Effect of host and inoculum patterns on take-all disease of wheat incidence, severity and disease gradient

Abstract

The importance of the spatial aspect of epidemics has been recognized from the outset of plant disease epidemiology. The objective of this study was to determine if the host spatial structure influenced the spatio-temporal development of take-all disease of wheat, depending on the inoculum spatial structure. Three sowing patterns of wheat (broadcast sowing, line sowing and sowing in hills) and three patterns of inoculum (uniform, aggregated and natural infestation) were tested in a field experiment, repeated over 2 years. Disease (severity, root disease incidence, plant disease incidence and, when applicable, line and hill incidences) was assessed seven times during the course of each season and the spatial pattern was characterized with incidence-incidence relationships. In the naturally infested plots, disease levels at all measurement scales were significantly higher in plots sown in hills, compared to plots sown in line, which were in turn significantly more diseased than plots with broadcast sowing. Disease aggregation within roots and plants was stronger in line and hill sowing than in broadcast sowing. Analysis of the disease gradient in the artificially infested plots showed that the disease intensified (local increase of disease level) more than it extensified (spatial spread of the disease), the effect of the introduced inoculum was reduced by 95% at a distance of 15 cm away from the point of infestation. Yield was not significantly affected by sowing pattern or artificial infestation

Characteristics and drivers of plant virus community spatial patterns in US west coast grasslands

“…While there is evidence for local dispersal of B/CYDVs from ‘spillover’ hosts (Power and Mitchell ), this and other studies showing plant disease aggregation often occur in assemblages of low plant diversity (Sone et al , Nessa et al ). Natural grasslands and other highly diverse ecological environments are likely to obscure aggregation caused by localized dispersal through mechanisms such as variation in host quality, vector foraging preferences, and the initial spatial distribution of disease inoculum (Caraco et al , Medel et al , Ferrari et al , Gosme and Lucas ). Regardless of diversity, longer‐lived plants can accumulate infections over time, resulting in random spatial patterns of disease (Raybould et al ).…”

Assessing Wheat Damage Caused by Gaeumannomyces graminis Using Plant Pathology Techniques, Image Analysis, and Satellite Data Image Analysis

“…Those fields were marked with a GPS device and samples were taken from patches of wheat heads. Samples were collected randomly in each field, from 20 patches of wheat heads, each patch marks as a 1x1m subplot, and six plants were sampled from each of the 20 subplots/sampling field [6]. Sampled plants were washed free of soil and examined for Take-all by isolated and identified (microscopic), the fungus from diseased tissues of the plants.…”

A new model for the pathozone of the take‐all pathogen, Gaeumannomyces graminis var. tritici

“…The pathozone was defined by Gilligan () as the volume of soil surrounding subterranean plant organs within which a propagule must occur if it is to have any chance of infecting the organ. It is an important concept in the epidemiology of soilborne diseases, not only from an applied point of view, for example modifying planting pattern so that the pathozone does not coincide with infected residues from the previous crop (Kabbage & Bockus, ; Gosme & Lucas, ) but also from an evolutionary perspective, because it represents the ability of a pathogen to initiate an epidemic and thus would play a crucial role in the evolution of a pathogen population if it varied across strains. The pathozone has been estimated empirically for a range of soilborne pests and pathogens using placement experiments, where propagules are placed at different distances from roots and the subsequent disease development is recorded (Gilligan & Simons, ; Bailey & Gilligan, ; Bailey et al , ).…”