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Review

A Comprehensive Review of White Rot Caused by Sclerotinia sclerotiorum: Pathogenicity, Epidemiology and Management

by
Zoltán András Boldizsár
*,
Levente Vörös
,
Wogene Solomon Kabato
,
Gábor Kukorelli
and
Zoltán Molnár
Albert Kázmér Faculty of Agricultural and Food Sciences, Széchenyi István University, Vár Square 2, 9200 Mosonmagyaróvár, Hungary
*
Author to whom correspondence should be addressed.
Agronomy 2026, 16(7), 688; https://doi.org/10.3390/agronomy16070688
Submission received: 17 February 2026 / Revised: 19 March 2026 / Accepted: 23 March 2026 / Published: 25 March 2026
(This article belongs to the Section Pest and Disease Management)
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Abstract

White mold caused by Sclerotinia sclerotiorum (Lib.) de Bary continues to threaten yield and quality and remains a stubborn, sometimes unpredictable constraint in many cropping systems. The pathogen’s broad host range and its capacity to persist for years as sclerotia mean that fields can carry risk long after visible symptoms fade. Disease development is often driven by short windows of favorable temperature and moisture that promote germination and ascospore release and dispersal, while myceliogenic infection from soil-borne sclerotia can also initiate disease directly. Yet dependable control is still undermined by durable inoculum, limited stable host resistance, variable biocontrol performance, and shrinking chemical options together with fungicide resistance risk. Here we consolidate current understanding and ongoing uncertainties around sclerotial formation and germination cues, the environmental drivers that shape epidemic onset, and the processes governing host colonization, including the roles of cell wall-degrading enzymes, oxalic acid, and redox regulation, as well as the continuing debate over necrotrophic versus hemibiotrophic phases. Management is considered from a practical perspective, covering cultural risk reduction, forecasting-guided fungicide programmes supported by resistance-management principles, and biological control strategies targeting sclerotia. Across systems, the evidence points to the same lesson: single tactics rarely remain reliable under field variability, whereas integrated packages that reduce soil inoculum and align interventions with risk are more durable. Future priorities include resolving early infection events, improving prediction of carpogenic germination under changing climates, increasing the consistency of biocontrol, and accelerating resistance breeding supported by genomic resources.

1. Introduction

White mold (white mould; Sclerotinia stem rot) caused by Sclerotinia sclerotiorum (Lib.) de Bary is a globally distributed and economically important disease across numerous crops. The pathogen is highly polyphagous, with reported infection on more than 400 plant species, including major hosts in Brassicaceae, Fabaceae, Solanaceae, Asteraceae and Apiaceae [1,2,3]. Beyond dicotyledonous crops, asymptomatic or endophytic growth has also been reported in several monocots [4], underlining the ecological breadth of the pathosystem [5]. Despite extensive research, severe outbreaks still occur and control outcomes remain inconsistent between seasons, regions and cropping systems [6].
A major reason for this persistence is the pathogen’s capacity to survive for years as melanised sclerotia in soil and plant residues, allowing disease risk to remain silent and then rapidly increase under favourable conditions [3,7]. Sclerotia support two epidemiologically distinct infection routes. Myceliogenic germination enables direct infection from soil-borne sclerotia [8], whereas carpogenic germination leads to apothecia formation and airborne ascospore release, which can drive canopy epidemics [9]. Epidemic development is often governed by short windows of conducive temperature and moisture, which makes prediction and timely intervention challenging in practice [10]. Importantly, ascospores typically require senescent or dead tissues as an initial substrate and generally do not infect healthy tissues directly; early saprotrophic colonisation can precede invasion of living host tissue [11]. Consequently, disease risk is shaped by the interaction of inoculum, crop phenology, canopy microclimate and transient wetness periods rather than by host presence alone.
Environmental regulation further contributes to variability. Temperature, soil moisture and pH influence vegetative growth, sclerotial development and the likelihood of carpogenic events [10,12]. Mechanistically, pH signaling has been linked to both development and virulence through regulatory pathways [13,14], and later work further supported relationships between environmental pH, sclerotial development and pathogenicity [15]. These interacting drivers help explain why management that performs well in one season or location may fail in another.
At the host–pathogen interface, S. sclerotiorum deploys multiple factors associated with tissue maceration and symptom development. Cell wall-degrading enzymes and other secreted components contribute to colonisation [16], while oxalic acid and redox-associated processes are central to disease progression and host manipulation [17,18,19]. Penetration commonly involves specialised infection structures such as appressoria and infection cushions, and establishment can be favoured by nutrient availability from flowers or other senescing tissues [20,21]. Although the interaction is often framed as necrotrophic, the timing and interpretation of early infection events remain debated, with implications for how we conceptualise colonisation phases and prioritise resistance targets [21,22].
From a management perspective, durable suppression is difficult because single tactics rarely remain reliable under field variability. Chemical control can be effective when well timed, yet performance depends strongly on canopy conditions and weather, and repeated reliance on limited modes of action increases resistance risk while regulatory pressure may further narrow available options [6,23,24]. Biological control, particularly approaches targeting sclerotia in soil, is attractive for inoculum reduction but can be inconsistent across field conditions [9,25,26]. These constraints support integrated strategies that combine agronomic risk reduction with chemical and biological tools aligned to epidemiological risk [6,23].
Recent reviews have provided valuable insights on S. sclerotiorum focusing on topics such as synthesis of virulence determinants and secreted effectors, the schizotrophic/endophytic lifestyle concept, sustainable management and resistance breeding advances [27,28,29,30]. Building on these advances, the present review focuses on the epidemic pathway and the practical decision points that determine field outcomes across crops and production contexts, linking epidemiological risk windows to the strengths and limitations of available management tools. We further address why field performance of biological control agents often remains inconsistent despite strong laboratory efficacy, and we connect current debates in infection biology with forecasting-guided, resistance-managed interventions to support integrated pest management. The aim of this review is to synthesise current knowledge while emphasising the biological, ecological and management complexity that underpins variable disease outcomes. We link life-cycle biology and inoculum persistence with environmental drivers of epidemic onset, summarise mechanistic insights into host colonisation and symptom development, and evaluate management options that integrate cultural, chemical and biological measures under resistance-management and risk-based decision making. By connecting these themes, we seek to clarify why white mold remains a critical challenge despite extensive research and to identify the most tractable knowledge gaps for future work.

