Crop Knowledge Master Fungi

Sclerotinia sclerotiorum

pink rot, white mold, water soft rot (Plant Disease Pathogen)
Hosts Distribution Symptoms Biology Epidemiology Management Reference


Stephen A. Ferreira, Extension Plant Pathologist

Rebecca A. Boley, Educational Specialist

Department of Plant Pathology,CTAHR

University of Hawaii at Manoa


Sclerotinia sclerotiorum is among the most nonspecific, omnivorous, and successful of plant pathogens. Plants susceptible to this pathogen encompass 64 families, 225 genera, and 361 species (Purdy, 1979). Some hosts are: cabbage, common bean, citrus, celery, coriander, melon, squash, soybean, tomato, lettuce, and cucumber.

There are some solitary reports of S. sclerotiorum on passion fruit, kiwi, and banana (Japanese apricot and peach showed symptoms after artificial inoculation).


S. sclerotiorum is geographically cosmopolitan and has a broad ecological distribution, though it is most common in temperate regions. It was originally believed to occur only in cool, moist areas, but is now known to occur in hot, dry areas as well.


The life cycle of Sclerotinia spp. occurs mostly in the soil; consequently, most host symptoms begin at the soil surface, though the fungus can also be transported by air. While symptoms can and do differ among host species, there are a number of similarities. The more common symptoms are water-soaked spots on fruits, stems, leaves, or petioles which usually have an irregular shape. These spots enlarge and a cottony mycelium covers the affected area. The fungus spreads and the plant becomes a soft, slimy, water-soaked mass. The cottony mycelium usually produces numerous sclerotia, black seed-like reproductive structures, a reliable diagnostic sign of Sclerotinia (these usually do not form until after host death).

In contrast to the water-soaked symptoms, the host may exhibit "dry" lesions on the stalk, stems, or branches, with an obvious definition between healthy and diseased tissues. The lesions enlarge and girdle the plant part. Distal portions of the plant become yellow, then brown, then die. The girdled portion is often the base of the plant which causes the plant to die. Sclerotia form within the stem pith cavities, fruit cavities, or between tissues (i.e., bark and xylem). Hosts that may be infected include beans, cabbage, carrots, celery, cucumbers, lettuce, onions, peas, pumpkins, squash, tomatoes, and others.

Listed below are specific host symptoms.


Pods can become infected, while on the plant and postharvest.


S. sclerotiorum on celery is called pink rot because the rotted, watery area that develops on mature celery is usually pinkish in color. The fungus attacks the basal crown and petioles. Plants appear to suddenly wilt and collapse in the field.


Outer leaves are infected first, then the fungus moves inward. Leaves wilt and fall from the head in succession. The heart may remain erect, but becomes a wet, slimy mass. S. minor (lettuce drop) causes similar symptoms and is more common than S. sclerotiorum.


Related pathogens include: Sclerotinia libertiana and Whetzelinia sclerotiorum.

Species of the genus Sclerotinia can function either as soilborne or airborne pathogens. Infections of above ground plant parts occur when sclerotia germinate to produce apothecia which in turn release airborne ascospores), At the soil-line, infection may result from either ascospore or sclerotial infection, while below ground infections result from mycelium produced from sclerotia.

Approximately 90% of the life cycle of Sclerotinia species is spent in soil as sclerotia. At certain times of the year, depending on the inherent nature of the fungus and various environmental factors, the sclerotia germinate and form either mycelium which can infect a host, or an apothecium. Infection of host plants by mycelium can occur at or beneath the soil-line. Sclerotia germinate in the presence of exogenous nutrients and produce hyphae which invade nonliving organic matter, forming mycelium which then infects living host tissues. Penetration of the host cuticle is achieved by mechanical pressure. Mycelium infection is unlikely to infect plants located more than 2 cm from a sclerotium.

Carpogenic germination produces an apothecium which releases ascospores that disseminate by air. Generally, 10-20 C is the optimum temperature range for carpogenic germination. Under favorable conditions, including adequate moisture, ascospores germinate within 3-6 hours of release. In one study, apothecia collected from the field discharged ascospores continuously for seven days in the laboratory. Ascospores infect nonliving host tissues, germinate, and inundate the nonliving plant part with mycelium. Then, the fungus invades healthy plant tissues with mycelium. After the plant or plant part dies, sclerotia are formed either on or in the plant. The sclerotia return to the soil for a "resting" period (which can be weeks or years) before they become active, which requires the appropriate environmental conditions.

Sclerotia are the structures which allow species of Sclerotinia to survive for long periods of time under adverse conditions. The black, melanized rind appears to act as a protectant from invasion by microorganisms. Soil temperatures, pH, and moisture appear to have little direct effect on their survival, though the combination of high temperatures and high moisture appears to encourage the degradation of sclerotia near the soil surface.

Many microorganisms in the soil have a detrimental effect on sclerotia. Coniothyrium minitans and some Trichoderma spp. have been established as destructive mycoparasites of Sclerotinia spp. It appears that secretion of -1,3 glucanase from C. minitans (and possibly from some Trichoderma spp.) degrades and lyses sclerotial tissues.


