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Primer on Sclerotinia

Saturday, January 15, 2005
filed under: Disease

Sclerotinia head rot made its presence known again in 2004 in much of northern North Dakota, northwestern Minnesota and southern Manitoba. The last time a widespread infection took place was in 1999. Cool temperatures and continued wet, cloudy weather in much of August through October provided the right conditions for the disease.

The outbreak in 1999 prompted considerable investment into finding solutions to this disease. The Sclerotinia Initiative, a federally funded research effort, was created with the assistance of Senators Johnson (S.D.) and Dorgan (N.D.). The Initiative annually provides research funding earmarked specifically for Sclerotinia on sunflower, canola, soybean, edible beans, peas and lentils.

Basics of the disease

The Sclerotinia fungus attacks over 400 crop plants, and in the upper Midwest these would primarily be canola, dry beans, soybeans, and sunflower, although even flax, potatoes, and sugarbeets can be infected.

Head rot in sunflower is solely dependent on wet weather conditions during and after bloom. The sclerotia (hard black material) in the soil from a previous infected crop (which may last for several years) needs continuous wet soil in the upper layer for approximately 7 to 14 days.

The wet soil allows the sclerotia to germinate and sprout small mushroom-like bodies. Once the mushrooms are produced, which are barely a quarter-inch across, millions of spores are blown by the wind to adjacent fields. The spores, technically called ascospores, are dependent on air movement and cloudy misty weather to survive. The spores are highly vulnerable to sunshine.

When the spore lands on a susceptible plant (canola, bean or sunflower) it requires dead or senescent (dying) plant material and water in order to germinate and grow. The dying flower parts, even pollen, are a good food base for the disease. Extended wet and cloudy periods will permit the disease to spread quickly through the head. Warm dry weather after infection, on the other hand, will greatly slow infection down. Thus, the initial infection and the level of severity of rot, on sunflower and other hosts, are highly dependent on weather during and after bloom.

Release of tolerant material and testing commercial hybrids

After the 1999 infection, the NSA, N.D. and S.D. State Universities and the USDA ARS Sunflower Unit developed misting systems at Carrington and Fargo N.D. and Brookings S.D. The irrigation systems, controlled by sensors and electronic controllers, duplicate the weather conditions for disease infection and growth to occur, keeping the plants continuously wet.

Each winter, thousands of spores are produced in the lab and these are sprayed onto each and every sunflower head in the test plots during bloom. The automated mist system ensures that the plants remain wet, 24 hours a day, for at least four weeks after inoculation. This is the most reliable approach to researchers for testing genetic material and existing commercial hybrids for disease tolerance.

While greenhouse testing of seedlings may be appropriate for other diseases, accurate evaluation of head rot resistance can only be done in the field with adult plants. Also, while natural infection can also provide useful information, it never seems to consistently occur in research plots.

One of the research goals is to identify resistant breeding material for new hybrids. USDA geneticist Jerry Miller and pathologist Tom Gulya have been testing a variety of materials for the last four years under the mist irrigation systems. They released improved oilseed germplasm to the commercial seed industry in 2003 – material which exhibited good head rot tolerance in the previous three years of testing.

Miller placed this germplasm into a hybrid. This year that hybrid had 3% head rot infection while the commercial resistant check had 24% disease and the susceptible check had 73% disease. The germplasm has been released to seed companies that are now crossing this tolerant material into their elite lines for future hybrid production. Miller and Gulya are continuing to test new lines for resistance and more releases are expected in the future, including Sclerotinia resistant germplasm for confection hybrids.

Researchers Robert Henson at Carrington and Marty Draper at Brookings along with USDA’s Gulya, have spent the last several years perfecting the disease inoculation and misting systems. “We are feeling a lot more confident with what we are doing,” says Henson. “There is a significant learning curve in this kind of testing system and we have worked out most of the ‘bugs.’ We now have data which shows there are hybrid differences. It has also allowed us to identify new breeding material that is consistently below the resistant checks.”

