OOS 23-3
Long-distance dispersal, disease spread, and initial epidemic conditions: Evidence from a fungal/plant pathosystem

Tuesday, August 11, 2015: 8:40 AM
342, Baltimore Convention Center
Christopher C. Mundt, Department of Botany and Plant Pathology, Oregon State University, Corvallis, OR

Epidemic invasions have substantial impacts on both ecosystem function and human welfare, and may become more frequent owing to globalization.  Pathogens demonstrating long-distance dispersal (LDD) are of particular concern, owing to their potential to rapidly spread over large spatial scales.  Understanding the establishment and spread of such diseases can contribute significantly to identifying appropriate disease control strategies. We have developed wheat stripe rust as an experimental model system in disease ecology, allowing us to experimentally manipulate pathogen and host genotypes in an environment conducive to infection and without interference from naturally-occurring inoculum. In past work,a simple model based on inverse power law dispersal described accelerating, instantaneous velocities of epidemics caused by pathogens with 'fat-tailed' dispersal kernels at spatial scales of <100 m in experimental wheat plots, as well as for historical plant and animal epidemics caused by LDD pathogens at the continental scale.  We also experimentally evaluated the effects of host abundance, host heterogeneity, and initial outbreak focus size on disease spread.


Our prior results suggest a dispersal pattern of strongly local deposition, but with extended tails that allow founding populations at long distance, a pattern that appears to be supported by direct field measurements. An implication of this dispersal pattern is that initial epidemic conditions at the outbreak focus are the primary drivers of subsequent epidemic spread, a hypothesis that has been experimentally tested in two ways. First, spatial manipulation of differing host genotypes showed that host susceptibility at the outbreak focus was the primary driver of subsequent epidemic spread, regardless of host susceptibility in the remainder of the population. In addition, experimental ring-culling in field experiments and computer simulations showed that culling must commence within a very short time after first disease appearance to be effective, and that size of ring culls has very little impact on subsequent disease spread. Our results are important to evaluating strategies for epidemic interventions and to predicting effects of landscape heterogeneity on spread of epidemic invasions.