Resistance to fungicides in field isolates and laboratory induced mutants of Pseudocercosporella herpotrichoides

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The in vitro response of a range of field isolates and laboratory mutants of Pseudocercosporella herpotrichoides to the benzimidazole fungicides carbendazim, benomyl and thiabendazole, the benzimidazole generating fungicide thiophanate-methyl, and two experimental fungicides, MDPC and diethofencarb was determined. Growth of benzimidazole-sensitive field isolates was completely inhibited by between 0·6 and 2·5 m carbendazim, while resistant isolates were able to grow in the presence of 1000 m carbendazim. Three distinct resistance phenotypes were recognized among laboratory mutants on the basis of response to carbendazim; low-level resistance (MIC 5–25 m), intermediate-level resistance (MIC 50–250 m) and high-level resistance (MIC > 1000 m). In all cases cross-resistance was observed to the other benzimidazoles although the level of resistance to thiabendazole was not precisely correlated with that to carbendazim. Negatively-correlated cross-resistance to MDPC was observed in all 17 benzimidazole-resistant field isolates tested but increased sensitivity to diethofencarb was found in only 14 of these strains. Considerable variation was seen in the phenylcarbamate response of laboratory mutants. Strains with high-level carbendazim resistance were either sensitive to both phenylcarbamates, sensitive only to MDPC or insensitive to both MDPC and diethofencarb. All intermediate-level resistance strains were insensitive to the phenylcarbamates. Most low-level resistance mutants were also insensitive to both compounds but some showed increased sensitivity to MDPC only. A group of mutants derived from one R-type field isolate exhibited very low resistance (MIC = 1·25 m) associated with greatly increased sensitivity to both phenylcarbamates. Spontaneous reversion to phenylcarbamate insensitivity in highly carbendazim-resistant strains was readily obtained. While some revertants were apparently back-mutations and had lost benzimidazole resistance, the majority retained a significant level of carbendazim resistance, and several showed enhanced resistance to carbendazim and thiabendazole. These results cast doubts on the successful field use of N-phenylcarbamates for the control of benzimidazole-resistant strains of the pathogen in the long term.