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United States Department of Agriculture

Agricultural Research Service

About Sclerotinia
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General Sclerotinia Information

 White Mold Sclerotinia sclerotiorum is a plant pathogenic fungus that causes important diseases known as white mold, Sclerotinia stem rot,  wilt or stalk rot, or Sclerotinia head rot on a wide variety of broadleaf crops.  It is commonly found damaging dry beans, sunflowers, soybeans, canola, peanut, and lentils. There are many other crops that are susceptible such as alfalfa, field pea, potato, mustard, safflower, flax, borage, crambe, buckwheat, chickpea, lupine, faba bean and numerous vegetables such
as lettuce and carrots. Some of these crops are rarely damaged by S. sclerotiorum, while other are quite susceptible. This pathogen is known to infect about 408 species of plants. Numerous weeds such as marsh elder, lambsquarters, pigweed, Canada thistle, sow thistle, and wild mustard are also hosts and can play a role in disease cycles.

There are two other species of Sclerotinia, S. trifoliorum and S. minor.  S. trifoliorum is known only on alfalfa and forage legumes in the south east and eastern USA, while S. minor is primarily a lettuce and peanut pathogen found in the eastern and western coastal areas. S. trifoliorum is similar in biology and morphology to S. sclerotiorum, but S. minor produces much smaller sclerotia and generally produces apothecia less frequently in nature.

The primary survival (overwintering) structure of S. sclerotiorum is the sclerotium. A sclerotium is a hard resting structure consisting of a light colored interior portion called a medulla and an exterior black protective covering called the rind. The rind contains melanin pigments which are highly resistant to degradation, while the medulla consists of fungal cells rich in β-glucans and proteins. The shape and size of sclerotia depend on the host and  where they are produced in or on infected plants.

What is the origin of sclerotia in a field? There are four primary methods that fields are infested with sclerotia. The most common is by  susceptible crops or weeds being infected by ascospores coming from adjacent infested fields. The fungus then produces sclerotia on those plants and some are returned to the soil when the field is harvested. Wind transported soil or crop debris infested with sclerotia are also known to contaminate adjacent fields. Contaminated machinery can introduce sclerotia into a field. Surface irrigation water or rain water moving naturally between fields can also move sclerotia to previously clean fields. Seed contaminated with sclerotia is another method of introducing the fungus into clean fields.

The basic disease cycle of Sclerotinia diseases begins with the overwintering of sclerotia in the soil. Sclerotia are conditioned to germinate by the overwintering process. In the growing season, overwintered sclerotia can germinate in one of two methods. Probably the most common is carpogenic germination which results in the production of a small mushroom called an apothecium. Carpogenic germination usually requires the sclerotia to be in wet soil for one to two weeks prior to germination. The apothecium forms spores called ascospores which are ejected into the environment. Most will fall on susceptible plants in the immediate area of the apothecia, but some can travel long distances by wind. Ascospores require free moisture plus a food base such as senescent  flower petals or damaged tissue to produce a small colony that can then infect the plant. The pathogen produces oxalic acid and numerous enzymes that break down and degrade plant tissue. The requirement of moisture for carpogenic germination and growth of the pathogen are reasons why rainy periods or irrigation are associated with outbreaks of disease on certain crops. Disease development is favored by moderate temperatures of 15 - 25 C.

The other method of germination  is myceliogenic, where the sclerotium produces mycelium.  A primary crop where myceliogenic germination plays a major role in the disease cycle is in Sclerotinia wilt of sunflower. Sclerotinia wilt is caused by sclerotia germinating and infecting the sunflower roots. Most other Sclerotinia or white mold diseases, such as on dry beans, soybean, canola and sunflower head rot are initiated by carpogenic germination and infection of above ground plants parts by ascospores.

How long do sclerotia survive in the soil? Few studies have quantified sclerotia survival in the field. There are many factors affecting survival such as soil type, previous crops, initial population of sclerotia and environmental conditions, but how and to what degree they affect survival is not well understood.  High temperature and high soil moisture combined are probably the two most deleterious environmental factors. Microbial degradation, however, is the principal reason for a decline in the populations of sclerotia. There are many fungi, bacteria and other soil organisms that parasitize or utilize sclerotia as carbon sources. One reason that crop rotation is recommended for Sclerotinia is to allow the natural microbial population to degrade sclerotia. Two important fungal parasites involved in the natural degradation of sclerotia are Coniothyrium minitans and Sporidesmium sclerotivorum. Both these fungi have been touted as possible biocontrol agents for sclerotia, and some commercial products are now available.

The effect of tillage on survival of sclerotia is poorly studied and no generalizations can be made to aid in management of the pathogen. There is evidence that leaving the sclerotia on the soil surface enhances degradation whereas burying the sclerotia enhances survival. It is thought that the more dramatic changes in temperature and moisture on the soil surface are deleterious to sclerotia.

Because of the numerous crops infected by this pathogen, there are many strategies for control. Fungicides have been use with some success such as with dry bean and canola. Crop rotation continues to be used for certain crops such as sunflower where inoculum densities in the soil play a major role in disease development. Host resistance has been an elusive goal of many control programs. Most Sclerotinia diseases are not controlled principally by host resistance. However, some moderate levels of host resistance such as in dry beans and soybean have been found and can aid in integrated control programs. Disease escape mechanisms via plant architecture also have a role in reducing disease. Cultural controls such as wider row spacing or lower plant populations that reduce the microclimate favorable for disease development are used with some crops. Sanitation practices such as with vegetable production, and clean seed programs to keep sclerotia out of seed lots are also useful practices in some crop production systems. Biological control has only recently been tried on a commercial scale, but the results of farmer’s acceptance of this method remains to be determined. Sclerotinia continues to be a very difficult pathogen to control.


