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White Mold
Phillip Wharton and William Kirk
Department of Plant Pathology, Michigan State University

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White mold, also called sclerotinia stem rot, is caused by the fungus Sclerotinia sclerotiorum (Lib.) de Bary. It is prevalent in the Pacific Northwest but in Michigan it is of secondary importance except in wet seasons or under excessive irrigation. The disease favors very moist conditions and is especially common in fields with overhead-irrigation such as by means of a center pivot. Agricultural practices that promote extensive canopy growth and keep relative humidity and free moisture in the crop canopy for extended periods of time and reduce wind movement, favor disease development.

Figure 1. White mold lesions (L) usually first appear on branches and stems in contact with the soil.  These become covered with a white cottony growth (arrows) and wilt. Figure 2. White mold lesions spread rapidly and can girdle stems causing foliage to wilt (arrows).

White mold symptoms first appear as water soaked lesions 14 to 20 days following row closure, depending on the cultivar and cultural practices. Lesions usually first appear in the intersections between the stem and branches, or on branches and stems in contact with the soil (Fig. 1). These become quickly covered with a white cottony growth that can spread rapidly to nearby stems and leaves if moisture is present for several hours. As lesions expand they can girdle stems causing foliage to wilt (Fig. 2). White mold is also often accompanied by bacterial stem rot, especially under wet conditions (Fig. 2). When conditions become dry, lesions dry out and turn beige, tan or bleached white in color and papery in appearance. As infected tissue decays, hard irregularly shaped resting structures called sclerotia form on the inside and outside of decaying tissue (Fig. 3). Sclerotia are usually to inch in diameter, start out white to cream in color and gradually turn black with age (Fig. 4). Stems are frequently hollowed out by the fungus leaving a papery shell to cover numerous sclerotia. Sclerotia eventually fall to the ground as infected stems dry out and the host plant dies. No stem rot symptoms are observed on below-ground tissues, i.e. roots, stolons or tubers.

Figure 3a.  As infected tissue decays, hard resting structures called sclerotia (S) form inside the decaying tissue. Figure 3b.  As infected tissue decays, hard resting structures called sclerotia (S) form outside the decaying tissue.

Disease cycle
White mold is caused by the soil-borne fungus Sclerotinia sclerotiorum. The pathogen causes disease in more than 400 different plant species. Host plants in Michigan include dry beans, soybeans, alfalfa, peppers and tomatoes, as well as some common weeds associated with potato production like lambsquarters, pigweed and nightshade. Sclerotinia sclerotiorum overwinters from one growing season to the next as sclerotia, but sclerotia can also survive in the soil for several years. Sclerotia require a conditioning period of cool temperatures before they can germinate, but these chilling requirements are easily met during Michigan winters.

Figure 4a. Sclerotia (S) are usually  to  inch in diameter and start out white to cream in color. Figure 4b. Sclerotia (S) are usually  to  inch in diameter and gradually turn black with age (b).

In late spring, sclerotia within 1 to 2 inches of the soil surface germinate when the crop canopy shades the ground, and soil moisture remains high for several days. After germination, small, pink to beige, flat to cup-shaped mushroom-like discs called apothecia are formed (Fig. 5). The fungus does not produce conidia (asexual spores), but ascospores (sexual spores) in the apothecia (Fig. 5). Ascospores are the primary source of inoculum in potato. Millions of ascospores (up to 8 million) are formed in each apothecium and under favorable conditions of temperature and humidity (cool, wet weather) they are forcibly ejected into the air (Fig. 5). Ascospores are dispersed by wind and air currents and can be spread throughout an entire field or to adjacent fields. Apothecia frequently occur in winter wheat fields that are cropped after potatoes, beans or another susceptible host and ascospores may be carried by wind currents from these fields to neighboring potato fields. In the Pacific Northwest, the peak period of ascospore release has been found to coincide with initial full bloom of potatoes. Ascospores are similar in size to pollen, and when being dispersed by air currents may be caught particularly well by potato blossoms. Potato blossoms and other plant parts such as petioles acquire ascospores while in/on the canopy. In high humidity and low air movement environments, ascospores germinate and infect these flowers and other contaminated plant parts as they senesce and drop to the ground or are trapped in the canopy. The fungus then grows out of the senescing tissues onto healthy stems and leaves in the lower parts of the canopy.

