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Phytophthora ramorum, cause of sudden oak death, has been distributed widely across the United States in horticultural situations, but is not established in forests outside of California and Oregon. Here, it has triggered widespread concern and, especially in Oregon, an intensive disease management programme. Now, we provide the first systematic evaluation of the efficacy of that effort. This paper evaluates four measures of the efficacy of Sudden Oak Death (SOD) local eradication treatments: inoculum availability; inoculum from tree species other than tanoak; disease spread from treated areas; and cumulative infested area with and without treatment. We conclude that local treatments demonstrably reduce local inoculum levels. Eradication of SOD from infested sites is difficult but not impossible. The disease usually does not persist after cutting infected trees but spread on the landscape continues because the pathogen may be present on undetected new infections for a year or two before whole tree symptoms are visible. This limits early detection and coupled with delays in completing eradication treatments, prolongs the chances for long‐distance aerial dispersal.

Sudden oak death, caused by Phytophthora ramorum (1,2), has been found for the first time in Oregon, killing tanoak, Lithocarpus densiflorus, trees. To our knowledge, this is the first report of the disease outside of the San Francisco to Monterey area in California, (300 km to the south). Nine areas of infestation, all within a 24-km2 area, were discovered on forest lands near Brookings, in southwest Oregon. Mortality centers ranged in size from 0.2 to 4.5 ha and included 5 to approximately 40 diseased trees. P. ramorum was isolated from stem cankers using Phytophthora-selective medium. Isolates had distinctive morphological features characteristic of P. ramorum, including abundant production of chlamydospores and caducous, semipapillate sporangia on solid media. Internal transcribed spacer (ITS) sequences of isolates of P. ramorum from Oregon were identical to ITS sequences of isolates from California (1). The pathogen also was isolated from necrotic lesions on leaves and stems of native Rhododendron macrophyllum and Vaccinium ovatum growing beneath diseased tanoaks. In July 2001, the disease was located by an aerial survey conducted cooperatively by the USDA Forest Service and Oregon Department of Forestry. All lands within 1.6 km (1 mile) of the mortality centers are subject to Oregon quarantine, which bars the transport of any host plant materials. An eradication effort is currently underway. Symptomatic plants and all known host plants within 15 to 30 m of symptomatic plants are being cut and burned in the first phase of this operation. The total treated area is approximately 16 ha. References: (1) D. M. Rizzo et al. Plant Dis. In press. (2) S. Werres et al. Mycol. Res. 105:1155, 2001.

Four 10- to 20-year-old plantations were precommercially thinned to determine the effects on tree growth and mortality caused by armillaria and heterobasidion root diseases. The plantations represented different species compositions with one each of (1) coastal Douglas-fir and noble fir, (2) Douglas-fir and western hemlock, (3) pure Douglas-fir, and (4) Shasta red fir and mountain hemlock. After 30 years, the probabilities of leave-tree survival and actual leave-tree survival (trees/ha [TPH]) were significantly (P ≤ 0.05) higher in thinned versus unthinned plots in one of the four plantations with no significant differences in the other three plantations. Most tree mortality was caused by armillaria root disease. Despite the high frequency of Heterobasidion occidentale in overstory stumps, only two leave trees in one plantation were killed by this fungus after 30 years. Quadratic mean diameter (QMD) growth and basal area (BA) (per ha) growth of leave trees were significantly (P ≤ 0.05) greater in thinned than in unthinned plots in one plantation for QMD and in three plantations for BA. Precommercial thinning does not appear to exacerbate the incidence of leave-tree mortality from armillaria or heterobasidion root diseases after 30 years, and leave-tree QMD and BA growth increased significantly in most but not all plantations for the tree species sampled. Armillaria and heterobasidion root diseases are not an impediment to precommercial thinning in plantations or stands similar to those we studied.

