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First Report of Fruit Rot of Pumpkin Caused by Fusarium solani f. sp. cucurbitae in Arkansas

June 2009 , Volume 93 , Number  6
Pages  669.2 - 669.2

V. L. Castroagudin, J. C. Correll, and R. D. Cartwright, Department of Plant Pathology, University of Arkansas, Fayetteville 72701

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Accepted for publication 31 March 2009.

During 2008, fruit rot of pumpkin (Cucurbita pepo L.) occurred on several cultivars in commercial fields in northeast and northwest Arkansas. Disease incidence ranged from 50 to 75% of the fruit, which were unmarketable. Symptoms included large (>10 cm), brown, corky lesions where the fruit was in contact with the soil. Initially, the lesions were water soaked. A cross section of the symptomatic fruit rind revealed a dry, brown, spongy rot with a light brown halo. Lesions finally became soft and wet, causing infected fruit to collapse. Masses of white mycelia surrounded advanced lesions. No rot symptoms were observed on the vines. Fusarium spp. were isolated from symptomatic fruit. Macroconidia obtained from field-infected fruit and pure potato dextrose agar (PDA) cultures of the predominant Fusarium sp. were morphologically similar. The straight, cylindrical, and robust macroconidia contained between five and seven septa. The apical cell was rounded and blunt and the basal cell was rounded. All three morphological types were tested for pathogenicity on mature fruit of cv. Sorcerer. Fruit were surface disinfected in 70% ethanol. Wounds were made (4 mm deep) in the fruit surface with a cork borer. Three wounds per isolate per fruit were inoculated with a PDA plug colonized with mycelium from a 3-day-old culture. Three replicated wounds were inoculated per isolate and four replicate fruit were used. After inoculation, the wounds were covered with saran wrap. The fruit were incubated at approximately 24°C and evaluated after 7 days. An uncolonized PDA plug was used as a negative control. After 7 days, only the predominant Fusarium sp. produced typical lesions, which were brown, water soaked, and approximately 3 cm in diameter. Fusarium spp. were recovered from the inoculated lesions. The colonies on PDA and macroconidia of the pathogenic Fusarium sp. were morphologically similar to the isolate inoculated and the ones recovered from field lesions. DNA was extracted from the same three isolates used in the pathogenicity test. A portion of the translation elongation factor 1α (TEF) gene was sequenced to verify the identity of the pathogenic isolates. On the basis of a comparison of the Fusarium-ID database at Pennsylvania State University (3), the pathogenic isolates had a 100% match with Fusarium solani f. sp. cucurbitae race 1, teleomorph Nectria haematococca mating population I, isolate NRRL 22098. F. solani f. sp cucurbitae was previously identified as the causal agent of crown and foot rot and a fruit rot of cucurbits and responsible for outbreaks on pumpkin fruit in Connecticut, Missouri, New York, and Ohio from 2001 to 2003 and again in Ohio in 2005 (2). In 2008, a higher average total of monthly precipitation was recorded late in the growing season in Arkansas, (13.7 cm in August and 23.7 cm in September). Although F. equiseti has previously been reported as a fruit rot pathogen of pumpkin in Arkansas (1), to our knowledge, this is the first report of F. solani f. sp cucurbitae as causal agent of pumpkin fruit rot in the state.

Reference: (1) J. C. Correll et al. Plant Dis. 75:751, 1991. (2) W. H. Elmer et al. Plant Dis. 91:1142, 2007. (3) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004.

© 2009 The American Phytopathological Society