scholarly journals QoI Resistance in Sugar Beet Powdery Mildew (Erysiphe betae) in Scandinavia

2019 ◽  
Vol 20 (3) ◽  
pp. 179-179 ◽  
Author(s):  
Thies Marten Heick ◽  
Anne Lisbet Hansen ◽  
Annemarie Fejer Justesen ◽  
Lise Nistrup Jørgensen

Powdery mildew caused by Erysiphe betae is one of the major fungal diseases in sugar beet in Denmark and Sweden. Frequent applications of fungicides mitigate the risk of powdery mildew epidemics and, consequently, reduce yield losses conferred by the disease. So far, mixtures of quinone outside inhibitors (QoIs) and triazoles have provided good efficacy against E. betae in field trials and common farming practice. However, development of fungicide resistance is a real risk, because only a limited number of active ingredients are available for the control of powdery mildew in sugar beet, and several other active ingredients are expected to be banned following reevaluation when the most recent European Union legislation is implemented. The G143A mutation associated with QoI resistance has been previously found in the United States. In this brief, its presence in Europe is reported for the first time. The current finding strongly encourages the adoption of anti-resistance strategies that minimize the spread of QoI resistance in sugar beet powdery mildew. Those strategies should be based on integrated pest management measures, including disease monitoring, the use of resistant cultivars, and the use of biological products. A sole reliance on QoI fungicides for sugar beet powdery mildew control should be avoided.

Plant Disease ◽  
2014 ◽  
Vol 98 (11) ◽  
pp. 1494-1502 ◽  
Author(s):  
Lynn Esther E. Rallos ◽  
Nels G. Johnson ◽  
David G. Schmale ◽  
Aaron J. Prussin ◽  
Anton B. Baudoin

Management of grape powdery mildew (Erysiphe necator) using quinone outside inhibitors (QoIs) has eroded in an increasing number of regions due to resistance development. To determine persistence of resistance when QoIs are withdrawn, competition assays were conducted on unsprayed grape plants (Vitis vinifera ‘Chardonnay’) by cycling mixtures of resistant and sensitive isolates characterized as genetically diverse based on microsatellite analyses. Under laboratory conditions, %G143A, quantified by quantitative polymerase chain reaction (qPCR), increased significantly, indicating competitiveness of the resistant fraction. To confirm competitiveness in the field, trials using potted plants were conducted. Percent G143A tended to decrease in one growing season, probably due to spore migration and mixing of populations with natural background inoculum. In a second season, QoI resistance persisted at high frequency for 4 weeks. Resistant populations were also found to persist in one vineyard without QoI application for four consecutive years. The frequency was still about 25% in the fourth year, with higher frequency (36%) in a hotspot section. QoI-resistant populations with >5% G143A also harbored Y136F in the cyp51 gene that confers some resistance to sterol demethylation inhibitors, another fungicide class for powdery mildew control. Double resistance could have been partly responsible for persistence of QoI resistance at this location.


Plant Disease ◽  
2001 ◽  
Vol 85 (7) ◽  
pp. 718-722 ◽  
Author(s):  
Sebastian Kiewnick ◽  
Barry J. Jacobsen ◽  
Andrea Braun-Kiewnick ◽  
Joyce L. A. Eckhoff ◽  
Jerry W. Bergman

Rhizoctonia crown and root rot, caused by the fungus Rhizoctonia solani AG 2-2, is one of the most damaging sugar beet diseases worldwide and causes significant economic losses in more than 25% of the sugar beet production area in the United States. We report on field trials in the years 1996 to 1999 testing both experimental fungicides and antagonistic Bacillus sp. for their potential to reduce disease severity and increase sugar yield in trials inoculated with R. solani AG 2-2. Fungicides were applied as in-furrow sprays at planting or as band sprays directed at the crown at the four-leaf stage, or four- plus eight-leaf stage, while bacteria were applied at the four-leaf stage only. The fungicides azoxystrobin and tebuconazole reduced crown and root rot disease by 50 to 90% over 3 years when used at rates of 76 to 304 g a.i./ha and 250 g a.i./ha, respectively. The disease index at harvest was reduced and the root and sugar yield increased with azoxystrobin compared with tebuconazole. The combination of azoxystrobin applied at 76 g a.i./ha and the Bacillus isolate MSU-127 resulted in best disease reduction and greatest root and sucrose yield increase.


