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First Report of Reduced Sensitivity to a QoI Fungicide in Apple Scab (Venturia inaequalis) in Virginia and Maryland

September 2012 , Volume 96 , Number  9
Pages  1,376.2 - 1,376.2

S. C. Marine , Department of Plant Pathology, Physiology and Weed Science, Virginia Polytechnic Institute and State University, Alson H. Smith, Jr. Agricultural Research and Extension Center, Winchester 22602 ; D. G. Schmale III , Department of Plant Pathology, Physiology and Weed Science, Virginia Polytechnic Institute and State University, Blacksburg 24061 ; and K. S. Yoder , Department of Plant Pathology, Physiology and Weed Science, Virginia Polytechnic Institute and State University, Alson H. Smith, Jr. Agricultural Research and Extension Center, Winchester 22602



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Accepted for publication 21 April 2012.

Apple scab caused by Venturia inaequalis (Cooke) Winter continues to be a significant concern for apple growers in Virginia and Maryland. Management of scab has relied on foliar fungicides including strobilurins (QoIs) such as trifloxystrobin (TFX). In recent years, populations of V. inaequalis with reduced sensitivity to the QoIs have been reported in other apple-growing regions of the United States (1,2). Although QoIs generally remain effective in the mid-Atlantic, concerns about the development of resistance in some Virginia and Maryland orchards prompted this study. Twenty-five isolates of V. inaequalis were obtained from scabby leaves from commercial and experimental orchards in Virginia in 2010 (n = 6) and 2011 (n = 14) and from a commercial orchard in Maryland (n = 5) in 2011. Orchards had previously been treated with QoI or sterol-inhibiting (SI) fungicides. Isolates of V. inaequalis were grown on potato dextrose agar (PDA) amended with 0, 0.1, or 1.0 μg ml–1 TFX with 100 μg ml–1 salicylhydroxamic acid (SHAM) and incubated at 19°C. Colony growth was measured weekly for 4 weeks. To account for the SI use at some orchards, isolates of V. inaequalis were also evaluated on PDA amended with 0, 0.5, or 1.0 μg ml–1 myclobutanil. Fungicide sensitivities were expressed as a percentage of the difference in colony growth using a discriminatory dose of 1.0 μg ml–1 TFX with SHAM or 1.0 μg ml–1 myclobutanil at 28 days. Isolates with <25% growth suppression (GS) were classified as fully resistant, whereas those with >70% GS were classified as sensitive. Isolates with 25 to 70% GS were classified as partially resistant. Effective concentration (EC50) values (TFX concentration inhibiting colony growth by 50%) were also calculated for a subset of fully resistant and sensitive isolates. Of the 25 isolates tested, six were fully resistant to TFX (mean EC50 value greater than 10.0 μg ml–1) and 10 were sensitive (mean EC50 value of 0.04 μg ml–1 ± 0.05 μg ml–1). Nine isolates were classified as partially resistant. Some isolates showed more than a 200-fold increase in resistance to TFX, and one isolate grew almost as well on 10.0 μg ml–1 TFX as on the unamended control (GS of 3%). Current-season use of QoIs on isolate source trees was significantly associated with a lack of sensitivity Ç2 (1) = 3.72 (P < 0.06). All six fully resistant isolates originated from QoI-treated commercial orchards, which had shown control failures. Seven of 10 isolates sensitive to QoIs originated from trees that had been treated with SIs during the isolation year. Resistance to myclobutanil was not significantly associated with resistance to TFX Ç2 (1) = 1.220 (P < 0.5), and only one isolate was resistant (i.e. >25% GS) to both. Despite the long history of QoI use at the experimental orchards, no isolates fully resistant to TFX were identified there. To our knowledge, this is the first report of V. inaequalis isolates with resistance to TFX in Virginia and Maryland. Since SI resistance has been documented in Virginia (3) and resistance to both the SI and QoI chemical classes is a concern in the mid-Atlantic region (4), tank-mixing or alternating QoIs with broad-spectrum fungicides with different modes of action is recommended.

References: (1). K. M. Cox et al. Phythopathology 99:S25, 2009. (2). K. E. Lesniak et al. Plant Dis. 95:927, 2011. (3) S. C. Marine et al. Plant Health Progress. doi:10.1094/PHP-2007-1113-01-RS, 2007. (4) E. E. Pfeufer and H. K. Ngugi. Phytopathology 102:272, 2012.



© 2012 The American Phytopathological Society