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Anthracnose of Sunflower Sprouts Caused by Colletotrichum acutatum in California

December 2009 , Volume 93 , Number  12
Pages  1,351.1 - 1,351.1

S. T. Koike, University of California Cooperative Extension, Salinas 93901; C. E. Fake, University of California Cooperative Extension, Auburn 95603; and J. C. Correll, University of Arkansas, Fayetteville 72701



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Accepted for publication 11 September 2009.

In California, sunflower (Helianthus annuus) is commercially grown and marketed as edible, germinated sprouts. Sunflower seeds are soaked overnight in water, drained, and seeded into a compost-based medium in flats. The flats are incubated for 3 days in low-light conditions until roots develop. Flats are then moved under filtered shade, with air circulation provided by fans, for 3 to 5 days. The germinated seedlings are finally grown in full sunlight for another 3 to 7 days and are then ready for market. Such sprouts can be consumed raw or cooked. In 2009, in Placer County, CA, a previously undescribed disease occurred on commercial organic sunflower sprouts. Symptoms were dark brown, irregularly shaped lesions on seedling cotyledons and stems. Fungal fruiting structures were not observed in diseased tissues. Isolations were carried out on symptomatic seedlings that were surface sanitized in 1.2% NaOCl and then rinsed in sterile distilled water (SDW). When placed on acidified potato dextrose agar (A-PDA), tissues consistently yielded one type of fungal organism. On A-PDA, isolates produced dark gray, aerial mycelium, acervuli, and single-celled fusiform conidia. Eight isolates were examined for sequence variation in the internal transcribed spacer (ITS) region and the intron in the glutamine synthetase (GS) gene (2). On the basis of spore morphology and a complete match (100%) of the ITS sequence and the GS intron sequence, all eight isolates were identified as Colletotrichum acutatum subgroup C1 represented by isolate ATCC MYA-662 (2). Six isolates were each tested for pathogenicity on sunflower by spraying a spore suspension (1 × 106 conidia/ml) onto sets (six-pack trays; one plant per cell) of plants at either cotyledon or first true-leaf stage. Each plant set was sprayed with approximately 5 to 8 ml of inoculum. Plants were incubated for 48 h in a humidity chamber and then maintained in a greenhouse. Control sunflower plants were sprayed with distilled water and otherwise treated similarly. After 14 days, inoculated cotyledons and true leaves developed lesions similar to those observed on commercial samples; C. acutatum was reisolated from these lesions. Control plants developed no symptoms. The experiment was repeated and the results were the same. To test for possible seedborne C. acutatum, sunflower seeds of the same commercial seed lot used to plant the affected crop were surface sanitized (1.2 % NaOCl for 60 s), rinsed in SDW, placed in incubation boxes (10.2 × 10.2 cm, clear acrylic, Hoffman Manufacturing, Inc., Jefferson, OR), and then processed according to a previously described freeze blotter assay (1). After testing 10 replications of 100 seeds each, no C. acutatum was detected. To our knowledge, this is the first report of anthracnose of sunflower sprouts in California and the first report of a sunflower disease caused by C. acutatum. This sprout production environment, consisting of high humidity, prolonged periods of high moisture, and low light, likely favored the disease. For the affected commercial sprouts crops, disease reached as high as 25% incidence and continues to be an intermittent problem.

References: (1) L. J. du Toit et al. Plant Dis. 89:4, 2005. (2) J. C. Guerber et al. Mycologia 95:872, 2003.



© 2009 The American Phytopathological Society