VIEW ARTICLE

Ecology and Epidemiology

Spatial and Temporal Patterns of Spotted Wilt Epidemics in Peanut. M. A. Camann, Department of Entomology, University of Georgia, Athens 30602; A. K. Culbreath(2), J. Pickering(3), J. W. Todd(4), and J. W. Demski(5). (2)(4)Departments of Plant Pathology and Entomology, Coastal Plain Station, University of Georgia, Tifton; (3)Department of Entomology, University of Georgia, Athens 30602; (5)Department of Plant Pathology, The Georgia Station, University of Georgia, Griffin. Phytopathology 85:879-885. Accepted for publication 30 May 1995. Copyright 1995 The American Phytopathological Society. DOI: 10.1094/Phyto-85-879.

The spatio-temporal patterns of spotted wilt disease in peanut, caused by thrips-vectored tomato spotted wilt tospovirus (TSWV), were analyzed by several methods. The spatial distributions of symptomatic plants were mapped at 2-wk intervals during two consecutive years in fields of the susceptible peanut cultivar Florunner and in the resistant cultivar Southern Runner. The disease frequency data were subjected to quadrat analyses, including indices of dispersion (variance/mean ratio and the negative binomial k parameter), comparison of frequency distributions of symptomatic plants to expected distributions derived from several models of spatial dispersion (binomial, Poisson, and negative binomial), and two-dimensional distance class analysis at each sampling interval. Although significant spatial aggregation of diseased plants was detected in most samples, random or nearly random clusters of infected plants that apparently arose from a continuous immigration of viruliferous vectors dominated spatial aspects of epidemic progress. Aside from smaller incidence of disease in the resistant compared to the susceptible cultivar, no effect of cultivar was noted in relation to spatial or temporal patterns of disease development in this pathosystem. Spotted wilt temporal progress was well described by monomolecular models of disease progress in each cultivar and year. The data and analyses were consistent with the hypothesis that most infections arise as a result of primary transmission and that there is limited secondary spread of TSWV after it becomes established in the field.