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Disease Cycle and Epidemiology

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Disease Cycle and Epidemiology

The fungus may infect roots of soybean seedlings soon after planting, but above ground symptoms of SDS in the midwestern USA rarely appear until mid-July, when soybean plants have reached reproductive stages. At this later time, the fungus penetrates into the vascular tissue of the plant (Roy et al., 1997). The fungus produces toxins in the roots that are translocated to the leaves. Often, symptoms first appear after heavy rains during reproductive stages; high soil moisture increases the disease severity (Xing and Westphal, 2006). The toxins cause foliar symptoms; the fungus itself does not invade the stems more than a few centimeters above the soil line (Roy et al., 1997).

The first noticeable symptoms of SDS are yellowing and defoliation of upper leaves. When symptoms first appear in a field, they may be confined to a few small areas or strips in the field, often in wetter or compacted areas (Figure 4), such as turn rows. Over the following two or three weeks, affected areas may enlarge and plants in other areas in the field may show symptoms. The extent of yield losses due to SDS depends on the severity and timing of disease expression relative to plant development in regards to yield components. If the disease develops early in the season, flowers and young pods will abort. When the disease develops later, the plant will produce fewer seeds per pod or smaller seeds. The earlier severe disease develops, the more the yield is reduced. Because the SDS fungus can persist in soil for long periods, larger areas of a field will show symptoms of the disease each growing season until most of the field is affected. No inoculum threshold levels of the pathogen have been developed, but the current hypothesis is that SDS will occur as long as the pathogen is present and conditions are conducive for the disease. SDS is more severe when the soybean cyst nematode (SCN, Heterodera glycines) is also present in a field and the cultivar is susceptible to both pathogens (Xing and Westphal, 2006). Both F. virguliforme and SCN are widespread. The close association of the pathogens is also apparent in the fact that the SDS pathogen can be isolated from cysts of SCN (Roy et al., 1997). It is not fully understood what implications this may have for the epidemiology of the disease. Production practices that maintain SCN at low levels may reduce the risk for SDS, but more research is necessary to better understand the nature of the interaction of the two pathogens. A field infested with the SDS pathogen should also be evaluated for SCN, and if SCN is present, a management strategy for both pests should be implemented.

Figure 4

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