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Root: dark-brown discoloration with rotting of tap root and lateral roots.
Seedling: pre- and post-emergence damping-off. In older seedlings and plants of highly susceptible cultivars a chocolate-brown canker extends from the base of the soil up the stem, plants wilt, the leaves turn yellow, and plants may die. In cultivars with high levels of partial resistance, the damage is restricted to the roots, plants may be stunted under high disease pressure.
Stem: a dark-brown discoloration extends upwards to as high as 10 nodes. Internal cortical and vascular tissues are discoloured.
Leaf: plants will turn yellow. The upper leaves become chlorotic and the plant wilts.
Cultural Control and Sanitary Methods
Installing drainage pipes deep in the soil to improve drainage and reduce soil flooding, and tillage practices that improve drainage and minimize soil compaction, can reduce disease severity (Dirks et al., 1980; Schmitthenner, 1985). There is increasing evidence that the disease is more severe under reduced tillage (Tachibana, 1983; Schmitthenner and Van Doren, 1985; Schmitthenner, 1988). Factors that may cause minor improvements in disease control are rotation, ridging and avoidance of high levels of fertility (Dirks et al., 1980; Schmitthenner and Van Doren, 1985; Schmitthenner, 1988). Some herbicides such as 2,4 DB (Schmitthenner, 1985), trifluralin (Duncan and Paxton, 1981) and sublethal rates of glyphosate (Keen et al., 1982) may increase severity. A study of integrated control suggested an optimum system of high-tolerance cultivars, good drainage, complete tillage, rotation with maize, and seed treatment with metalaxyl (Schmitthenner, 1988).
Thirteen single genes for resistance to P. sojae (Rps) have been identified of which eight are in allelic series (Diers et al., 1992). From these thirteen Rps genes only eight (Rps1a, Rps1b, Rps1c, Rps1k, Rps2, Rps3a, Rps6 and Rps7) have been incorporated in commercial soyabean cultivars. Following the deployment of each single Rps gene, races of P. sojae were subsequently identified that had a susceptible interaction with the Rps gene. Single Rps genes have been effective for 8 to 15 years depending on inoculum density and environmental conditions (Schmitthenner, 1985). Recently, potential new sources of resistance were identified, but the number or Rps genes present in these sources of resistance and the location on the soyabean chromosome has yet to be determined (Lohnes et al., 1996; Kyle et al., 1998; Schmitthenner et al., 1999; Dorrance and Schmitthenner, 2000). With limited sources of new single gene resistance available, the length of time that single Rps genes are effective and the subsequent development of more complex P. sojae populations, other types of resistance need to be explored. Various methods of transferring resistant genes have been examined ( Wehrmann et al., 1988; Kilen and Keeling, 1990).
Partial resistance (also termed field resistance, general resistance or tolerance) has been shown to be effective against all races of P. sojae (Tooley and Grau, 1982; Schmitthenner, 1985). This resistance is also thought to be rate-limiting (Tooley and Grau, 1982, 1984). Differences in yield among cultivars in P. sojae-infested soil have been attributed to the degree of partial resistance present in the cultivar (Tooley and Grau, 1984; St. Martin et al., 1991).
Cultivars with partial resistance are very susceptible to seedling damping-off (Schmitthenner and Walker, 1979). In Ohio, the first tolerant cultivars have not lost yield potential over 11 years, and there is no evidence for the development of super races (Schmitthenner, 1985). However, repeated planting of cultivars with partial resistance can increase disease severity due to a build-up of inoculum (Anderson, 1986). There is also evidence that some forms of tolerance may be race-specific (Thomison et al., 1988).
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:
Phytophthora root rot is particularly severe in northern soyabean production areas of the USA. After the first outbreak in Ohio in the 1950s, resistant cultivars provided effective control until about 1972. The use of high yielding, but highly susceptible cultivars, led to a build-up of new races and a second disease outbreak occurred, which peaked in 1978 with approximately 50% of the Ohio crop affected and average yield reduced by 536 kg/ha (Schmitthenner and Walker, 1979; Schmitthenner, 1985). Severe losses also occurred on 5 million acres in the lower Mississippi Valley at that time (Kilen, 1977). Later estimates indicated that approximately 5 million hectares were infested in the north central region and 3 million hectares in other areas of USA, with losses of up to 100% possible in individual fields (Schmitthenner, 1989). Losses as high as 96.8% have been demonstrated experimentally by comparing yields in untreated plots with those in plots protected by the fungicide metalaxyl (Anderson and Buzzell, 1982; Tooley and Grau, 1984). Disease incidence (percentage symptomatic plants) has been related to severity and expressed in a regression equation (Tooley and Grau, 1984; Grau, 1985). One study indicated that plant stand reduction was related to loss in yield under low disease incidence, but factors other than stand affected yield at high disease incidence (Moots et al., 1988b). In addition to the use of susceptible cultivars, the other overriding factor that favours disease development is flooded conditions (Athow 1985; Schmitthenner, 1985, 1988, 1989).
The disease was reported as widespread in Queensland, Australia, particularly in poorly drained, heavy-textured soils. Losses were normally <20%, but 50-90% of plants were killed in some fields (Rose et al., 1982). A crop loss study indicated yield losses up to 72% in cultivars not protected by fungicides under conditions of natural infection in the field (Ryley et al., 1989).