scholarly journals Monitoring Fungicide Sensitivity of Cercospora beticola of Sugar Beet for Disease Management Decisions

Plant Disease ◽  
2010 ◽  
Vol 94 (11) ◽  
pp. 1272-1282 ◽  
Author(s):  
Gary A. Secor ◽  
Viviana V. Rivera ◽  
M. F. R. Khan ◽  
Neil C. Gudmestad

Cercospora leaf spot, caused by the fungus Cercospora beticola Sacc., is the most serious and important foliar disease of sugar beet (Beta vulgaris L.) wherever it is grown worldwide. Cercospora leaf spot first caused economic damage in North Dakota and Minnesota in 1980, and the disease is now endemic. This is the largest production area for sugar beet in the United States, producing 5.5 to 6.0 million metric tons on approximately 300,000 ha, which is 56% of the sugar beet production in the United States. This Plant Disease feature article details a cooperative effort among the participants in the sugar beet industry in this growing area and represents a successful collaboration and team effort to confront and change a fungicide resistance crisis to a fungicide success program. As a case study of success for managing fungicide resistance, it will serve as an example to other pathogen–fungicide systems and provide inspiration and ideas for long-term disease management by fungicides.

2020 ◽  
Vol 21 (4) ◽  
pp. 230-231 ◽  
Author(s):  
Danilo L. Neves ◽  
Martin I. Chilvers ◽  
Tamra A. Jackson-Ziems ◽  
Dean K. Malvick ◽  
Carl A. Bradley

Frogeye leaf spot, caused by Cercospora sojina, is an important disease of soybean (Glycine max) in the United States. An important tactic to manage frogeye leaf spot is to apply foliar fungicides. Isolates of C. sojina were collected from soybean fields in one county in Michigan, three counties in Minnesota, and 10 counties in Nebraska in 2019, and they were tested for resistance to quinone outside inhibitor (QoI) fungicides using a discriminatory dose assay, a PCR assay, and DNA sequencing. Results of the testing indicated that QoI fungicide-resistant isolates were detected in isolates from all counties. Testing results also indicated that the G143A mutation was responsible for the QoI fungicide resistance. This is the first report of QoI fungicide-resistant C. sojina isolates in Michigan, Minnesota, and Nebraska and expands the geographical distribution of QoI fungicide-resistant C. sojina isolates to 18 states in total.


Plant Disease ◽  
2009 ◽  
Vol 93 (1) ◽  
pp. 108-108 ◽  
Author(s):  
A. J. Caesar ◽  
R. T. Lartey ◽  
D. K. Berner ◽  
T. Souissi

