In 2000 and 2001, commercial carrots (Daucus carota L.) cv. Cellobunch grown in organic soils in Ontario, Canada, developed water-soaked, dark olive-green lesions on leaves that were in contact with soil. Lesions spread rapidly to petioles and adjacent leaves when prolonged moist conditions occurred within the canopy and persisted through harvest. A soft rot lesion was observed on the crown of one carrot root in the field, but no disease symptoms were detected on carrot samples in cold storage. Symptoms on leaves and roots of carrots were similar to sclerotinia rot caused by Sclerotinia sclerotiorum, a common disease in the area, except for the signs of sparser mycelia and smaller sclerotia. White mycelium and irregular, black sclerotia (0.5 to 2 mm) that formed on the surface of diseased leaf and root tissues were plated on potato dextrose agar (PDA) and incubated at 20 ± 1°C. Within 3 to 4 days, numerous mycelial clumps developed throughout the surface of white colonies and within 5 to 7 days these clumps developed into sclerotia. The pathogen was identified as S. minor Jagger (1). In the growth-room, young and senescing leaves of eight carrot (cv. Cellobunch) plants and 20 surface-disinfested roots were inoculated with 5-mm mycelial disks from the margins of colonies of one isolate of S. minor or S. sclerotiorum grown on PDA. A control treatment of an equal set of test units inoculated with sterile PDA plugs was also included. Inoculated plants and roots were incubated at 21 ± 1°C and ≈100% relative humidity for 21 days. Plants inoculated with S. minor, lesions, mycelial clumps, and sclerotia developed on the surface of leaves and petioles 1, 2, and 10 days postinoculation, respectively and were similar to those observed in the field. Lesions progressed faster on senescing leaves and reached the base of the petiole within 7 days, however, infection of the rosette or crown did not occur under these test conditions. In roots, lesions, mycelia, and sclerotia were observed 2, 4 and 10 days postinoculation, respectively, and sclerotia sometimes adhered in large aggregate crusts. S. minor was reisolated from infected tissues, completing Koch's postulates. Carrots inoculated with S. sclerotiorum yielded similar symptoms, but the white mycelium grew into cotton-like, dense mats and produced large (5 to 10 mm) individual sclerotia. Carrot has been previously reported as a host of S. minor (2), but to our knowledge, this is the first report demonstrating the occurrence of sclerotinia rot of carrot caused by S. minor in Ontario. S. minor may not cause damage to carrots in storage, but may affect yield by weakening the tops needed for efficient mechanical harvest. Carrot crops where S. minor was identified are typically rotated with onions (Allium cepa L.), which is not a host of S. minor (2). However, this 1-year rotation is unlikely to suffice for reducing the accumulation of sclerotial inoculum in soil. The knowledge of the occurrence and prevalence of S. minor in carrot crops is a valuable consideration when planning to incorporate carrots in rotation with other hosts of S. minor.
References: (1) L. M. Kohn. Mycotaxon 9:365, 1979. (2) M. S. Melzer et al. Can. J. Plant Pathol. 19:272, 1997.
