Bishop, G.

The ongoing spread of X-disease, which is associated with ‘ Candidatus Phytoplasma pruni’, has resulted in severe economic losses for cherry and stone fruit growers in the U.S. Pacific Northwest in the last decade. Given that this pathogen is transmitted by polyphagous leafhopper species, primarily Colladonus montanus ssp. reductus and C. geminatus in the Pacific Northwest, alternative plant hosts present a significant management concern. Here, we surveyed phytoplasma incidence in non- Prunus plants found in and around stone fruit orchard borders and compared these results to the leafhopper feeding patterns through gut content analysis. We confirmed ‘ Ca. P. pruni’ infection in 21 plant species from 15 families. Of these, 15 species were commonly found in the diets of phytoplasma-carrying leafhoppers. Due to the abundance of common plant species, including Taraxacum, Malva, and Trifolium spp., alternative hosts were found across all growing seasons, although ‘ Ca. P. pruni’ titer was low (<102 cells) in most of these hosts. No geographic patterns were identified; instead, phytoplasma incidence and spread at individual orchards was related to the management of annual and biennial host species, thus removing preferred leafhopper feeding hosts. These data suggest that alternative host removal, along with the removal of infected trees, is an effective means of slowing disease spread.

‘Candidatus Phytoplasma pruni’ infection in cherries causes small, misshapen fruit with poor color and taste, rendering the fruit unmarketable. However, this is a disease with a long development cycle and a scattered, nonuniform symptom distribution in the early stages. To better understand the biology as well as the relationship between pathogen titer and disease expression, we carried out seasonal, spatial, and temporal examinations of ‘Ca. P. pruni’ titer and distribution in infected orchard-grown trees. Sequential sampling of heavily infected trees revealed marked seasonal patterns, with differential accumulation in woody stem and leaf tissues and, most notably, within fruit in the early stages of development from bloom to pit hardening. Furthermore, mapping phytoplasma distribution and titer in trees at different stages of infection indicated that infection proceeds through a series of stages. Initially, infection spreads basipetally and accumulates in the roots before populating aerial parts of the trees from the trunk upward, with infection of specific tissues and limbs followed by an increasing phytoplasma titer. Finally, we observed a correlation between phytoplasma titer and symptom severity, with severe symptom onset associated with three to four orders of magnitude more phytoplasma than mild symptoms. Cumulatively, these data aid in accurate sampling and management decision-making and furthers our understanding of disease development.