The herbaceous perennial Lepidium draba L. is an invasive weed of rangelands and riparian areas in North America and Australia. As of 2002, it had infested 40,500 ha of rangeland in Oregon and large areas in Wyoming and Utah. Little is known of plant pathogens occurring on L. draba, especially in the United States, that could be useful for biological control of the weed. Leaf spots were first noted on a stand of L. draba near Shepherd, MT in 1997. The spots were mostly circular but sometimes irregularly shaped and whitish to pale yellow. The pathogen was erroneously assumed to be Cercospora beticola since its morphological traits closely resembled that species and the area had large fields of sugar beet with heavy Cercospora leaf spot incidence. Diseased leaves of L. draba were collected in 1997 and 2007. Conidia, borne singly on dark gray, unbranched conidiophores produced on dark stromata late in the season, were elongate, hyaline, multiseptate, 38 to 120 × 2 to 6 μm (mostly 38 to 50 × 2 to 5 μm) and had bluntly rounded tips and wider, truncate bases. These characteristics were consistent with the description of C. bizzozeriana Saccardo & Berlese (2). To isolate the fungus, spores were picked from fascicles of conidiophores with a fine-tipped glass rod, suspended in sterile water, and spread on plates of water agar. Germinated spores were transferred to potato dextrose agar (PDA). The ITS1, 5.8S, and ITS2 sequences of this fungus (GenBank Accession No. EU887131) were identical to sequences of an isolate of C. bizzozeriana from Tunisia (GenBank Accession No. DQ370428). However, these sequences were also identical to those of a number of Cercospora spp. in GenBank, including C. beticola. We also compared the actin gene sequences of the Montana isolate of C. bizzozeriana (GenBank Accession No. FJ205397) and an isolate of C. beticola from Montana (GenBank Accession No. AF443281); the sequences were 94.6% similar, an appreciable difference. For pathogenicity tests, cultures were grown on carrot leaf decoction agar. Aqueous suspensions of 104 spores per ml from cultures were sprayed on 6-week-old L. draba plants. Plants were covered with plastic bags and placed on the greenhouse bench at 20 to 25°C for 96 h. Koch's postulates were completed by reisolating the fungus from the circular leaf spots that appeared within 10 days, usually on lower leaves. Spores of C. bizzozeriana were also sprayed on seedlings of sugar beet, collard, mustard, radish, cabbage, and kale under conditions identical to those above. No symptoms occurred. After the discovery of the disease in 1997, plants of L. draba in eastern Montana, Wyoming, and Utah were surveyed from 1998 to 2003 for similar symptoms and signs, but none were found. This, to our knowledge, is the first report of C. bizzozeriana in the United States. The initial report of the fungus in North America was from Manitoba in 1938 (1). It has recently been reported as occurring on L. draba in Tunisia (4) and Russia (3) and is reported as common in Europe (2). A voucher specimen has been deposited with the U.S. National Fungus Collections (BPI No. 878750A). References: (1) G. R. Bisby. The Fungi of Manitoba and Saskatchewan. Natl. Res. Council of Canada, Ottawa, 1938. (2) C. Chupp. A Monograph of the Fungus Genus Cercospora. C. Chupp, Ithaca, NY, 1953. (3) Z. Mukhina et al. Plant Dis. 92:316, 2008. (4) T. Souissi et al. Plant Dis. 89:206, 2005.


Plant Disease ◽  
2014 ◽  
Vol 98 (7) ◽  
pp. 1004-1004 ◽  
Author(s):  
M. D. Bolton ◽  
O. T. Neher

The $2.1 billion United States sugar beet (Beta vulgaris L.) industry is the primary provider of domestic sucrose. Sugar beet powdery mildew is caused by Erysiphe polygoni DC and occurs principally in sugar beet growing regions in the western United States. In these regions, the quinone outside inhibitor (QOI) fungicides pyraclostrobin (Headline, BASF, NC) and trifloxystrobin (Gem, Bayer Crop Science, NC) have been important tools to manage powdery mildew since registration in 2002 and 2005, respectively. However, researchers in Idaho reported poor disease management despite QOI application starting in 2011. In 2013, a research plot near Parma, ID, containing natural powdery mildew infection received treatments of pyraclostrobin, trifloxystrobin, or was untreated (control). Since there was no significant reduction in disease levels between QOI-treated blocks and untreated control blocks, experiments were conducted to clone a partial fragment of the E. polygoni cytochrome b (cytb) gene to gain insight into the molecular basis of QOI resistance in this pathosystem. The primers MDB-920 (5′-CACATCGGAAGAGGTTTATA-3′) and MDB-922 (5′-GGTATAGATCTTAATATAGCATAG-3′) were designed based on consensus sequences of several fungal cytb genes obtained from GenBank (data not presented) and used to amplify a 575-bp fragment of the E. polygoni cytb gene using DNA isolated from 12 infected leaf samples collected in September 2013 from the Parma research plot. Each sample consisted of three leaves harvested from three plants (one leaf per plant) in an experimental block. All DNA extraction, PCR, and sequencing procedures were as described previously (1). PCR products derived from six QOI-treated samples and six untreated samples were sequenced directly. Without exception, all QOI-treated samples harbored a point mutation at nucleotide position 143 that encoded a G143A mutation compared with cytb sequence from untreated samples. The two identified cytb haplotypes have been deposited in GenBank under accession numbers KF925325 and KF925326. This is the first report of QOI resistance and the associated cytb G143A mutation in E. polygoni. The G143A mutation has been reported in most QOI-resistant pathogens to date (2). When the G143A mutation dominates in a pathogen population, there is a consistent association with a loss of disease management despite QOI application (3). Careful monitoring and judicious use of QOI fungicides will be necessary to ensure QOI fungicides remain efficacious for sugar beet powdery mildew management in the United States. References: (1) M. D. Bolton et al. Pest Manag. Sci. 69:35, 2013. (2) N. Fisher and B. Meunier. FEMS Yeast Res. 8:183, 2008. (3) U. Gisi et al. Pest Manag. Sci. 58:859, 2002.