Sclerotinia in Soybeans
 White Mold on Soybeans

White mold of soybeans is a common disease caused by the fungus Sclerotinia sclerotiorum. It can cause major seed yield reductions when soybeans are planted in infested soil and there is a dense plant canopy with prolonged periods of wet weather (a major factor in disease development). The disease is rarely observed during dry periods in July and August. Besides seed yield reductions, the disease also results in reduced seed quality and seed contaminated with the black sclerotia of the fungus. Sclerotinia overwinters as sclerotia in soil.

The sclerotia germinate to form small mushrooms called apothecia that produce spores termed ascospores. The ascospores infect senescing flower tissue and then infect the stems of the plant; disease is closely tied to flowering.

Symptoms usually are observed after the canopy has closed. Dead plants are generally the first symptom observed. An inspection under the canopy will reveal a cottony, white mycelial (fungus threads) growth on stems, leaves or pods. Lesions develop on main stems and side branches. Stems appear bleached and sometimes shredded from advanced decay. Large sclerotia form in and on diseased tissue. Seeds in diseased pods are usually shriveled and may be infected by the fungus or replaced by sclerotia.

When a field with white mold is harvested the seed is almost always contaminated with sclerotia. Yield losses usually occur when incidence of disease is 15% or greater. Yield losses can range from to 1.3 to 3.7 bu/A for every 10% increase in disease incidence. The pathogen has an extensive host range of over 370 plant species and causes diseases on a wide variety of crops such as sunflower, dry bean, canola, alfalfa, buckwheat, lupine, mustard, potato, Jerusalem artichoke, safflower, lentil, flax, field peas and many vegetables. There are also many common broadleaf weed hosts such as marsh elder, lambsquarters, pigweed, Canada thistle and wild mustard.  The fungus that causes white mold on soybean is the same one that causes white mold of sunflower, dry beans, canola, and other crops.


The most important controls for white mold of soybean are to choose less susceptible cultivars, avoid planting on soils heavily infested with Sclerotinia, and to maintain open rows so air movement through the crop reduces plant wetness. Cultural practices, such as wider rowspacing, which reduce environmental conditions favoring disease are helpful. Orienting the rows toward the prevailing wind, for example, will help dry the crop following precipitation. Under very prolonged rainy periods or in protected areas such as along shelterbelts where humidity is higher, disease may develop even in an open canopy.

Soybean fields should be monitored for disease incidence. Check the seed hopper at harvest for the presence of sclerotia. As disease begins to increase in a field, the rotation time to non-susceptible crops such as small grains and corn should be increased. Crop rotation will reduce populations of sclerotia in soil, but will not entirely eliminate the pathogen. Do not plant highly susceptible crops such as drybeans and sunflowers during the rotation. If you rent land, find out the disease and cropping history before making planting decisions.

Although common soybean cultivars adapted for this region are susceptible to white mold, some cultivars are less susceptible than others. Information on cultivar susceptibility is available from the NDSU Extension Service. Do not use seed from a white mold infected crop. Seed quality could be low, and sclerotia may be introduced into the field along with the seed. Also, maintain good control of broadleaf weeds, since they can be hosts of Sclerotinia. When growing soybeans under irrigation avoid practices that favor a dense canopy and free water on the plant during flowering, since these will create ideal conditions for disease development.

SOURCE: NDSU Extension Service Circular A-1172



Sclerotinia in Dry Edible Beans
 Sclerotinia on Dry Edible Beans White mold is a sporadic disease which is most serious when wet weather occurs at flowering. When the surface soil is wet, the hard black survival structures, called sclerotia, germinate to form tiny mushroom-like bodies that liberate millions of wind-borne spores. These spores colonize dead bean tissue, particularly the dead blossoms, then the fungus invades green tissues, causing a watery soft rot. In wet weather infected tissues are tan colored and soft, with

tufts of fluffy white fungal growth.

These tufts of "white mold" develop into hard black bodies, the sclerotia, some of which survive many years in the soil. Leaves of infected plants turn yellow and wilt. In dry weather affected stems have a bleached or whitish appearance. Infected seed is discolored, chalky and lightweight.

White mold is favored by rainy weather before and at flowering, moderate temperatures and long periods of high humidity, and keeping the lower canopy of plants wet more or less continuously for up to two days.


Crop rotation is important but of only modest value in areas of intensive bean production, since the spores may blow in from nearby infested fields. Benlate and Topsin M are registered for white mold control. They are more effective when applied before infection occurs. Early bloom is the best time to apply these fungicides. Good canopy penetration is required so that the blossoms and lower stems are covered with fungicide. The most economical method is band application using drop nozzles, high pressure and high gallonage. High pressure broadcast application is not quite as effective but can also be used when band application is impractical. Aerial application using 7½-10 gpa also can be effective. Widely spaced rows may help enhance drying in the canopy. Upright varieties dry more quickly and may escape severe infection in years with conditions that are marginal for white mold development. Deep plow infected bean crop refuse and clean harvest equipment between fields. Avoid short rotations or rotation with other susceptible crops, especially beans, sunflower, canola, lentils and soybeans.

SOURCE: NDSU Extension Service Circular A-1133


Sclerotinia in Sunflower
 Sclerotinia Wilt

The Sclerotinia diseases are some of the most important diseases of sunflower in the Northern Great Plains. Three diseases are recognized in the field: Sclerotinia wilt, middle stalk rot, and head rot. Wilt is distinct because it begins as a root rot, whereas Sclerotinia head rot and middle stalk rot are above-ground diseases caused by airborne spores. All three diseases are caused by the same organism, Sclerotinia sclerotiorum, a very destructive fungus which is often called the "white mold" fungus.

Sclerotinia sclerotiorum is a serious problem not only in areas where sunflower and dry bean have been cultivated for many years, but also in areas where irrigated susceptible crops are grown. As production of sunflower in North Dakota moved west, there was an increase in the incidence and severity of Sclerotinia diseases in areas with no previous history of the pathogen. This fungus can be a serious problem in the drier sunflower production areas.

