Soil structure and soil‐borne diseases: using epidemiological concepts to scale from fungal spread to plant epidemics

Abstract

SummaryMany epidemics of root diseases involving soil fungi depend on the interplay between fungal growth and the spatial and temporal heterogeneity of the soil environment. Colonization or infection of a root occurs at fine scales with growth and movement of fungal mycelia through soil. However, epidemics are observed at coarser scales, and depend on a cascading spread through populations of roots. We briefly review conventional analyses of soil-borne epidemics and argue that these treat soil physical conditions at scales too coarse to be meaningful for interactions between soil, plants and fungi, and fail to consider the effect of soil physical conditions on the underlying epidemiological processes. Instead, we propose a conceptual epidemiological framework that integrates spatial scales and use this to review the effect of soil structure on the dynamics of soil-borne pathogenic fungi. Using the soil-borne fungal plant pathogen Rhizoctonia solani as an example, we demonstrate that invasion of fungi into host populations is critically affected by environmental conditions operating at each of two scales: (i) at the microscopic scale (mm À cm) the fungus preferentially explores certain pathways in soil, and small changes in soil physical conditions make the fungus switch from small, dense colonies to large, sparse and rapidly expanding ones; (ii) at the larger scale (cm À dm) a critical density of susceptible hosts is required, in excess of which fungi switch from non-invasive to invasive spread. Finally, we suggest that the approach will increase the applicability of research dealing with microscopic soil-plant-microbe interactions towards the solution of large-scale epidemiological problems.

Observer-dependent variability of the thresholding step in the quantitative analysis of soil images and X-ray microtomography data

“…Soil scientists rapidly seized that opportunity (e.g., Jongerius et al, 1972;Murphy et al, 1977a,b). They continued to do so in the 1980s (e.g., Ringrose-Voase and Bullock, 1984), after the development of personal computers, and particularly in the 1990s, as inexpensive scanners, digital cameras, and versatile image manipulation software made it increasingly straightforward to acquire images and to analyze them (often with the help of fractal geometry), for a variety of purposes (e.g., Hallaire and Cointepas, 1993;Bielders et al, 1996;Deleporte et al, 1997;DeLeo et al, 1997;Beaudet-Vidal et al, 1998;Baveye, 2002;Ohrstrom et al, 2002;Dathe and Baveye, 2003;Ohrstrom et al, 2004;Morris and Mooney, 2004;Pendleton et al, 2005;Persson et al, 2005;Wantanaphong et al, 2006;Lipsius and Mooney, 2006;Vogel et al, 2006;Otten and Gilligan, 2006;Jacobson et al, 2007;Marcelino et al, 2007;Mooney and Morris, 2008;Papadopoulos et al, 2008;Persson and Olsson, 2008;Tarquis et al, 2008). In recent years, synchrotronbased X-ray computed tomography (CT) and table-top X-ray micro-CT scanners have allowed researchers to visualize in 3 dimensions the structure and composition of soils at micrometric resolutions, and have enabled significant advances to be made in our understanding of the functioning of soils at previously unexplored spatial scales (e.g., Garnier et al, 1998;Baveye et al, 2002;Elliot and Heck, 2007a,b;Sleutel et al, 2008).…”

Landscape epidemiology of plant diseases

“…Finally, in the case of heteroecious pathogens, the presence of alternative hosts may be required to allow the pathogen to locally complete its life cycle. Host density is recognized as a major factor driving disease epidemics and theoretical studies have focused on determining a threshold below which a pathogen cannot invade a population of susceptible individuals (McCallum et al 2001;Otten & Gilligan 2006). The dependence of plant disease incidence on the local density of the host is documented in forests (Gilbert et al 1994;Bell et al 2006;Emiko Condeso & Meentemeyer 2007) or in grasslands (Knops et al 1999;Mitchell et al 2002).…”

Epidemiological History of Cypress Canker Disease in Source and Invasion Sites

“…The policy of not planting cypress species susceptible to bark canker over large surfaces has represented a form of disease control, capable of minimizing the build-up of the pathogen inoculum; and the lack of continuity of host species has probably limited the spread of disease in the following years. Host density is recognized as a major factor driving disease epidemics, and some studies have determined a threshold below which a pathogen cannot invade a population of susceptible individuals [53,54].…”