Figure 5. The disease cycle of the white mold pathogen Sclerotinia sclerotiorum.

When warm and dry soil conditions are not favorable for the production of apothecia and ascospores, sclerotia may germinated directly producing mycelia that grows and infects adjacent (about inch) plant tissues, occasionally affecting the crown area of potato plants early in the growing season. While mycelium from sclerotia can infect the crown area of potato stems, ascospores are unable to infect potato foliage or stems directly, even under ideal conditions. As the fungus colonizes healthy tissue it produces water soaked lesions with white cottony growth and sclerotia form in the decaying infected tissue as described above. The disease cycle is repeated when a susceptible host grows in close proximity to the sclerotia.

Monitoring and control
Effective management of white mold requires implementation of an integrated disease management approach. The disease can controlled primarily through the use of cultural practices and foliar fungicides.

Cultural control
Cultural practices, such as eradication of weed hosts and crop rotation with non-susceptible hosts like corn, or weak hosts such as small grains will help minimize sclerotinia rot in subsequent potato plantings. However, since Sclerotinia sclerotia can survive for several years in the soil it may be necessary to grow non-susceptible hosts in long rotations to reduce inoculum levels significantly. With these rotations, sclerotia will germinate, but the fungus will not have a suitable host to infect and will not be able to continue its life cycle. If a field has a history of white mold, avoid rotating into susceptible hosts such as dry beans, soybeans, alfalfa or canola.

Good fertility management to prevent excessive canopy development will also suppress white mold. As such, cultivars that naturally produce thicker, dense canopies are at higher risk of white mold, than those that produce sparser canopies.

Since this disease is favored by high humidity and free water in the crop canopy, proper irrigation management is a critical factor in dealing with potential white mold problems. Irrigation strategies that reduce humidity and free moisture in the canopy and allow the soil surface to dry will help decrease white mold. As such irrigating in cool cloudy weather should be avoided and irrigation should be timed to allow plants time to dry before nightfall. Cultural practices that help to prevent late blight disease development will also help in white mold management.

Biological control
Use of the biological control agent Conithirium minitans, a parasite of S. sclerotiorum sclerotia, to reduce the sclerotia bank in the soil has yielded conflicting results between the regions where the experiments were conducted. In Wisconsin, applications of C. minitans in bean fields have repeatedly reduced white mold incidence significantly on bean plants. Conversely, no reduction in apothecial numbers were observed in potato fields in the Columbia Basin of Washington State and hence disease incidence was not affected. Furthermore, the migration of ascospores generated from apothecia emerging in neighboring, and more distant fields, to potato fields seems to be more substantial in the Pacific Northwest than Wisconsin. Nevertheless, if applied prior to the planting of rotational crops susceptible to S. sclerotiorum, C. minitans is likely to reduce the in-field inoculum, especially if the applications are repeated over a number of seasons. However, the use of this biological control agent is not compatible with fumigation. Additionally, deep tillage and hilling of fields will re-distribute sclerotia across soil profiles, thus bringing to the top sclerotia that have not been exposed to the biological control agent. Therefore, it is essential to repeat the application of C. minitans over a number of years to reduce the sclerotia bank accumulated in the field. Even if a field is not intended for potato production, it may be of benefit to reduce the sclerotia bank in such a field, as ascospores are able to migrate to neighboring, and more distant, fields and result in high disease incidence.

Chemical control
The most widely cultivated commercial cultivars of potato are equally susceptible to Sclerotinia stem rot. In the absence of resistant cultivars, chemical control with fungicides remains the most effective management tactic. Effective fungicide products include Iprodione (a.i. iprodione), Botran (a.i. dichloran), Omega (a.i. fluazinam), Quadris (a.i. azoxystrobin), Topsin (a.i. thiophanate-methyl) and Endura (a.i. boscalid). Field, greenhouse and in-vitro experiments have shown that there are no significant differences in the effectivness of these compounds. Application of these fungicides at initial full bloom are effective in reducing the number of infected stems. However, application of the same fungicides made at or prior to row closure following label recommendations were found to offer erratic protection at best.

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© 2013, P.S. Wharton, Michigan State University.
Page Last Updated - 08 May 2013