An Overview of Sudden Death Syndrome

Updated in 2025, this version replaces the previous An Overview of Sudden Death Syndrome (Archived) publication.

Sudden death syndrome (SDS) is one of the most well-known diseases across much of the soybean-producing regions of the U.S. and Ontario, Canada. Its impact, however, varies considerably. In some areas, SDS occurs in most fields and can contribute to significant statewide yield losses, while in others it remains sporadic or uncommon.

Fusarium virguliforme and several additional closely related Fusarium species cause SDS. SDS symptoms are similar to those caused by some other soybean pathogens, which can make it difficult to diagnose in the field. The presence of additional pathogens, such as soybean cyst nematode (SCN), can also exacerbate symptoms of SDS.

This publication examines the symptoms of SDS, describes conditions favorable for SDS development, explains how SDS differs from other plant problems that may resemble it, and recommends management practices.

Signs and Symptoms

Foliar Symptoms

The first symptoms of SDS appear on the leaves as yellow spots between leaf veins (Figure 1), known as interveinal chlorosis. These spots can expand and progress to turn brown, which is called interveinal necrosis. Leaf veins remain green (Figure 2). Symptoms are most noticeable later in the season, typically during the reproductive growth stages.

As the symptoms of SDS progress, leaves die and prematurely fall from the plant, while petioles remain attached to the stem (Figure 3). These advanced symptoms most often develop during the later reproductive growth stages. Pods and seed may abort, and surviving seed may be smaller. Foliar symptoms of SDS can resemble those of many other diseases (Table 1).

Root and Stem Symptoms/Signs

Plants infected by fungi causing SDS can have discolored and decaying roots even when no noticeable foliar symptoms are present. Compared with a healthy root system—which is typically larger and has more extensive lateral roots—SDS-affected roots are often reduced and deteriorated. The woody tissue of the taproot (cortex) may range from brown to dark gray, while the pith in the upper portion of the stem remains white (Figure 4).

Several soybean diseases can cause foliar symptoms similar to SDS, making it important to closely examine the stem and root for an accurate diagnosis (see Table 1). Red crown rot (RCR, caused by Calonectria ilicicola) resembles SDS but is distinguished by red discoloration at the lower stem and root that is sometimes accompanied with small reddish orange spherical fungal fruiting bodies (perithecia). If the stem pith (center) is brown and discolored, the disease might be brown stem rot (BSR, caused by Cadophora gregata) rather than SDS. However, it is important to note that a single plant can be infected by multiple pathogens, including those that cause SDS, RCR, and BSR. When soils are wet, the SDS fungi can reproduce on the root surface, sometimes producing masses of spores that are purple-blue and visible to the naked eye (Figure 5).

Disease Cycle

The fungi that cause SDS survive the winter in crop residue and soil (Figure 6). Early in the season, the fungus can infect soybean roots, sometimes within a few days of seed germination. Infection is favored by wet soils and relatively cool temperatures, often below about 60–65 °F (15–18 °C) during early vegetative growth, which promote root infection and colonization by the pathogen.

Foliar symptoms develop because toxins produced by the SDS pathogens move through the plant's water-conducting vessels (xylem) to the leaves. These symptoms typically appear after flowering, but they have been observed during early soybean growth stages on highly susceptible varieties or when conditions are cool and wet after emergence (Figure 7).

Hot and/or dry conditions in the spring or summer can delay or stop SDS symptom development. When SDS symptoms are severe, plants may defoliate prematurely, although petioles remain attached to the stem.

Conditions that Favor Disease

Cool and wet field conditions shortly after planting favor early root infections and SDS development. Frequent or heavy rains midseason can favor early symptom expression. Irrigated fields are at higher risk for SDS.

The presence of soybean cyst nematode (SCN; Heterodera glycines) in the same field where SDS is observed can increase the severity of SDS symptoms (Figure 8). Therefore, fields with SDS should be tested for SCN. Research has linked the presence of SCN with greater levels of SDS and increased yield losses. However, SDS can occur independently of SCN, and vice versa.

