Sclerotinia Stem Rot (SSR) impacts hundreds of plant species worldwide. This disease is caused by a widespread fungus that causes rapid decay in many economically important crops, including soybeans, canola, and sunflowers. Yield losses can be substantial for producers in affected regions. Understanding the progression of this disease is essential for protecting crops.
Identifying Sclerotinia Stem Rot
The initial signs of Sclerotinia Stem Rot often appear as small, water-soaked lesions near the nodes or where senescing flower petals have adhered to the stem. These lesions quickly expand, wrapping around the stem and turning pale gray or white as the fungus spreads. Since the fungus compromises the vascular system, the foliage above the infection point often wilts suddenly and prematurely, turning brown while the stem remains bleached.
A definitive sign is the appearance of fluffy, white, cottony growth, known as mycelium, on the surface of the infected stem during high humidity. This fungal colonization leads to the soft decay and shredding of the pith tissue inside the stem. The stem becomes hollowed out and brittle, making infected plants prone to lodging and collapse.
The most conclusive sign is the formation of hard, black, irregular resting structures called sclerotia. These structures develop both on the outside of the stem and internally within the hollowed cavity. Sclerotia resemble mouse droppings, ranging in size up to two centimeters, and serve as the primary survival mechanism for the fungus. Their presence confirms the infection cycle is complete and the pathogen is prepared for long-term dormancy.
The Pathogen’s Life Cycle and Spread
The fungus Sclerotinia sclerotiorum survives long-term primarily as sclerotia buried within the top few inches of the soil profile. These resting structures are resilient and can remain viable in the soil for several years, often lasting five to eight years. This extended dormancy allows the pathogen to persist even when non-host crops are grown, posing a constant inoculum threat to future susceptible crops.
Sclerotia germinate when conditions are favorable, typically involving soil temperatures between 50 and 68 degrees Fahrenheit (10–20°C) and continuous soil moisture for at least 10 days. Instead of infecting roots directly, the sclerotium undergoes carpogenic germination, producing small, tan or orange, cup-shaped structures called apothecia. The emergence of these apothecia, which look like tiny mushrooms, marks the beginning of the infectious phase above ground.
The apothecia release millions of microscopic, airborne spores known as ascospores into the crop canopy. These spores are carried by air currents and serve as the primary source of initial plant infection. Ascospores cannot penetrate healthy plant tissue; instead, they require a food source to establish infection.
Infection occurs when ascospores land on dead or senescing plant material, such as dropped flower petals lodged on the stem. The fungus colonizes this dead tissue first, using the nutrients to generate enzymes needed to breach the living plant stem. This dependence on petals means that the timing of flowering is the most vulnerable period for most susceptible crops.
Integrated Disease Management Strategies
Managing Sclerotinia Stem Rot begins with disrupting the sclerotia survival cycle through cultural practices like crop rotation and strategic tillage. A minimum rotation of three to five years with non-host crops, such as corn or small grains like wheat, is recommended to starve the fungus of susceptible hosts while the sclerotia naturally degrade over time.
While deep tillage can temporarily bury sclerotia below the depth from which apothecia can emerge, subsequent plowing can bring viable sclerotia back to the surface. Therefore, a consistent approach, whether deep burial or no-till, is more effective than alternating methods that redistribute the inoculum.
Canopy management is an indirect strategy for controlling the disease by altering the microclimate within the crop. Reducing planting density or using wider row spacing improves air circulation, which promotes faster drying of the plant surface and soil. Since apothecia germination and ascospore infection require prolonged periods of moisture, any practice that reduces canopy humidity makes the environment less conducive for fungal activity.
Chemical control relies entirely on preventative fungicide application, as the pathogen becomes shielded from topical treatments once it establishes inside the stem. Fungicides must be applied during the window when flower petals are being produced and are susceptible to ascospore colonization. This typically corresponds to the initial flowering stages, such as the R1 to R3 stages in soybeans or 10 to 50 percent bloom in canola.
Successful chemical management requires precise scouting and timely application within a few days of the optimal window to ensure the protective residue is present when the petals drop. Effective fungicidal products generally belong to the DMI (Demethylation Inhibitors) or SDHI (Succinate Dehydrogenase Inhibitors) chemical groups, which interfere with fungal cell growth and respiration.
These systemic products are absorbed by the plant and translocated to the susceptible tissues, providing a protective barrier against germinating ascospores. Growers utilize predictive models that factor in local weather data to optimize application timing. Resistance management is also necessary, requiring the rotation of different fungicide modes of action to maintain efficacy.
Sanitation practices, such as cleaning harvesting equipment when moving between fields, prevent the mechanical transfer of sclerotia to uninfested areas. Biological control agents, including certain strains of Coniothyrium minitans or Trichoderma species, are commercially available and can be applied to the soil. These beneficial fungi act as mycoparasites, directly attacking and degrading the sclerotia in the soil, thus reducing the pathogen’s long-term survival rate.