Sclerotinia sclerotiorum attacks approximately 374 species of broadleaf plants. The row crops commonly damaged in the Northern Great Plains are sunflower and dry bean; however, many other crops are susceptible, such as soybean, buckwheat, flax, lentils, pea, potato, mustard, crambe, rapeseed or canola, Jerusalem artichoke and safflower. Not all of these other crops are as susceptible to S. sclerotiorum as sunflower and some are rarely damaged. Many broadleaf weeds

such as marsh elder, common lambsquarters, redroot pigweed, Canada thistle and wild mustard also are hosts.

Sclerotinia Wilt

Description: Characteristic symptoms include sudden wilting of leaves, root rot and a basal stem canker (Figure 61 JPEG; 21.6Kb). Wilting plants are often first observed just prior to flowering, but about 60 to 70 percent of the wilted plants appear after flowering and are commonly found adjacent to each other. The time required from incipient wilt to complete wilting may be four to seven days.

A tan, greyish or green-brown canker forms at the base of the plant and eventually girdles the stem (Figure 62 JPEG; 28.5Kb). As decay progresses, the stalk becomes bleached with a shredded appearance and the pith is decayed. Plants lodge easily during high winds. Inside and often outside at the base of the stem hard, black resting bodies of the fungus called sclerotia [about 0.12 to 0.25 inch (3 to 6 mm) in diameter] can be found (Figure 63 JPEG; 22.7Kb). The presence of sclerotia provides a positive identification of the disease. Decay of lateral roots and tap roots is obvious. During wet weather, white mycelium (mold) often develops at the base of the stem, hence the name "white mold."

Disease Cycle: Sclerotinia sclerotiorum overwinters as sclerotia in the soil or in plant debris. When sunflower roots come in contact with sclerotia, the sclerotia germinate, infect and decay the roots, the fungus grows up into the stem, and the plant wilts and dies. Contact between roots of adjacent plants within rows allows the fungus to spread from plant to plant. The fungus generally does not move between rows. Sunflower is the only crop S. sclerotiorum consistently infects through the roots. Other susceptible crops are infected mainly by spores on above-ground parts of the plant.

Sclerotia are formed in the decayed stem pith and on the roots as the plant dies. These sclerotia are then returned into the soil during tillage operations and serve as sources of inoculum for the next susceptible crop. Sclerotia can be spread from field to field through wind-blown soil, moving surface water, on farm implements and rarely as contaminants in commercial seed.

Sclerotia survive in the soil and fields can remain infested for many years. The higher the inoculum density (i.e., the number of sclerotia in the soil), the longer the period a field will remain infested. Populations of sclerotia begin to decline when fields are planted with non-hosts. Although the effect of tillage practices on sclerotia survival is little understood, preliminary research suggests minimum till will enhance the degradation of sclerotia.

The most important factor affecting incidence of wilt is inoculum density. Research in North Dakota has shown that an inoculum density of 0.1 sclerotia per liter (about one quart) of tillage layer soil can result in about 10 percent wilted plants. An inoculum density of 1.0 sclerotia per liter of soil would result in about 60 to 70 percent wilted plants in the standard hybrid 894. In practical terms, this means that low levels of the fungus in the soil will cause substantial sunflower losses. Soil moisture and temperature during the growing season are not critical factors affecting wilt incidence. Plant population in the range between 15 to 30 thousand plants per acre (37-74 thousand plants per hectare) on 30- or 36-inch (76- or 91-cm) rows is not a factor affecting disease incidence (percentage of plants that are diseased), although solid-seeding should be avoided. Lodging of wilted plants, however, increases at high plant populations.

Damage: Wilt is the most important of the three diseases caused by Sclerotinia. Wilt occurs whenever sunflower is planted on Sclerotinia-infested soil and can cause severe yield loss. For example, in two fields in North Dakota with 80 percent and 60 percent incidence of wilt, yield was reduced by 79 percent and 50 percent, respectively, in the hybrid 894. Infected plants usually die rapidly. Surviving plants may or may not produce seed, depending on when infection occurs. The heads on wilted plants generally are smaller than those on healthy plants and seed weights are lower. On the average, infected plants yield less than 50 percent of healthy plants. Equally important, however, is that Sclerotinia wilt leads to increased levels of sclerotia in the soil, which can result in the removal of fields from sunflower production for many years. Sclerotinia diseases, therefore, affect future production and economic gain from sunflower and other susceptible crops and disrupt rotation schedules.

Sclerotinia Middle Stalk Rot and Head Rot

Description: Middle stalk rot is usually first observed at the middle to mid-upper portion of the stalk during flowering and continues until maturity. It begins as a tan to gray water-soaked lesion which eventually girdles and decays the stalk (Figure 64 JPEG; 25.7Kb). The stalk usually bends over at the point of decay and the tissues above the canker die. During wet weather, a dense white mycelium and some sclerotia often will be produced both inside and outside the stalk. The affected tissues become bleached and will have a shredded appearance.

The first symptoms of head rot usually are the appearance of water-soaked spots or bleached areas on receptacles (the fleshy back of the head). The fungus can decay the entire receptacle and the seed layer falls away leaving only a bleached, shredded skeleton interspersed with large sclerotia (Figure 65 JPEG; 28.1Kb). These bleached, skeletonized heads are very obvious in the field, even from a distance. During combining, infected heads often shatter and any remaining seeds are lost. Usually, the seeds are not decayed but many are empty. The large sclerotia in the heads may be 0.5 inch (12 mm) or greater in diameter and many are harvested along with the seed (Figure 66 JPEG; 25.6Kb). Large sclerotia mixed in with seed confirms that a field contained head rot.

