Abstract
An experimental iprodione fungicide,3-(3,5dichlorophenyl)- N-(1-methylethyl)-2,4-dioxo-1-imidazolidinecarboxamide, controls Fusarium blight of Kentucky bluegrass ( Poa pratensis L.), but it also amplifies the proportion of crowns colonized by Fusarium and the number of its propagules in soils. In contrast, the disease, the proportion of infected crowns, and the numbers of propagules in soil are generally suppressed by benomyl, methyl 1-(butylcarbamoyl)-2-benzimidazolecarbamate. Triadimefon, 1-(4-chlorophenoxy)-3,3-dimethyl-1-(1H-1,2,4-triazol-1-yl)-2-butanone, also controls the disease but is not stimulatory or inhibitory of fusaria. Iprodione and benomyl were studied for their effects on growth and sporulation of Fusarium acuminatum isolated from diseased crowns; iprodione had no or slightly stimulatory effects, and benomyl greatly suppressed these processes, except in a benomyl-tolerant strain. Toxicities of iprodione and benomyl to 1555 identified Fusarium isolates from Kentucky bluegrass turf were determined, as were the toxicities of iprodione to 23 turfgrass pathogens. Of the Fusarium spp, only F. solani was significantly inhibited by iprodione, whereas all were inhibited by benomyl. Iprodione-sensitive fungi included species of Bipolaris, Corticium, Curvularia, Drechslera, Rhizoctonia, Sclerotinia, and Typhula. Insensitive fungi included Colletotrichum, Fusarium, Gaeumannomyces, and Pythium. Investigations with selective fungicides indicate that the primary causal agent of Fusarium blight is not among the fusaria, and that re-interpretation of the disease and its etiology is necessary.
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