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Research.

Etiology of Canker and Dieback of Sweet Cherry Trees in Washington State. K. M. Regner, former Graduate Research Assistant, Irrigated Agricultural Research and Extension Center, Prosser, WA 99350. D. A. Johnson, and D. C. Gross. Associate Plant Pathologist, Irrigated Agricultural Research and Extension Center, Prosser, WA 99350, and Associate Plant Pathologist, Department of Plant Pathology, Washington State University, Pullman 99164-6430. Plant Dis. 74:430-433. Accepted for publication 21 December 1989. Copyright 1990 The American Phytopathological Society. DOI: 10.1094/PD-74-0430.

Canker and dieback were found in most sweet cherry orchards surveyed between 1985 and 1987 in eastern Washington. Cytospora canker was the principal canker disease, on the basis of disease symptoms and the recovery of Cytospora cincta and, infrequently, C. leucostoma from canker specimens. Pathogenicity tests showed that most isolates of C. cincta were highly virulent, colonizing over 75% of the stem circumference in 12 mo and causing cankers up to 11.5 cm long. Inoculation studies with C. cincta demonstrated that canker expansion was greatest from February to May; moderate expansion occurred during the summer, and little or no appreciable expansion in the autumn and winter months. In contrast, the bacterial canker pathogen, Pseudomonas syringae pv. syringae, was not isolated from cankers in orchards where disease was endemic, and inoculations in the spring (but not those in the fall) resulted in the formation of cankers, which usually remained active only until summer. It was concluded that P. s. pv. syringae and C. cincta do not coexist for extended periods in cankered tissues and that C. cincta is largely responsible for canker and dieback in sweet cherry orchards in Washington State.