Disease Cycle: If soil moisture is high for seven to 14 days, sclerotia in the upper several inches of soil can germinate to form small mushrooms called apothecia. These apothecia produce ascospores for a week or more if soil moisture remains high. The ascospores are ejected into the air, carried by the wind, and may land on sunflower or other susceptible plants. Apothecia can be found between June and September but usually are not observed until after the crop canopy has completely covered the rows. Apothecia are formed under canopies of many crops, including small grains, corn, potato, dry bean, soybean and sunflower (Figure 67 JPEG; 20.1Kb).

Ascospores require a film of water and a food base such as dead or senescing plant tissue to germinate and infect, and are also known to infect through wounds. On the stem, the ascospores apparently come in contact with a food base (such as dead pollen) and water that accumulates in the stem-leaf axil and infection occurs. Infection may also occur on a damaged leaf, and the fungus will grow down the petiole into the stem. Infection of sunflower by ascospores is similar to the process by which S. sclerotiorum infects dry beans, soybean and other susceptible crops. Ascospores infect the receptacle of the sunflower head via the developing florets and decay the entire head. The pathogen can infect the seed and survive as mycelium (thread-like strands of the fungus) in the seed coat, but evidence suggests that infected seed is not an important means of spreading of the fungus.

Damage: Head rot and middle stem rot occur sporadically and only following long periods of wet weather. Usually they are not as serious as wilt in the Northern Great Plains, although they can cause yield losses. Rotted, intact heads may yield up to one-third less than healthy heads and are very susceptible to shattering, so additional seed is lost during combining. Head rot also causes a decrease in oil content and an increase in free fatty acid content. The sclerotia that form in diseased stalks and heads are returned into the soil at harvest and can cause Sclerotinia diseases in sunflower or other crops in following years, magnifying the damage. Many sunflower fields with no history of Sclerotinia became infested due to ascospore infection followed by a return of sclerotia to the soil.

Management of Sclerotinia Diseases: Because occurrence of middle stem rot and head rot is sporadic, disease control is usually aimed at control of wilt. The most important tools for managing the Sclerotinia diseases of sunflower are planting in non-infested soil and preventing buildup of sclerotia in soils. Prevention is done principally through monitoring of fields for Sclerotinia diseases and crop rotation. No totally resistant hybrids are currently available. However, commercial seed companies are in the process of developing hybrids that are moderately to highly resistant to Sclerotinia wilt. There is no chemical registered for control of wilt and none that is economic. There are no fungicides currently registered in North Dakota for control of ascospore infection of sunflower. The following is a summary of disease management recommendations:

  • Sunflower should not be planted on land already infested with sclerotia. Fields that have been planted to susceptible crops such as dry bean or soybean could be infested, especially if in an area where Sclerotinia is common.
  • Planting certified seed minimizes the danger of introducing sclerotia into fields that are free of Sclerotinia. Avoid solid seeding and high plant populations.
  • Fields of susceptible crops should be monitored for disease incidence. Sunflower fields should be scouted about four weeks after flowering to assess incidence of wilt. A later date is even better, but as dry-down proceeds, it becomes harder to evaluate infected plants. A final scouting should occur prior to harvest to assess incidence of middle stalk rot and head rot. In other susceptible crops such as dry bean, it may be necessary to carefully search beneath the canopy to see sclerotia being formed. Accurate records of disease incidence and crop rotations are necessary for managing this pathogen.
  • Rotations to a nonsusceptible crop such as small grains, corn or sorghum are necessary when disease appears (see section on rotations). Crop rotation is the most important management procedure. The rotation interval will depend upon disease incidence. A three to five-year rotation may be necessary with low disease incidence (less than 10 percent), while six to eight years or longer might be needed at higher disease incidence. A dryland field with 10 percent wilted sunflower plants might require a four to five-year rotation to nonsusceptible crops to reduce the incidence of wilt to about 5 percent. The incidence of wilt should not be permitted to exceed 1 to 2 percent before starting a rotation to non-host crops. A low incidence of wilt increases substantially after several years of continuous sunflower and long rotations are then needed when there is a high level of sclerotia. Broadleaf weeds should be controlled.
  • If sunflower is to be planted on Sclerotinia-infested soils, choose the least susceptible commercial hybrids available.
  • Sunflower should not be planted adjacent to a field infested the previous year because this may serve as a source of ascospores for head and middle stalk rots.

SOURCE: NDSU Extension Service Circular PP-840 * Goes to a non-federal site


Sclerotinia Stem Rot in Canola
 Sclerotinia Stem Rot in Canola Field Sclerotinia stem rot has been the most serious disease of canola in North Dakota and Minnesota in recent years, with average incidence (percent infected plants) as high as 19 percent in North Dakota in 1993 and 19 percent in Minnesota in 1997. Estimated state-wide losses from Sclerotinia were as high as 13 percent in North Dakota (1993) and 13 percent in Minnesota (1997). In severely infected fields losses were estimated as high as 50 percent.

Although Sclerotinia has always been a threat to canola production, it has become more serious as canola production has increased and wet weather has favored disease development in recent years.



Sclerotinia stem rot develops late in the season, with the first visual symptoms appearing by the end of flowering. Dead and lodging plants occur singly or in patches in infected fields (Figure 1 JPEG; 27.2Kb). Infections of individual plants usually develop around cast petals. The infections may produce a target pattern of light brown, mushy tissues. Infections may spread from infected leaf petioles or branches to larger stems. Infected areas eventually become bleached or white and the tissues become shredded (Figure 2 JPEG; 14.4Kb). If the main stem is infected, plants may die early, reducing seed production, and plants may lodge. Hard black bodies which resemble rat droppings may be produced in infected stems. These are known as sclerotia (Figure 3 JPEG; 13.8Kb). They are helpful in identifying Sclerotinia, but may not be present in every infected stem.

