and Pickett 1966, Laosuwan andAtkins 1977) and/or semi-arid

Pathogenicity tests were performed on 11 genotypes of Coffea arabica using single‐isolate suspensions of Colletotrichum Kahawae obtained from 90 monoconidial isolates. The objective of this study was to estimate the proportion of pathogenic variation corresponding 10 differences in aggressiveness and virulence (races). A large part of the variation in the pathogen population was due to aggressiveness. The differential effects were too small to suggest conclusively that races exist. This paper discusses the possible causes for the observed small differential interaction and suggests breeding strategies that not only prevent possible adaptation of the pathogen to resistant varieties but also limit variation for resistance due to differences in aggressiveness of the pathogen.

Forty-eight inbred lines of maize with varying levels of resistance to gray leaf spot (GLS) were artificially inoculated with Cercospora zeina and evaluated to characterize partial disease resistance in maize under field conditions from 2012 to 2014 across 12 environments in western Kenya. Eight measures of disease epidemic—that is, final percent diseased leaf area (FPDLA), standardized area under the disease progress curve (SAUDPC), weighted mean absolute rate of disease increase (ρ), disease severity scale (CDSG), percent diseased leaf area at the inflection point (PDLAIP), SAUDPC at the inflection point (SAUDPCIP), time from inoculation to transition of disease progress from the increasing to the decreasing phase of epidemic increase (TIP), and latent period (LP)—were examined. Inbred lines significantly (P < 0.05) affected all measures of disease epidemic except ρ. However, the proportion of the variation attributed to the analysis of variance model was most strongly associated with SAUDPC (R2 = 89.4%). Inbred lines were also most consistently ranked for disease resistance based on SAUDPC. Although SAUDPC was deemed the most useful variable for quantifying partial resistance in the test genotypes, the proportion of the variation in SAUDPC in each plot was most strongly (R2 = 93.9%) explained by disease ratings taken between the VT and R4 stages of plant development. Individual disease ratings at the R4 stage of plant development were nearly as effective as SAUDPC in discerning the differential reaction of test genotypes. Thus, GLS rankings of inbred lines based on disease ratings at these plant developmental stages should be useful in prebreeding nurseries and preliminary evaluation trials involving large germplasm populations.

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