Plant Disease ◽  
2017 ◽  
Vol 101 (1) ◽  
pp. 254-254
Author(s):  
J. H. Joa ◽  
K. C. Seong ◽  
I. Y. Choi ◽  
S. E. Cho ◽  
H. D. Shin

Plant Disease ◽  
2012 ◽  
Vol 96 (11) ◽  
pp. 1621-1628 ◽  
Author(s):  
L. A. Miles ◽  
T. D. Miles ◽  
W. W. Kirk ◽  
A. M. C. Schilder

Powdery mildew, caused by Erysiphe necator, is the most common and destructive disease of grapes (Vitis spp.) worldwide. In Michigan, it is primarily controlled with fungicides, including strobilurins (quinone outside inhibitors [QoIs]). Within the United States, resistance to this class of fungicides has been reported in E. necator populations in some east coast states. Among 12 E. necator isolates collected from five Michigan vineyards in 2008, one carried the G143A single-nucleotide mutation responsible for QoI resistance. This isolate was confirmed to be resistant in a conidium germination assay on water agar amended with trifloxystrobin at 0.001, 0.01, 0.1, 1, 10, or 100 μg/ml and salicylhydroxamic acid (100 mg/liter). The mutant isolate was able to germinate on media amended with 100 μg/ml trifloxystrobin, whereas a representative wild-type isolate did not germinate at concentrations higher than 0.1 μg/ml. In 2009, 172 isolates were collected from a total of 21 vineyards (juice and wine grapes): three vineyards with no fungicide application history (baseline sites), six research vineyards, and 12 commercial vineyards. QoI resistance was defined as the effective concentration that inhibited 50% of conidial germination (EC50) > 1 μg/ml. Isolates from baseline sites had EC50 values mostly below 0.01 μg/ml, while isolates that were highly resistant to trifloxystrobin (EC50 > 100 μg/ml) occurred in five research and three commercial wine grape vineyards at frequencies of 40 to 100% and 25 to 75% of the isolates, respectively. The G143A mutation was detected in every isolate with an EC50 > 1 μg/ml. These results suggest that fungicide resistance may play a role in suboptimal control of powdery mildew observed in some Michigan vineyards and emphasizes the need for continued fungicide resistance management.


Plant Disease ◽  
2017 ◽  
Vol 101 (6) ◽  
pp. 941-947 ◽  
Author(s):  
Anika Bartholomäus ◽  
Stefan Mittler ◽  
Bernward Märländer ◽  
Mark Varrelmann

Rhizoctonia solani (AG 2-2 IIIB) is the causal agent of Rhizoctonia root and crown rot, a disease that causes severe economic problems in sugar beet growing areas worldwide. In the United States, azoxystrobin is the most important active ingredient for fungicidal control of R. solani in sugar beet, showing efficacy superior to other substances. First reports on resistance development in R. solani, however, underline the importance of a careful fungicide resistance management. For this reason, the efficacy of a new fungicide mixture of azoxystrobin and difenoconazole was compared with a fungicide containing only azoxystrobin. Field trials were carried out under natural infection conditions as well as with inoculation in the years 2012, 2013, and 2014. Evaluation of the disease severity and the obtained white sugar yield of different sugar beet cultivars demonstrated that both fungicide treatments possess a similar efficacy, reducing the diseased beet surface by up to 78% and preventing yield losses. Additionally, a real-time PCR assay, based on DNA extracts from representative soil samples (250 g), was used to directly determine the effect of chemical treatment and plant cultivar on the soil-borne inoculum. Fungicide application significantly reduced the concentration of soil-borne inoculum by up to 97%. Furthermore, the results demonstrated that the cultivation of a susceptible cultivar significantly increases the concentration of R. solani in the soil by a factor of 200. In conclusion, the study implies that only a combination of resistant cultivar and fungicide application can prevent an accumulation of R. solani inoculum under conducive conditions in infested fields.