Blackleg is another common disease that also may cause lodging. Blackleg produces black lesions on the stem. The internal root tissues of blackleg-infected plants turn dark gray to black or have dark gray streaks in them. Blackleg infections near the soil surface may result in stem breakage at or near the soil surface (Figure 4 JPEG; 12Kb). This contrasts to Sclerotinia, which produces shredded white stem tissues with stem bending or breakage at a height of 6 to 18 inches above the soil but no symptoms in the roots (Figure 5 JPEG; 36Kb). For more information about blackleg, see Extension Circular PP-1367. *Goes to a non-federal Web site 

Disease Cycle. The Sclerotinia fungus, Sclerotinia sclerotiorum, produces sclerotia in the stems. Although there may not be many sclerotia produced per stem, the total production of sclerotia per acre may be quite high, up to 40 or 50 pounds (Schatz, unpublished data). Sclerotia fall to the soil at harvest and survive on or in the soil for several years.

If the soil is at or above field capacity for 10 to 14 days, the sclerotia may germinate to produce tiny mushroom-like bodies that resemble golf tees. These fruiting bodies, called apothecia, produce millions of airborne spores (Figure 6 JPEG; 13.4Kb). The spores can be produced not only in canola fields, but also in fields of other crops, including small grains. The spores escape from the canopy and may be wind borne to nearby fields. The spores can survive long enough to be blown from field to field.

The spores do not infect healthy green plant tissue but need a dead or dying food source. As canola petals die and fall onto lower portions of the plant, any spores on the dead petals may germinate and begin to grow if the canopy stays wet for long periods of time. Once growth is established on the cast petals the fungus invades the surrounding tissues. Infections in canola may continue to spread as long as the canopy remains wet. Sclerotinia development may cease in hot or dry weather, but it can resume once cooler, wet weather returns. Sclerotia are produced in the infected stems and later drop to the soil (Figure 7 GIF; 8.22Kb).

Environment. Wet weather preceding flowering and at flowering favors disease development. At least 1 to 2 inches of rain are required in the 10 to 14 days before flowering to saturate the surface soil and stimulate formation of apothecia. The foliage in the canopy must be wet for most of two days for the petals to be colonized and infection to occur. If wet weather continues, the infection will continue to spread. Dry weather will stop further spread. Temperatures in the 70s are more favorable than higher temperatures. Infection and development does not occur at temperatures of 86 degrees Fahrenheit or higher.

Survival. The pathogen survives as sclerotia in or on the soil. Some sclerotia may survive as long as four to six years. Each year some sclerotia die. They may die due to freezing and thawing or wetting and drying, especially if they are near the soil surface. Various soil microorganisms may colonize the sclerotia and kill them.

Hosts. Many broadleaved plants are hosts of Sclerotinia. Sunflower, dry bean, canola, crambe, and soybean are some of the best hosts and support the greatest buildup of sclerotia in the soil. Chickpea and lentil are also quite susceptible but support less buildup of sclerotia in the soil. Field pea is less susceptible and flax is much less susceptible. Many broad-leaved weeds are also susceptible, including lambsquarters, Canada thistle, ragweed and marsh elder. Members of the grass family including small grains, corn and grassy weeds are immune.

Crop Rotation. Crop rotation is important, but the sclerotia survive for long periods in the soil, and the spores may blow into canola fields from nearby fields. Large concentrations of susceptible crops and several years with wet weather will contribute to a buildup of Sclerotinia in an area. Try to avoid more than one highly susceptible crop in a rotation, including canola, crambe, sunflower, dry bean or soybean. Semi-leafless pea supports less buildup of Sclerotinia than does the vining types and may be acceptable in a rotation with canola. Flax and buckwheat are less susceptible. In irrigated trials at Carrington, N.D. (Schatz, unpublished) no sclerotia were produced in flax; therefore flax appears to be a relatively safe crop in rotation with canola.

Tillage. Some studies indicate that sclerotia near the soil surface break down faster than those buried deeper; other studies indicate that infection is greatest when sclerotia are left on the soil surface. In any case, sclerotia that are within an inch of the soil surface are capable of producing apothecia, which liberate spores that may start new infections. Deep tillage may be used to bury sclerotia after a susceptible crop has been heavily infected; this practice will help to reduce Sclerotinia spore showers in subsequent years if the sclerotia remain deeply buried, but not if deep tillage is used the following year. Burial of sclerotia may or may not result in longer survival of sclerotia. If deep tillage is used to bury sclerotia, shallow tillage should be used for the next two or three years to assure that sclerotia are not returned to the soil surface where they can produce apothecia and liberate spores. Deep tillage is of limited value if used on only a few fields in an area that has many infested fields; it may be more effective if practiced area-wide.

Biological Control. Intercept is a biological control product registered for control of Sclerotinia. It contains Coniothyrium minitans, a fungus which attacks the sclerotia in the soil and kills them. Several months are required for the fungus to kill the sclerotia. Since this product is new, very little field data is available from North Dakota and Minnesota on how well it controls Sclerotinia.

Varieties. Although all varieties are susceptible some are less susceptible than others, and will perform better under moderate to severe disease pressure. Research has been initiated to test for varieties that are less susceptible. Some varieties are available that are apetalous, that is they have no petals. This removes a major food source for Sclerotinia, and apetalous varieties escape a severe infection incidence. Apetalous varieties may be useful if they yield as well as conventional varieties.

Fungicides. Quadris was registered for suppression of Sclerotinia on canola in March of 1999, Ronilan was registered in June of 2000 and Topsin M was registered in June of 2002. Other fungicides may be registered within the next several years. Information on fungicides currently registered is available in the most current edition of the North Dakota Field Crop Fungicide Guide (PP-622), from county extension offices, NDSU and University of Minnesota Research Extension Centers, the Northern Canola Growers Association and the Minnesota Canola Council.

