1 - General Sclerotinia Information
2 - Sclerotinia in Soybeans
3 - Sclerotinia in Dry Edible Beans
4 - Sclerotinia in Sunflower
5 - Sclerotinia Stem Rot in Canola
6 - Sclerotinia in Lentils
7 - Sclerotinia in Dry Peas
8 - Sclerotinia in Chick Peas
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
The primary survival (overwintering) structure ofS. 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.
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