Clonally propagated monoculture crop plants facilitate the emergence and spread of new diseases. Plant pathogens cause disease by the secretion of effectors that function by repressing the host defense response. While the last few decades have seen a huge increase in our understanding of the role effectors play in mediating plant-pathogen interactions, the combinations of effectors required for the establishment of plant disease and that account for host specificity are less well understood. Breeding genetic resistance is often used to protect plants from disease but it is frequently evaded by rapidly evolving pathogens. Pseudomonas syringae pv. actinidiae (Psa) which causes bacterial canker disease of kiwifruit has spread rapidly throughout the world’s kiwifruit orchards, particularly those growing cultivars of Actinidia chinensis . Other Actinidia species including A . arguta display strong resistance conferred by recognition of effectors delivered by Psa. We explore the depth and dynamics of Psa effector recognition by A . arguta and show that there is a trade-off between losses of effector recognition by A . arguta versus the retention of pathogenicity. Our findings should aid in the understanding of how to breed durable resistance into perennial plants challenged by swiftly evolving pathogens.