Plant Disease ◽  
2007 ◽  
Vol 91 (7) ◽  
pp. 847-851 ◽  
Author(s):  
H.-Y. Liu ◽  
R. T. Lewellen

Beet necrotic yellow vein virus (BNYVV) is the causal agent of rhizomania in sugar beet (Beta vulgaris). The virus is transmitted by the plasmodiophorid Polymyxa betae. The disease is controlled primarily by the use of partially resistant cultivars. During 2003 and 2004 in the Imperial Valley of California, partially resistant sugar beet cultivars with Rz1 allele seemed to be compromised. Field trials at Salinas, CA have confirmed that Rz1 has been defeated by resistance-breaking isolates. Distinct BNYVV isolates have been identified from these plants. Rhizomania-infested sugar beet fields throughout the United States were surveyed in 2004–05. Soil surveys indicated that the resistance-breaking isolates not only existed in the Imperial Valley and San Joaquin Valley of California but also in Colorado, Idaho, Minnesota, Nebraska, and Oregon. Of the soil samples tested by baited plant technique, 92.5% produced infection with BNYVV in ‘Beta 6600’ (rz1rz1rz1), 77.5% in ‘Beta 4430R’ (Rz1rz1), 45.0% in ‘Beta G017R’ (Rz2rz2), and 15.0% in ‘KWS Angelina’ (Rz1rz1+Rz2rz2). Analyses of the deduced amino acid sequence of coat protein and P-25 protein of resistance-breaking BNYVV isolates revealed the high percentage of identity with non-resistance-breaking BNYVV isolates (99.9 and >98.0%, respectively). The variable amino acids in P-25 proteins were located at the residues of 67 and 68. In the United States, the two amino acids found in the non-resistance-breaking isolates were conserved (AC). The resistance-breaking isolates were variable including, AF, AL, SY, VC, VL, and AC. The change of these two amino acids cannot be depended upon to differentiate resistance-breaking and non-resistance-breaking isolates of BNYVV.


Plant Disease ◽  
2005 ◽  
Vol 89 (12) ◽  
pp. 1362-1362
Author(s):  
B. Jacobsen ◽  
M. R. Johnston ◽  
H. C. Weltzien

Wide spread powdery mildew infections on sugar beets were observed at the Southern Agricultural Experiment Station in Huntley, MT during September, 2003. Throughout the area, lower leaves were frequently heavily covered by the vegetative stage of the fungus with plants at the edge of the field having clearly visible abundant mature (black) and immature (brown) globose ascocarps on the leaf surfaces and stems. The fruiting structures had mostly branched appendages and were imbedded in the superficial mycelium. Their diameter ranged from 70 to 100 μm. Each ascocarp contained five to eight asci with one to four ascospores (mostly three) per ascus. Elliptical ascospores were hyaline and measured 20 to 25 μm long and 12 to 20 μm wide. On the basis of the descriptions given for isolates from Idaho and Colorado (1) and the usage of Erysiphe polygoni DC for powdery mildew on sugar beet in the United States, this isolate may be classified as E. polygoni DC. However, measurements taken show that ascocarps, asci, and ascospores also fall within the range of E. betae (Vanha) Weltz. as described by Weltzien (2). We strongly suggest that these species be compared by using rDNA analysis of the ITS region to determine whether they are separate species. If survival of the ascocarps and the viability and pathogenicity of the ascospores can be confirmed, epidemics of sugar beet powdery mildew could be understood as local and regional events that are not dependant on long distance dispersal of conidiospores. The occurrence of the perfect stage also could lead to the more frequent appearance of new races through genetic recombination. References: (1) J. J Gallian and L. E. Hanson. Plant Dis. 87:200, 2003. (2) H. C. Weltzien. Phytopathol. Z. 47:123, 1963.


