What is sudden death syndrome? 

Sudden death syndrome (SDS) is one of the most important diseases of soybean in the Midwest.  The disease was first observed in Arkansas in 1971, and has subsequently been reported throughout most soybean growing areas of the United States.  SDS was first documented in Wisconsin in 2005, and has become more common and severe since that time.  The disease is most severe when soybeans are planted into cool, wet soils, and when midsummer rains saturate the soil.  SDS often occurs in fields where soybean cyst nematode (SCN) is present.

What does sudden death syndrome look like? 

The first noticeable symptoms of SDS are chlorotic (i.e., yellow) blotches that form between the veins of soybean leaflets.  These blotches expand into large, irregular, chlorotic patches (also between the veins), and this chlorotic tissue later dies and turns brown.  Soon thereafter, entire leaflets will die and shrivel.  In severe cases, leaflets will drop off leaving the petioles attached.  Taproots and below-ground portions of the stems of plants suffering from SDS, when split open, will exhibit a slightly tan to light brown discoloration of the vascular (i.e., water-conducting) tissue.  The pith will remain white or cream-colored.  In plants with advanced foliar symptoms of SDS, small, light blue patches will form on taproots and stems below the soil line.  These patches are spore masses of the fungus that causes the disease.

Foliar symptoms of SDS can be confused with those of brown stem rot (see UW Plant Disease Facts D0026, Brown Stem Rot of Soybean).  However, in the case of brown stem rot (BSR), the pith of affected soybean plants will be brown.  In addition, roots and lower stems of plants suffering from BSR will not have light blue spore masses.

Once symptoms of SDS are evident, yield losses are inevitable.  Yield losses can range from slight to 100%, depending on the soybean variety being grown, the plant growth stage at the time of infection, and whether or not SCN is present in a field.  If SDS occurs after reproductive stages R5 or R6, impact on yield is usually minimal.  If SDS occurs at flowering however, yield losses can be substantial.  When SCN is present, the combined damage from both diseases can be substantially more than the sum of the damage expected from the individual diseases.

Where does sudden death syndrome come from? 

SDS is caused by the soilborne fungus, Neocosmospora phaseoli (synoym:  Fusarium virguliforme, Fusarium solani f. sp. glycines).  N. phaseoli can overwinter freely in the soil, in crop residue, and in the cysts of SCN.  The fungus infects soybean roots (by some reports as early as one week after crop emergence) and is generally restricted to roots as well as stems near the soil line.  N. phaseoli does not invade leaves, flowers, pods or seeds, but does produce toxins in the roots that move to the leaves, causing SDS’s characteristic foliar symptoms.

How can I save a soybean crop with sudden death syndrome? 

SDS cannot be controlled once plants have become infected.  Foliar fungicides and fungicide seed treatments have no effect on the disease.

How can I avoid problems with sudden death syndrome in the future?  

Use SDS-resistant varieties whenever possible in fields with a history of the disease.  If SDS and SCN are both problems in the same field, planting an SCN-resistant soybean variety may also be beneficial in managing SDS.  Avoid planting too early.  Wisconsin growers typically prefer to plant soybeans before May 10 to extend the length of the growing season and maximize yields.  However, planting when soils are cool and wet makes plants more vulnerable to infection by N. phaseoli.  Improve soil drainage by using tillage practices that reduce compaction problems.  Rotation, while useful in managing other soybean diseases, does not appear to significantly reduce the severity of SDS.  Even after several years of continuous production of corn, N. phaseoli populations typically are not reduced substantially.  Research from Iowa State University has shown that corn (especially corn kernels) can harbor the SDS pathogen.

For more information on sudden death syndrome of soybean: 

Contact the University of Wisconsin Plant Disease Diagnostics Clinic (PDDC) at (608) 262-2863 or pddc@wisc.edu.

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What is soybean vein necrosis disease? 

Soybean vein necrosis disease (SVND) is a relatively recent discovery in soybean.  SVND was first described in 2008 in Tennessee, but has since been confirmed in several other states including Arkansas, Delaware, Illinois, Iowa, Kentucky, Maryland, Michigan, Mississippi, Missouri, New York, Pennsylvania and Virginia.  SVND was confirmed in Wisconsin in 2012.  Researchers do not know if SVND can lead to significant yield reductions.

What does soybean vein necrosis disease look like? 

Soybean plants with SVND exhibit vein clearing (i.e., lightening of vein color) and chlorosis (i.e., yellowing), as well as mosaic patterns (i.e., blotchy light and dark areas) on affected leaves.  Initially, symptoms develop around the veins of leaves and eventually expand outward.  As the disease progresses, vein and leaf browning and necrosis (i.e., death) occur.

Where does soybean vein necrosis disease come from? 

SVND is caused by Soybean vein necrosis virus (SVNV).  SVNV is in the viral genus Tospovirus.  This group of viruses includes common vegetable viruses [e.g., Tomato spotted wilt virus (see UW Plant Disease Facts D0117, Tomato Spotted Wilt of Potato) and Iris yellow spot virus] and ornamental viruses [e.g., Impatiens necrotic spot virus (see UW Plant Disease Facts D0067, Impatiens Necrotic Spot)] that can cause severe damage and substantial loss of yield and crop quality.  Tospoviruses tend to have wide host ranges and are transmitted by several species of thrips.  SVNV is transmitted primarily by soybean thrips (Neohydatothrips variabilis), and to a lesser extent by tobacco thrips (Frankliniella fusca) and Eastern flower thrips (Frankliniella tritici).  SVNV may have been introduced to Wisconsin as thrips moved north on wind currents from the southern United States.

