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Ecology and Epidemiology

Disease Progress, Defoliation, and Spatial Pattern in a Multiple-Pathogen Disease Complex on White Clover. Scot C. Nelson,Former graduate research assistant, Department of Plant Pathology, North Carolina State University, Raleigh 27695-7616, Current address: University of Hawaii, Department of Plant Pathology, 3190 Maile Way, St. John 313, Honolulu 96822; C. Lee Campbell, professor, Department of Plant Pathology, North Carolina State University, Raleigh 27695-7616. Phytopathology 83:419-429. Accepted for publication 6 January 1993. Copyright 1993 The American Phytopathological Society. DOI: 10.1094/Phyto-83-419.

Disease progress, host growth and defoliation, and spatial patterns for a multiple pathogen, leaf spot disease complex on white clover (Trifolium repens) were monitored in four 6-wk growth periods during 1990–1991 in a natural, 10-ha pasture of white clover and tall fescue (Festuca arundinacea) in North Carolina. The disease complex comprised summer blight (Rhizoctonia solani), black spot (Pseudomonas andropogonis), Stagonospora leaf spot (Stagonospora meliloti), Cercospora leaf spot (Cercospora zebrina), Curvularia leaf spot (Curvularia trifolii), anthracnose (Colletotrichum trifolii), sooty blotch (Polythrincium trifolii), and rust (Uromyces sp.). Estimates of disease severity (percent leaf area diseased) for the disease mixture and leaf area (cm²) were obtained twice per week for 20 leaves on each of 512 plants in four plots. Each plot consisted of two proximal, square 8 × 8 lattices of 64 plants of the virus-susceptible cultivar Regal and the Southern Regional Virus Resistant (SRVR) white clover germ plasm in an existing sward of tall fescue. SRVR populations are resistant to alfalfa mosaic virus, clover yellow vein virus, and peanut stunt virus. A disease severity/leaf area rating scale with 45 categories (nine for disease severity, five for leaf area) was used to estimate percent leaf area diseased and total leaf area (cm²) for each leaf sampled. Also in 1991, disease severity and leaf area were estimated once per week for all individual leaves on 20 plants each of Regal and SRVR during each growth period. Most progress curves for disease incidence (percent of plants diseased) and severity were nonmonotonic, and poor fits were obtained to linearized, classic growth-curve models (logistic, Gompertz, monomolecular). Incidence of virus-infected plants was significantly greater for most plots of Regal than for the SRVR germ plasm; however, both host populations were similar with regard to shape of progress curves and overall disease values (disease maxima and AUDPC) for the leaf spot disease complex. No differences were detected between virus-free and virus-infected plants in total AUDPC for leaf spot severity per 6-wk epidemic. Interactions between host growth (leaf expansion or leaf addition) and defoliation accounted for observed declines in leaf spot severity between consecutive disease assessments. Loss of diseased tissue (defoliation) occurred most often as disease severity increased in the latter part of each growth period, and in patches or near plot edges. Spatially, values for disease severity indicated strongly nonrandom patterns for diseased plants at most assessment dates. Temporal shifts in cluster size and shape were associated with increasing disease severity, or with defoliation. A blocked-quadrat variance procedure detected aggregation for leaf spot severity at several, concurrent spatial scales.