White mold of carrot is mainly caused by Sclerotinia sclerotiorum, while Sclerotinia nivalis is rarely reported. This study provides the first molecular confirmation of S. nivalis on carrot in Russia, expanding knowledge of its global distribution. rDNA-ITS sequencing (100% identity with reference strains) and phylogenetic analyses confirmed the isolate as S. nivalis. The growth, sclerotia formation, temperature response, pathogenicity, and fungicide sensitivity of four Sclerotinia strains (S. sclerotiorum from carrot, rapeseed, and soybean, and S. nivalis from carrot) were compared. S. nivalis showed slower growth, smaller but more numerous sclerotia (2–5 mm), and an optimal temperature of 15 °C, lower than S. sclerotiorum (25 °C). The soybean strain S. sclerotiorum SC382 was the most aggressive, causing 62% necrosis of carrot leaves and complete root decay within 9 days, while S. nivalis and the carrot isolates showed moderate aggressiveness. The S. nivalis SM8 strain was four times less sensitive to fluazinam (EC₅₀ = 0.0107 µg/mL) than S. sclerotiorum, whereas sensitivity to boscalid and pyraclostrobin varied. These findings confirm S. nivalis as a new causal agent of carrot white mold in Russia and demonstrate the potential of Sclerotinia strains from soybean and rapeseed to infect carrot, emphasizing the need for species-level monitoring and adapted control strategies.

A hyperparasite was observed on Venturia inaequalis during a survey in Krasnodar region, South Russia. Morphological characterization using light microscopy and molecular characterization by sequencing ITS region of nuclear ribosomal DNA and phylogenetic analysis revealed the identity of the pathogen as Trichothecium roseum. This is the first record of hyperparasite Trichothecium roseum on Venturia inaequalis from Russia.

Sugar beet cercospora leaf spot (CLS), caused by the fungus Cercospora beticola, is among the most economically important diseases of sugar beet, and the effectiveness of chemical disease management depends on the susceptibility of pathogen populations to fungicides. In this study, isolates of C. beticola from the Russian Federation were characterized based on QoI resistance, molecular detection of the G143A mutation, and phenotypic variability in radial growth, colony morphology, and aggressiveness. A total of 46 leaf samples were surveyed, and 196 isolates were obtained, from which a representative subset of 48 isolates was selected for detailed analysis. The selected isolates were characterized for in vitro radial growth and colony morphology, assessed for aggressiveness on sugar beet leaves, and tested for sensitivity to azoxystrobin based on EC50 values. The G143A mutation was detected by allele-discriminating real-time PCR and confirmed by sequencing of the cytB region. The G143A mutation was identified in 41 of 48 isolates (85.4%). In the mycelial bioassay, all isolates had EC50 values above 0.2 µg/mL, and 38 of 48 isolates (79.2%) had EC50 values exceeding 100 µg/mL. Additional validation with SHAM in a subset of 35 isolates did not alter the qualitative interpretation of resistance. Considerable variability was also observed in radial growth rate, aggressiveness, and colony appearance among isolates. These findings indicate widespread QoI resistance in the analyzed Russian isolate collection and provide a structured baseline for regional resistance monitoring and for more cautious use of FRAC 11 fungicides in integrated sugar beet disease-management programs.