Sclerotinia rot affects a wide range of plants particularly non-woody species. Sclerotinia rot is caused by S. sclerotiorum. Sclerotinia rot can affect plants at any stage of production including seedlings, mature plants and harvested products. Plants with senescing or dead tissue are particularly susceptible to infection.

Symptoms

The infected area of a plant initially takes on a dark green or brown water-soaked appearance, then may become paler in color. Dense white cottony mycelium usually develops and the plant begins to wilt and eventually dies. Resting or survival structures (sclerotia) are produced externally on affected plant parts and internally in stem pith cavities. The sclerotia are hard, black, irregular in shape, mostly 2-4 mm in size, and difficult to see once incorporated into the soil.

Disease sources and spread

The life-cycle of S. sclerotiorum includes both a soil-borne and an air-borne phase. Sclerotia of S. sclerotiorum can survive in the soil for ten years or more. They germinate to produce small funnel-shaped fruiting bodies (apothecia) that are approximately 1 cm in diameter. Apothecia produce air-borne spores, which can cause infection when they land on a susceptible host plant, either via flowers, or by direct germination on leaves. Occasionally, infection of stem bases can occur when fungal strands (mycelium) develop directly from Sclerotia near the surface. New sclerotia develop in infected plant tissue and when the plant dies they remain on the soil surface or may become incorporated during subsequent soil cultivation.

Conditions for Infection

After a period of cold conditions in winter, sclerotia, overwintering in the top 5 cm of the soil, germinate from spring onwards to produce apothecia, when soil temperatures are 10°C or higher and the soil is moist. Sclerotia do not germinate in dry soil or when the soil temperature is above 25°C. Sclerotia buried below 5 cm in the soil are less likely to germinate. Once apothecia are fully formed, spore release can occur in the light or dark but is temperature dependent, so tends to peak around midday. Apothecia can last about 20 days at 15 to 20°C but shrivel after less than 10 days at 25°C. For flowering herbs, spores landing on petals and stamens germinate rapidly (germination within 3-6 hours and infection within 24 hours) in optimum conditions of 15-25°C, continuous leaf wetness and high humidity within the crop. Subsequent infection of leaves and stems depends on petals falling and sticking on leaves. The risk of infection is increased if the leaves are wet because this causes more petals to stick. Infected dead or senescing petals provide nutrients for the invasion of the fungus into leaves and stems. For non-flowering herbs, infection is mainly by air-borne spores landing directly on leaves. Spores can survive on leaves for several weeks until conditions favorable for leaf infection occur. Spore germination and infection depend on the presence of nutrients on leaves, either from plant wounds or senescing plant material. As for flowering herbs, the optimum spore germination and infection conditions are 15-25°C with continuous leaf wetness and high humidity. Once plant infection has occurred, rapid disease progression is favoured by warm (15-20°C) and moist conditions in dense crops.

Sclerotinia Infection Model

Carpogenic germination of sclerotia is stimulated by periods of continuous soil moisture. Apothecia are formed on the soil surface from which ascospores are released into the air. Infection of most crop species is principally associated with ascospores but direct infection of healthy, intact plant tissue from germinating ascospores usually does not occur. Instead, infection of leaf and stem tissue of healthy plants results only when germinating ascospores colonize dead or senescing tissues, usually flower parts such as abscised petals, prior to the formation of infection structures and penetration. Myceliogenic germination of sclerotia at the soil surface can also result in the colonization of dead organic matter with subsequent infection of adjacent living plants. However, in some crops, for example sunflower myceliogenic germination of sclerotia can directly initiate the infection process of the roots and basal stem resulting in wilt. The stimulus for myceliogenic germination and infection in sunflower is not known but likely depends on nutritional signals in the rhizosphere derived from host plants.

