Abstract Bacterial canker disease (BCD) of sweet cherry ( Prunus avium L.) represents one of the most complex and persistent patho-systems in perennial fruit crops. It is primarily caused by genetically diverse lineages within the Pseudomonas syringae species complex, including but not limited to P. syringae pv. syringae ( Pss ), P. amygdali pv. morsprunorum ( Pam ), and P. avellanae ( Pav ). This study reviews the taxonomic evolution, ecological diversity, and epidemiological behavior of these pathogens across global cherry-producing regions. Pathogen population surveys reveal that distinct P. syringae lineages dominate in different agroclimatic zones, influenced by frost frequency, precipitation, and host genotype. The disease cycle integrates pathogen epiphytic persistence, opportunistic invasion via natural, pruning, or frost wounds, and overwintering in cankers and buds. P. syringae further weakens host defense by disrupting the bud’s deep supercooling mechanism through ice-nucleation-active (INA) proteins, initiating freezing injury at −1.5 to −2°C and predisposing tissues to necrosis and systemic colonization. This freezing-induced damage leads to blossom blast, resulting in floral necrosis, poor fruit set, and early-season spur dieback. Recent advances are driving a shift from conventional copper-based management toward integrated, precision-based strategies for BCD in sweet cherry. These include targeted cultural, chemical, and biological approaches, enhanced by insights into host-pathogen interactions, stable resistance loci in Prunus germplasm, and climate-informed epidemiological modeling. Information © The Authors 2026.
Manna et al. (Thu,) studied this question.