2. Economic Importance and Global Impact

White mold is an extremely destructive disease that can cause substantial yield losses. Infected plant parts may become completely unmarketable, and the thousand-seed weight and oil content of oilseed crops often decrease, resulting in serious economic losses [6]. Depending on the geographic location and the crop, yield losses can reach 80% [31]. In soybeans, the incidence of the disease clearly correlates with the magnitude of yield loss—an increase of 10% in incidence may result in yield losses of up to 260 kg/ha in certain cultivars—and the quality parameters of the harvested product, such as thousand-seed weight, protein content and oil content, can also decline [32]. Similar trends have been reported in several studies on oilseed rape: for each 1% increase in white mold incidence, yield decreases by an average of 13.13 kg/ha [33]. In sunflowers, average losses may be around 10–20%, but yield losses of 50–100% can also occur during epidemics [34]. Due to this variability, the disease has a particularly significant impact in regions where large areas of susceptible crops are grown and there are frequent periods of a conducive canopy microclimate.
White mold is found all over the world and has been reported in major temperate production regions. In practice, it is most economically relevant in countries where susceptible broadleaf crops are grown and where flowering-stage conditions regularly favor ascospore-driven epidemics. In North America, the disease has been repeatedly reported as one of the most important constraints on soybean production in major producing areas, including the United States and Canada [35]. In South America, extensive multi-season field datasets from Brazil further highlight the prevalence of white mold pressure in soybean systems and the context-dependent nature of control outcomes [36]. In Europe, S. sclerotiorum remains a significant pathogen of oilseed rape in key production areas, while in Australia inoculum is now widespread in canola regions and can cause substantial losses under favorable conditions [37].
From a food security and sustainable agriculture perspective, white mold is particularly relevant because it affects major oilseed and protein crops and can generate substantial, recurrent production shocks that reduce harvested output and compromise quality across seasons. In soybean systems, for example, estimated yield losses attributed to S. sclerotiorum were reported to total approximately USD 5.5 billion (without inflation adjustment) between 1996 and 2023, highlighting the scale at which this disease can influence supply and profitability in key protein chains [38]. Recent syntheses also emphasise that the sporadic but severe nature of outbreaks can indirectly increase input intensity, yet sustainable management requires integrated, risk-based packages that reduce excessive pesticide use while maintaining effective control. In oilseed rape, decision-support developments that identify high- and low-risk windows for fungicide application have been shown to reduce unnecessary treatments while maintaining control, supporting more sustainable production systems under variable epidemic pressure [39].

