C.O.R.N. Newsletter 2013-28

Our OSU Extension Agronomy State Field Specialist have assembled the following list of questions concerning sudden death syndrome and its widespread development across Ohio this year.  I’ve (Anne Dorrance) done my best to address most of them, although for some the “jury” is still out as we await data from this season’s trials.

Does seed treated with a fungicide reduce the level of infection for SDS?  Particularly fludioxonil which is listed as excellent on Fusarium, and if so, on average what length of protection to soybean seedlings could be expected ( ie. 7 days, 10 days)?

The jury is still out on the use of seed treatments for early season control of sudden death syndrome.  All of my data for seed treatments and Fusarium comes from F. graminearum, which is really a seed rotter.  F. virguliforme, the causal agent of SDS – is a root rotter, and can infect roots over the course of the season.  Seeds and seedlings are the most vulnerable stage to many pathogens, after this time the plants defense mechanisms will hopefully be able to pick up the slack.  There are a number of new seed treatments, including some that are biological, that may have more or longer activity.  We will see how this year’s studies go.

How good are the soybean genetic resistance genes in preventing infection?

In one word, excellent!  There is very good resistance to SDS now and as we can see from our field trials this year it is effective from the early to late season stages.  I need to remind everyone though – disease severity is directly linked to the presence of soybean cyst nematode and new findings indicate root knot nematode as well.  Managing SCN populations is very important to managing SDS.

How many races? I read that preliminary research Identified more than a dozen different Fusarium virguliforme.

There are no races – in the classic terminology in which an isolate will act differentially with a host that has R-genes, like we have with Phytophthora sojae.  Resistance to Fusarium virguliforme is a type of partial resistance and is effective against all strains.  The Leandro lab and colleagues at Iowa State University reported that there is variability within the F. virguliforme populations found in the US which was identified with molecular markers and different levels of aggressiveness (ability to cause disease), but natural variation is expected.

The very strong relationship of SCN to SDS is well documented - is this also true for Brown Stem Rot?

This strong relationship relates to the increase in severity of the disease in the presence of SCN.  Yes, this is also true for brown stem rot.  Brown stem rot and SDS have very similar foliar symptoms.

Plant area/Symptom	Brown Stem Rot	Sudden Death Syndrome
Pith	Brown	White
Tap root	White	Gray, sometimes with blue spores
Root Rot	Absent	Present

 

Studies from Japan, Iowa State and Univ. of Wisconsin all indicate that disease severity of BSR is greater when SCN is present.  However, most of our varieties now have SCN resistance and there is some reduction in overall symptom development – albeit the relationship is quite complicated.

Another facet that also influences brown stem rot symptom development is soil pH.  A study at the University of Wisconsin very nicely demonstrated that severity was greater when soils are low in phosphorus and potassium and soil pH is below 6.5

Malvick from Minnesota found many fields that with plants infected with both SDS and BSR; have found similar results in Ohio?

Numerous times, we have recovered both the SDS and BSR pathogens from the same plant- since 1997.

Seedlings are very susceptible to SDS infection according to Leandro of Iowa, but what about infection in later growth stages when SCN may be more active ?

SCN is very active and can sense the plants as soon as they have been planted.  For our studies with SCN, to get accurate population data – we try to sample within 24 hours of planting or many of the eggs will have already hatched.

When I examine SDS foliar symptom infected plants, the base of the plant may show brick red lesions characteristic of Rhizoctonia; have other pathogens been linked to SDS; or are these likely secondary fungi with Fusarium the primary disease causing agent?

We see this brick red coloration in response to several soybean pathogens, including Sclerotinia, occasionally Phytophthora.  This could be dual infections, all of these pathogens are in the soil and the conditions that favor one also favor these other pathogens.  This could also be part of the plants attempt to defend itself.  Glyceollin,  the key plant compound that is made, is toxic to many fungi and oomycetes.  We often see this red at the edge of the infection sites, the compound turns red once it comes into contact with sunlight.  Our own Dr. Terry Graham – Emeritus Professor in the Dept. of Plant Pathology has done an enormous amount of research on this compound.

The link between soil compaction and SDS is established; Given this link, can we also say that stress on the plant (too wet) may also contribute to SDS?

This relates more to the conditions that favor fungal growth, ability to form spores, and ability to infect plants.  Compaction helps keep the soil wet for a longer period of time, and takes longer to dry out.  The roots have a very difficult time penetrating this.  A very nice study at Southern Illinois University demonstrated that on heavy soils, breaking up that compaction layer reduced overall disease severity. For high yield production systems, field quality, and drainage are key to obtaining high yields.

Why is SDS appearing in new areas and not in areas where it has been observed in the past?

This is quite common with plant diseases, it all relates to the disease triangle.  Is the variety planted in those historic sites resistant to SDS, and are the SCN populations lower than when the symptoms were prevalent the last time.  For SDS to develop in a field, high levels of SDS inoculum AND SCN populations, a SDS susceptible host as well as heavy rains shortly after planting are needed. My thought and recommendation for producers, once you have SDS, always select a variety with resistance to SDS and SCN for future plantings.