Deciphering Kiwifruit Bacterial Canker: Molecular Insights, Host–Pathogen Dynamics, and Innovative Management Strategies

Abstract

Kiwifruit bacterial canker, caused by Pseudomonas syringae pv. actinidiae (Psa), severely threatens global kiwifruit production. Psa uses type III secretion, effectors, biofilms, and hormone manipulation to suppress the host immunity and achieve successful colonization. In response, kiwifruit activates multilayered defense systems involving pattern-triggered immunity, effector-triggered immunity, structural barriers, reactive oxygen species signaling, and hormone-mediated defense pathways. However, these immune mechanisms remain insufficiently validated in Actinidia species, limiting the translation of molecular findings to practical field applications. This review summarizes Psa epidemiology, pathogenicity, host defense (phenylpropanoids, lignin, and resistance inducers such as sulfur/saccharin), and integrated management strategies. Control measures include copper, antibiotics, biocontrol, induced resistance, microbiome engineering, CRISPR, and predictive-disease modeling. Several translational gaps persist, such as inconsistent efficacy, resistance to control measures, varying regulations, and insufficient long-term studies. Future priorities include precision diagnostics, resistance monitoring, region-specific integrated disease management, robust field trials, durable resistance breeding, and global collaboration for sustainable management.