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Rice Blast Epidemics Initiated by Infested Rice Grain on the Soil Surface

June 2001 , Volume 85 , Number  6
Pages  612 - 616

D. H. Long , Field Research Biologist, Zeneca Ag Products, Southern Regional Technical Center, Leland, MS 38756 ; J. C. Correll , Professor, Department of Plant Pathology, University of Arkansas, Fayetteville 72701 ; F. N. Lee , Professor, Rice Research and Extension Center, Stuttgart, AR 72160 ; and D. O. TeBeest , Professor, Department of Plant Pathology, University of Arkansas, Fayetteville 72701

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Accepted for publication 16 February 2001.

Field experiments were conducted in 1996 and 1997 with a marked strain of Pyricularia grisea to determine if inoculum from infested rice grain could cause primary infections and sustain a rice blast epidemic during the growing season by giving rise to leaf, collar, and neck symptoms. The marked strain, a sulfate nonutilizing (sul) mutant of P. grisea, was grown on autoclaved rice seed for 7 days at 25°C. Infested rice grains were applied to the soil surface at the time of plant emergence (approximately 10 days after planting) at densities of 0, 0.5, 5, 25, and 50 grains per 0.1 m2 in plots planted to the blast susceptible cv. M-201. Leaf blast symptoms were first detected in the plots containing infested grain 35 days after plant emergence in both 1996 and 1997. The sul mutant was isolated from more than 90% of the lesions sampled from rice seedlings 35 to 45 days after plant emergence. Leaf blast increased more rapidly in plots with 25 and 50 infested grains per 0.1 m2 than in plots with less inoculum pressure (0.5 and 25 infested grains per 0.1 m2), although in 1996, leaf blast incidence recorded at midseason in plots containing 0.5 and 5 infested grains per 0.1 m2 was 41 and 55%, respectively. At the end of both seasons, the sul mutant was recovered from over 90% of the leaf, collar, and neck blast lesions except for one sample date in 1996. Rice blast was not detected in the control plots (no infested grain) in 1997 and not until 65 days after planting in 1996. Comparisons of disease progress on leaves between the marked strain and the parental wild-type strain under field conditions indicated that development of disease caused by the sul mutant was similar to disease caused by the wild-type strain.

© 2001 The American Phytopathological Society