Stem rot of soybean caused by Sclerotinia sclerotiorum (Lib.) de Bary was not recognized as an important problem in the North Central Region of the United States until severe outbreaks occurred in 1992, 1994, and 1996 (2). Although sclerotia mixed with seeds are known to be important to the spread of this disease, the role of internally infested soybean seed in dissemination of the disease is unknown. Tu (1) demonstrated in dry bean, which differs from soybean in seed size and plant architecture, that internally infected seeds are important to the spread of the disease, by producing sclerotia in the soil after the seeds are planted. Experiments were conducted to determine if sclerotia are formed in soils from internally infected soybean seeds. Soybean seed from a field with 70% disease severity were collected and sorted into three classes: (i) normal quality seed, which included moderate or good seed; (ii) poor quality seed (shriveled and/or whitish); and (iii) seed of regular size with visible mycelial mats (S. sclerotiorum or Peronospora manshurica (Naumov) Syd. in Gäum) on the seed coat. Transfer of surface-disinfested seeds to potato dextrose agar and subsequent production of sclerotia showed that 2, 44, and 6% of the seed from each respective class were infested with S. sclerotiorum. One hundred seeds from each of these classes were planted into sterilized and nonsterilized soil at a rate of 5 seeds per pot. Toothpicks were placed to identify the location of each seed, and seeds were covered with 2 cm of soil. Pots were placed in growth chambers with a 14-h photoperiod under two temperature regimes: (i) at 20°C; and (ii) at 10°C for 10 days and then raised to 20°C. Soil was kept saturated by periodically top watering the pots for the first 10 days and bottom watering after that. Two weeks after planting, seeds were examined for formation of sclerotia and the percentages of seeds from which sclerotia were formed were calculated. The experiments were conducted four times. One to two (occasionally three) sclerotia were found in place of each seed that did not germinate. Sclerotia were mainly found from seeds of poor quality, with an average of 12% seeds that produced sclerotia. The frequency of sclerotia found in normal quality seeds was 0.4%, and no sclerotia were found from seeds with mycelial mats. The sclerotia were 2.36 ± 1.07 mm in width, 3.33 ± 1.11 mm in length, and 6.8 ± 3.7 mg in weight, with an averaged germination rate of 88% 8 months after production. Sclerotia production frequencies were 11.4 and 15.4% for temperature regimes (i) and (ii), respectively. Higher percentages of sclerotium production were found in sterilized soil (15.6%) than nonsterilized soil (7.5%). Our results indicate the possibility of internally infected soybean seeds as a means for field-to-field dissemination of S. sclerotiorum.
References: (1) J. C. Tu. J. Phytopathol. 121:40, 1988. (2) X. B. Yang. ICM Newsl. 18, 1997.