3. Symptomatology and Diagnostics

S. sclerotiorum is an aggressive pathogen that can rapidly induce necrosis, the death of cells and tissues, in plants. The fungus produces numerous enzymes, including endo- and exo-pectinases, cellulases, hemicellulases and proteases, which facilitate its colonisation of the host and the rapid degradation of the cell wall [16]. In addition to cell wall-degrading enzymes (CWDEs), oxalic acid (OA) production also plays a key role in infection [13]. Proteins secreted by the pathogen also play a fundamental role in initiating infection. Following infection, a sequence of regulated events leads to ‘programmed cell death’ in the infected parts of the host plant. Many studies have focused on the mechanisms that S. sclerotiorum uses to infect host plants. A precise understanding of these processes could contribute significantly to the development of improved control strategies.
The timing of identification of the pathogen is critical for managing and preventing the disease it causes. Diseases are primarily diagnosed based on the symptoms induced by the pathogen. As S. sclerotiorum infects a wide range of plant species, the symptoms are largely similar across different hosts. The dense, cottony, white mycelium is easily identifiable and is most often observed on infected plant parts, particularly under wet, humid conditions. In the early stages of infection, water-soaked lesions can be observed, which become progressively paler and necrotic over time, often showing concentric ring patterns before the development of a mycelial coating [40]. White mycelial masses and the hard-walled survival structures formed from them, the sclerotia, are frequently present within the tissues [41].
As with other host plants, symptoms of infection in sunflowers (Helianthus annuus) may occur in several forms and appear at different plant parts at different crop growth stages. For example, infection at the stem base can cause sudden wilting before or during flowering. Throughout the growing season, symptoms can develop on any part of the stem at any time, but most frequently towards the middle to end of the season [42]. The pathogen can also infect the inflorescence and the head as well. In this case, the head develops patchy, water-soaked rot and subsequently disintegrates. Large sclerotia, up to several centimeters in size, form within it and, as they coalesce around the seeds, create a lattice-like black structure [42].
In oilseed rape (Brassica napus), it causes greyish-white lesions to appear on the stem and/or pods. Hard, black sclerotia typically form within the stem. Infected plants are prone to lodging, which complicates harvesting and contributes to yield losses [6]. Representative symptoms and structures are shown in Figure 1.
Sclerotia that develop within plant tissues can vary in shape, but are generally rounded. They can range in size from 2 mm to 2 cm [43].
Colonies grown on PDA (Potato Dextrose Agar) rapidly expand to form white, cottony aerial mycelia. At the expanding edges of the colonies, sclerotia form radiating lines and concentric rings, and the hyphae are hyaline, branched and multinucleate [44]. A sclerotium produces one or multiple tan-to-amber apothecia; apothecial asci are cylindrical and contain eight unicellular, hyaline, elliptical ascospores, typically 9–14 µm × 3–6 µm [45].
Beyond symptom observation and culture-based identification, molecular assays are increasingly being used to confirm the presence of S. sclerotiorum and qualify inoculum in plant samples. Quantitative PCR assays have been developed to detect and measure pathogen DNA from infected tissues. When combined with crop stage and weather conditions, these assays support early assessment of infection pressure and enable risk-based decisions [46]. Isothermal amplification approaches such as loop-mediated isothermal amplification (LAMP) provide rapid detection with minimal equipment and have been validated for S. sclerotiorum in fungal cultures and plant/soil DNA extracts. This makes them a practical option for faster confirmation outside of specialized laboratories [47].
Innovative sensor-based methods are also being explored to enable earlier, non-destructive detection and spatial localization of infection. Hyperspectral imaging has been used to identify S. sclerotiorum infection in oilseed rape tissue using chemometric or machine learning classification. This demonstrates the potential to distinguish between healthy and infected tissue before symptoms become visually apparent under controlled imaging conditions [48,49].

4. Pathogen Biology and Life Cycle

Although the primary inoculum originates from sclerotia, epidemics are not strictly monocyclic, because carpogenic germination can produce apothecia and release ascospores repeatedly under favourable conditions. The sclerotium is the starting element of its life cycle and can remain viable for a long period. Sclerotia can germinate in two ways: myceliogenically (directly) or carpogenically (indirectly). The two infection routes and key life-cycle transitions are summarized in Figure 2. Myceliogenic germination is stimulated by exudates produced by plant roots. This infection route is commonly referred to as primary infection. In the soil, the mycelium directly infects plant roots and the stem base. This leads to wilting, plant death, and consequently, yield loss [8].
In the case of carpogenic germination, infection is initiated by ascospores that are released from apothecia, which develop from sclerotia. Regardless of their size, sclerotia can undergo carpogenic germination over multiple years, and can form apothecia during the process. Each apothecium produces a large number of asci, each of which contains eight ascospores. Once these ascospores are discharged into the air, they can infect the above-ground parts of cultivated plants [9]. Ascospores deposited on flowers may germinate in response to the stimulatory effect of sugary floral exudates. Subsequent colonisation of the inflorescence leads to its destruction. Beyond the inflorescence, the pathogen can also infect the leaves, spreading to the petiole and then to the stem. This causes the most characteristic symptom: stem rot. Under favourable conditions, the pathogen can spread from the initial infection site to other parts of the plant, and then to uninfected plants. Ascospores are unable to infect healthy tissues directly. In order to germinate and penetrate the host plant, they must first colonise dead or senescent plant tissues saprotrophically. Only then can they infect healthy tissue [11]. In practice, this occurs when the pathogen initially colonises senescing, damaged or detached leaves and/or inflorescences that remain in direct contact with healthy plant parts.
As mentioned above, this pathogen can also infect via the mycelium on the soil surface or a few centimeters below it. The growing hyphae colonise dead organic matter in a saprotrophic manner and then infect living plant tissues [21].
The life cycle concludes with the formation of sclerotia, which, as mentioned above, remain viable even under adverse conditions. A sclerotium consists of three clearly distinguishable parts that confer high resilience:
  • The thick, hard outer black rind contains large amounts of melanin, which plays an important protective role against external environmental factors. Melanin can also influence the virulence of certain pathogens; however, there is currently no scientific evidence to support this for S. sclerotiorum [50].
  • The middle layer (the cortex) contains fewer pigmented cells and maintains connectivity between the outer and inner layers. It also serves a storage function [7].
  • The medulla is the innermost, lighter-coloured layer, composed of thin-walled cells forming loose tissue. Its primary function is to store nutrients, and the processes of germination originate from there [3].
Three main phases can be identified in the formation of a sclerotium. First, hyphae aggregate to form a white sclerotial mass. In the second stage, these foci enlarge. The third and final stage is maturation (or ageing), during which melanin is produced in the outer layer and the survival structure hardens.