We gathered baseline data to assess alder tree damage in western Oregon riparian ecosystems. We sought to determine if Phytophthora-type cankers found in Europe or the pathogen Phytophthora alni subsp. alni, which represent a major threat to alder forests in the Pacific Northwest, were present in the study area. Damage was evaluated in 88 transects; information was recorded on damage type (pathogen, insect or wound) and damage location. We evaluated 1445 red alder (Alnus rubra), 682 white alder (Alnus rhombifolia) and 181 thinleaf alder (Alnus incana spp. tenuifolia) trees. We tested the correlation between canopy dieback and canker symptoms because canopy dieback is an important symptom of Phytophthora disease of alder in Europe. We calculated the odds that alder canopy dieback was associated with Phytophthora-type cankers or other biotic cankers. P. alni subsp. alni (the causal agent of alder disease in Europe) was not identified in western Oregon; however, Phytophthora siskiyouensis was isolated from Phytophthora-type cankers which were present on 2% of red alder trees and 3% of white alder trees. The odds of canopy dieback were 5.4 and 4.8 times greater for red and white alder (respectively) with Phytophthora-type canker symptoms than in trees without such cankers. The percentage of trees with canopy dieback was 51%, 32%, and 10% for red, white, and thinleaf alder respectively. Other common damage included wounding, foliar pathogens and insects on red alder. This is the first report of Phytophthora canker of alder in United States forests and first report of P. siskiyouensis isolation from alder in forests anywhere.

Non-native diseases of dominant tree species have diminished North American forest biodiversity, structure, and ecosystem function over the last 150 years. Since the mid-1990s, coastal California forests have suffered extensive decline of the endemic overstory tree tanoak, Notholithocarpus densiflorus (Hook. & Arn.) Manos, Cannon & S. H. Oh (Fagaceae), following the emergence of the exotic pathogen Phythophthora ramorum and the resulting disease sudden oak death. There are two central challenges to protecting tanoak: 1) the pathogen P. ramorum has multiple pathways of spread and is thus very difficult to eradicate, and 2) the low economic valuation of tanoak obscures the cultural and ecological importance of this species. However, both modeling and field studies have shown that pathogen-centric management and host-centric preventative treatments are effective methods to reduce rates of spread, local pathogen prevalence, and to increase protection of individual trees. These management strategies are not mutually exclusive, but we lack precise understanding of the timing and extent to apply each strategy in order to minimize disease and the subsequent accumulation of fuels, loss of obligate flora and fauna, or destruction of culturally important stands. Recent work identifying heritable disease resistance traits, ameliorative treatments that reduce pathogen populations, and silvicultural treatments that shift stand composition hold promise for increasing the resiliency of tanoak populations. We suggest distinct strategies for pathogen invaded and uninvaded areas, place these in the context of local management goals, and suggest a management strategy and associated research priorities to retain the biodiversity and cultural values associated with tanoak.

Sudden oak death (SOD) caused by Phytophthora ramorum was first discovered in Oregon forests in July 2001. There appear to have been three separate introductions of P. ramorum into Oregon; in approximately 1998, 2008, and 2014. The most recent of these was the EU1 clonal lineage; all others were the NA1 clonal lineage. Since 2001 an interagency team has been attempting to eradicate the pathogen though a program of early detection (aerial and ground surveys, stream baiting) and destruction (herbicide treatment, felling and burning) of infected and nearby host plants; the program has evolved over time. Post-treatment monitoring indicates that although the pathogen has been eliminated from many of the sites, spread continues. From 2001 to 2015 the quarantine area expanded from 23 km2 to 1,333 km2, where it remains to date. Within a 145 km2 Generally Infested Area near the center of the quarantine area, most sites have not been treated and the disease has been allowed to intensify and spread. Where eradication treatments have stopped, canopy tanoak mortality increased from nearly zero to 87 percent during the 2012-2016 period. Managing sudden oak death in Oregon forests is challenging for many reasons and Oregon’s program is likely to change in the future.

Summary Phytophthora species were surveyed by collecting soil samples and placing bait leaves in selected streams during June–October in the years 2005, 2006 and 2010 at three sites in oak forests in Diqing Tibetan Autonomous Prefecture of NW Yunnan province, China. Seventy-three isolates of Phytophthora spp. were recovered from 135 baited leaf samples and 81 soil samples. Eight Phytophthora species were identified by observation of morphological features and ITS1-5.8S-ITS2 rDNA sequence analysis. The eight taxa included two well-known species P. gonapodyides and P. cryptogea, two recently described species P. gregata and P. plurivora, two named but as yet undescribed taxa, P. taxon PgChlamydo and P. taxon Salixsoil, and two previously unrecognized species, Phytophthora sp.1 and P. sp.2. The most numerous species, P. taxon PgChlamydo, and the second most abundant species, P. taxon Salixsoil, were recovered at all three sites. Phytophthora cryptogea was detected only once at site Nixi. Phytophthora gregata and P. sp.2 were isolated from a stream only at site Bitahai, while the other three species were each found at two sites. Phylogenetic analysis revealed that the isolates belonged to three ITS clades, one species including six isolates in clade 2, six species including 66 isolates in clade 6 and one species in clade 8. There was a relatively rich species and genetic diversity of Phytophthora detected in the investigated regions where the forest biotic and abiotic factors affecting the growth and evolution of Phytophthora populations were diverse.

