Sudden Death Syndrome

Sudden Death Syndrome (SDS), a disease in soybean plants, quickly spread across the southern United States in the 1970s, eventually reaching most agricultural areas of the US. SDS is caused by a Fusarium fungi, more specifically the soil borne root pathogen Fusarium virguliforme, formerly known as Fusarium solani f. sp. glycines.[1]. Losses could exceed hundreds of millions of dollars in US soybean markets alone making it one of the most important diseases found in Soybeans across the US.[1]

Not to be confused with Sudden arrhythmic death syndrome.

Importance

In the US, SDS was first found in 1971 in Arkansas and in other southern states within a few years.[2] In 1993, a SDS epidemic broke out in Illinois and some locations in Iowa, where 100% infection rates were found, causing large reductions in yields.[2] Currently, SDS is the most important disease in soybeans across the US, affecting soybeans in almost all states where soybeans are grown. Nationally, yield losses have ranged from 20-30 million bushels over the past 10 years, with local variation due to the large range factors that determine the severity of the disease.[3] If conditions are conducive to this pathogen, yield losses can be devastating. In 2010, SDS ran wild throughout the Midwest because of the cool and wet conditions.[4] In 2013 alone, studies showed a loss of 25 million bushels across the US.[4] These yield losses are primarily from root deterioration causing a reduction in nutrient uptake, loss of photosynthetic area, and flower or pod abortion, causing reduction in seed numbers.[5]

Symptoms and signs

Most of the SDS symptoms can be confused with other factors like nutrient deficiencies and some other diseases like brown stem rot and stem canker.[3] Usually the first symptom seen is interveinal chlorosis, which is the yellowing of the plant material between the leaf veins.[6] When leaves begin to die, puckering and mottling can also be observed along with the chlorosis.[2] As severity increases, necrosis (death of cells) occurs and eventually these leaves will fall off, leaving only petioles left on the stem.[7] If the conditions are right (cool and wet), these symptoms can appear suddenly, causing large yield reductions. Normally, this is seen in mid or late July around the time of flowering and pod production.[4]

In addition to foliar symptoms, the stem of the soybean plant can show symptoms as well. If a soybean stem with SDS is split, the pith will be visibly white while the cortical tissue around the pith will be tan to light brown in color.[3][1] If the pith is brown in color (or if the whole stem looks brown on the inside), it is likely that the plant has brown stem rot, rather than SDS.[3]

Along with the above ground foliar and stem symptoms, the roots usually show some kind of rotting and decrease in vigor compared to other healthy soybean roots.[1] If soil conditions are moist, roots are also likely to show blue masses of spores (macroconidia) around the taproot just below the soil surface.[1] Blue fungal masses, found along with the foliar and stem symptoms, are strong diagnostic indicators for SDS.[1]

Disease cycle

F. virguliforme overwinters as asexual macroconidium and chlamydospores and currently no research has found a successful sexual stage with this pathogen.[1] When conditions are favorable, these spores germinate on seedling roots and infect the plant. From the V1 to R1 stages (seedling to first flower) of soybean growth, the fungus colonizes within the plant cortex and only goes up the stem a few inches above the soil surface.[1] Toxins are produced when the pathogen colonizes the lower parts of the soybean cortex. These toxins travel up the xylem to the leaves, causing leaf chlorosis and necrosis, eventually leading to leaf and pod drop.[6][1]

Blue Fungal spore masses are produced on the roots of the plant where macroconidia are formed. Macroconidia are one of the overwintering phases of the pathogen and can persist in the soil and plant residue for many years.[1] Between growing seasons, F. virguliforme is also found in the form of chlamydospores in the crop residue and freely in the soil.[1] These thick walled overwintering structures can withstand large temperature fluctuations within the soil and even resist desiccation.[1]

Environmental factors

Cool, wet field conditions shortly after planting favor the infection of soybean seedlings.[6] This increases disease establishment and poses a higher threat to the crop yield. In addition to early cool and wet conditions, frequent or heavy rains in the middle of the growing season can speed up the expression of SDS symptoms.[6] Being that this pathogen favors these wet conditions, increased risk is acquired when fields are irrigated as well as low-lying fields that are at risk of flooding and having soil compaction issues.[6][5]

Disease development

F. virguliforme is a soil borne pathogen that starts by infecting the roots of soybean seedlings after germination. The fungus then moves up the plant and infects the vascular tissue, causing a brown color within the cortex around the pith of the plant a few inches above the soil surface.[1] Toxins are produced by the fungus when it colonizes the cortex and are sent up the stem to the leaves, causing the above ground symptoms around first flower during mid-summer.[1] While infection occurs early in the season, symptoms do not normally appear until mid-summer.[5]

SDS also has a synergistic relationship with Soybean Cyst Nematode (SCN). Fields that have SCN presence have more severe SDS symptoms.[6] While it is not known exactly how the two interact, it is known that symptoms of SDS are more severe when SCN are present in the field and that F. virguliforme can be isolated from a SCN that is found in the same area as this pathogen.[1]

Management

The best way to manage SDS is with a resistant variety.[1] One issue is that most resistant varieties are only partially resistant so yield reductions may still occur.[1] Another issue is that the plant needs resistance for SDS and SCN in order to gain true resistance because of their synergistic relationship and most varieties do not have resistance for both.[4] Aside from resistance, the only other ways to control SDS are management practices.

These include:

• Avoid planting in cool, wet conditions[4]
• Plant later when the soil has warmed up[3]
• Try avoiding soil compaction as it creates wet spots in the soil that can increase plant stress and SDS infection rates[3]
• Managing for SCN as this nematode often occurs alongside F. virguliforme[3]
• Deep tillage to break up compaction and help the soil warm faster[3]

One common management tactic used in other pathogen management plans is crop rotation. In some cases, disease severity can be reduced but most often it is not effective.[4] This is because of chlamydospores and macroconidia as they can persist in soils for many years.[6]

Fungicides are another common product used to control fungal pathogens. In-furrow applications and seed treatments with fungicides have some effect in decreasing disease instance but in most cases, the timing isn't right and the pathogen can still infect the plants.[1] Foliar applications of fungicides have no effect on disease suppression for SDS because the fungi are found in the soil and mainly the roots of the plants. Most foliar fungicides do not move downward through plants, therefore having no effect on the pathogen.[1]

References

1. "Sudden death syndrome of soybean". www.apsnet.org. Retrieved 2016-11-16.
2. "Foliar symptom expression in association with Fusarium virguliforme, causal agent of soybean sudden death syndrome". www.plantmanagementnetwork.org. Retrieved 2016-11-15.
3. "Sudden Death Syndrome" (PDF). www.iasoybeans.com. Iowa Soybean Association. 2010.
4. "Wanted for Yield Robbery: Sudden Death Syndrome". United Soybean Board. Retrieved 2016-11-16.
5. "Crop Focus: Sudden Death Syndrome of Soybeans" (PDF). www.pioneer.com. Pioneer Agronomy Services. 2010.
6. "SDS - Crop Protection Network". Crop Protection Network. Retrieved 2016-11-15.
7. Corn and Soybean Field Guide. 2013. p. 172.