5. Environmental and Climatic Drivers of Disease Development

The formation of sclerotia is influenced by several external and environmental factors, including the quantity and quality of available nutrients, and primary metabolic processes. However, sclerotia primarily form when mycelial growth is constrained for some reason [43].
The most favourable nutrients for sclerotial formation are glucose, yeast extract, peptone, ascorbic acid and casein. Media supplemented with calcium and sodium may also be suitable for this process. The environmental temperature has a strong influence on sclerotial development: 20 °C is considered optimal, whereas formation is more limited above 25 °C and below 20 °C [51].
Temperature is also critically important for infection. It is a key factor in determining which crops are affected and at what stage of development the disease emerges [10].
pH also significantly affects sclerotial formation and growth. Sclerotial development is slightly inhibited under neutral or alkaline conditions; the most favourable range is acidic (pH 4–5.5) [12]. The accumulation of OA produced by the fungus lowers the pH of the environment, thereby promoting the formation of survival structures [13]. Consistent with this, studies have shown that S. sclerotiorum mutants deficient in OA do not form sclerotia in vitro and are unable to infect plants [14]. Furthermore, lowering the environmental pH does not restore sclerotial formation in these mutants, indicating that pH alone is not a determining factor in pathogenicity.
Field soil conditions determine whether S. sclerotiorum persists as a practical threat by influencing both sclerotial survival and carpogenic potential. The soil moisture regime, texture and organic matter content affect the sclerotia, while soil microbial communities can reduce the viable inoculum over time through antagonism, competition and parasitism [6,52]. The physical placement of sclerotia within the soil affects the emergence of apothecia, because carpogenic germination and successful apothecia formation generally require sclerotia to be located close to the soil surface. Therefore deeper burial can limit emergence [53,54]. These soil effects can help to explain why disease pressure can differ between fields that have had similar cropping histories, but have different soil structure, moisture dynamics and tillage regimes.
Humidity and canopy microclimate are equally important factors in the initiation and spread of epidemics during the growing season. High relative humidity and prolonged leaf wetness within dense canopies promote ascospore germination and early saprotrophic establishment on flowers and other senescing tissues, prior to the invasion of healthy tissue [6,29]. Short moisture-favourable periods around flowering and canopy closure often determine whether epidemics develop and how rapidly lesions expand. This contributes to sporadic but severe outbreaks and inconsistent outcomes [29].

