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

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Abstract
Spores of laboratory isolates of Botrytis cinerca did not germinate on potato‐dextrose agar (PDA) containing 5 μg/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 grey mould, germinated normally on PDA containing 100 μg/ml vinclozolin. The fungicide concentrations that reduced the mycelial growth rate of these resistant strains by 50% ranged from 1‐0 to 4‐9 μg/ml for six dicarboximides and dicloran. These values were between nine and 26 times greater than the values for sensitive strains (0.10‐0.27 μg/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 four to 19 times on fungicide‐free PDA, 36 were stable in their resistance. In four in vivo systems, various plant parts were treated with dicarboximide fungicides (500–2500 μg/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 apparently resulted from selection pressure imposed on the pathogen population by exclusive and extensive use of dicarboximides under conditions favouring grey mould epidemics on protected crops.