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Oral: Initial epidemic conditions and long-distance spread of disease.


Dispersal at Multiple Scales: A Key to Outbreak of Disease Epidemics
C. Mundt (1); (1) Oregon State University, OR, USA

A simple model based on inverse power law dispersal describes accelerating, instantaneous velocities of epidemics caused by pathogens with 'fat-tailed' dispersal kernels both in experimental field plots with wheat stripe rust, as well as for plant and animal epidemics at the continental scale. Disease spread has been found to be independent of spatial scale of study, and proportional to the size of the epidemic outbreak. Coupled with our studies of landscape heterogeneity on wheat stripe rust epidemics, this simple models suggests highly local deposition that makes disease increase largely independent of disease levels in other parts of the population, but with extended “fat tails” that result in an accelerating epidemic front. An implication of such dispersal patterns is that epidemic spread will be determined largely by initial epidemic conditions. This has been confirmed experimentally through field studies of wheat stripe rust. The degree of epidemic spread was determined by the degree of host susceptibility in the outbreak focus, rather than by the degree of susceptibility in the remainder of the plots. Further, culling of outbreak foci showed no effect on epidemic spread unless implemented early in the first generation of secondary spread, and size of ring-culls had no apparent impact on epidemic spread.