Timing. Effective suppression of Sclerotinia requires timely application of a fungicide. Quadris should be applied at 10-25 percent bloom, or three to seven days after initiation of bloom. There will be 10 to 18 flowers on the main stem of Argentine canola when it is at 10-25 percent bloom. Quadris should be applied before or as the first petals begin to fall. Late application of Quadris is less effective than timely application.

Ronilan and Topsin M should be applied at 20-50 percent bloom, or four to eight days after initiation of bloom. There will be 14 to 16 flowers on the main stem at 20 percent bloom and 20 or more (includes any flowers that have dropped off) at 30 percent bloom . The 50 percent bloom stage is the time of maximum color development in the crop. At that stage there will be pods on the lower one third of the main stem. Once the crop is beyond 50 percent bloom, Ronilan and Topsin M are less effective for Sclerotinia control. Fungicide trials in 2001 and 2002 indicated that both Ronilan and Topsin M were more effective when applied at 35-50 percent bloom than when applied earlier.

Rates. Quadris should be applied at 9.6 to 13.8 fl oz/A. The 9.6 fl oz rate has been supported by the registrant, Syngenta, and may provide adequate control if applied before any petals begin to fall. Results with Quadris have been variable, however.

Ronilan should be applied at 10.6 to 16 oz/A. Extensive data from North Dakota, Minnesota and Canada indicates that the 12 oz rate provides excellent and consistent Sclerotinia suppression under even severe disease pressure. The 10.6 oz rate is slightly less effective, but may be adequate for moderate disease pressure.

Topsin M should be applied once at 1-2 lb/A at 20-50 percent bloom or twice at 1 lb/A for each application, with the first application at 20-30 percent bloom and the second at 40-50 percent bloom. One application of the 1 lb rate has performed very well at 35-50 percent flowering in most trials in Minnesota and North Dakota.

Spray decisions. Fungicides for suppression of Sclerotinia are expensive and the decision to spray should be made only when: 1) yield potential is above normal (at least 40 bushels or 2,000 lb/A) if canola prices are minimal, 2) weather leading to early bloom has been wet (at least 1-2 inches of rain in the two weeks prior to early bloom), 3) more rain or high humidity is expected, and 4) Sclerotinia has been a problem in recent years in fields currently planted to canola or in fields nearby. A fungicide is more likely to be needed if canola is on tight rotations (three years or less) or if other susceptible crops were in the rotation.

A Sclerotinia risk map, similar to that used in Canada, was initiated in 2001 for North Dakota and northwest Minnesota. The risk map is posted on the Northern Canola Growers Association Web site:

and the NDSU Web site:

The risk map site contains three maps: a map showing the growth stage of canola, a map showing soil moisture and where the soil is at field capacity, and a map showing the risk from Sclerotinia.

Sclerotinia Stem Rot Checklist

A risk assessment checklist follows. This checklist was duplicated, with permission, from the Web site of the Canola Council of Canada.

When to complete the checklist:
Fill out the checklist and assess the crop shortly after first flower. First flower occurs when 75 percent of the canola plants have three open flowers on the main stem. Usually this occurs during the last week of June or the first week of July.


How to complete the checklist:
Read each question and circle the point value assigned to the answer you choose. Count up the points for each question and enter the total for each section. Answer all the questions in this section.


Section One


1. Have you had good looking crops at flowering and poor yields at harvest, even though growing conditions were favorable?

Yes - 20 No - 0

2. Have you seen sclerotinia stem rot in your crops in previous years?

Yes - 20 No - 10

3. Have you heard of sclerotinia problems in your area in the past two to three years?

Yes - 10 No - 5

4. Have you seen black sclerotes in your harvested seed in the past two to three years?

Yes - 20 No - 10

5. In previous years have your canola crops lodged?

Heavily - 20
Moderately - 10
Lightly - 0

6. Do you see large swaths at harvest but get low yield?

Yes - 10 No - 0


7. If you sprayed a sclerotinia fungicide in previous years, what were the results?

Better crop - 20
No difference - 0


Total points for section one = __________



If you scored 60 or more in this section you probably had sclerotinia stem rot in your canola crops. Proceed to section two with a 60 or more score.

Section Two


8. When you walk through the crop during the morning at the beginning of flowering are your boots and pant legs wet when you come out?

Yes - 20 No - 10

9. Have you had wet weather in the immediate area within 2 to 3 weeks prior to flowering that allowed the soil to remain moist for extended periods?

Yes - 20 No - 10

10. Were apothecia found in the field, around the field, or in any neighboring cereal or canola fields where canola was grown in the previous 1 to 3 years?

Yes - 20 No - 10

11. Do you feel it will be dry throughout the flowering stage of the crop?

Highly likely - 0
Moderately likely - 10
Not likely - 20


Total points for section two = __________



If you had a high score in section one and more than 50 for section two, you should consider applying a fungicide to protect your crop again sclerotinia stem rot.

Section Three


12. What is the condition of your stand of canola in terms of height, vigor and uniformity?

Excellent - 20
Good - 10
Fair - 5
Poor - 0

13. When you walk through your crop, how dense is the canopy?

Light - 0
Moderate - 10
Very Dense - 20

14. What is the yield potential of the stand?

10 - 20 bu/ac - 0
20 - 30 bu/ac - 10
Greater than 30 bu/ac - 20

15. In previous years, when your yield potential was 30+ bu/ac, what were the actual yields?

Greater than 30 bu/ac - 0
20 - 30 bu/ac - 20


Total points for section three = __________


If you have scored 50 or higher in section three, along with high scores from the first and second sections (60 and 50 plus respectively), it may be worthwhile to protect your crop against sclerotinia stem rot. If you scored less than 50 in the last section it is not likely worth applying a foliar fungicide.

Permission by the Canola Council of Canada to reproduce this checklist is gratefully acknowledged.


