Population Biology of Plant Pathogens

Abstract

Population change in plant pathogens is driven by environmental factors, especially wetness and temperature, and by intrinsic and induced host resistance. For pathogens except those of woody tissue, turnover of host tissue, and decline in pathogen population during periods when the host is absent or conditions unsuitable for infection produce intrinsic fluctuations in populations. Movement of propagules to new hosts is much more efficient in denser host stands, introducing density dependence at a larger scale. The reduction of host populations by a successful pathogen both allows space for other plants to grow, and introduces selective forces increasing resistance in the host. This gives rise to a coevolutionary race between host and pathogen, resulting in both diversity and turnover of genetic elements involved in defence signalling. Rare movement of pathogens between subpopulations of a metapopulation introduces a further birth–death process causing fluctuations in disease and selection pressures on relevant genetic elements. Key Concepts: Population densities of plant pathogens are set by the balance between pathogen infection and host turnover. Populations of plant pathogens are rarely stable, but cycle from high to low across seasons. Environmental factors modulate or limit but do not regulate pathogen abundance. Asexual reproduction is often associated with shorter distance dispersal mechanisms and sexual reproduction with longer distance mechanisms. Density‐dependence acts at the level of the individual host, the host population and within metapopulations. Pathogens increase biodiversity by disadvantaging common hosts. Coevolution between host and pathogen leads to continuing change and diversity in pathogenesis related parts of the genome. When a pathogen encounters a susceptible host not coevolved with it – for example, through trade – a dramatic drop in host density may occur.