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.
Boldizsár et al. (Wed,) studied this question.
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