SOURCE: Arthur Lamey, Professor Emeritus, North Dakota State University and Carl A. Bradley, Extension Plant Pathologist, North Dakota State University, NDSU Extension Service Circular PP-1201 (Updated Version: Sclerotinia of Canola pp 1410) *Goes to a non-federal Web site


Sclerotinia in Lentils
 White Mold On Lentil


White mold of lentil occurs from early flowering to pod setting, usually in highly productive fields with tall, dense stands of lentils. The disease is favored by wet and cool conditions especially on lower ground where dense canopies usually develop. Because winter lentils are exposed to the prolonged wet and cool spring weather, white mold is likely to be more common and more severe in winter lentils than in spring-sown lentils.

Lentil plants infected by white mold first appear bleached near infection site on stems, leaves and stems turn brown to tan, die prematurely. Infected areas are covered with white fluffy mold on infected area Figure 1 (JPEG; 17.5Kb).  Dark brown to black sclerotia develop inside and often outside of the infected plants Figure 2 (JPEG; 16.8Kb).

The pathogen

The pathogen that causes white mold is the fungus Sclerotinia sclerotiorum.  It produces sclerotia that survive adverse conditions Figure 3 (JPEG; 5.48Kb). Sclerotia are hard and black bodies of mycelium, irregular in shape and like mouse droppings in appearance.  Inside the sclerotia is white to pink mycelium which can re-grow under favorable conditions. Under cool and moist soil conditions usually provided by dense canopy, sclerotia germinate either directly by means of mycelium which can infect adjacent lentil plants or they produce small mushroom-like structure called apotheria, which eject ascospores into the air through wind or rain splash.  The ascospores will land on lentil plants and start new infection. This pathogen is known to infect more than 400 plant species. A population of the white mold pathogen obtained from a single lentil field from eastern Washington showed considerable genetic diversity as measured by mycelial incompatibility.

Disease cycle

The sclerotia survive in the soil. During cool and wet conditions, sclerotia can germinate by means of mycelium and infect plant roots. More often, under dense conopy which provides moist and cool conditions, sclerotia germinate by means of mushroom-like apothecia. Apothecia produce and eject ascospores into the air and ascospores may land on plants and start new infection. Infected plant become brown and tan in the infected area and the plant may wilt.  Under dense plant conditions, white fluffy mycelium develop on affected areas, hence the disease name white mold.  The fungus develops more sclerotia on infected plants. During harvest the sclerotia can be either shaken to the ground Figure 4 (JPEG; 891Kb) or collected with grains.  Seeds contaminated with sclerotia may spread the disease to new production areas.


Although all lentil cultivars are susceptible to infection by S. sclerotiorum, cultivars do show different tolerance levels to this disease. Field and greenhouse evaluations of lentil cultivars have shown that significant differences in response to white mold exist among lentil cultivars.  Certain cultivars performed consistently better than others in both field and greenhouse conditions conducted in Washington and Oregon.  The cultivars that consistently showed tolerance to white mold include Pennel and CDC Sovereign. In fields where white mold is of a problem in the past, cultivars with tolerance to white mold should be selected for planting as a disease management practice.

Disease management

  1. Plant lentils in fields where no white mold is observed previously and plant seeds free of sclerotia.
  2. Long term (five year or longer) rotation with cereal crops (but not with other legumes) will help reduce inoculum potential. The pathogen does not infect common cereal like wheat, barley, but it infects other legumes and crucifers like peas, and canola.
  3. Plant lentil cultivars that show some tolerance to white mold. Cultivar Pennel is more tolerant to white mold in our greenhouse and field evaluations.
  4. For seed production and in areas where the disease is very severe, fungicides may be sprayed.  Fungicides Ronilan and Endura showed strong inhibition of white mold growth in our laboratory tests. Check fungicide restrictions before spraying.


Beniwal, S. P. S., Baya’s, B., Weigand, S., Makkouk, Kh., Saxena, M. C. 1993.  Field Guide to Lentil Disease and Insect Pests. International Center for Agricultural Research in the Dry Areas, Aleppo, Syria 107 pages.

Chen, W., Grunwald. N., McPhee, K. and Muehlbauer, F. 2003. Field evaluation of lentil cultivars for resistance for Sclerotinia sclerotiorum, 2002. Biological and Cultural Tests for Control of Plant Diseases (online.) Report 18:F010. DOI:10.1094/BC18. The American Phytopathological Society, St. Paul, MN.

Chen, W., Grunwald, N., McPhee, K. and Muehlbauer, F. 2003. Evaluation of lentil cultivars for resistance to white mold. 2003 Sclerotinia Initiative Annual Meeting Abstract Page 17.

Chen, W., Myers, J., McPhee, K. and Muehlbauer, F. 2005. Field Evaluation of Lentil Cultivars for Tolerance to Sclerotinia sclerotiorum, 2004. Biological and Cultural Tests for Control of Plant Diseases (online.) Report 20: Submitted. The American Phytopathological Society, St. Paul, MN.


Weidong Chen and Fred Muehlbauer
Grain Legume Genetics and Physiology Research Unit
USDA-Agricultural Research Service
303 Johnson Hall, Washington State University
Pullman, WA 99164


 White Mold on Lentil 1  White Mold on Lentil 2  White Mold on Lentil 3  White Mold on Lentil 4


Sclerotinia in Dry Peas
 White Mold on Peas

White mold of pea occurs worldwide under wet conditions on foliage and stems with excessive vine growth. White mold is caused by Sclerotinia sclerotiorum, a fungal pathogen that has a wide range of host plants including many cultivated crops such as beans, Brassica spp., vegetables, potato, sunflower, soybean, and pea.

The pathogen infects stems, leaves and flowers that are in contact with the ground due to lodging.  It produces prominent black sclerotia within mycelium and in cavities of infected stems. Sclerotia can germinate and produce mycelium for infection, but they most often develop apothecia, a sexual fruiting body produced after a period of dormancy. Within the apothecia, asci develop which eventually release ascospores into the air. The disease is most severe at the late growth stage when plants are flowering and the canopy is closed.

