Laboratory-induced fungicide resistance to benzimidazole and azole fungicides in Cercospora beticola

Strains of Cercospora beticola resistant to sterol 14α-demethylation inhibitors (DMI) were found 30 times more frequently than strains resistant to carbendazim (MBC) following mutagenesis. In contrast, pathogenicity and resistance tests under greenhouse conditions revealed only 16% of the highly resistant DMI resistant strains to be pathogenic as compared to 67% of the highly resistant MBC resistant strains which were pathogenic. Strains selected on one DMI fungicide were cross-resistant to all other DMI fungicides tested but were not highly resistant to fenpropimorph which inhibits the 14-reductase and the 8-7 isomerase step in sterol biosynthesis. The DMI sensitive parent strain contains ergosta-5,7-dienol, not ergosterol, as its primary sterol. In 24 of 25 different C. beticola isolates which were resistant to flusilazole, the major sterol present was ergosterol. All strains accumulated 14α-methyl sterols as a result of DMI fungicide treatment, suggesting that the 14α-demethylase enzyme was still sensitive to the fungicide. The results of this laboratory study indicate that resistance to DMI fungicides is incremental and associated with reduced fitness, and may suggest that there is a greater risk of resistance development to benzimidazoles than to DMI fungicides.