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Ecology and Epidemiology

Analysis of Disease Progress of Citrus Canker in Nurseries in Argentina. T. R. Gottwald, Research plant pathologist, U.S. Department of Agriculture, Agricultural Research Service, Horticultural Research Laboratory, Orlando, FL 32803; L. W. Timmer, and R. G. McGuire. Professor and postdoctoral research associate, University of Florida, Citrus Research and Education Center, Lake Alfred 33850. Phytopathology 79:1276-1283. Accepted for publication 16 June 1989. 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, 1989. DOI: 10.1094/Phyto-79-1276.

Three nursery plots of Duncan grapefruit, Pineapple sweet orange, and Swingle citrumelo rootstock were established in Concordia, Entre Rios, Argentina, to study the temporal increase and spatial spread of citrus bacterial canker from a single focal point. Focal trees of each cultivar were inoculated with Xanthomonas campestris pv. citri, the causal agent of Asiatic citrus bacterial canker, and planted in the center of each plot. Disease increase over time was measured as either disease severity (proportion of leaves infected per plant) or disease incidence (proportion of plants infected). Exponential, monomolecular, logistic, Gompertz, and Weibull models were tested for appropriateness by nonlinear regression analysis. The Gompertz model was superior for describing increase in disease incidence and disease severity in all three citrus nurseries. The rate of disease increase was greater in the most susceptible host, Duncan grapefruit, than in less susceptible hosts, Pineapple orange or Swingle. Disease spread coincided with rain splash dispersal and a rapid increase in the apparent infection rate after windblown rainstorms. Rate of disease spread was independent of wind direction. Aggregation of diseased plants was observed in all three nurseries throughout the duration of the tests. Aggregation of individuals appeared to be equivalent between and across rows, indicating that splash dispersal of inoculum was not impeded by between-row distances. Secondary foci were established early in the epidemics and soon overcame the effect of the original focus of disease. The slope of linearized disease gradients, [—ln(—ln(y)) = a + b ln(x), where y = disease incidence and x = distance from the focus of infection in meters, fluctuated over time because of disease-induced defoliation of severely infected plants. Defoliation of more severely diseased plants near the focus subsequently resulted in positive disease gradient slopes for the susceptible Duncan grapefruit nursery as disease levels near the focus diminished.