Incidence and severity of peach rusty spot were monitored throughout the growing seasons of 1999 to 2001. Graphical and statistical analysis revealed that disease increased from the shuckoff stage of fruit development until 60 days after full bloom; epidemics typically lasted from 17 to 30 days. An analysis of fruit growth indicated that the early-season epidemic coincided with the first stage of stone fruit development, physiologically characterized as the period of cell division. During this period, as fruit growth slowed and approached initiation of pit-hardening, the rate of disease increase slowed. Since fruit infection was greatest during the period of fruit growth, disease progression was modeled as a function of plant growth instead of time. Temporal analysis revealed that the logistic function was appropriate for describing both growth processes, and a synchronous logistic/logistic composite disease progression/fruit growth model was fit to all data sets. No change in disease levels occurred during midseason, which coincided with the second stage of fruit development, a period of slow growth. Subsequently, disease incidence and severity significantly declined on average by 26% and 1.3 lesions per fruit, respectively, during the 20 to 30 days prior to harvest. This decline phase coincided with the third stage of fruit growth, the period of cell enlargement and coloration. These disease reductions may be related to physical changes in fruit size and pigmentation, as opposed to resistance development, causing younger, less established lesions to become undetectable.
Different numbers of consecutive fungicide applications, beginning at petal fall and continuing into the summer, were examined for their effect on rusty spot epidemics. Disease progressions for each fungicide level were quantified by fitting either the logistic or monomolecular model. When the weighted absolute infection rate (ρ) and maximum disease level (Kmax) parameters were expressed as functions of the number of applications, the logistic decline model provided the best fit for five of six data sets. This model described a gradual decrease in ρ and Kmax in response to the initial fungicide application, a rapid decline in parameter values with the addition of one or two applications, and a diminished parameter response as fungicide applications continued toward the end of the epidemic. Based on examination of model behavior across all 3 years of the study, adequate management was achieved with a total of three to five fungicide applications. Additional analyses of area under the disease progress curve and final disease intensity at harvest supported these results and indicated that further reduction in fungicide usage may be possible. Unlike earlier findings, rusty spot did not significantly decrease fruit volume or weight at midseason or at harvest; as lesion density increased, fruit volume remained constant. The relationship between disease incidence and lesion density within any given year was best explained by the zero-intercept version of the exponential model. However, comparison of model parameters across years revealed significant seasonal variation. Nevertheless, the incidence-lesion density relationships were fairly uniform across years at incidence values below 0.5, where lesion density increased gradually and in a near-linear fashion.
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