Under these conditions, a humid microclimate in the lower pea canopy is produced, that is conducive to disease development.  Senescent flowers are considered to be the initial nutrient source for infection.  Once infection has started, the pathogen can quickly infect all plant parts.

To control white mold, seed used for planting should be free of sclerotia. Dicarboximide can be used as a protectant fungicide during the flowering stage in fields with known risk of white mold.  Pea cultivars with semi-leafless traits may offer advantage for reducing white mold. Rotation with cereal crops, but not with many of the broad leaf crops such vegetables, beans, soybean and oilseed rape, can reduce inoculum build-up in the soil. No resistant cultivars of pea are available although resistance in some plant introduction accessions has been reported. 

Source: Grünwald, N. J., W. Chen, and R. C. Larsen. 2004. Pea Diseases and their Management. In Disease Management of Fruits and Vegetables. II. Vegetable Diseases, edited by S. A. M. H. Naqvi and K. G. Mukerji. Dordrecht, The Netherlands: Kluwer Academic Publishers.


Sclerotinia in Chick Peas


White mold of chickpea can occur at either seedling stage or at flowering and pod filling stages depending on the environmental conditions and possible the pathogen species involved. At seedling stage, the disease occurs at the base of the stem causing symptoms like collar rot. Often white mycelial growth around the stem on soil surface is visible Figure 1 (JPEG; 1.44Mb). Affected plants wilt and die Figure 2 (JPEG; 1.38Mb) and Figure 3 (JPEG; 1.38Mb). Black sclerotia in various shape and sizes form on dead or dying chickpea stems right above or below the soil line Figure 4 (JPEG; 1.21Mb).  The disease at the seedling stage is common in central California in the early spring, and serious losses due to this disease have been observed there.  However, in the Pacific Northwest and the northern Great Plains, the disease is more common at the flowering and pod filling stage (Chen et al. 2006).  Infection starts at upper stem or on senescent flowers. Infected stems become pale in colour like bleaching, and the symptom spreading both upward and downward along the stems Figure 5 (JPEG; 633Kb).  Under heavy canopy and humid conditions, white puff mycelial growth becomes conspicuous Figure 6 (JPEG; 313Kb) and Figure 7 (JPEG; 403Kb), and black irregular-shaped sclerotia may form and are visible on the stems.  The plant parts above the infection wilt and die.  Disease infected fields show appearance of chlorotic and dying branches or whole plants scattered in the field.

The pathogens

White mold of chickpea is caused by Sclerotinia sclerotiorum in the Pacific Northwest and the Great Plains.  However, both S. sclerotiorum and S. minor are reported to cause white mold of chickpea in Arizona (Matheron and Porchas, 2000).  The species of Sclerotinia responsible for the seedling stage disease in Central California could be different based on our preliminary studies and remains to be identified (Njambere et al., 2006). In all cases, the pathogens produce black and irregularly shaped fruiting bodies of sclerotia that survive adverse conditions, and the sclerotia can either germinate directly or produce apothecia and ascospores that can be spread by wind, land on plant parts and initiate new infection.

The disease cycle

All the pathogens survive adverse conditions or between crop seasons as the black sclerotia in soil or from infested seed lots.  At appropriate conditions, the sclerotia may germinate by one of two means. Sclerotia can germinate directly by means of mycelium in the soil and infect chickpea stems. After appropriate conditioning like periods of low temperature and moisture, sclerotia could also germinate by means of apothecia bearing ascospores in asci.  Ascospores are blown and spread by wind and land on stems or flowers to initiate new infection. Within season spread of the disease may occur directly from infected plant to health plants through direct contact under dense crop canopy conditions.  In the case of stem base infection, the pathogen may spread to adjacent plants through mycelial growth under wet soil conditions if plants are close to one another (like 2 to 3 inches apart).


The disease at seedling stage is mainly caused by direct germination of sclerotia in the soil. Therefore management practices that can reduce sclerotial density in the soil will be effective in reducing the disease. Considering the longevity of sclerotia in soil and wide host range of the pathogen.  Long-term rotations with cereal crops when possible will reduce the inoculum (sclerotia) density.

Chickpea cultivars in California do show differential reactions to white mold in the field. Some are more resistant or more tolerant than others based on field observations. Therefore, the tolerant cultivars should be chosen when possible especially in fields with history of white mold. However, specific experiments are needed to demonstrate and confirm the resistance/tolerance of the cultivars that seem to perform better in the field.

The disease at the flowering and pod filling stages is favoured by excessive vegetative growth and cool moist conditions.  No resistance to this stage of disease has been observed among chickpea cultivars. Fungicide application could be an option used to control white mold, but the economical viability of fungicide application for controlling white mold on chickpea remains to be demonstrated. Rotation and agronomical practices that reduce or delay canopy closure will help reduce the disease.


  • Chen, W., Schatz, B, Henson, B., McPhee, K. E., and Muehlbauer, F. J. 2006. First report of Sclerotinia stem rot of chickpea caused by Sclerotinia sclerotiorum in North Dakota and Washington. Plant Disease 90: 114. Link
  • Matheron, M. E., and Porchas, M. 2000. First report of stem and crown rot of garbanzo caused by Sclerotinia minor in the United States and by Sclerotinia sclerotiorum in Arizona. Plant Disease 84: 1250. Link
  • Njambere, E., Chen, W., Frate, C, Temple, S.R., and Muehlbauer. F.J. 2006. Diversity of Sclerotinia isolates from chickpea from central California.  Phytopathology 96: S85. About

Contributed By

Weidong Chen
Grain Legume Genetics and Physiology Research Unit
Pullman, WA 99164


Last Modified: 5/2/2012