Swiss needle cast (SNC), an important fungal disease of Douglas-fir (Pseudotsuga menziesii (Mirb.) Franco), has increased in severity throughout its natural and introduced range over the last half century. The role of climate change and forest management practices in the increase is unclear. We analyzed tree-ring chronologies from six late-successional Douglas-fir stands in the western Oregon Coast Range using time-series intervention analysis (TSIA) to address how climate relates to the impact of SNC on tree growth. Tree-ring chronologies of western hemlock (Tsuga heterophylla (Raf.) Sarg.), a species not susceptible to the fungus Phaeocryptopus gaeumannii (Rhode) Petrak, were used as a climate proxy in the TSIA. We found that growth reductions associated with SNC dated back to the 1590s, the earliest record in our dendritic data. Growth reductions were synchronous across the six sites, indicating that the disease severity was largely influenced by climatic conditions. SNC impact peaked in 1984–1986 at all six study sites, followed by unprecedented disease impacts of 100% in 1996 and 2004 at one site, while decreasing to previous levels at the other five sites. Our SNC index of impact significantly correlated with winter and summer temperatures and summer precipitation. Winter conditions were more strongly associated with disease impact at wetter, cooler sites, whereas summer conditions were more important at less humid, warmer sites. With climate change, SNC impacts are likely to increase in coastal areas where June–July precipitation is much higher than the P. gaeumannii-limiting threshold of ∼110 mm, and decrease where summer precipitation is at or below the threshold. Warmer winters will increase disease severity at higher elevation, north along the coast from northern Oregon to British Columbia, and at inland sites where current winter temperatures limit fungal growth.

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We constructed a mixed-species community designed to simulate roadside and field edge plant communities and exposed it to glyphosate drift in order to test three hypotheses: (1) higher fitness in transgenic Brassica carrying the CP4 EPSPS transgene that confers resistance to glyphosate will result in significant changes in the plant community relative to control communities; (2) given repeated years of glyphosate drift selective pressure, the increased fitness of the transgenic Brassica with CP4 EPSPS will contribute to an increase in the proportion of transgenic progeny produced in plant communities; and (3) the increased fitness of Brassica carrying the CP4 EPSPS transgene will contribute to decreased levels of mycorrhizal infection and biomass in a host species (Trifolium incarnatum). Due to regulatory constraints that prevented the use of outdoor plots for our studies, in 2005 we established multispecies communities in five large cylindrical outdoor sunlit mesocosms (plastic greenhouses) designed for pollen confinement. Three of the community members were sexually compatible Brassica spp.: transgenic glyphosate-resistant canola (B. napus) cultivar (cv.) RaideRR, glyphosate-sensitive non-transgenic B. napus cv. Sponsor, and a weedy B. rapa (GRIN Accession 21735). Additional plant community members were the broadly distributed annual weeds Digitaria sanguinalis, Panicum capillare, and Lapsana communis. Once annually in 2006 and 2007, two mesocosms were sprayed with glyphosate at 10% of the field application rate to simulate glyphosate drift as a selective pressure. After two years, changes were observed in community composition, plant density, and biomass in both control and treatment mesocosms. In control mesocosms, the weed D. sanguinalis (crabgrass) began to dominate. In glyphosate drift-treated mesocosms, Brassica remained the dominant genus and the incidence of the CP4 EPSPS transgene increased in the community. Shoot biomass and mycorrhizal infection in Trifolium incarnatum planted in 2008 were significantly lower in mesocosms that had received glyphosate drift treatments. Our results suggest that, over time, glyphosate drift can contribute to persistence of Brassica that express the CP4 EPSPS transgene and that increased representation of Brassica (a non-mycorrhizal host) within plant communities may indirectly negatively impact beneficial ecosystem services associated with arbuscular mycorrhiza.

The fungal pathogen, Phaeocryptopus gaeumannii, causing Swiss needle cast (SNC) occurs wherever Douglas‐fir is found but disease damage is believed to be limited in the U.S. Pacific Northwest (PNW) to the Coast Range of Oregon and Washington (Hansen et al., Plant Disease, 2000, 84, 773; Rosso & Hansen, Phytopathology, 2003, 93, 790; Shaw, et al., Journal of Forestry, 2011, 109, 109). However, knowledge remains limited on the history and spatial distribution of SNC impacts in the PNW. We reconstructed the history of SNC impacts on mature Douglas‐fir trees based on tree‐ring width chronologies from western Oregon. Our findings show that SNC impacts on growth occur wherever Douglas‐fir is found and is not limited to the coastal fog zone. The spatiotemporal patterns of growth impact from SNC disease were synchronous across the region, displayed periodicities of 12–40 years, and strongly correlated with winter and summer temperatures and summer precipitation. The primary climatic factor limiting pathogen dynamics varied spatially by location, topography, and elevation. SNC impacts were least severe in the first half of the 20th century when climatic conditions during the warm phase of the Pacific Decadal Oscillation (1924–1945) were less conducive to pathogen development. At low‐ to mid‐elevations, SNC impacts were most severe in 1984–1986 following several decades of warmer winters and cooler, wetter summers including a high summer precipitation anomaly in 1983. At high elevations on the west slope of the Cascade Range, SNC impacts peaked several years later and were the greatest in the 1990s, a period of warmer winter temperatures. Climate change is predicted to result in warmer winters and will likely continue to increase SNC severity at higher elevations, north along the coast from northern Oregon to British Columbia, and inland where low winter temperatures currently limit growth of the pathogen. Our findings indicate that SNC may become a significant forest health problem in areas of the PNW beyond the coastal fog zone.