2021 ◽  
Author(s):  
Rebecca Spanner ◽  
Jonathan Neubauer ◽  
Thies M. Heick ◽  
Michael Grusak ◽  
Olivia Hamilton ◽  
...  

Cercospora leaf spot (CLS) is a globally important disease of sugar beet (Beta vulgaris L.) caused by the fungus Cercospora beticola. Long-distance movement of C. beticola has been indirectly evidenced in recent population genetic studies, suggesting potential dispersal via seed. Commercial sugar beet “seed” consists of the reproductive fruit (true seed surrounded by maternal pericarp tissue) coated in artificial pellet material. In this study, we confirmed the presence of viable C. beticola in sugar beet fruit for 10 of 37 tested seed lots. All isolates harbored the G143A mutation associated with quinone outside inhibitor resistance and 32 of 38 isolates had reduced demethylation inhibitor sensitivity (EC50 > 1 µg/ml). Planting of commercial sugar beet seed demonstrated the ability of seed-borne inoculum to initiate CLS in sugar beet. Cercospora beticola DNA was detected in DNA isolated from xylem sap, suggesting the vascular system is used to systemically colonize the host. We established nuclear ribosomal internal transcribed spacer region amplicon sequencing using the MinION platform to detect fungi in sugar beet fruit. Fungi from 19 different genera were identified from 11 different sugar beet seed lots, but Fusarium, Alternaria, and Cercospora were consistently the three most dominant taxa, comprising an average of 93% relative read abundance over 11 seed lots. We also present evidence that C. beticola resides in the pericarp of sugar beet fruit, rather than the true seed. The presence of seed-borne inoculum should be considered when implementing integrated disease management strategies for CLS of sugar beet in the future.


Plant Disease ◽  
2020 ◽  
Vol 104 (6) ◽  
pp. 1654-1661 ◽  
Author(s):  
Subidhya Shrestha ◽  
Jonathan Neubauer ◽  
Rebecca Spanner ◽  
Mari Natwick ◽  
Joshua Rios ◽  
...  

Cercospora leaf spot (CLS), caused by the fungal pathogen Cercospora beticola, is the most destructive disease of sugar beet worldwide. Although growing CLS-tolerant varieties is helpful, disease management currently requires timely application of fungicides. However, overreliance on fungicides has led to the emergence of fungicide resistance in many C. beticola populations, resulting in multiple epidemics in recent years. Therefore, this study focused on developing a fungicide resistance detection “toolbox” for early detection of C. beticola in sugar beet leaves and mutations associated with different fungicides in the pathogen population. A loop-mediated isothermal amplification (LAMP) method was developed for rapid detection of C. beticola in infected sugar beet leaves. The LAMP primers specific to C. beticola (Cb-LAMP) assay was able to detect C. beticola in inoculated sugar beet leaves as early as 1 day postinoculation. A quinone outside inhibitor (QoI)-LAMP assay was also developed to detect the G143A mutation in cytochrome b associated with QoI resistance in C. beticola. The assay detected the mutation in C. beticola both in vitro and in planta with 100% accuracy. We also developed a probe-based quantitative PCR (qPCR) assay for detecting an E198A mutation in β-tubulin associated with benzimidazole resistance and a probe-based qPCR assay for detection of mutations in cytochrome P450-dependent sterol 14α-demethylase (Cyp51) associated with resistance to sterol demethylation inhibitor fungicides. The primers and probes used in the assay were highly efficient and precise in differentiating the corresponding fungicide-resistant mutants from sensitive wild-type isolates.


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