Phytophthora ramorum, the causal agent of sudden oak death and ramorum blight, is known to exist as three distinct clonal lineages which can only be distinguished by performing molecular marker-based analyses. However, in the recent literature there exists no consensus on naming of these lineages. Here we propose a system for naming clonal lineages of P. ramorum based on a consensus established by the P. ramorum research community. Clonal lineages are named with a two letter identifier for the continent on which they were first found (e.g., NA = North America; EU = Europe) followed by a number indicating order of appearance. Clonal lineages known to date are designated NA1 (mating type: A2; distribution: North America; environment: forest and nurseries), NA2 (A2; North America; nurseries), and EU1 (predominantly A1, rarely A2; Europe and North America; nurseries and gardens). It is expected that novel lineages or new variants within the existing three clonal lineages could in time emerge.

We followed the local intensification and dispersal of Phytophthora ramorum Werres, De Cock, Man In't Veld in Oregon tanoak (Lithocarpus densiflorus (Hook Arn.) Rehd.) forests from its initial detection in 2001 through 2006, co- incident with a continuing eradication effort. The initial infested area included nine scattered sites below 400 m elevation, close to the Pacific Ocean near Brookings, Oregon. In subsequent years, one-half of new infections were within 122 m of a previous infection, and 79% of the newly detected trees occurred within 300 m of a previously identified tree. Dispersal up to 4 km was occasionally recorded. Initial infection occurred in the upper crowns of tanoak trees. The pathogen was re- covered in rainwater collected beneath diseased tanoak trees in every month from November 2006 through October 2007. Twenty-four multilocus microsatellite genotypes were identified among 272 P. ramorum isolates collected from Curry County. Genotypic analysis provided independent estimates of time of origin of the Oregon infestation, its clustered distri- bution, and dispersal distances. In all sampling years, 60%-71% of the isolates belonged to the same multilocus genotype. In 2001, 12 genotypes were detected and new genotypes were identified in each of the subsequent years, but all isolates belonged to the same clonal lineage. Knowledge of local intensification of the disease and long-distance dispersal should inform both Oregon eradication efforts and national quarantine regulations. Resume´ : Nous avons suivi la progression locale et la dispersion de Phytophtora ramorum Werres, De Cock, Man In't Veld dans des forets de lithocarpe de Californie (Lithocarpus densiflorus (Hook. Arn.) Rehd.) en Oregon depuis que la maladie a etedetectee pour la premiere fois, en 2001, jusqu'en 2006, pendant que se poursuivait les efforts d'eradication. Les zones initialement infectees incluaient neuf stations dispersees en dessous de 400 m d'altitude, aproximitede l'ocean Pacifique, pres de Brookings en Oregon. Au cours des annees qui ont suivi, la moitiedes nouvelles infections etaient sit- uees amoins de 122 m d'une infection precedente et 79% des arbres nouvellement infectesetaient situesamoins de 300 m d'un arbre dejainfecte´. La dispersion de la maladie a occasionnellement eteobservee sur une distance pouvant aller jus- qu'aquatre kilometres. L'infection initiale s'est produite dans la partie superieure de la cime des lithocarpes. Le cham- pignon pathogene a eteretrouvedans l'eau de pluie collectee sous les lithocarpes malades achaque mois, de novembre 2006 aoctobre 2007. Vingt-quatre genotypes multilocus de microsatellites ont eteidentifies parmi les 272 isolats de P. ra- morum collectes dans le comtede Curry. L'analyse genotypique a fourni des estimations independantes du moment du de´- but de l'infection en Oregon, de sa repartition en grappes et des distances de dispersion. Durant toutes les annees

The population structure and ecological roles of the indigenous pathogen Phellinus weirii, cause of laminated root rot in conifer forests of western North America, are examined. This pathogen kills trees in slowly expanding mortality centers, creating gaps in the forest canopy. It is widespread, locally abundant, and very long-lived. It is among the most important disturbance agents in the long intervals between stand-replacing events such as wildfire or harvest in these ecosystems and shapes the structure and composition of both wild and managed forests. Trees are infected and killed regardless of individual vigor. Management of public lands is changing dramatically, with renewed emphasis on natural forest structures and processes but pathogens, especially root rot fungi, remain a significant challenge to “ecosystem management.”