The infection process
Infection of healthy tissue depends on the formation of an appressorium, which may be simple or complex in structure depending on the host surface. In most cases, penetration is directly through the cuticle and not through stomata. Appressoria develop from terminal dichotomous branching of hyphae growing on the host surface and consist of a pad of broad, multi-septate, short hyphae that are orientated perpendicular to the host surface to which they are attached by mucilage. Complex appressoria are often referred to as infection cushions. Although earlier workers considered penetration of the cuticle to be a purely mechanical process there is strong evidence from ultrastructural studies that enzymatic digestion of the cuticle also plays a role in the penetration process. Little is known about S. sclerotiorum cutinases, however, the genome encodes at least four cutinase-like enzymes (Hegedus unpublished). A large vesicle, formed at the appressorium tip prior to penetration, appears to be released into the host cuticle during penetration. After penetration of the cuticle, a subcuticular vesicle forms from which large hyphae fan outgrowing over and dissolving the subcuticular wall of the epidermis.

Infection by enzymatic degradation of the epidemic cells: Oxalic acid works in concern with cell wall degrading enzymes, such as polygalacturonase (PG), to bring about the destruction of host tissue by creating an environment conducive for PG attack on pectin in the middle lamella. This in turn releases low molecular weight derivatives that induce the expression of additional PG genes. Indeed, overall PG activity is induced by pectin or pectin-derived monosaccharides, such as galacturonic acid, and is repressed by the presence of glucose. Examination of the expression patterns of individual Sspg genes has revealed that the interplay among PGs and with the host during the various stages of infection is finely co-ordinated. (Dwayne D. Hegedus *, S. Roger Rimmer: Sclerotinia sclerotiorum: When ‘‘to be or not to be’’ a pathogen? FEMS Microbiology Letters 251 (2005) 177–184)

Looking for Climate Conditions for Infection of S. sclerotiorum has to take consideration of the apothecia formation, the sporulation, the direct infection by apothecia (even if it does not take place very frequently) and the infection from established mycelia by enzymatic degradation of the epidemic cells .

Apothecia formation and sporulation takes place if a rain of more than 8 mm is followed by a period of high relative humidity lasting longer than 20 hours at optimum temperature of 21°C to 26°C.

Direct Infection by Apothecia can be expected after a leaf wetness period followed by 16 hours of relative humidity higher than 90% under optimum 21°C to 26°C (“appressoria infection”). Whereas saprophytic growth followed by enzymatic degradation of the epidermic cells (“hydrolytic infection”) can be expected under a slightly lower relative humidity of 80% lasting for a period of 24 hours under optimum conditions of 21°C to 26°C.

Literature:

• Lumsden, R.D. (1976) Pectolytic enzymes of Sclerotinia sclerotiorum and their localization on infected bean. Can. J. Bot. 54,2630–2641.
• Tariq, V.N. and Jeffries, P. (1984) Appressorium formation by Sclerotinia sclerotiorum: scanning electron microscopy. Trans. Brit. Mycol. Soc. 82, 645–651.
• Boyle, C. (1921) Studies in the physiology of parasitism. VI. Infection by Sclerotinia libertiana. Ann. Bot. 35, 337–347.
• Abawi, G.S., Polach, F.J. and Molin, W.T. (1975) Infection of bean by ascospores of Whetzelinia sclerotiorum. Phytopathology 65, 673–678.
• Tariq, V.N. and Jeffries, P. (1986) Ultrastructure of penetration of Phaseolus spp. by Sclerotinia sclerotiorum. Can. J. Bot. 64, 2909– 2915.
• Marciano, P., Di Lenna, P. and Magro, P. (1983) Oxalic acid, cell wall degrading enzymes and pH in pathogenesis and their significance in the virulence of two Sclerotinia sclerotiorum isolates on sunflower. Physiol. Plant Pathol. 22, 339–345.
• Fraissinet-Tachet, L. and Fevre, M. (1996) Regulation by galacturonic acid of ppectinolytic enzyme production by Sclerotinia sclerotiorum. Curr. Microbiol. 33, 49–53.

Practical Use of the Sclerotinia Model

The White Leg Infection Model shows the periods when the formation of apothecia are expected. If these periods are consistent with the flowering period of rapeseed or canola we have to expect S. sclerotiorum infections during a moist period. The spores formed in the apothecia might be available for one to several days. The opportunity of infections is indicated by the calculation of the infection progress for direct or indirect infections by appressoria or enzymatic cell wall degradation. If the infection progress line reaches 100% an infection has to be assumed. These infections should be covered preventative or a fungicide with a curative action against S. sclerotiorum has to be used.