6. The Infection Mechanisms of the Pathogen

We define S. sclerotiorum as a necrotrophic pathogen; however, recent studies suggest that it is actually a hemibiotrophic pathogen. During the initial phase of infection, after crossing the cuticle, necrosis of the infected tissue does not begin immediately. Instead, the pathogen develops biotrophically in the apoplastic space before necrosis is initiated. Therefore, infection proceeds in two distinct phases, whereby the pathogen bypasses the host’s defence mechanisms prior to killing host cells [22]. Beyond the necrotrophy–hemibiotroph dichotomy, the recently proposed schizotrophic framework suggests, that S. sclerotiorum may adopt different interaction modes depending on the host and environmental context. This offers a useful way of reconciling seemingly conflicting infection models [28]. A schematic representation of the proposed two-phase infection process of S. sclerotiorum within host tissues is shown in Figure 3.
The conversion of hyphae into appressoria is essential for establishing an infection in healthy tissue. Hyphae can develop from either sclerotia or ascospores produced in apothecia, but in all cases the presence of external nutrients is required—primarily flowers or other senescing tissues [20]. Depending on the characteristics of the host plant surface, the fungus may form simpler or more complex appressoria. Simple appressoria are formed when branching develops at the tip of hyphae growing on the host surface. These structures are short and often branched further, attaching perpendicularly to the host surface via mucilage [21].
Complex appressoria, or infection cushions, develop from a single hyphal tip. This process involves several stages, including the swelling of the mycelium, slowed growth and the formation of new mycelium branches. The result is a dense, cushion-like structure that facilitates fungal penetration into host tissues [55] and supports adhesion to the host surface [56]. Previous studies have demonstrated that these infection cushions facilitate the breach of the host’s outer protective layer through mechanical pressure and/or the secretion of cell wall-degrading enzymes if a compatible interaction is established between the fungus and the host plant [20].
When an incompatible interaction occurs between the fungus and the host plant, one of the plant’s most important defense strategies is to prevent the formation of infection cushions. This inhibits the penetration and spread of S. sclerotiorum within the plant’s tissues, highlighting the crucial role of infection cushions in establishing an infection. The hyphae that form the cushions are usually flatter and thicker. Thin, needle-like formations develop from these structures, which penetrate the host tissues only beneath the infection cushion or the complex appressorium [57].
In complex appressoria, the hyphal tips are densely organised. These individual hyphal ends initiate independent penetration attempts towards the host plant. The concentration of multiple hyphal tips at a single site increases the local accumulation of toxins, hydrolytic enzymes and defence-suppressing compounds, as opposed to simple appressoria [22]. Penetration pegs that develop from appressoria can breach the cuticular layer through a combination of mechanical pressure and enzymatic degradation. However, these pegs alone cannot penetrate deeply enough to reach the epidermal cells beneath them [18].
Bulbous and multilobed vesicles develop from the penetration pegs, producing subcuticular infectious hyphae. These hyphae spread horizontally beneath the cuticle, driving the progression of infection [22]. The subcuticular hyphae of S. sclerotiorum can traverse multiple cell layers before killing the epidermal cells [58]. This indicates that a transient biotrophic lifestyle is established during the early stage of infection, beginning approximately 12–24 h after infection [19].
During the initial phase of infection, the pathogen evades or suppresses the host plant’s defenses through physical and chemical means. The activation of specific S. sclerotiorum genes blocks the host immune response, preventing recognition of the pathogen [59]. This early biotroph-like stage is crucial for subsequent necrotrophic development.
Smaller branches form from the hyphae growing subcuticular, which then penetrate the epidermal and mesophyll layers [22]. Following the successful spread of these secondary hyphae, S. sclerotiorum transitions to a necrotrophic phase [59], during which large amounts of reactive oxygen species (ROS), toxins and CWDEs are produced. These compounds rapidly destroy the epidermal cell wall, resulting in necrotic symptoms becoming apparent [17,19,60].
Recent syntheses emphasise that the virulence of S. sclerotiorum is driven by a coordinated suite of factors rather than by any single determinant. These factors include OA, CWDEs activity (pectin-degrading enzymes such as polygalacturonases) and an expanding repertoire of secreted proteins that modulate host immunity and cell death pathways [27].
Functionally characterized effectors now provide concrete examples of these strategies. For example, SsCVNH (S. sclerotiorum cyanovirin-N homologue) promotes virulence by targeting host’s redox-related defences (class III peroxidase AtPRX71) while SsPEIE1 (S. sclerotiorum Plant Early Immunosuppressive Effector 1) suppresses host immunity via HIR-associated processes. More recently, SsCm1 originally annotated as a chorismate mutase-related effector but shown to lack chorismate mutase activity, was found to stabilize MORF2 and interfere with chloroplast-linked immunity illustrating how effectors can adjust growth–defense trade-offs during infection [61,62,63].
Of the various virulence factors, the relationship between the production of OA and the development of white mold is a key focus of current research [64]. The pathogen can modify the pH of its surroundings by acidifying the local environment. As previously mentioned, this trait is closely linked to infectivity, as OA-deficient mutants are unable to infect or exhibit reduced virulence [15]. However, strains with limited OA production can still infect the host to some extent. This suggests that OA primarily functions as a colonisation-promoting factor rather than being an indispensable prerequisite for infection.
When considered in isolation, OA is not directly toxic to plant cells. Instead, it plays a far more nuanced role in pathogenesis by modulating host physiology in ways that create favourable conditions for the growth of S. sclerotiorum [65]. OA influences multiple host processes, including promoting cell wall degradation by enhancing polygalacturonase activity, inhibiting plant defence enzymes, suppressing the oxidative burst, disrupting the regulation of stomatal guard cell closure, mediating pH signalling, inducing apoptosis-like cell death and altering the redox status of plant cells [66,67,68]. The production of OA and the subsequent acidification are consistent with the infection strategy of S. sclerotiorum, as reducing the apoplastic pH to levels that are favourable for the pathogen weakens the cell wall and facilitates enzymatic breakdown [69].
Previous findings clearly indicate that S. sclerotiorum uses OA to induce programmed cell death. The first step in this process involves the fungus establishing a reducing environment in the host cell. This neutralises the host’s defence responses, inhibits the oxidative burst and prepares the infection site. During the early stages of infection, the fungus suppresses the host’s defence mechanisms by promoting the accumulation of ROS and the deposition of callose in host tissues. At the same time, the fungus absorbs calcium ions (Ca2+), which are released during cell wall collapse. This protects fungal hyphal development from excessively high Ca2+ concentrations [70].
In the later stages of infection, OA suppresses the activity of antioxidant enzymes, stimulates the production of ROS and damages host cell membranes [71]. Given this, it can be concluded that OA supports the success of S. sclerotiorum infection at multiple points.
Taken together, the high-resolution infection timelines and transcriptomic and cytological evidence support a model in which S. sclerotiorum can pass through an early asymptomatic or biotroph-like phase before necrotic expansion. The broader schizotrophic framework highlights that infection can shift in response to the host and environmental context [19,22,28,65,66].
Similarly, the most consistent interpretation of the OA literature is stage-dependent: OA enhances colonization efficiency by shaping pH and redox conditions as well as modulating host cell death. However, its apparent indispensable nature varies with infection context and experimental system. The practical implication is that variability at field-level is to be expected unless management aligns interventions with the narrow risk windows when establishment on senescent substrates transitions to invasion of living tissues. Resolving these timing and context dependencies remains a key knowledge gap for both forecasting and achieving long-term control [14,15,18,27,69,72,73].

