| Abstrakt: |
Pathogen invasions pose a growing threat to ecosystem stability and public health. Guidelines for the timing and spatial extent of control measures for pathogen invasions are currently limited, however. We conducted a field experiment using wheat (Triticum aestivum) stripe rust, caused by the wind-dispersed fungus Puccinia striiformis, to study the extent to which host heterogeneity in an initial outbreak focus influences subsequent disease spread. We varied the frequency of susceptible host plants in an initial outbreak focus and in the non-focus of experimental plots, and observed the progress of epidemics produced by artificial inoculation. The frequency of susceptible hosts in the initial outbreak focus increased the spread of stripe rust in the experimental plots, while frequency of susceptible hosts outside the initial outbreak focus did not. This suggests that factors influencing pathogen reproduction in the initial outbreak focus are key to the control of epidemics of stripe rust. Two mechanisms may underlie the field results. The first is the continuing, direct infection of susceptible hosts in areas outside the initial outbreak focus by disease propagules arriving from the initial outbreak focus. The second is highly local proliferation of disease caused by direct descendants of colonizing individuals originating from the initial outbreak focus. We considered these two alternatives in simulations of a generalized pathogen exhibiting fat-tailed dispersal, similar to P. striiformis. Simulations showed a dominant effect of conditions in the initial outbreak focus, in agreement with the field experiment, but indicated that, over time, this dominance may erode. Analysis of the duration of focal dominance led to the conclusion that both mechanisms contribute to the phenomenon of focal dominance, and that the frequency of susceptible hosts in the initial outbreak focus had a stronger influence when the proportion of propagules that remained local during dispersal was higher. Overall, our results suggest that targeting pathogen reproduction in the initial outbreak focus will have a disproportionately large impact on subsequent epidemic spread. |
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