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Stimulatory Effects of Flusilazole on Virulence of Sclerotinia sclerotiorum.

Flusilazole, a member of the demethylation inhibitor fungicides, is highly efficacious for control of Sclerotinia sclerotiorum. To achieve judicious applications of flusilazole, its hormetic effects on virulence of S. sclerotiorum were investigated. Flusilazole sprayed at concentrations from 0.02 to 0.5 μg/ml caused statistically significant (P < 0.05) stimulatory effects on virulence of S. sclerotiorum to potted rapeseed plants, and the maximum stimulation magnitudes were 11.0 and 10.7% for isolates GS-7 and HN-24, respectively. Studies on the time course of the infection process showed that a stimulatory effect on virulence could be discerned at 18 h postinoculation, indicating a direct stimulation mechanism rather than an overcompensation for initial inhibitions. In order to determine whether the stimulations were caused mainly by effects of flusilazole on S. sclerotiorum or on rapeseed plants, mycelia grown on flusilazole-amended potato dextrose agar (PDA) media were inoculated on leaves of rapeseed plants without spraying the fungicide. Mycelium radial growth on PDA supplemented with flusilazole at concentrations from 0.005 to 0.16 μg/ml was inhibited by 10.11 to 48.7% for isolate GS-7 and by 4.1 to 24.9% for isolate HN-24. Observations with a scanning electron microscope showed that flusilazole in PDA at 0.04 and 0.08 μg/ml caused slightly deformed mycelia and twisted mycelial tips. Nevertheless, after inoculating on leaves of potted rapeseed plants, virulence of the inhibited mycelia was statistically significantly (P < 0.05) greater than that of the nontreated control, and the maximum stimulation magnitudes were 16.2 and 19.8% for isolates GS-7 and HN-24, respectively. Studies on a physiological mechanism for virulence stimulations showed that tolerance to hydrogen peroxide did not increase significantly for mycelia grown on flusilazole-amended PDA, thus excluding the possibility of tolerance to reactive oxygen species as a potential mechanism for virulence stimulations.