7. Management and Control Strategies

To successfully control the pathogen, it is important to consider the key processes in its life cycle. These include reducing baseline soil inoculum, preventing establishment during the growing season and maintaining long-term efficacy through resistance-managed interventions. A practical, risk-based integrated management workflow is presented in Figure 4.
From a grower’s perspective, one of the most important control options is crop rotation and soil-related practices. Since the pathogen spends around 90% of its lifespan in the soil in the form of sclerotia [2], tillage and crop rotation are key to reducing the sclerotial load in soil and mitigating the risk of S. sclerotiorum infection [23]. However, crop rotation alone cannot effectively reduce the amount of overwintering forms if additional interventions are not applied within the disease cycle. As S. sclerotiorum can infect several hundred host plant species, crop rotation will only be effective if weeds acting as alternative hosts are also adequately suppressed [72]. The choice of tillage system is also critical, as sclerotia present in the soil can only produce apothecia from a depth of 2–3 cm; those buried deeper do not germinate [10]. Sclerotial viability may be reduced by manipulating soil moisture: suitable temperatures combined with a higher moisture content [74] and dry soil conditions [73] can decrease viability. This is highly relevant from a research perspective; however, its practical significance is limited.
In practice, control can be divided into two main categories: the management of myceliogenic, soil-borne infections and plant protection treatments that prevent ascospore-driven infections. Soil-based control primarily targets reducing sclerotia, as these structures are the main source of inoculum for ascospore infections. Control using biological agents can be particularly effective as sclerotia are usually found in the top layer of soil, are relatively large and the pre-sowing period provides flexibility for scheduling applications [26].
Trichoderma asperellum is one of the most commonly used biological control products. It can interfere with S. sclerotiorum at multiple points by reducing the pathogen’s viability through competition for nutrients and ecological niche. This antagonist fungus also produces antifungal metabolites and, due to its mycoparasitic properties, it can degrade the mycelium of other fungal species [75]. T. asperellum can be applied in various ways: its spores can be mixed with soil amendments or organic manure and incorporated into the soil, or it can be used as a seed treatment. The latter method promotes early establishment in the rhizosphere during the initial growth stages and may therefore provide earlier protection against soil-borne pathogens than other application methods [76]. Recent syntheses further emphasise that the field performance of Trichoderma-based products depends heavily on formulation choices and on multi-strain or multicomponent inoculants, however reproducibility remains a key practical constraint [77,78].
Another biological control agent that is used in practice is Coniothyrium minitans, which specifically targets sclerotia. It penetrates beneath the thick, hard rind by enzymatic degradation, ultimately destroying the structure and reducing the amount of inoculum in the soil. C. minitans breaks down the sclerotial wall using chitinases and β-1,3-glucanases, thereby supporting effective parasitism [25]. However, its efficacy is strongly influenced by environmental factors such as soil moisture and temperature. A recent review highlights the renewed interest in using C. minitans to manage S. sclerotiorum, while moisture and temperature sensitivity as well as the timing of application remain the main factors affecting its effectiveness in the field [52].
The backbone of control measures against S. sclerotiorum remains chemical control, which has undergone substantial changes in recent decades. In the second half of the 20th century, chlorothalonil and thiabendazole formed the basis of control programmes [1], followed by benomyl and carbendazim, which initially demonstrated exceptional efficacy against S. sclerotiorum. However, these benzimidazoles were selected by pathogen populations for resistance, which compromised their effectiveness. In Europe, these active ingredients were withdrawn due to toxicological concerns [23]. From the 1990s onwards, iprodione became increasingly important and remained a key active ingredient for decades. However, its efficacy has decreased in several countries, limiting its long-term usefulness [6].
Currently, three groups of active ingredients are used to control white mold. Combining these can substantially improve efficacy while reducing the risk of resistance development. Most products include DMI (triazole) fungicides, with tebuconazole, difenoconazole and prothioconazole playing a fundamental role in control programmes. Their main advantage is their reliable preventive and curative activity [24].
Many products also include strobilurin (QoI) fungicides; however, they are limited in that they do not provide adequate control when used alone. One of their advantages is that they can improve a crop’s tolerance to abiotic stress [6].
Carboxamides (SDHI fungicides), including boscalid and fluopyram, are currently considered to be among the most important and effective active ingredients against white mold [76].
When discussing control strategies, it is important to distinguish between theoretically effective factors and those that can be consistently applied in practice. While the importance of crop rotation, soil tillage and weed management is emphasised across studies, their effectiveness is often limited. The formation and persistence of sclerotia are well documented and depend on the combined effects of temperature, humidity, soil moisture and tillage practices [10,12,74]. Given that the pathogen spends a substantial proportion of its life cycle as sclerotia in the soil, crop rotation and soil cultivation can be considered core pillars of risk reduction [2,23]. Nevertheless, the exceptionally broad host range often limits the practical effectiveness of crop rotation, as weeds can act as alternative hosts and sustain inoculum levels [3,72]. Consequently, reducing soil inoculum pressure is usually a slow process and is often overlooked in short-term on-farm decision-making.
One argument in support of using biological agents such as Trichoderma asperellum and Coniothyrium minitans in the field is that they target sclerotia in the soil, which are the primary source of inoculum. This addresses the starting point of the epidemiological process [9,25,26]. However, variability in field conditions (e.g., soil moisture, temperature and microbial competition) often results in lower, less predictable efficacy than that observed in laboratories [9,26]. Conversely, the case for chemical control is its more consistent performance and ease of integration into crop protection programmes. Nevertheless, a significant counterargument is the risk of resistance development, and the unsustainability of a fungicide-centred strategy in the long term [6,23,24]. Therefore, the above approaches are likely to be effective only within an integrated strategy combining agronomic risk reduction, biological and chemical control, and forecasting-based fungicide use [76]. A recent example of this is the development of a field-level Sclerotinia risk forecasting system for winter oilseed rape in Germany. This system integrates crop phenology and disease development, demonstrating how risk-based timing can be implemented under variable weather conditions while reducing unnecessary applications and maintaining control [39]. Several emerging approaches aim to reduce dependence on repeated fungicide use and to improve control under variable field conditions. RNA-based technologies are advancing rapidly. For example, spray-induced gene silencing (SIGS) has been demonstrated against S. sclerotiorum using dsRNA constructs that target essential fungal genes. Recent studies have also highlighted actionable targets and delivery concepts for white mold suppression [79,80,81].
In parallel, host-induced gene silencing (HIGS), in which the host plant produces RNA molecules that silence essential fungal genes during infection, and combined SIGS–HIGS strategies are being explored in oilseed rape, to achieve stable resistance, when regulatory adoption constraints can be addressed [82].
Hypovirulence-associated mycoviruses, such as S. sclerotiorum hypovirulence-associated DNA virus 1 (SsHADV-1), represent another promising area of research, as there is evidence that viral infection can reduce the virulence of the pathogen, and in some cases, lead to beneficial outcomes. However, deployment will depend on factors such as stability, transmission and consistency on a large scale [83].
Finally, botanical fungicides and nanomaterials are being investigated as lower-impact alternatives or complements to conventional chemistry, but evidence is still at the laboratory stage and requires field-relevant data [84].
Taken together, these approaches demonstrate that the reliable suppression of white mold is rarely achieved by a single tactic, but rather by integrated agronomic, biological, chemical and risk-based decision support tools, which are applied according to the crop, inoculum pressure and environmental conditions. The main management tools discussed in this section are summarized in Table 1.

