Aetiology of dryberry disease of boysenberry in New Zealand

Abstract

Abstract Studies indicated that Peronospora sparsa (Synonym P. rubi), causal agent of dryberry disease of boysenberry and other brambles, overwintered primarily as a ‘systemic’ cortex infection of canes, crowns, roots, and buds. The disease cycle started each spring with the production of internally infected shoots from infected root crown, and cane buds. Abundant sporangia (‘conidia’) were observed m the field on these diseased shoots, predominantly on the undersides of the first few leaves formed. By contrast sporulation on overwintered cane surfaces was sparse. ‘Systemic’ infection was confined to the outer cortex parenchyma and appeared to keep pace with cell division at apical meristems. Unfolding leaves were invaded during warm wet conditions causing typical leaf symptoms, including distortion. Systemic cane infection was often indicated by a red streaking of stems and petioles linking successively diseased leaves on a shoot. Secondary infections of flowers and developing berries during wet warm weather were initiated from flowering onwards primarily by conidia produced on diseased shoots and producing the dryberry phase. Diseased berries then became an important source of inoculum for new cycles of berry infection. Spores were produced on the protected pith surfaces in split berries, on the inner calyx surfaces, and on the lower druplets protected by the calyx. Heavy sporulation often occurred before disease symptoms were obvious on green bernes. After harvest, infection of developing primocanes lying on the ground continued by internal mycelial growth and spore infection. Oospores were only found on the root surfaces in dead cortex cells.