Some crop production practices may also increase the risk of SDS development. Early planted fields, or fields with low concentrations of soil nutrients, low pH, poor drainage, or moderate to severe soil compaction are at greater risk of SDS.

Yield Losses and Impact

Yield losses due to SDS can be highly variable and depend on several factors, including the environment, the timing of symptom development, the susceptibility of a soybean variety to the disease, and the levels of SCN present in the field. SDS can weaken plants and cause premature defoliation. Infected plants may also produce fewer and smaller seeds (Figure 9).

Yield losses can be substantial in years when cool, wet soil conditions follow planting of susceptible varieties in fields with a history of SDS and SCN. Although root infection often occurs early, foliar symptoms typically develop after flowering (beginning at R3) and are most damaging when they appear during the mid reproductive growth period (R3–R5). If foliar symptoms do not appear until R6 (full-seed) or if seasonal environmental conditions are unfavorable for SDS development, yield losses are often minimal. Losses are rarely field-wide because SDS commonly occurs in patches in the field (Figure 10).

Diagnosis and Management

Diagnosing SDS can be challenging, because other diseases and disorders cause symptoms similar to SDS (see Table 1). Foliar symptoms alone are not sufficient for diagnosis. It is important to inspect plants closely, dig and inspect roots, and split stems open to examine for internal stem discoloration.

After splitting stems, the pith of a plant infected with SDS will be white even when roots are severely rotted (Figure 4). The cortex typically shows brown to gray discoloration. A laboratory diagnosis may be needed to distinguish SDS from other soybean diseases and disorders.

SDS management strategies include planting soybean varieties with resistance to SDS, managing SCN, using effective fungicide seed treatments, improving soil drainage in fields with recurring SDS, rotating crops, avoiding or reducing soil compaction, and maintaining proper pH and fertility levels. An integrated SDS management strategy is essential, as no single tactic is likely to provide complete control when conditions are favorable for SDS development.

Resistant Varieties

There are no soybean varieties completely resistant to SDS, but partially resistant varieties are available (Figure 11). Planting the most resistant varieties available that also fit the farming operation and environment is the foundation of a SDS management program. Keep in mind that planting partially resistant varieties does not guarantee complete control of SDS, but it can help minimize yield losses.

Weather and field conditions influence the severity of SDS, even in partially resistant varieties. Most soybean breeding programs have focused on evaluating SDS resistance based on foliar symptoms. Less is known about resistance to root rot, and the relationship between root rot and foliar symptoms is not well understood. Some varieties with excellent resistance to foliar symptoms of SDS can have significant root rot.

Seed Treatments

Foliar fungicides and most seed treatments are not effective at reducing SDS. However, several seed treatment fungicides, including cyclobutrifluram (Victrato®, Syngenta), fluopyram (ILEVO®, BASF), and pydiflumetofen (Saltro®, Syngenta), have demonstrated efficacy against SDS. These products have consistently reduced SDS severity and protected yield on susceptible varieties compared to base seed treatments in research trials conducted by Extension plant pathologists across the North Central United States and Ontario, Canada.

Manage SCN

SCN populations have been associated with SDS and may increase severity of the disease. Practices that reduce SCN, such as planting SCN-resistant varieties and rotating crops, may delay SDS onset and reduce disease severity.

Tillage and Drainage

Minimizing soil movement may slow the spread of the SDS fungus to new fields. Improving drainage and soil structure, and reducing compaction, can also help alleviate SDS symptom severity.

Tillage in compacted areas may reduce SDS severity and can allow soils to warm more quickly in the spring. However, some research indicates that SDS severity is reduced in no-till fields. The impact of tillage on soil erosion and quality should always be considered when using it to manage SDS.

Crop Rotation

Rotating to corn does not typically reduce SDS in subsequent soybean crops. Corn and several other crop and weed species can maintain or even increase the SDS fungus in the soil. A number of other legume species can also be hosts of the SDS fungus and develop root rot, including alfalfa, pinto bean, navy bean, white clover, and red clover.

