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Cercospora kikuchii can infect soybean seeds, pods, stems and leaves, but is most commonly found on the seed (Sweets, 2008).
On seeds, the disease is characterized by irregular blotches varying from light to dark purple and ranging from a tiny spot to the entire area of the seed coat. These discolorations are often accompanied by wide cracks in the seed coat, usually extending transversely along the seed.
When diseased seeds germinate, the cotyledons often become shrivelled and dark purple. Initial symptoms on cotyledons may be observed 10-15 days after sowing (Sasaki, 1982). Cotyledonary infection spreads to stems of young seedlings, producing a dark, diseased area which may later encircle the stem. Usually these young infected seedlings are killed. Plants which survive are often stunted and appear weaker than healthy plants.
Reddish-purple, angular to irregular spots occur on both upper and lower surfaces of infected primary and secondary leaves. These vary from a pin-point spot to irregular patches up to 1 cm diameter. When infections are numerous, leaves become yellow prematurely. Upper leaves exposed to the sun may initially demonstrate a light purple appearance. This discoloration can deepen and extend over the entire upper leaf surface, giving affected leaves a leathery, dark, reddish-purple appearance.
On older plants, young infections on stems and petioles appear as slightly sunken, irregular, reddish-purple areas, 1 to several millimetres long. Several infected areas may coalesce so that the lesion completely encircles the stem or petiole. Premature defoliation may result from severe petiole infection. Maturing pods show minute, reddish to reddish-purple areas which later become purplish-black.
Yields are usually not reduced but a high percentage of seed stain may be evident at harvest (Sweets, 2008).
Cultural Control and Sanitary Methods
Late maturity reduced disease incidence in Korea (Kwon et al., 1977; Oh and Kwon, 1981) and Japan (Koyama and Yunoki, 1977). In the United States delays in harvest did not affect the disease (Wilcox et al., 1974), whereas in Japan the disease was more severe at later harvest time with poorer drying conditions in the field. Storing seeds insufficiently dried also increased the number of infected seeds (Suzuki, 1985). Competition from cocklebur had little effect on disease (Kirkpatrick et al., 1983), and in Brazil the disease was not affected by weed development (Dhingra and da Silva, 1978a). In one study disease was reduced under a no-till cropping regime (Tyler and Overton, 1981). Potassium fertilizer reduced seed infection in some reports (Camper and Lutz, 1977; Ito et al., 1993) but had no effect in others (Andrews and Svec, 1976; Svec et al., 1976).
Studies of resistance to purple seed stain across different maturity groups have been complicated by difficulties in distinguishing between resistance and environmental effects (Koyama and Yunoki, 1977; Oh and Kwon, 1981; Okabe et al., 1990; Roy and Abney, 1976). PI 80837, however, has consistently shown a high degree of resistance (Roy and Abney, 1976; Wilcox et al., 1975). A study of the relative importance of genotype and environment, using crosses of PI 80837 x Amsoy, showed that the incidence of seed infection is under moderately strong genetic control and can be reduced by selection for resistance (Wilcox et al., 1975). The length of the R7-R8 period during major pod and seed dry down was associated consistently with the incidence of seed infection by C. kikuchii. Among genotypes with near-identical maturities, soyabeans resistant to seedborne diseases had shorter R7-R8 intervals and a greater rate of moisture loss than susceptible soyabeans (Ploper et al., 1992). Numerous cultivars, such as Morgan, have been registered as resistant to C. kikuchii (Kenworthy, 1988).
Variability in susceptibility to leaf infection was detected in a greenhouse inoculation study (Walters, 1980b; Walters, 1985). Histological aspects of resistance have been studied in Japan (Fujita and Suzuki, 1988). Resistance in wild soyabean (Glycine soja) seems to be controlled by two dominant genes that could possibly be utilized in G. max by interspecific hybridization (Fujita et al., 1988). The inheritance of resistance to purple stain disease was studied in the parents and F2 progeny of SJ2 (resistant) x Chiang Mai (susceptible). Segregation ratios fit a 3:1 ratio indicating that purple stain disease was under the control of a singe gene (Jordan et al., 1992).
Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:
Purple seed stain occurs wherever soyabeans are grown throughout the world (Agarwal, 1981). The seed phase of the disease does not adversely affect yields or other agronomic characteristics (Wilcox et al., 1975), but the discoloration symptom affects marketability of the seed, whether it is used for planting or processing. This is a significant concern in Japan (Suzuki, 1985) and in the United States where grain grades are reduced by purple seed stain (Wilcox et al., 1975). Substantial crop losses have been attributed to the leaf phase of the disease in southern regions of the United States (Walters, 1980b; Walters, 1985). Younger soybean plants (of maturity groups III and IV) were more susceptible than older plants (maturity group V) to Cercospora leaf blight (Alloatti, 2009).