Sudden Death Syndrome of Soybean

Sudden Death Syndrome of Soybean

Sudden death syndrome (SDS) is a relatively "new" disease of soybean. It was first discovered in Arkansas in 1971. The first reported epidemic, with losses as high as 50%, occurred in the early 1980's. The disease is distributed primarily in the Mississippi, Missouri and Ohio River valleys of the United States. Sudden death syndrome has been identified in Arkansas, Alabama, Georgia, Illinois, Indiana, Iowa, Kansas, Kentucky, Mississippi, Missouri, Ohio, Tennessee and Wisconsin. The disease has also been found in Argentina and Brazil. Sudden death syndrome is commonly found in fertile fields with high yield potential. It is caused by blue-pigmented strains of Fusarium solani f. sp. glycines form. nov. Isolates of the fungus recovered from soybean vary in their virulence. Other hosts of the pathogen include green bean, lima bean, mung bean and cowpea. The fungus is a soilborne pathogen that survives between seasons as chlamydospores in the soil. These structures have also been recovered from overwntering cysts of the soybean cyst nematode (Heterodera glycines). The exact mode of host penetration has not been proven but evidence indicates that it is achieved by direct penetration. Infection may occur in seedlings that are 2 to 3 weeks old. The fungus is found primarily in the root cortical tissue and rarely progresses beyond the crown. The vascular system (stele) may be invaded after substantial root degradation has occurred. A bluish mat of macroconidia forms on the stem and roots near the soil line when soil moisture is high. Chlamydospores are produced in cortical tissue and are released into the soil when it is sloughed off and degrades. Macroconidia washed into the soil may also convert to chlamydospores. Plants under stress tend to be more susceptible to infection than healthy ones. Infection is greatest in saturated soils at a temperature range of 55-65oF. SDS is more severe when the early part of the growing season is cool and wet or plants are irrigated. Disease incidence is higher in no-till fields than those under conventional tillage. This situation is probably the result soil conditions remaining cooler and wetter with no-till. Other conditions that affect SDS severity are planting date and nematode injury. Early planted soybeans generally suffer more injury than those planted later. The positive correlation between soybean cyst nematode injury and SDS severity was noted by some of the first researchers to study the disease. While the presence of H. glycines tends to exacerbate problems with SDS is not a required component for successful establishment of F. solani f. sp. glycines in its host.

Symptoms

Aboveground symptoms of SDS are commonly visible midway through the growing season. Leaf symptoms consist of chlorotic patches or streaks between the veins. Affected areas enlarge or may coalesce and become necrotic. In severe cases the midrib and main lateral veins may be the only green areas left. Leaf blades may curl up or be shed with petioles remaining attached. Leaf symptoms are produced in response to phytotoxins produced by the fungus. Foliar symptoms are evident on upper leaves first. They are usually visible when plants begin reproductive development (R5). Symptom development and death occurs rapidly on susceptible cultivars under optimum environmental conditions and hence the name "Sudden Death Syndrome". Dead plants are seen in patches throughout the field or scattered evenly. Other aboveground symptoms include flower or pod abortion and small seed size in pods that survive to maturity. External stem symptoms consist of a blue mat of spores near the soil line. Internally, vascular tissue has a gray to reddish-brown discoloration but the pith remains white. The discoloration may extend from the taproot to several nodes aboveground. Roots near the soil line may also be covered with a mat of bluish spores. They may be discolored, decayed and poorly nodulated and are easily pulled from the ground.

Plant Health Management

Resistant Cultivars.

Resistant cultivars have been identified and are often those that are also resistant to soybean cyst nematode.

F. solani

glycines

Improve soil drainage.

Control plant stress.

Two main ways to control stress are to reduce soil compaction and control plant pathogenic nematodes, especially soybean cyst nematodes.

References

McGee, D.C. 1992. Soybean diseases. A reference source for seed technologists. APS Press, St. Paul, MN. 151 pp.

Roy, K.W. 1997. Fusarium solani on soybean roots: Nomencalture of the causal agen of sudden death syndrome and identity and relevance of F. solani form B. Plant Dis. 81:259-266.

Roy, K.W. Rupe, J.C., Hershman, D.E., and Abney, T.S. 1997. Dudden death syndrome of soybean. Plant Dis 81:1100-1111.

Sinclair,J.B. and Backman, P.A.,eds. 1989. Compendium of soybean diseases, 3rd ed. APS Press, St. Paul, MN. 106 pp.

Wrather, J.A., Kendig, S.R., Anand, S.C., Niblack, T.L. and Smith, G.S. 1995. Effects of tillage, cultivar, and planting date on percentage of soybean leaves with symptoms of sudden death syndrome. Plant Dis. 79:560-562.

Useful Links

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Caveat

This description is presented for information only and no endorsement is intended for products listed, nor criticism meant for products not mentioned. Always consult the product label before purchasing and using any pesticide.

Material contained on the Links from the page are the responsibility of the linked page's author(s).

This page was researched and drafted by: Jane Christensen, Department of Plant Pathology, University of Nebraska-Lincoln

Disease images were provided by: Dr. David Wysong, Department of Plant Pathology, University of Nebraska-Lincoln

Questions, Comments, Complaints and Complements?

This page is authored and maintained by:
Dr. J.E. Partridge, Department of Plant Pathology, University of Nebraska-Lincoln

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