Resistance to 3,5‐dichlorophenyl‐N‐cyclic imide (‘dicarboximide’) fungicides in the grey mould pathogen Botrytis cinerea on protected crops*

Abstract

Spores of laboratory isolates of B. cinerea did not germinate on potato-dextrose agar (PDA) containing 5 .mu.g/ml dicarboximide fungicides (iprodione, vinclozolin, procymidone, Serinal, Co 4462, Co 6054). Spores from diseased cucumbers, tomatoes, strawberries and eggplants, from greenhouses where iprodione and vinclozolin failed to control gray mold, germinated normally on PDA containing 100 .mu.g/ml vinclozolin. The fungicide concentrations that reduced the mycelial growth rate of these resistant strains by 50% ranged 1.0-4.9 .mu.g/ml for 6 dicarboximides and dichloran. These values were 9-26 times greater than the values for sensitive strains (0.10-0.27 .mu.g/ml). Mycelial growth of resistant strains was inhibited at lower fungicide concentrations than was spore germination. On average, resistant strains grew 25-30% slower than sensitive strains. Dicarboximide-resistant strains were all resistant to benomyl but sensitive to prochloraz. Of 37 resistant strains transferred 4-19 times on fungicide-free PDA, 36 were stable in their resistance. In 4 in vivo systems, various plant parts were treated with dicarboximide fungicides (500-2500 .mu.g/ml) and then inoculated with mycelial plugs. Protection was observed against sensitive strains of B. cinerea but not against dicarboximide-resistant strains. Lesion development of resistant strains was often slower than that of sensitive strains. The emergence of resistant strains resulted from selection pressure imposed on the pathogen population by exclusive and extensive use of dicarboximides under conditions favoring gray mold epidemics on protected crops.