivity of the hosts to their surrounding populations and tracked spatio-temporal disease progression throughout the 2014 growing season. We coupled our survey of infection with intensive sampling of the pathogen. The field-collected samples were genotyped using a SNP panel to reveal genetic diversity within these populations. We then analyzed the relationship between pathogen genetic diversity (i.e., rarified strain richness), host connectivity, and epidemic severity (i.e., maximum infection rate) in the populations using mixed-effects modeling.

Results/Conclusions

We found that epidemics reached greater severity in populations containing higher pathogen genetic diversity. Pathogen genetic diversity varied greatly among populations, ranging from only a single strain detected in 20% of the populations to 19 strains in the most diverse population. Host connectivity also affected epidemic severity: well-connected host populations had more severe epidemics than more isolated populations. These relationships were robust even though pathogen genetic composition varied greatly across our study populations, often with no overlap in pathogen strains between populations. One potential explanation for our findings is that higher strain richness in diverse pathogen populations may facilitate the infection of additional host genotypes, enhancing the growth of the epidemic. High connectivity may exacerbate this process by facilitating the arrival of new pathogen strains from surrounding populations. Our results suggest that pathogen genetic diversity may be an important general factor determining epidemic severity, especially in wild populations where host resistance is typically highly diverse.