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First Report of Geotrichum candidum as a Pathogen of Sweetpotato Storage Roots from Flooded Fields in North Carolina and Louisiana

June 2002 , Volume 86 , Number  6
Pages  695.3 - 695.3

G. J. Holmes , North Carolina State University, Department of Plant Pathology, P.O. Box 7616, Raleigh 27695-7616 ; and C. A. Clark , Louisiana State University, Department of Plant Pathology and Crop Physiology, Baton Rouge 70803-1720



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Accepted for publication 20 March 2002.

In October 1997, samples of diseased sweetpotato (Ipomoea batatas (L.) Lam.) roots from storage were submitted for diagnosis to the Plant Disease and Insect Clinic at North Carolina State University. Two organisms were detected from soft rotted roots: Rhizopus stolonifer (Ehrenb.:Fr.) Vuill. (cause of Rhizopus soft rot) and Geotrichum candidum Link. Attempts to duplicate a soft rot by stab-inoculation of sweetpotato roots with a pure culture of G. candidum were unsuccessful. In Louisiana, following heavy rains due to Tropical Storm Frances in 1998, sweetpotato roots exhibiting a cortical tissue collapse at time of harvest were submitted to Louisiana State University for disease identification. Isolations from lesion margins consistently yielded G. candidum. Attempts to reproduce the disease by stab-inoculation produced only a few restricted lesions 5 to 15 mm in diameter. In 1999, rains from hurricanes Dennis, Floyd, and Irene caused extensive flooding in sweetpotato-growing areas of the North Carolina Coastal Plain. Extensive losses occurred in many fields due to a condition known as “souring,” and G. candidum was frequently detected sporulating on the surface of soured roots. This provided a clue for reproducing the disease artificially (1). In 2000, the disease was successfully reproduced. Sterile, wood toothpicks were dragged across a pure culture of G. candidum and inserted (1.5 cm deep) into the mid-section of sweetpotato (cv. Beauregard) roots. Roots were submerged in water at room temperature (23°C) for 24 to 48 h. Each of four roots was inoculated four times, and sterile toothpicks were stabbed into the controls. Additional controls consisted of an inoculated root that was not submerged in water, and a root that was not wounded or inoculated but submerged in water. Following submersion, roots were incubated at room temperature for 5 days. The experiment was repeated. Isolations from diseased tissues consistently yielded G. candidum. Symptoms consisted of slightly sunken, circular lesions, typically 15 to 50 mm in diameter. In cross-section, diseased tissue surrounding the wound was darkened, soft (but not watery), and extended 1 to 20 mm on either side of the wound. None of the controls showed signs of decay. These symptoms are consistent with but do not represent the full range of symptoms observed in the field. Souring of sweetpotato is likely the result of a complex of factors including predisposition of roots by water-saturated soil and the pathogenic effects of G. candidum. To our knowledge, this is the first known report of rot caused by G. candidum on sweetpotato in the United States. G. candidum was reported on sweetpotato in India, but no pathogenicity tests were reported (2).

References: (1) E. Cohen and J. W. Eckert. Plant Dis. 75:166, 1991. (2) N. C. Mandal and M. K. Dasgupta. Indian J. Mycol. Plant Pathol. 10:31, 1980.



© 2002 The American Phytopathological Society