Sudden Death of Soybeans (SDS)// here is the normal content // ?>
Sudden death syndrome (SDS) caused by the fungus Fusarium virguliforme, was first discovered in 1971 in Arkansas. Since that time the disease has spread throughout the soybean growing areas of the United States. SDS was first identified in Delaware in the early 2000’s. SDS can cause yield losses up 100% under appropriate conditions; however, its impact in Delaware is not currently severe or significant. This article will discuss how to diagnose SDS, the disease cycle of the pathogen, and management recommendations.
Plants suffering from SDS typically do not present symptoms until after flowering (R1). Early symptoms of the disease include mottling and crinkling of the leaves. As the disease progresses the leaf tissue between the veins turns yellow/brown, while the veins remain green (Figure 1). Soon thereafter the leaves shrivel and fall from the plant, but the petioles remain intact (Figure 2). If the plant is removed from moist soil tiny blue structures may be visible at the base of the stem . These are spore masses produced by the fungus. In most cases diagnosis is completed by sectioning the lower portion of the stem lengthwise. The cortex of a stem infected with SDS will be streaked with tan/light brown lesions, and pith of infected plants retains a white coloration.
Symptoms of SDS can be confused with other pathogens of soybean including charcoal rot and brown stem rot; however, for these diseases the leaflets tend to remain attached to the stems . Stems infected with charcoal rot fungus contain round black/gray structures that look like tiny bits of coal. In cases of brown stem rot, the pith (central section of the stem) is discolored but not the cortex (outer section). Plants suffering from chemical burn will not present symptomatic stems.
F. virguliforme overwinters in the residue or free soil as recalcitrant chlamydospores, which are resistant to a wide range of temperatures and stresses. Changes in soil temperature signal the fungus to emerge from chlamydospores and infect roots of young seedlings. Initial infection occurs in seedlings planted cool, moist soils, and cortical infection occurs between V1 and V6. When plants reach early reproductive stages the pathogen colonizes the cortex more thoroughly, and toxins are produced that are translocated to foliage. These toxins are responsible for the characteristic interveinal necrosis often seen in leaves of SDS infected soybeans . Symptoms often appear during heavy rains during the reproductive stages and disease is favored by high soil moisture. Consequently, the disease typically is present in areas of the field that are poorly drained (low lying or compacted areas). The disease is spread short distances on mechanical equipment, workers boots, etc), and spores can be disseminated very short distances in rain.
SDS is often found in association with Soybean Cyst Nematode and the pathogen can be isolated from within cysts of SCN. Disease severity is most severe when SCN and SDS are found together . This is likely because stress caused by SCN feeding on roots further weaken the plant, predisposing it to SDS infection.
The options for management of SDS are limited. Within season management of the disease is not possible. Between season management is achieved by the use of resistant cultivars, cultural practices, and SCN management.
Some soybean cultivars are more tolerant to SDS than others and resistance ratings can be obtained from seed dealers or directly from seed companies. A variety should be used that has both SDS and SCN resistance.
Because SDS is most severe when seeds are planted into cool, wet soils, planting full season beans later in the spring or planting double crop beans may reduce levels of SDS. Disease severity is related to time of infection, being most severe when seedlings are infected at early vegetative stages . Therefore practices that enhance the establishment and growth of seedlings may reduce SDS. SDS is often most severe in wet areas. Improving drainage in wet areas and reducing soil compaction can help reduce the effects of SDS and improve yields.
Some research indicates that reduced tillage can reduce levels of SDS . In these studies, the greatest levels of SDS reduction occurred when minimal tillage was combined with crop rotation. Crop rotation used alone is not likely to have an effect on SDS because of the ability for chlamydospores to survive in soil for several years.
Chemical control: The seed treatment iLeVO has some activity against SDS. Current data indicates that this seed treatment can provide some benefit in terms of yield protection when used in fields with a history of SDS and low levels of SCN. Stunting may occur, but yields should not be affected. Currently this treatment has not been evaluated in mid-Atlantic soils.
- A., Westphal., et al., Sudden death syndrome of soybean. The Plant Health Instructor, 2008.
- Brar, H.K., S. Swaminathan, and M.K. Bhattacharyya, The Fusarium virguliforme Toxin FvTox1 Causes Foliar Sudden Death Syndrome-Like Symptoms in Soybean. Molecular Plant-Microbe Interactions, 2011. 24(10): p. 1179-1188.
- Xing, L.J. and A. Westphal, Effects of crop rotation of soybean with corn on severity of sudden death syndrome and population densities of Heterodera glycines in naturally infested soil. Field Crops Research, 2009. 112(1): p. 107-117.
- Gongora-Canul, C.C. and L.F.S. Leandro, Plant Age Affects Root Infection and Development of Foliar Symptoms of Soybean Sudden Death Syndrome. Plant Disease, 2011. 95(3): p. 242-247.
- Westphal, A., Sustainable Approaches to the Management of Plant-parasitic Nematodes and Disease Complexes. Journal of Nematology, 2011. 43(2): p. 122-125.
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