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Epidemiological Analysis of Take-All Decline in Winter Wheat

July 2009 , Volume 99 , Number  7
Pages  861 - 868

D. J. Bailey, N. Paveley, J. Spink, P. Lucas, and C. A. Gilligan

First and fourth authors: INRA--Agrocampus Rennes, UMR BiO3P, BP 35327, F-35653 Le Rheu Cedex, France; second author: ADAS, High Mowthorpe, Duggleby, Malton, North Yorkshire YO17 8BP, UK; third author: ADAS Rosemaund, Preston Wynne, Hereford HR1 3PG, UK; and fifth author: Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge, CB2 3EA, UK.

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Accepted for publication 23 February 2009.

Take-all dynamics within crops differing in cropping history (the number of previous consecutive wheat crops) were analyzed using an epidemiological model to determine the processes affected during take-all decline. The model includes terms for primary infection, secondary infection, inoculum decay, and root growth. The average rates of root production did not vary with cropping history. The force of primary infection increased from a low level in 1st wheat crops, to a maximum in 2nd to 4th wheat crops, and then to intermediate levels thereafter. The force of secondary infection was low but increased steadily during the season in first wheat crops, was delayed but rose and fell sharply in 2nd to 4th wheat crops, and for 5th and 7th wheat crops returned to similar dynamics as that for 1st wheat crops. Chemical seed treatment with silthiofam had no consistent effect on the take-all decline process. We conjecture that these results are consistent with (i) low levels of particulate inoculum prior to the first wheat crop leading to low levels of primary infection, low levels of secondary infection, and little disease suppression; (ii) net amplification of inoculum during the first wheat crop and intercrop period; (iii) increased levels of primary and secondary infection in subsequent crops, but higher levels of disease suppression; and (iv) an equilibrium between the pathogen and antagonist populations by the 5th wheat, reflected by lower overall rates of primary infection, secondary infection, disease suppression and hence, disease severity.

The American Phytopathological Society, 2009