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Asiatic Citrus Canker: Spatial and Temporal Spread in Simulated New Planting Situations in Argentina. T. R. Gottwald, Research plant pathologist, Agricultural Research Service, U.S. Department of Agriculture, Orlando, FL 32803; R. G. McGuire(2), and S. Garran(3). (2)Assistant plant pathologist, University of Florida, Institute of Food and Agriculture Sciences, Lake Alfred, FL 33850; (3)Instituto Nacional de Tecnologia Agropecuaria, Concordia, Entre Rios, Argentina. Phytopathology 78:739-745. Accepted for publication 10 December 1987. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1988. DOI: 10.1094/Phyto-78-739.

Single replant trees, one each of cultivars Marsh grapefruit and Valencia orange, were inoculated with a rifampicin-resistant strain of Xanthomonas campestris pv. citri. These inoculated trees were planted in the center of two plots each consisting of 187 trees (approximately 1.0 m tall) of the corresponding cultivar. Spread of epiphytic bacteria from the focal trees was monitored by immunofluorescence microscopy, and incidence of diseased trees was determined by observing visual symptoms. Disease was first detected 49 days after diseased trees were placed in the field. Initial disease spread was highly directional and associated with high winds and blowing rain in mid-January. Subsequent spread was less rapid and generally nondirectional. Monomolecular, logistic, and Gompertz models were tested for goodness-of-fit to disease progress data. The Gompertz model was superior in describing the increase of citrus canker over time. The rate of disease increase (Gompertz rate parameter, k) was 0.005 and 0.009 per day for orange and grapefruit plots, respectively. Disease gradients of —ln(—ln(y)) = a — b log10 m, where y = disease severity (%) and m = distance from the disease focus of infection in meters, varied over time from –0.713 to –1.237 and from +0.048 to –1.856 for orange and grapefruit plots, respectively. The rate of disease progress also was affected by disease-induced defoliation. Disease gradients steepened over time as a result of disease-induced defoliation that often exceeded 90% on individual trees.