Centre for Plant Biodiversity Research, CSIRO-PI, PO Box 1600, Canberra, ACT 2601, Australia

Pathogens have an enormous range of effects on the ecology of their hosts, causing simple reductions in numbers, inducing changes in the genetic structure of populations, mediating changes in the structure and species composition of communities, and even influencing the rate and direction of successional change.

The interactions that produce these changes occur at a multitude of spatial scales. The most obvious level is that occurring within individual populations where hosts and pathogens potentially have a direct and immediate selective effect on each other. However, individual populations rarely occur in isolation, with most plant species, and hence most pathogens, occurring in a multitude of populations (a metapopulation) scattered across the landscape. Where dispersal is essentially global, the interaction between host and pathogen will tend to behave much as a single population, albeit one that is unevenly distributed into a series of spatially discrete patches in the environment. Alternatively, when dispersal is very local, individual host-pathogen populations may be so widely separated that they are totally isolated from one another. However, at intermediate levels of dispersal, extinction and colonization processes are likely to play a major role, such that the evolutionary trajectory of the host-pathogen metapopulation may be quite different from that of the component local populations.

An obvious feature of such partly independent dynamics is seen in the patchiness of disease which is commonly seen in natural host-pathogen associations. Typically, some host populations may remain infected for long periods of time, while in others the pathogen may only persist for short periods - its longer-term presence in a particular host population being dependent on a continuing process of recolonization from other sites. This asynchrony of disease incidence and severity may occur at a variety of spatial scales ranging from that between adjacent populations to differences between subregions of the overall metapopulation.

Asynchrony in disease occurrence reflects not only the spatial fragmentation of populations but also variation in life history attributes of host and pathogen that affect their respective abilities to disperse and persist. The interaction between spatial structure and the relative scale at which hosts and pathogens disperse is likely to play a major role in determining the evolution of resistance/viruience structures.