Air-borne ascospores are the most important means of spread. Mycelium from sclerotia can also cause infection, but usually this mode of infection stays within an area. Moving contaminated soil (on farm equipment, shoes, infected seedlings) and fertilizing with manure from animals fed infected plant debris, are two common ways of spreading sclerotia or mycelium from place to place. Irrigation also has been shown to be involved in the spread of Sclerotia spp. from field to field. Irrigation transported sclerotia remained viable for at least 10-21 days in flowing water. In addition, seed may be an infective source, either from contaminating sclerotia or internal mycelium. However, support for this method of transmission is questionable.



Although potential for biological control exists, most reports are based on laboratory observations and little information is available on field situations. Coniothyrium minitans and Trichoderma spp. are the only parasites that have been studied to any extent, and are reported to be able to control S. sclerotiorum in sunflower fields effectively. It appears that secretion of -1,3 glucanase from C. minitans degrades and lyses sclerotial tissues. In one study, the first field trial provided good results, but subsequent trials gave poorer results due to low temperatures and unsatisfactory moisture conditions during the trial. Other fungi that have shown effectiveness against Sclerotinia in culture are: Gliocladium roseum, Trichothecium roseum, Fusarium spp., Mucor spp., Alternaria spp., Epicoccum spp., and Penicillium spp. However, the effectiveness of these fungi under natural conditions is uncertain.

Preventing the build up of humidity beneath and between the foliage of susceptible crops is one way to thwart infection. Wider row spacing of plants, use of wire trellis supports to raise foliage from the ground, and pruning of branches, are some ways to decrease humidity. Field trials using these methods are encouraging and control could be improved by using fungicides in combination with these practices.

Crop rotation is a necessary practice for minimizing many diseases. However, it is not an effective for control of Sclerotinia diseases because of the longevity of soil borne sclerotia. In addition, tilling generally assures the presence of sclerotia at or near the soil surface.

Resistant cultivars are essentially nonexistent, but there are people working towards that goal. Currently most work has been on beans and germ-plasm resistance.


Benomyl has been reported to control Sclerotinia diseases of sunflower, cabbage, and beans. Results suggest that plant coverage rather than systemic movement of benomyl is important for good control. Another study reported that benomyl provided good control for both aerial and basal infection of tomatoes at 100g/100L, but did not control disease development on cauliflower. When benomyl was applied at a rate of 50g/100L and 1% white oil was applied as well, control was similar to the 100g/100L. DCNA gave unsatisfactory control at commercial applications. In addition, a separate study found that benomyl's effectiveness is often diminished because of microbial degradation of the compound in soil. The fungicide thiram (TMTD), when applied with benomyl, delayed degradation. Thus, TMTD may prolong the effectiveness of benomyl in soil. A reduction in apothecial emergence as a result of the combined treatment was observed in the field.

Dicarboximide fungicides Roval (iprodione), Ronilan (vinclozolin), and procymidine (on celery) currently (1989) provide effective disease control on lettuce, peanuts, etc. There are mixed reports on the effectiveness of iprodione on celery. Some studies have reported reasonable control of Sclerotinia, but phytotoxic effects that cause the harvest to be downgraded have also been reported (when applied at 1g a.i./2 liters water/m2 initially, then five subsequent sprays at 750 g a.i./1500 liters water/ha at 14-day intervals). These fungicides appeared to control S. sclerotiorum largely by restricting the development of established lesions.

Unfortunately, in vitro development of resistance to these fungicides has been reported by some investigators. One study tested a number of fungicides for soil borne Sclerotinia control in order to demonstrate that other fungicides had good control potential similar to that of Roval and Ronilan. Lettuce plants at the 3-4 leaf stage were inoculated with sclerotia. Fungicide treatments were applied to the entire surface immediately and again 2-3 weeks later. Roval and Ronilan were consistently among the most effective, but others that provided equivalent disease control were CGA-449, SC-0858, SDS-65311, Bay HWG 1608, and Spotless.

Due to mechanical harvesting, post harvest damage of fruits occurs, which increases the chance for infection. Dipping the fruit in chemicals (heated dicloran or thiabendazole) has been recommended. Storage of produce in controlled atmospheres of oxygen and carbon dioxide at approximately 2 C has also been found to reduce wastage.


Abawi, G.S. and R.G. Grogan. 1979. Epidemiology of diseases caused by Sclerotinia species. Phytopathology 69:899-904.

Adams, P.B. and W.A. Ayers. 1979. Ecology of Sclerotinia species. Phytopathology 69:896-899.

Huang, H.C. 1985. Factors affecting myceliogenic germination of sclerotia of Sclerotinia sclerotiorum. Phytopathology 75:433-437.

MacNab, A.A., A.F. Sherf, and J.K. Springer. 1983. Identifying diseases of vegetables. The Pennsylvania State University, University Park, Pennsylvania. 62pp.

Mordue, J.E.M. and P. Holliday. 1976. Sclerotinia sclerotiorum. CMI descriptions of pathogenic fungi and bacteria. No. 513.

Purdy, L.H. 1979. Sclerotinia sclerotiorum: history, diseases and symptomatology, host range, geographic distribution, and impact. Phytopathology 69:875-880.

Steadman, J.R. 1979. Control of plant diseases caused by Sclerotinia species. Phytopathology 69: 904-907.

Yarden, O., Y. Ben-Yephet, J. Katan, and N. Aharonson. 1986. Fungicidal control of Sclerotinia sclerotiorum in soil with a combination of benomyl and thiram. Plant Disease 70:738-742.



APRIL 1992



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