First and sixth authors: Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge, CB2 3EA. U.K.; second author: ADAS, High Mowthorpe, Duggleby, Malton, North Yorkshire YO17 8BP U.K.; third and fourth authors: Division of Agricultural and Environmental Sciences, University of Nottingham, Sutton U.K.; and fifth author: Bonnington Campus, Loughborough, Leicestershire LE12 5RD U.K.; and ADAS Rosemaund, Preston Wynne, Hereford HR1 3PG. U.K.
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Accepted for publication 30 August 2004.
Epidemiological modeling is used to examine the effect of silthiofam seed treatment on field epidemics of take-all in winter wheat. A simple compartmental model, including terms for primary infection, secondary infection, root production, and decay of inoculum, was fitted to data describing change in the number of diseased and susceptible roots per plant over thermal time obtained from replicated field trials. This produced a composite curve describing change in the proportion of diseased roots over time that increased monotonically to an initial plateau and then increased exponentially thereafter. The shape of this curve was consistent with consecutive phases of primary and secondary infection. The seed treatment reduced the proportion of diseased roots throughout both phases of the epidemic. However, analysis with the model detected a significant reduction in the rate of primary, but not secondary, infection. The potential for silthiofam to affect secondary infection from diseased seminal or adventitious roots was examined in further detail by extending the compartmental model and fitting to change in the number of diseased and susceptible seminal or adventitious roots. Rates of secondary infection from either source of infected roots were not affected. Seed treatment controlled primary infection of seminal roots from particulate inoculum but not secondary infection from either seminal or adventitious roots. The reduction in disease for silthiofam-treated plants observed following the secondary infection phase of the epidemic was not due to long-term activity of the chemical but to the manifestation of disease control early in the epidemic.
© 2005 The American Phytopathological Society