This year the plot at Brookings was severely damaged at the seedling stage and had to be destroyed. So that means just one misting location with results in 2004. But the Langdon, N.D. performance trial had a large amount of head rot through natural infection. Comparing the results of the two sites clearly points out that the misting site location is a ‘worst case scenario.’ Of 15 commercial hybrids that were in both locations, only one hybrid had more disease in Langdon than Carrington. Head rot averaged 62% at Carrington and 35% at Langdon across common hybrids.

The graph provides comparisons between the two locations. It is noteworthy to point out that one commercial hybrid had 21% infection at Carrington and 17% at Langdon. This hybrid has consistently had low levels of disease in previous year tests at Carrington, according to Henson. He further points out that the entry with the lowest disease incidence in 2004 was an experimental confection hybrid. “This is a good indication that the breeders are making good progress. We just have to be able to reliably quantify it,” says Gulya.

Plans for the future

It is going to be important for farmers to see a hybrid rating system in the very near future says Stan Buxa, a member of the NSA board of directors and a farmer near Harvey N.D. “We as farmers are already making judgments and comparisons on what we are seeing in the fields. We need scientific data to either support or reject our observations,” says Buxa.

The plan is to expand the number of misting systems next year in an effort to get more reliable data. In addition to the Carrington and Brookings sites, additional misting locations are planned for Morden, Manitoba and Langdon. Efforts are underway to find one additional location. Gulya says that hopefully there will be some consistency between sites within a certain range. “By using artificial inoculation plus mist irrigation, we hope that the disease rankings of hybrids will be similar at all locations, allowing both growers and seed companies to view the data with confidence.”

Along with the head rot trials, Gulya is coordinating a multi-site effort to evaluate hybrids for resistance to Sclerotinia stalk rot. Thus, in the near future, growers can pick up a copy of a university hybrid yield trial publication and also see its performance against both Sclerotinia head rot and stalk rot. – Larry Kleingartner

Common Questions about Sclerotinia Head Rot

Q: I had head rot this year. Will I get it next year or the years later when I rotate this field back to sunflower?

A: Planting any susceptible crop in a field with Sclerotinia present the previous year increases risk, but head rot will develop only if weather conditions are right.

Q: What kind of weather is needed for infection?

A: Continuous wet soils for 7 to 14 days prior to or sunflower bloom are required for the sclerotia to form the mushrooms that result in head rot infection. Additionally, prolonged cloudy wet periods are required for the initial infection and subsequent disease development.

Q: Can the spores come from a neighboring field?

A: Yes, under the right conditions of extended wet and cloudy periods, the spores can be blown from field to field. Thus, the further a sunflower field is planted from a field known to have Sclerotinia the previous year, the less chance of head rot.

Q: Why do some plants have no disease while the next plant is totally destroyed by head rot?

A: It depends a lot on timing and some luck. The spore has to land on dead plant material to grow.

Q: One field had no or little head rot while another field of the same hybrid was nearly devastated. Why did that happen?

A: It is likely a matter of timing during bloom and a spell of wet weather. A day or two can make a significant difference in levels of infection.

Q: There seems to be hybrid differences in levels of infection. Is that true?

A: There are definite differences among hybrids. Seed companies may be hesitant to promote head rot tolerance without sufficient testing. That is why it is important to have multiple testing locations to confirm field observations.

Q: Can I plant sunflower on last year’s soybean ground and be eligible for crop insurance? What about canola or edible beans?

A: Yes for soybeans. You must keep a crop year between sunflower and edible beans and canola to be eligible for insurance.

Q: Will a fungicide be available in the future?

A: There is one fungicide labeled but efficacy remains a question. Field testing started this year and results are not available at this time. Testing of fungicides is being conducted at the misting sites for a large number of products.

Q: Is this a U.S. problem only?

A: No, it is international. Sclerotinia head rot is seen on sunflowers in every area of the world, and is considered a major problem. The Kansas/Colorado sunflower production region seldom has head rot problems because the weather is not conducive to extended wet and cloudy periods in August/September.

Q: Is there any hope that this problem will be eliminated in the near future?

A: Probably not eliminated but it should be greatly reduced in the near future. There is a core research group working on this disease in a number of crops including sunflower. There are efforts under way to identify resistant genes that can be mapped. Once that is accomplished then researchers can simply take a cotyledon and determine if the resistant gene(s) are present.

Compiled by Larry Kleingartner

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