One study in Iowa suggested that a more diverse rotation can reduce SDS. In this study, adding a third year into the corn-soybean rotation (where either alfalfa or an alfalfa/red clover mixture were planted) reduced the amount of SDS that developed in the subsequent soybean crop. Incorporating small grain crops into the rotation can also reduce SDS severity. Further research is needed to understand the effects of crop rotation and cover crops on SDS.

Planting Date

A traditional SDS management approach is to delay planting fields with a history of SDS, allowing the soil to warm up and dry down, thereby reducing conditions that favor infection by the SDS fungus and subsequent symptom development. Although delaying planting can lower the risk of early root rot, its effect on reducing foliar symptoms is less consistent. Additionally, research shows that delayed planting can reduce yield potential, often to a greater extent than the yield loss from SDS. Therefore, delayed planting, or planting high-risk fields last, should be considered only in fields with an extremely severe history of SDS.

Soil Nutrition

Soil fertility levels may affect SDS occurrence and severity, although published research is somewhat unclear on how different fertilizer applications and fertility levels affect the disease. Maintaining proper soil fertility levels is important for reducing plant stress and maintaining overall plant health, which may help decrease the occurrence of soybean diseases such as SDS.

Irrigation

High soil moisture levels within a few days after planting increase the risk of infection by the SDS pathogen, and irrigation during the mid-late soybean reproductive growth stages (R3-R6) may increase SDS foliar symptoms. Farmers should be aware that over-irrigation during the reproductive stages can increase the risk of SDS.

Table 1. Comparisons of symptoms of sudden death syndrome (SDS) and other soybean diseases and disorders.

Diseases and other conditions that appear similar to sudden death syndrome

Brown Stem Rot (caused by Cadophora gregata)

Brown stem rot (BSR) foliar symptoms include yellowing and necrosis between veins. The stem symptoms include brown, discolored pith tissue, especially near nodes of soybean stems.

How to distinguish BSR from SDS: plants with BSR will have discoloration in the pith of the stem. BSR does not cause rotted roots.

Fusarium Wilt (caused by Fusarium oxysporum)

Plants with Fusarium wilt have brown vascular tissue in the roots and stem. Leaves turn yellow and die but remain attached to the stem. Plants eventually wilt and possibly die. Fusarium wilt is frequently observed in Ontario, Canada, but may be present in other northern states, especially in wet years.

How to distinguish Fusarium wilt from SDS: Fusarium wilt does not cause interveinal chlorosis on leaves and the leaves stay attached to the plant after they die.

Red crown rot (caused by Calonectria ilicicola)

Red crown rot (RCR) leads to root and lower stem rot that often appears in patches after R3. Infected plants may show interveinal chlorosis and necrosis, reddish stem discoloration and red fungal fruiting bodies (perithecia) under moist conditions, and severe root rot that can stunt plants or cause premature death.

How to distinguish RCR from SDS: RCR causes reddish lower stem and root discoloration that may be accompanied with white hyphae and reddish orange spherical fungal fruiting bodies (perithecia), while plants with SDS do not have these symptoms and signs.

Root-knot Nematode (caused by Meloidogyne spp.)

Root-knot nematodes (RKN) particularly the southern root-knot nematode (M. incognita) can cause foliar symptoms resembling SDS, including yellow and necrotic spots. Affected plants are stunted, and their root system exhibits extensive galling.

How to distinguish RKN from SDS: Examine the root system for galls - these are characteristic of RKN and do not occur with SDS.

Southern blight (caused by Agroathelia rolfsii)

Southern blight causes sudden wilting and yellowing, accompanied by a dark, girdling stem lesion at the soil line. White, fanlike fungal growth and small sclerotia on the lower stem and surrounding soil are characteristic features.

How to distinguish southern blight from SDS: It can be differentiated by the presence of white mycelial mats and numerous sclerotia at the plant base, which are not produced by the SDS pathogen.

Stem Canker (caused by Diaporthe aspalathi and D. caulivora)

Stem canker symptoms can include leaves with necrosis between leaf veins or completely wilted leaves and stems generally after R5.5.

