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Sclerotinia Stem Rot

Sclerotinia stem rot or white mold of soybeans is a disease caused by the fungus Sclerotinia sclerotiorum.  The disease can cause major seed yield reductions or even completely destroy a crop when soybeans are planted in infested soil and there is a dense plant canopy with prolonged periods of wet weather. Yield losses usually occur when incidence of disease is 15 % or greater. In most years throughout North Dakota, Sclerotinia stem rot is only a minor to moderate problem for growers, and the disease is rarely observed during drought years. Wet weather is a major factor in disease development. It has been a persistent problem in irrigated soybeans. Besides seed yield reductions, the disease also results in reduced seed quality and seed contaminated with the black sclerotia of the fungus. Seed contamination can be a serious problem for exported seed since it may result in rejection of the seed lot at foreign ports of entry. Furthermore, sclerotia returned to the soil can affect other crops in the rotation. Sclerotinia stem rot can be managed by growers through an understanding of the pathogen and disease cycle.

Symptoms

Symptoms usually are not observed until the crop canopy between rows has closed, creating a humid microclimate. Wilting and withering of leaves followed by death of plants are usually the first symptoms observed. A close inspection under the plant canopy will reveal a cottony, white mycelial (fungus threads) growth on stems, leaves or pods . Lesions develop on main stems and side branches. Eventually, lesions girdle the stems and the plant parts above die. Stems appear bleached and sometimes shredded from advanced decay. Large, black sclerotia of varying shapes and sizes will form from the white mycelium growing on plant tissue. Sclerotia also form in the stem pith and have a characteristic cylindrical shape. Seeds in diseased pods are usually shriveled and may be infected by the fungus, or replaced by black sclerotia. The seed is usually contaminated with sclerotia when infected plants are harvested.

The Pathogen

The fungus 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 (rapeseed), potato, alfalfa, buckwheat, lupine, mustard, Jerusalem artichoke, safflower, lentil, flax, field peas and many vegetables. In North Dakota it is rare to find this pathogen causing serious damage on some of these crops such as flax and potato. There are also many common broadleaf weed hosts such as marsh elder, lambsquarter, pigweed, Canada thistle and wild mustard. The fungus that causes white mold on soybean is the same one that causes white mold or Sclerotinia disease of sunflower, dry beans, canola, and other crops. Sclerotinia sclerotiorum overwinters principally as sclerotia in soil. The sclerotia germinate to form small tan to brown mushrooms called apothecia (about one-eighth to one-fourth inch in diameter) . These produce spores termed ascospores which initiate the disease on soybean and other susceptible crops.

Disease Cycle

Moisture and flowering are critical factors in disease development. Disease usually does not occur before the closing of the crop canopy, because a dense canopy promotes cool temperatures and a humid microclimate around the stems and maintains high soil moisture following rain or irrigation. Initiation of disease is also closely associated with flowering. Following seven to 14 days of high soil moisture, sclerotia within the upper several inches of soil will germinate to form the mushroom-like apothecia. A single sclerotium can produce several apothecia. The apothecia will forcibly eject their ascospores into the air where they will be carried by air currents to soybean plants. The most important source of ascospores is from apothecia produced within the field, but ascospores can blow in from adjacent or nearby fields. One apothecium can produce enormous quantities of ascospores over several days. Ascospores survive for short periods on plant tissue but do not overwinter. Ascospores require a film of water and a food base such as dead or senescing flower tissues to germinate and grow before they infect the plant. Flower tissue is the most important food base for initiating infections. Often infections will start in stem axils where senescing flower tissues have fallen and lodged. Infections may also occur through wounds caused by hail or other injury. A film of water on the plant surface promotes development of lesions and increases the amount of tissue damage. Initial disease development generally requires greater than 40 hours of continuous plant surface wetness, but once disease is started, shorter periods of wetness will allow lesion development. This is the reason disease is associated with lengthy periods of cloudy, humid, rainy weather. As plant surfaces dry, the progress of disease is slowed. Cool temperatures between 59 and 75 degrees Fahrenheit favor disease development. The greater the density of the plant canopy the more favorable the environmental conditions are for disease. Solid seeded soybeans and lodged crops are therefore more prone to disease development. Sclerotia will be formed as the mycelium grows in and on the plant tissues. These sclerotia will not germinate to form more apothecia during the season, but rather will be returned to the soil during harvest and tillage operations and will over-winter to become inoculum (source of infective fungus) for a future susceptible crop. Sclerotia are highly resistant structures and survive for long periods in soil.

Quelle: http://www.ndsu.edu_pubweb_bernelso_soydiseases_sclerotinia.shtml_REAL_LT_p_REAL_GT_
Quelle: http://www.ndsu.edu/pubweb/~bernelso/soydiseases/sclerotinia.shtml

Sclerotinia SteamRot In FieldClimate the model for Sclerotinia is calculated in dependence of a rainy periods, the relative humidity and temperature as well as leaf wetness. During long wet periodes an infection through the establishing of an appressorium by the fungal pathogen is recommended. Another way of infection is called "hydrolytic infection". This way is based on the release of hydrolytic enzymes that sequentially degrade the plant cuticle, middle lamellae, and primary and secondary cell walls and entire the plant. Model described in detail on this page.