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Dynamics of Primary and Secondary Infection in Take-All Epidemics

January 1999 , Volume 89 , Number  1
Pages  84 - 91

D. J. Bailey and C. A. Gilligan

Department of Plant Sciences, University of Cambridge, Downing Street, Cambridge, CB2 3EA, England, U.K.

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Accepted for publication 4 October 1998.

Using a combination of experimentation and mathematical modeling, the effects of initial (particulate) inoculum density on the dynamics of disease resulting from primary and secondary infection of wheat by the take-all fungus, Gaeumannomyces graminis var. tritici, were tested. A relatively high inoculum density generated a disease progress curve that rose monotonically toward an asymptote. Reducing the initial inoculum density resulted in a curve that initially was monotonic, rising to a plateau, but which increased sigmoidally to an asymptotic level of disease thereafter. Changes in the infectivity of particulate inoculum over time were examined in a separate experiment. Using a model that incorporated terms for primary and secondary infection, inoculum decay, and host growth, we showed that both disease progress curves were consistent with consecutive phases dominated, respectively, by primary and secondary infection. We examined the spread of disease from a low particulate inoculum density on seminal and adventitious root systems separately. Although seminal roots were affected by consecutive phases of primary and secondary infection, adventitious roots were affected only by secondary infection. We showed that the characteristic features of disease progress in controlled experiments were consistent with field data from crops of winter wheat. We concluded that there is an initial phase of primary infection by G. graminis var. tritici on winter wheat as seminal roots grow through the soil and encounter inoculum, but the rate of primary infection slows progressively as inoculum decays. After the initial phase, there is an acceleration in the rate of secondary infection on both seminal and adventitious roots that is stimulated by the increase in the availability of infected tissue as a source of inoculum and the availability of susceptible tissue for infection.

© 1999 The American Phytopathological Society