How to distinguish stem canker from SDS: A plant with stem canker often has a characteristic red lesion on the outside of the stem. The lesion will typically start at a node above the soil line and extend both upwards and below the soil line. The stem interior can also show discoloration where lesions are present.

Taproot decline (caused by Xylaria necrophora)

Taproot decline (TRD) causes interveinal chlorosis and necrosis, premature plant death, and severe root deterioration in which much of the root system snaps off and remains in the soil. Infected roots often show black fungal growth (called stroma), and humid conditions can produce distinctive “dead man’s fingers” on residue or at the plant base.

How to distinguish taproot decline from SDS: Unlike SDS, TRD is characterized by roots that break off easily and have black stroma, often accompanied by “dead man’s fingers,” which do not occur with SDS. TRD symptoms can appear anytime from seedling stages through R6, whereas SDS symptoms typically do not appear until the reproductive stages.

White Mold (Sclerotinia stem rot — caused by Sclerotinia sclerotiorum)

White mold is typically more of a problem in years with rainy and cool environmental conditions that occur at flowering. Lesions develop on the nodes and expand up the stems. Leaves often die and remain attached to the stem.

How to distinguish white mold from SDS: Plants with white mold have white fungal growth on the outside of stems. In addition, the white mold fungus produces sclerotia that are hard and black.

Late-season Potassium Deficiency

Patches of soybean with yellow leaves may appear in soils that have low potassium levels. Soybean cyst nematode and Diaporthe spp. may increase symptoms. Symptoms include yellowing that begins at the leaf margins of the uppermost trifoliates.

How to distinguish potassium deficiency from SDS: The foliar symptom pattern of potassium deficiency differs from that of SDS, and plants lacking potassium will not show the stem and root discoloration associated with SDS.

Demethylation Inhibitor (DMI; Triazole) Fungicide Injury

Foliar SDS-like symptoms can occur following applications of certain DMI fungicides, especially when conditions are hot and dry and oftentimes more so when an adjuvant is included with the fungicide.

How to distinguish DMI fungicide injury from SDS: Check the pattern of symptom development and field activities; symptoms from DMI fungicide injury are confined to leaves and do not affect stems and roots.

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Acknowledgments

Authors

Daren Mueller, Iowa State University; Carl Bradley, University of Kentucky; Martin Chilvers, Michigan State University; Dylan Mangel, University of Nebraska; Madalyn Shires, South Dakota State University; Adam Sisson, Iowa State University; Damon Smith, University of Wisconsin-Madison; Albert Tenuta, OMAFA; and Kiersten Wise, University of Kentucky

Reviewers

Tom Allen, Mississippi State University; Alyssa Betts, University of Delaware; Mandy Bish, University of Missouri; Travis Faske, University of Arkansas; David Langston, Virginia Tech; Horacio Lopez-Nicora, The Ohio State University; Dean Malvick, University of Minnesota; Trey Price, LSU AgCenter; Camilo Parada Rojas, Cornell University; Edward Sikora, Auburn University; Terry Spurlock, University of Arkansas; Darcy Telenko, Purdue University; Richard Wade Webster, North Dakota State University; and Jean Williams-Woodward, University of Wyoming.

Sponsors

The Soybean Disease Management series is a multi-state collaboration sponsored by the North Central Soybean Research Program (NCSRP) through the Soybean Checkoff. This project was funded in part through Growing Forward 2 (GF2), a federal-provincial territorial initiative. The Agricultural Adaptation Council assists in the delivery of GF2 in Ontario. The authors thank the United States Department of Agriculture - National Institute of Food and Agriculture, the Grain Farmers of Ontario, and United Soybean Board for their support. Contributors to this series come from land-grant universities in the North Central states and Canada.

How to cite: Mueller, D., Bradley, C., Chilvers, M., Mangel, D., Shires, M., Sisson, A., Smith, D., Tenuta, A., and Wise, K. An Overview of Sudden Death Syndrome. 2025. Crop Protection Network. CPN-1011. Doi.org/10.31274/cpn-20190620-028.