Pre- and post-infection activity of azoxystrobin, pyraclostrobin, mefenoxam, and phosphite against leather rot of strawberry, caused by Phytophthora cactorum, was determined under greenhouse conditions. Strawberry plants (cv. Honeoye) were grown in pots, and attached fruit at the green-to-white stage of development were used in evaluations. Plants and fruit were sprayed to runoff with the above-mentioned fungicides either before (protectant) or after (curative) inoculation with a zoospore suspension (105 zoospores/ml) of P. cactorum. Inoculated plants with fruit were placed in a mist chamber for 12 h to ensure infection. Fungicides were applied at either 2, 4, or 7 days before inoculation or 13, 24, 36, or 48 h after inoculation. Incidence (proportion of diseased fruit) was recorded 6 days after inoculation. Azoxystrobin and pyraclostrobin provided protectant activity for up to 7 days before inoculation, but only slight curative activity when applied 13 h after inoculation. Phosphite and mefenoxam also provided protection for up to 7 days, as well as curative activity of at least 36 h. There were no significant differences in protectant activity among the QoI fungicides azoxystrobin and pyraclostrobin, phosphite and mefenoxam.
Sensitivities of 89 isolates of Phytophthora cactorum, the causal agent of crown rot and leather rot on strawberry plants, from seven states (Florida, Maine, North Carolina, Ohio, Oregon, South Carolina, and New York) to the QoI fungicide azoxystrobin were determined based on mycelium growth and zoospore germination. Radial growth of mycelia on lima bean agar amended with azoxystrobin at 0.001, 0.01, 0.1, 1.0, 10, and 30 μg/ml and salicylhydroxamic acid (SHAM) at 100 μg/ml was measured after 6 days. Effect on zoospore germination was evaluated in aqueous solutions of azoxystrobin at 0.005, 0.01, 0.05, 0.1, 0.5, and 1.0 μg/ml in 96-well microtiter plates by counting germinated and nongerminated zoospores after 4 h at room temperature. SHAM was not used to evaluate zoospore sensitivity. The effective dose to reduce mycelium growth by 50% (ED50) ranged from 0.16 to 12.52 μg/ml for leather rot isolates and 0.10 to 15 μg/ml for crown rot isolates. The Kolmogorov-Smirnov test showed significant differences (P < 0.001) between the two distributions. Zoospores were much more sensitive to azoxystrobin than were mycelia. Differences between sensitivity distributions for zoospores from leather rot and crown rot isolates were significant at P = 0.05. Estimated ED50 values ranged from 0.01 to 0.24 μg/ml with a median of 0.04 μg/ml. Experiments with pyraclostrobin, another QoI fungicide, demonstrated that both mycelia and zoospores of P. cactorum were more sensitive to pyraclostrobin than to azoxystrobin. Sensitivities to azoxystrobin and pyraclostrobin were moderately but significantly correlated (r = 0.60, P = 0.0001).
Efficacy of azoxystrobin, pyraclostrobin, mefenoxam, and potassium phosphite for control of strawberry leather rot, caused by Phytophthora cactorum, was evaluated on a commercial farm. Foliar sprays of azoxystrobin, pyraclostrobin, and potassium phosphite were applied weekly from bloom through harvest and mefenoxam was applied twice as a soil drench at early plant growth and at fruit set. All fungicide treatments had significantly less leather rot than the untreated control and there were no significant differences in leather rot incidence between any fungicide treatment during both years of testing. Mefenoxam (Ridomil Gold) and potassium phosphite (ProPhyt) are currently registered for control of strawberry leather rot in the U.S. Although they are registered for use on strawberry, leather rot is not on the azoxystrobin (Abound) or pyraclostrobin (Cabrio) labels. Results from these studies indicate that both of these strobilurin fungicides provide excellent control of strawberry leather rot. Accepted for publication 28 November 2004. Published 7 January 2005.
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