Evol Ecol Res 1: 681-701 (1999)     Full PDF if your library subscribes.

The spatial scale of pathogen dispersal: Consequences for disease dynamics and persistence

Peter H. Thrall* and Jeremy J. Burdon

Centre for Plant Biodiversity Research, CSIRO – Plant Industry, GPO Box 1600, Canberra, ACT 2601, Australia

Author to whom all correspondence should be addressed.
e-mail: thrall@pi.csiro.au


Plant pathogens exhibit a diverse array of life histories and dispersal mechanisms. The latter suggests that, in nature, there will be a broad range of spatial scales over which hosts and pathogens interact (e.g. soil-borne pathogens to aerially dispersed rusts). Variation in the spatial scale of such interactions is likely to have consequences for disease dynamics and pathogen persistence, and therefore coevolution of host and pathogen. We investigated disease dynamics and persistence using a spatially explicit simulation model that incorporated local dispersal of host and pathogen approximating the range of spatial structures seen in nature (i.e. many small isolated populations with very local dispersal to single large populations with some substructuring with global dispersal). Our results show that the spatial scale of pathogen dispersal is an important factor in determining the probability of disease persistence, as well as spatial and temporal patterns of incidence. Disease persistence was highest at relatively local scales of dispersal; at higher scales, not only was disease persistence less likely, but disease also caused major reductions in the fraction of sites occupied by the host. The nature of the dynamics also varied with the spatial scale of dispersal, with temporal changes in disease presence across the metapopulation showing endemic patterns at low scales of dispersal, but epidemic patterns when pathogen dispersal was over broader scales. It has been argued that the genetic diversity of host–pathogen systems with respect to resistance and virulence will depend on the probability of encounter rates between particular host and pathogen genotypes. Our results suggest that encounter rates, and therefore genetic diversity, are also likely to be heavily influenced by the spatial scale of the interaction.

Keywords: endemic, epidemic, metapopulation, population asynchrony.

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