Importance
Soybean sudden death syndrome (SDS) was first discovered in Arkansas in 1971, but was not recognized as a serious soybean disease until 1984. Since that time, the disease has been confirmed in 9 states including Alabama, Arkansas, Illinois, Indiana, Kentucky, Louisiana, Missouri, Mississippi and Tennessee. While SDS is not a serious problem every year, severe infections can reduce yields by as much as 80%. These losses result from premature defoliation, flower and pod abortion, pod drop and reduced seed size. Indirect yield losses and seed quality problems may also be a factor due to higher levels of pod- and stem-infecting fungi where plants die prematurely as a result of SDS.
SDS has appeared in 20 west Kentucky counties since 1984. The most severe episodes of the disease have occurred in highly productive river bottom fields, especially those with a history of soybean cyst nematode (SCN) infestation. Early-planted full season soybeans are more often and more severely affected than are double crop soybeans or late planted full season soybeans.

Cause
Initially, the cause of SDS was elusive, with mechanical, cultural, environmental and biological factors all considered as possible causes. Early studies involving soil fumigation indicated that the origin was biological. Subsequent work in Arkansas and Mississippi proved that SDS is caused by a strain of the common soil fungus Fusarium solani (FS-A). This result has been confirmed by work in Indiana and Missouri and is now generally accepted.
Although FS-A is the primary organism associated with SDS, other pathogens may also be involved in disease development. The most studied of these is the soybean cyst nematode. Mississippi researchers found that while SCN is not required for severe SDS to occur, SCN at sufficient levels exacerbates foliar symptoms, leading to early and severe SDS. This finding is important, since the disease's timing and severity, relative to soybean development, determines how much yields are reduced.
In addition to SCN, other soybean pathogens (foliar and root/stem infecting) are being studied for their potential role in SDS development. Preliminary data suggest that any stress factor (biological, mechanical or environmental) may magnify SDS symptom expression and cause SDS-affected plants to deteriorate earlier and more severely (i.e. to die prematurely).

Symptoms
Foliar
Symptoms first appear as random, irregularly-shaped yellow blotches of various sizes. Blotches occur between the veins of leaflets and can start at any level in the canopy of plants. As the disease progresses, blotches run together and begin to turn brown. At first this effect is most pronounced in the tops of plants. At this stage the disease becomes recognizable from the road.
With time, you see large dead areas between the veins with the veins remaining green. Affected leaflets eventually die and either stay on the plant or fall to the ground. In the latter case, the petioles remain attached and the plants look as though they have been fed on by grasshoppers.
Severe defoliation in the early to mid-reproductive stages may be accompanied by flower and pod abortion and drop of developing pods. Fully expanded pods, although they may ripen prematurely, rarely drop off the plants. Premature ripening, however, may lead to higher levels of pod- and stem-infecting fungi which could indirectly lower yields or seed quality.

Root and Stem Symptoms
In addition to foliar symptoms, roots and stems of plants with SDS also show characteristic symptoms. Root symptoms precede foliar symptoms and appear as a general deterioration of taproots and lateral roots. Nitrogen-fixing nodules also deteriorate and are non-functional. The internal portion of affected taproots turns a milky gray-brown. This general discoloration extends up the stem for several nodes, but the stem's core remains healthy (i.e. white).

Cause
SDS symptoms are the result of root infections by FS-A. The fungus cannot be isolated from tissue above the soil line. Recent research has indicated that foliar symptoms are the result of a fungus-produced plant toxin. The fact that plants occasionally recover after showing earlier foliar symptoms further suggests toxin activity.

Disease Development
Symptoms of SDS can begin in plants at almost any stage of development; however, in Kentucky symptoms rarely develop before the mid pod fill stages. While the name "sudden death syndrome" suggests the plants' rapid and complete demise, death, if it occurs, can come very slowly or affected plants may recover. Hot and dry weather during pod development is most often associated with the remission of SDS symptoms.
SDS is most prevalent and severe during wet, cool growing seasons. Crops planted early when soil moisture and temperatures are higher and lower, respectively, also seem to be at greatest risk. However, severe SDS has been noted in late-planted soybeans.
The link between soil moisture and SDS, while suspected by many, was confirmed through work in Mississippi. Workers there found that root infection by FS-A was highest and SDS more severe under conditions of continuous, high soil moisture during the early vegetative stages of crop development. It is common to be able to isolate FS-A from soybean roots as little as 2 weeks after planting. Thus, under field conditions, a long period exists between root infection by FS-A and the development of foliar symptoms.
SDS typically begins in fields as spots ('hot spots') or streaks. This may be followed by symptom development throughout the field. Although the reason behind the development of hot spots is not clear, researchers speculate that these areas in fields are most favorable to root infection by FS-A and/or the development of symptoms. Conditions which favor these processes are still being worked out, but probably include higher soil moisture, higher SCN populations, and slowed or enhanced root development, among other factors.
Research in Kentucky and field observations throughout the mid south indicate that cropping sequence has little effect on SDS development. This is probably due to the widespread distribution of FS-A and its ability to survive for long periods in the roots of many crop and weed plants, in plant residues and in the soil. However, a questions remains as to rotation's effect on other diseases which may indirectly affect SDS. It seems logical that moderating any stress factor by crop rotation would lessen the potential for severe SDS to occur. This, however, has yet to be proved.
Cultivars differ in their response to SDS; however, researchers have had a hard time pinning down a consistently favorable response from many cultivar. This situation is not likely to change until we better understand the factors favoring and determining SDS severity. The development and use of environmentally-controlled tests for the rapid screening of soybeans against FS-A, should help identify cultivars with the highest and most consistent level of resistance. The long-term goal is to identify resistance genes and begin an SDS breeding program using either conventional breeding techniques or biotechnology.

Control
While control measures for SDS are still under development, using the following practices, in an integrated approach, should help reduce the disease's overall impact.
•Plant cultivars which have performed well in the presence of SDS. To determine which cultivars to plant, use test results from as many locations and years as possible. Give preference to cultivars with resistance to other important diseases in your area.
•Plant more than one cultivar, preferably from different maturity groups.
•For full season soybeans, delay planting for as long as possible. Early May plantings are at generally higher risk than are late May/early June plantings.
•Plant parts of fields or different cultivars at different times.
•Use any cultural practices which reduce plant stress (good fertility and weed control) and control other diseases which might augment the effects of SDS (e.g. SCN).
•Improve drainage in field.
•Harvest affected fields in a timely fashion.