8. Conclusions and Future Perspectives

Due to its outstanding adaptability, it is clear that S. sclerotiorum remains one of the most important, complex and difficult-to-control plant pathogens. Its broad host range and global distribution are due, on the one hand, to the exceptional longevity of sclerotia, and on the other, to the pathogen’s flexibility, which enables it to persist and infect under diverse climatic conditions. Importantly, disease outcomes are often determined by the alignment of long-term inoculum pressure and short, crop stage specific microclimate along the epidemic pathway. This helps to explain the sporadic yet severe nature of outbreaks, as well as the variable performance of single tactics under field conditions. Although several conflicting interpretations have been published in recent years, further research into the pathogen’s infection strategy could lead to more effective management options. It could also help identify the most realistically targetable decision points in integrated, risk-based programmes.
Future work should prioritise resolving early infection events and the functional boundary between biotroph-like and necrotrophic phases, improving mechanistic understanding of sclerotial conditioning and carpogenic germination under variable climates, and increasing the consistency of biocontrol performance under field conditions. In parallel, advancing resistance breeding (including identification and deployment of novel resistance sources) and strengthening decision-support systems for timing interventions will be key to reducing input dependence while maintaining economically effective control. In addition, emerging concepts such as RNA-based approaches (HIGS/SIGS), hypovirulence-associated mycoviruses, and lower-impact active ingredients or formulations require further evaluation in a field context. This should particularly consider delivery, stability, timing and cost, in order to determine how these concepts can complement established management strategies.

Author Contributions

Conceptualization, Z.A.B., L.V., W.S.K., G.K. and Z.M.; literature search, Z.A.B., L.V., W.S.K., G.K. and Z.M.; literature synthesis, Z.A.B., L.V., W.S.K., G.K. and Z.M.; writing—original draft preparation, Z.A.B., L.V., W.S.K., G.K. and Z.M.; writing—review and editing, Z.A.B., L.V., W.S.K., G.K. and Z.M.; visualization, Z.A.B., L.V., W.S.K., G.K. and Z.M. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Conflicts of Interest

The authors declare no conflict of interest.