How can I save a soybean crop with soybean vein necrosis disease? 

Currently very little is known about SVND.  Thus there are no specific management practices recommended for SVND at this time.

How can I avoid problems with soybean vein necrosis disease in the future?  

Currently no specific control recommendations are in place.  Researchers at universities across the country are attempting to determine what impact SVNV will have.  Additional research is needed to determine how SVNV affects soybeans, how it is transmitted, how it overwinters, and what can be done to slow its spread.

For more information on soybean vein necrosis disease:  

Contact the University of Wisconsin Plant Disease Diagnostics Clinic (PDDC) at (608) 262-2863 or pddc@wisc.edu.

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What is soybean rust? 

Soybean rust is an extremely serious fungal disease of soybean that was first reported in the continental United States in November of 2004.  The disease has never been reported in Wisconsin.  Soybean rust had previously been reported in Asia, Australia, Africa and South America, where yield losses due to the disease ranged from 10 to 80%.  In addition to soybean (Glycine max), soybean rust affects approximately 90 other plant species in the legume family.  In Wisconsin, other potential hosts include snap and kidney bean (Phaseolus vulgaris), American bird’s-foot trefoil (Lotus unifoliolatus), crimson clover (Trifolium incarnatum), Korean clover (Kummerowia stipulacea), white clover (Trifolium repens), purple crownvetch (Coronilla varia), Chinese lespedeza (Lespedeza cuneata), lupine (Lupinus spp.), pea (Pisum sativum), rattlebox (Crotalaria spp.), yellow sweetclover (Melilotus officinalis), ticktrefoil (Desmodium spp.), and winter vetch (Vicia villosa).

What does soybean rust look like? 

Initial symptoms of soybean rust include formation of small, gray spots on soybean leaves, particularly on the undersides of leaves.  Spots are most likely to occur first on lower leaves where conditions are more favorable for spores to germinate and infect.  Infections can also occur on petioles, stems and pods.  Spots increase in size over time and change color from gray, to tan or reddish-brown.  Tan lesions mature to form small pimple-like structures (called pustules) on the lower leaf surface.  Pustules contain powdery, tan spores that give the leaves the appearance that they have dandruff.  Reddish-brown lesions are composed of primarily necrotic (i.e., dead) tissue and typically have only a limited number of pustules.  As plant canopies close and pods begin to set, the soybean rust fungus can rapidly spread from lower to upper foliage of plants.  Other diseases of soybean including brown spot [see UW Plant Disease Facts, Brown Spot (Septoria Leaf Spot)], bacterial pustule and particularly downy mildew could potentially be confused with soybean rust.

Where does soybean rust come from?  

Soybean rust is caused by the fungi Phakopsora pachyrhizi and Phakopsora meibomiae.  P. pachyrhizi is the more aggressive of the two species, and the fungus that was introduced into the continental United States in 2004.  P. pachyrhizi is thought to have been brought to the U.S. through hurricane activity in the late summer of 2004.  Soybean rust fungi must overwinter on living plant tissue.  Therefore, if soybean rust fungi ever reach Wisconsin, they are not likely to survive Wisconsin winters.  In the South, however, plants such as kudzu (Pueraria montana var. lobata) can serve as overwintering hosts.  Soybean rust spores produced on these plants could be moved north each year by prevailing winds, as is known to occur with other rust fungi (e.g., the corn rust pathogen).  Soybean rust fungi may eventually reach Wisconsin via this route.  This movement of spores via prevailing winds could occur each year, thus making soybean rust a recurring problem.

How do I save a soybean plants infected with soybean rust? 

If you suspect that your soybeans are suffering from soybean rust, proper diagnosis is crucial to document the presence of the disease in Wisconsin.  Contact the UW-Madison Plant Disease Diagnostics Clinic (https://pddc.wisc.edu/) about submitting a sample for diagnosis.  Keep in mind however that once soybean plants are infected and the soybean rust fungus has begun to produce spores, control of the disease is difficult and significant yield losses are likely.  Fungicides with “curative” properties are registered for use against soybean rust in Wisconsin.  However, curative fungicides have a very limited ability to eliminate existing disease and by the time soybean rust is observed, these products will likely not provide adequate control.  Therefore, every attempt should be made to prevent infections (see below), rather than to attempt to control soybean rust after infections have occurred.

How do I prevent problems with soybean rust? 

Plant soybeans as early as possible, so that if soybean rust does occur, plants are as mature as possible when infection occurs, and yield loss can be minimized.  Researchers throughout the soybean-producing regions in the United States monitor for soybean rust each growing season (see https://soybean.ipmpipe.org/soybeanrust/).  Watch for reports of the disease to the south of Wisconsin and consider preventative fungicide treatments as the rust fungus approaches the state.  Products containing chlorothalonil, strobilurins and triazoles (the latter two types of active ingredients often combined into a single product) are labeled for preventative control of soybean rust.  Combining strobilurins with triazoles helps reduce the risk of selecting for variants of the soybean rust pathogen that will no longer be controlled by these active ingredients.  If you decide to use fungicides for control, be sure to select a formulation that is labeled for use on soybeans, and be sure to read and follow all label instructions of the fungicide that you select to ensure that you use the fungicide in the safest and most effective manner possible.

For more information on soybean rust: 

Contact the University of Wisconsin Plant Disease Diagnostics Clinic (PDDC) at (608) 262-2863 or pddc@wisc.edu.

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