White Mold in Dry Bean

White mold occurs in most areas of the world where beans are grown, except the warm, humid tropics, and is often highly destructive. Crop losses may reach 100%.  The disease typically becomes serious in crops that have a dense canopy, in fields with a history of the disease, and in seasons when cool, moist conditions occur during and after flowering.

Symptoms

Infected flowers may develop a white, cottony appearance as mycelium grows on the surface.  Lesions on pods, leaves, branches, and stems are initially small, circular, dark green, and water-soaked but rapidly increase in size, may become slimy, and may eventually encompass and kill the entire organ. Under moist conditions, these lesions may also develop a white, cottony growth of external mycelium. Affected tissues dry out and bleach to a beige or white that contrasts with the normal light tan color of senescent tissue.  The epidermis easily sloughs off when the stem or pod is rubbed.  Cushions of white mycelium (immature sclerotia) develop into hard, black sclerotia in and on infected tissue. Entire branches or plants may be killed.

Causal Organism

White mold is caused by Sclerotinia sclerotiorum (Lib.) de Bary, an ascomycete fungus that infects over 400 plant species.  Mycelium is hyaline, septate, and branched.  Sclerotia are globose to C-shaped to cylindric (2-15 X 2-30 mm), depending on where they are formed in or on the plant, with a black outer rind and a white inner cortex. One or more apothecia may arise from a sclerotium. Apothecia are ocher to light tan in color.  The receptacle is 2-10 mm wide, flat to concave when young, and flat to convex at maturity; it tapers to form a stipe 1-2 mm wide and 3-30 mm long. Asci are cylindrical, have a thickened apex possessing a pore channel, and contain eight ascospores. Ascospores are 4-6 X 9-14 um, uniseriate, hyaline, ellipsoid, and biguttulate; and contain 2-4 nuclei. Eight to ten million ascospores may be produced from an apothecium. Microconidia are globose, hyaline, 2-4 um in diameter; produced from phialides in sporodochia, on hyphae, or from the surface of the hymenium or culture. The role of microconidia is not known and conidia are not produced. S. sclerotiorum is homothallic and exhibits clonality.

Disease Cycle and Epidemiology

Sclerotia may survive in soil for 5 or more years. Under suitable conditions of temperature, light, and moisture, sclerotia within 5 cm of the soil surface germinate to produce a stipe(s) which develops an apothecium(ia).  Ascospores are released from turgid asci, often simultaneously by "puffing”. Ascospores germinate and colonize flowers and other tissues that are senescing, and the mycelium from colonized tissues invades adjacent organs. Flower parts often fall onto pods, leaves, branches, and stems and provide nutrients required by the fungus to penetrate these organs.  Infected tissues are rapidly killed and become dry and bleached.  Limited spread of the fungus from one plant to another may occur by mycelial growth between tissues in contact.  Sclerotia form in or on infected tissues and may fall to the soil, remain in crop debris, or be removed with harvested seeds or pods. The fungus may continue to grow and cause disease in green beans in transit and in storage (nesting).

Sclerotia are preconditioned to produce apothecia by exposure to moist, cool (4°C) or freezing conditions for several weeks. To produce apothecia, preconditioned sclerotia require moist soil (water potentials greater than -5 bars) for 1 to several weeks at temperatures of 11-20°C.   Apothecia can produce ascospores for 5-10 days.  Apothecia generally do not develop or persist until a dense crop canopy has formed to provide a cool, moist microclimate.  Ascospores may be released by changes in relative humidity or by physical disturbance of the apothecium. Most ascospores produced within a field are deposited within the crop canopy.  Externally produced wind-blown ascospores may also contribute to limited infection in the bean crop.

Dissemination of the pathogen occurs by aerial transport of ascospores; irrigation water carrying mycelium, ascospores, and sclerotia; and infected or infested seed. The wide host range of the pathogen leads to widespread contamination of fields through crop or weed infection, and the subsequent production of sclerotia.

Ascospores can survive on plant surfaces for up to 2 weeks, and mycelium in infected blossoms may remain viable for a month. Disease develops from 5-30°C and most rapidly at 20-25°C, especially in the presence of moisture.

Control

Some bean cultivars and breeding lines, such as Ex Rico 23 and G122, are less susceptible than other cultivars, but immunity to white mold is not known in common bean. Resistance has been found in P. coccineus and is being transferred to P. vulgaris. Plants with an upright growth habit and an open architecture can avoid the disease.   

A fungicide spray, such as thiophanate-methyl, applied during the flowering period is another disease management strategy. However, disease control is difficult with dry edible beans where plants develop lush, viny growth and the flowering period extends over several weeks. Sprays applied before or after flowering are less effective.

Rotation with non-host crops, such as cereals and corn, may reduce disease by reducing the prevalence of initial inoculum. However, inoculum may be present from a previous host or be maintained on weeds, carried into the field by wind, irrigation water, or insects such as bees. The disease may be reduced by practices that reduce plant surface and soil moisture, and reduce canopy density.  Examples of these practices are planting rows parallel to the prevailing wind, avoiding excessive and late-season irrigation and excessive amounts of nitrogenous fertilizer, and using wide row spacing. Timely harvest, followed by rapid cooling and storage of healthy pods at 7-10°C, can provide simple and effective control of white mold in snap beans.  Coniothyrium minitans and other biological control agents provide possible future disease management strategies.

PHOTOS: Dr. Howard Schwartz, Colorado State University Plant Pathologist

Selected References

Boland, G. J., and Hall, R. 1987. Epidemiology of white mold of white bean in Ontario. Can. J. Plant Pathol. 9:218-224.

Boland, G. J. and Hall, R. 1994.  Index of plant hosts of Sclerotinia sclerotiorum. Can. J. Plant Pathol. 16:93-108.

Kohli, Y., Morrall, R. A. A., Anderson, J. B., and Kohn, L. M. 1992. Local and trans-Canadian clonal distribution of Sclerotinia sclerotiorum on canola. Phytopathology 82: 875-880.

Kohli, Y., Brunner, L. J., Yoell, H., Milgroom, M. G., Anderson, J. B., Morrall, R. A. A., and Kohn, L. M. 1995.  Clonal dispersal and spatial mixing in populations of the plant pathogenic fungus Sclerotinia sclerotiorum.  Mol. Ecol. 4: 69-77.

Morton, J. G., and Hall, R. 1989. Factors determining the efficacy of chemical control of white mold in white bean. Can. J. Plant Pathol. 11:297-302.

Proceedings of Sclerotinia 2001 – The XI International Sclerotinia Workshop, 8th–12th July 2001, York, England Central Science Laboratory.  192 pp. www.bspp.org.uk

Steadman, J. R. 1983. White mold-A serious yield-limiting disease of bean. Plant Dis. 67:346-350.

Tu, J.C. 1997.  An integrated control of white mold (Sclerotinia sclerotiorum) of beans with emphasis on recent advances in biological control. Bot. Bull. Acad. Sin. 38:73-76.

Willetts, H. J., and Wong, J. A.-L. 1980. The biology of Sclerotinia sclerotiorum, S. trifoliorum, and S. minor with emphasis on specific nomenclature. Bot. Rev. 46:101-165.

(Prepared by R. Hall and J. R. Steadman, Revised by J. R. Steadman and G. Boland)

SOURCE: 2004.  White Mold. Section in the Compendium of Bean Diseases, 2nd Edition, Edited by H. F. Schwartz, J. R. Steadman, R. Hall and R. Forster.  Amer. Phytopath. Society, St. Paul, MN.