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Figure 1. Representative symptoms and diagnostic structures of white mold. (A) Mycelium under microscope (B) Colony morphology on PDA (C) Sclerotia collected from infected sunflower heads (D) Stem lesion on oilseed rape (E) Stem lesion on sunflower (F) Head rot on sunflower.
Figure 1. Representative symptoms and diagnostic structures of white mold. (A) Mycelium under microscope (B) Colony morphology on PDA (C) Sclerotia collected from infected sunflower heads (D) Stem lesion on oilseed rape (E) Stem lesion on sunflower (F) Head rot on sunflower.
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Figure 2. Life cycle of S. sclerotiorum illustrating carpogenic and myceliogenic germination routes of sclerotia.
Figure 2. Life cycle of S. sclerotiorum illustrating carpogenic and myceliogenic germination routes of sclerotia.
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Figure 3. Schematic overview of the infection process and phase transition of S. sclerotiorum within host tissues.
Figure 3. Schematic overview of the infection process and phase transition of S. sclerotiorum within host tissues.
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Figure 4. Risk-based integrated management workflow for white mold.
Figure 4. Risk-based integrated management workflow for white mold.
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Table 1. Main management tools against white mold across crops and production systems.
Table 1. Main management tools against white mold across crops and production systems.
MethodTreatmentPrimary TargetCropsCountriesReferences
Agronomic practiceCrop rotationBaseline soil inoculum and break in host continuityGlycine max, Brassica napus, Helianthus annuusMultiple countries[6,29,38]
Tillage/burial of sclerotiaApothecial emerge and positioning of sclerotia in the soil profileBrassica napus, Glycine maxGermany Multiple countries[29,85]
Weed host managementAlternative hosts and inoculum carryover between cropsGlycine max, Brassica napus, Helianthus annuusMultiple countries[29,38]
Canopy management (row spacing, plant density, irrigation management)Canopy humidity, leaf wetness duration and infection window around floweringGlycine max, Brassica napusUnited States Canada Australia Multiple countries[29,38,86]
Biocontrol agentTrichoderma spp.Soil inoculum, early establishment, integrated suppressionBrassica napus, Solanum tuberosum, Glycine maxPoland
Mexico
Brazil		[76,87,88]
Coniothyrium minitansSclerotinia, soil inoculum reductionBrassica napus, multiple hostsPoland
Multiple countries		[52,76]
Chemical controlDMI fungicidesAscospore-driven infection during susceptible growth stagesBrassica napus, Glycine maxMultiple countries[6,29,38]
QoI fungicidesAscospore-driven infection during susceptible growth stagesBrassica napus, Glycine maxMultiple countries[6,38]
SDHI fungicidesAscospore-driven infection during susceptible growth stagesBrassica napus, Glycine max, Phaseolus vulgarisMultiple countries, United States[6,38,89]
Decision support toolWeather based forecasting (DSS)Timing of fungicide application and risk-window identificationBrassica napus, Glycine maxGermany
Canada
Multiple countries		[39,85,86]
Host resistancePartially resistant/tolerant cultivarsReduced susceptibility, risk reduction Glycine max, Brassica napusUnited States
Multiple countries		[29,38,86]
RNA-based emerging controlSpray-induced gene silencing (SIGS)Essential fungal genes, virulence pathwaysExperiments in broadleaf hostsExperimental[79,80,81]
Host-induced gene silencing (HIGS)Fungal virulence genes expressed during host colonizationExperimental systemsExperimental[82]
Emerging biological controlHypovirulence-associated mycovirus (SsHADV-1)Pathogen fitness/virulence reductionS. sclerotiorum isolates, experimental evaluationUnited States[83]
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Boldizsár, Z.A.; Vörös, L.; Kabato, W.S.; Kukorelli, G.; Molnár, Z. A Comprehensive Review of White Rot Caused by Sclerotinia sclerotiorum: Pathogenicity, Epidemiology and Management. Agronomy 2026, 16, 688. https://doi.org/10.3390/agronomy16070688

AMA Style

Boldizsár ZA, Vörös L, Kabato WS, Kukorelli G, Molnár Z. A Comprehensive Review of White Rot Caused by Sclerotinia sclerotiorum: Pathogenicity, Epidemiology and Management. Agronomy. 2026; 16(7):688. https://doi.org/10.3390/agronomy16070688

Chicago/Turabian Style

Boldizsár, Zoltán András, Levente Vörös, Wogene Solomon Kabato, Gábor Kukorelli, and Zoltán Molnár. 2026. "A Comprehensive Review of White Rot Caused by Sclerotinia sclerotiorum: Pathogenicity, Epidemiology and Management" Agronomy 16, no. 7: 688. https://doi.org/10.3390/agronomy16070688

APA Style

Boldizsár, Z. A., Vörös, L., Kabato, W. S., Kukorelli, G., & Molnár, Z. (2026). A Comprehensive Review of White Rot Caused by Sclerotinia sclerotiorum: Pathogenicity, Epidemiology and Management. Agronomy, 16(7), 688. https://doi.org/10.3390/agronomy16070688

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