The putative center of origin of Plasmopara viticola, the causal agent of grape downy mildew, is eastern North America, where it has been described on several members of the family Vitaceae (e.g., Vitis spp., Parthenocissus spp., and Ampelopsis spp.). We have completed the first large-scale sampling of P. viticola isolates across a range of wild and cultivated host species distributed throughout the above region. Sequencing results of four partial genes indicated the presence of a new P. viticola species on Vitis vulpina in Virginia, adding to the four cryptic species of P. viticola recently recorded. The phylogenetic analysis also indicated that the P. viticola species found on Parthenocissus quinquefolia in North America is identical to Plasmopara muralis in Europe. The geographic distribution and host range of five pathogen species was determined through analysis of the internal transcribed spacer polymorphism of 896 isolates of P. viticola. Among three P. viticola species found on cultivated grape, one was restricted to Vitis interspecific hybrids within the northern part of eastern North America. A second species was recovered from V. vinifera and V. labrusca, and was distributed across most of the sampled region. A third species, although less abundant, was distributed across a larger geographical range, including the southern part of eastern North America. P. viticola clade aestivalis predominated (83% of isolates) in vineyards of the European winegrape V. vinifera within the sampled area, indicating that a single pathogen species may represent the primary threat to the European host species within eastern North America.

Limited information is available on the spread dynamics of grapevine red blotch virus (GRBV, genus Grablovirus, family Geminiviridae) in vineyards. In this study, we investigated red blotch disease progress in three vineyards with a disparate initial inoculum prevalence. Secondary spread was documented in Cabernet Sauvignon and Cabernet franc vineyards in California, but not in a Merlot vineyard in New York. Increase in annual disease incidence (4.8, 0.13, and 0%) was unrelated to the estimated initial source of inoculum at planting (1, 40, and 40%) in the Cabernet franc, Cabernet Sauvignon, and Merlot vineyards, respectively. Limited genetic diversity of GRBV populations in newly infected vines supported localized spread in California vineyards, and suggested the planting material as the primary source of inoculum. Among the community of hemipteran insects visiting two of the three study vineyards, populations of Spissistilus festinus, the vector of GRBV, were absent in the Merlot vineyard and low in the Cabernet Sauvignon vineyard. Furthermore, all cover crop samples collected from GRBV-infected California vineyards each spring of 2016 to 2018, particularly legume species which are preferred hosts of S. festinus, tested negative for GRBV, suggesting a minimal role, if any, in GRBV spread as inoculum reservoirs. Together our findings illustrate differential disease progress in distinct vineyard ecosystems, and support the elimination of virus inoculum sources as an actionable disease management strategy across vineyards.

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