Plant Disease ◽  
2018 ◽  
Vol 102 (12) ◽  
pp. 2586-2591 ◽  
Author(s):  
Xuewen Feng ◽  
Mizuho Nita ◽  
Anton B. Baudoin

The protectant fungicide quinoxyfen has been used against grape powdery mildew (Erysiphe necator) in the United States since 2003. In 2013, isolates of grape powdery mildew with reduced quinoxyfen sensitivity (here designated as quinoxyfen lab resistance or QLR) were detected in a single vineyard in western Virginia, USA. Field trials were conducted in 2014, 2015, and 2016 at the affected vineyard to determine to what extent quinoxyfen might still contribute to disease control. Powdery mildew control by quinoxyfen was similar to, or only slightly less than, that provided by myclobutanil and boscalid in all three years. In 2016, early- versus late-season applications of quinoxyfen were compared to test the hypothesis that early-season applications were more effective, but differences were small. A treatment with two early quinoxyfen applications, at bloom and 2 weeks later, followed by a myclobutanil-boscalid plus a low dose of sulfur rotation provided slightly better control of foliar disease incidence than treatments containing four quinoxyfen applications or two midseason or two late quinoxyfen applications supplemented by myclobutanil and boscalid applications; severity differences were small and nonsignificant. Metrafenone and benzovindiflupyr generally provided excellent powdery mildew control. The frequency of QLR in vines not treated with quinoxyfen slowly declined from 65% in 2014 to 46% in 2016. Further research is needed to explain how, despite this QLR frequency, quinoxyfen applied to grapes in the field was still able to effectively control powdery mildew.


Plant Disease ◽  
2011 ◽  
Vol 95 (4) ◽  
pp. 494-494 ◽  
Author(s):  
L. E. Hanson ◽  
J. M. McGrath

Powdery mildew (Erysiphe polygoni DC [synonym E. betae {Vanha} Weltzien]) affects several different crops of Beta vulgaris, including sugar beet, Swiss chard, and table beet. The disease has been prevalent in many sugar beet-growing areas of the United States since the first major epidemic in beet in 1974 (3). Powdery mildew in the United States was primarily associated with the asexual stage of the pathogen until the perfect stage was found, first in western states such as Idaho and Colorado (2), then in more Midwestern states such as Nebraska, and most recently in North Dakota (1). Similar to North Dakota, powdery mildew has not been a major problem in the Michigan growing area. It does appear sporadically, particularly on sugar beets that have not been sprayed to control other foliar diseases. In 2010, powdery mildew infection on sugar beet was observed in late August in a field in the Saginaw Valley of Michigan. Plants were inspected periodically for the presence of the sexual stage. In early October, sugar beet and Swiss chard plants with heavy powdery mildew infection also were observed at the Michigan State University (MSU) Horticultural Demonstration Gardens in East Lansing and on sugar beet at the MSU Plant Pathology and Botany research farms. On both the Saginaw Valley sugar beet and Swiss chard on the MSU campus, ascomata were observed on a few leaves in mid-October. No ascomata were found on sugar beet at the other two locations. The majority of ascomata were dark brown to black when located, although a few light tan ascomata were observed on the Swiss chard. Ascomata varied from 70 to 100 μm in diameter. Asci contained one to four hyaline or golden yellow ascospores similar to those described in other growing regions on sugar beet (1,2). No ascomata had been detected on powdery mildew-infected sugar beet from either the Saginaw Valley or the MSU research farms the previous two years. These results appear to indicate a spread of the ability to form the perfect stage eastward from the western United States. This may be due to movement of one mating type because E. polygoni has been reported to be heterothallic on some crops (4). The presence of the perfect stage indicates that sexual recombination could occur in E. polygoni on Beta species in Michigan, creating the potential for more rapid development of new strains that might vary in fungicide sensitivity and response to host resistance. References: (1) C. A. Bradley et al. Plant Dis. 91:470, 2007 (2) J. J. Gallian and L. E. Hanson. Plant Dis. 87:200, 2003. (3) E. G. Ruppel. Page 13 in: Compendium of Beet Disease and Insects. E. D. Whitney and J. E. Duffus, eds. The American Phytopathological Society, St. Paul, MN, 1986. (4) C. G. Smith. Trans. Br. Mycol. Soc. 55:355, 1970.


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