Sclerotinia stem rot or white soybean mold is a disease. The cause of this disease is the fungus Sclerotinia Sclerotiorum. The disease can cause a significant reduction in yield or can even completely destroy the crop if you plant soybeans in contaminated soil and there is a dense vegetation cover with a long period of wet weather. Crop losses usually occur when the incidence rate is 15% or more. For many years in North Dakota, sclerotinia stem rot is a minor problem or a problem of medium importance for farmers, and the disease rarely occurs during the drought period.
Wet weather is a major factor in the development of the disease. It was a constant problem in soybean plantations with irrigation. In addition to reducing the yield of seeds, the disease also leads to a decrease in the quality of seeds and contamination of the seeds with black sclerotia of the fungus. Seed contamination can be a serious problem for the export, as it can lead to the rejection of the seed lot in foreign ports of entry. Moreover, sclerotia in the soil can affect other cultures in the rotation. Farmers can gain control over this disease only if they understand the pathogen and the cycle of the disease itself.
Symptoms usually are not obvious until the row spacing closes, creating a humid microclimate. Withering and drying out of leaves with subsequent death of plants is usually the first notable symptoms. A thorough examination under the canopy of the plant will demonstrate the growth of a white fluffy mycelium (fungal fiber) on stems, leaves or pods. Damage develops on the main stems and lateral branches. After all, the damages surround the stems, and the parts of the plants above are dying.
The stems seem discolored and sometimes fragment from a progressive lesion. Large black sclerotia of various shapes and sizes form from a white mycelium growing on plant tissue. Sclerotia also form in the core and have a characteristic cylindrical shape. Seeds in affected pods usually are shriveled and can be infected with a fungus, or absorbed by black sclerotia. Sclerotia usually infect seeds, when harvesting infected soybean plants.
The fungus has a wide range of “hosts” (which it can parasitize on), which includes more than 370 species of plants, and causes diseases in a wide variety of crops, such as: sunflower, dry beans, rape, potatoes, alfalfa, buckwheat, lupine, mustard, Jerusalem artichoke, safflower, lentils, flax, field peas and many vegetables. In North Dakota, this pathogen is rare, causing serious damage to some of these crops, such as for example, flax and potatoes. There are also many common broadleaf weeds that can be the “host” of this fungus, such as the late lactate (Iva Annua), Chenopodium album, Amaranthus spp., Canadian thistle, and wild mustard.
The fungus that causes white mold on soybeans is the same that causes white mold or sclerotinia disease of sunflower, dry beans, rape, and other crops. Sclerotinia Sclerotiorum hibernates predominantly in the form of sclerotia in the soil. Sclerotia sprouts, forming small brown mushrooms, called apothecia (1/8 to 1/4 inch in diameter). They produce spores called ascospores, which initiate diseases on soybeans and other susceptible crops.
Moisture and flowering are critical factors in the development of the disease. The disease usually does not occur until the plants close, as a dense dome promotes cool temperatures and a moist microclimate around the stems and maintains high soil moisture after rain or irrigation.
The onset of the disease is also close to flowering. After 7-14 days of high soil moisture, sclerotia germinate in the upper few inches of the soil, forming mushroom-shaped apothecia. One sclerotia can cause several apothecia. Apothecia will forcefully squeeze its ascospores into the air, where it transports by air currents to soybean plants.
The most important source of ascospores is apothecia in the field, but ascospores can transfer from neighboring fields. One apothecia can produce a huge amount of ascospores for several days. Ascospores survive for short period on plant tissue, but do not overwinter. Ascospores require an aqueous membrane and food base, such as dead or sensitizing floral tissues, to germinate and grow before infecting the plant.
Flower tissue is the most important food base for initiating infections. Infections often begin in the sinuses of the stem, where the decayed floral tissues have settled. Infections can also occur through damage caused by hail or other factors. Water on the surface of the plant contributes to the development of damage and increases the amount of tissue damage.
Development of the Disease
The initial development of the disease usually requires more than 40 hours of continuous moisture on the plant surface, but as soon as the disease begins, shorter periods of humidity will allow the lesion to develop. That’s why the disease is associated with prolonged periods of cloudy, wet, rainy weather. As the plant surface becomes dry, the progress of the disease slows down. Cold temperatures between 59 and 75 degrees Fahrenheit favor the development of the disease. The greater the density of the vegetation cover, the more favorable the environmental conditions are for the disease.
Sclerotia will form as the mycelium grows in the tissues of plants. This sclerotia will not germinate to form more apothecia during the season, but rather return to the soil during harvesting and tillage operations and will hibernate there to become an inoculant (a source of infectious fungus) for a future sensitive harvest. Sclerotia is a highly resistant structure that is long-lived in the soil.
In FieldClimate the model for sclerotinia is calculated depending on the rainy periods, relative humidity and temperature, as well as the moisture content of the leaves. During a prolonged period of wet weather, infection is recommended by creating an appressorium with a fungal pathogen. Another way of infection is “hydrolytic infection”. This base of this method is on the release of hydrolytic enzymes. They consistently destroy the plant membrane, the middle cell walls, the primary and secondary cell walls, and the entire plant.