Abstract

Walnut blight, caused by Xanthomonas arboricola pv. juglandis, is present in all walnut growing regions of Australia, and has been responsible for significant losses of walnut fruits in Tasmania. The pathogen has been isolated from buds just prior to bud-burst in Tasmania, and disease symptoms on fruit of introduced cultivars of Juglans regia are similar to those observed in other growing regions of the world. This review focuses on the approach taken to model disease progression and describes how these models can help interpret the efficacy of spray programs, identify key factors influencing epidemic development and build tools for supporting decisions about spray timing. Considerable differences in the temporal progression of disease incidence on cvs Franquette and Vina fruits were found between three growing years in Tasmania, with incidences near harvest ranging from 19 to 100%. Final disease incidence was correlated positively to the quantity of rainfall during the first 4 weeks after bud-burst. Disease incidence was then used for modelling these epidemics because incidence on half full-size diameter fruit accounted for 97% of the variance in yield of Vina walnuts. The monomolecular growth model with K = 1 obtained a good fit for the ten epidemics analysed. In a dry year, two sprays of copper-based biocide (300 g/kg of copper hydroxide formulated with 150 g/kg mancozeb) applied one week apart from 5% terminal bud-burst provided commercially acceptable control whereas up to nine sprays in a wetter year failed to control this disease. It was concluded that copper-based biocides could be timed strategically and according to the slow rate of disease development in drier years.

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