Alan Kanaskie

Sudden oak death caused by Phytophthora ramorum in Oregon.

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.

Standardizing the Nomenclature for Clonal Lineages of the Sudden Oak Death Pathogen, Phytophthora ramorum

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.

Stream Monitoring for Detection of Phytophthora ramorum in Oregon Tanoak Forests

Stream monitoring using leaf baits for early detection of Phytophthora ramorum has been an important part of the Oregon Sudden Oak Death (SOD) program since 2002. Sixty-four streams in and near the Oregon quarantine area in the southwest corner of the state were monitored in 2008. Leaves of rhododendron (Rhododendron macrophyllum) and tanoak (Lithocarpus densiflorus) were placed in mesh bags, and bags were floated in streams. Leaf baits were exchanged every 2 weeks throughout the year. Leaves were assayed by isolation on selective medium and by multiplex rDNA internal transcribed spacer polymerase chain reaction (ITS PCR). The two methods gave comparable results, but multiplex PCR was more sensitive. P. ramorum was regularly recovered at all seasons of the year from streams draining infested sites 5 years after eradication treatment. In streams with lower inoculum densities, recovery was much higher in summer than in winter. P. ramorum was isolated from streams in 23 watersheds. When P. ramorum was detected, intensive ground surveys located infected tanoaks or other host plants an average of 306 m upstream from the bait station. P. ramorum was isolated from stream baits up to 1,091 m from the probable inoculum source.

Ten-year growth and mortality in young Douglas-fir stands experiencing a range in Swiss needle cast severity

Swiss needle cast, a foliar disease caused by the Ascomycete Phaeocryptopus gaeumannii (T. Rohde) Petr., con- tinues to afflict Douglas-fir (Pseudotsuga menziesii (Mirb.) Franco) in north coastal Oregon. Permanent plots were installed in 1998 to assess growth impacts and monitor disease severity. Gross periodic annual increment was measured for three 2- year growth periods and one 4-year growth period and ranged from 0.37 to 31.74 m 3 ·ha -1 ·year -1 . Foliage retention, defined as the average number of annual needle age classes held by a tree, was also estimated as an index of disease severity. As- suming negligible losses in stands with maximum needle retention (approximately 3.9 years), growth losses in net periodic annual increment reached slightly over 50% in stands with the lowest needle retention (approximately 1 year). Mixed-effects regression models supported a consistent relationship between foliage retention and both gross and net periodic annual in- crement among the four growth periods. Periodic annual mortality ranged from 0 to 19.12 m 3 ·ha -1 ·year -1 but was not signif- icantly influenced by Swiss needle cast as measured by average foliage retention. Minimum and maximum foliage retention has fluctuated annually from 1998 to 2008 on the permanent plots, but growth losses at a given level of foliage retention ap- pear to have remained stable. Estimated growth losses are similar to those reported for comparable levels of defoliation by other agents.

Influence of Bravo fungicide applications on wood density and moisture content of Swiss needle cast affected Douglas-fir trees

Wood density, moisture content, tracheid width and cell wall size were examined in trees from plots that were sprayed for 5 years with chlorothalonil (Bravo 1 ) fungicide to reduce the impact of Swiss needle cast (SNC) and from trees in adjacent unsprayed plots. The unsprayed (more heavily diseased) trees had significantly narrower sapwood, narrower growth rings, lower sapwood moisture content, and narrower tracheid cell wall thickness than did the sprayed (less heavily diseased) trees. Moreover, unsprayed trees had altered earlywood density—earlywood width relationships, higher latewood proportion, and higher overall wood density than the sprayed trees. We hypothesize: (1) that the decreased moisture content of diseased trees results from their poor carbon economy resulting in insufficient energy (photosynthate) to reverse sapwood embolisms, and (2) SNC decreases wood density relative to growth rate. # 2003 Elsevier B.V. All rights reserved.

Spatial and Temporal Analysis of Populations of the Sudden Oak Death Pathogen in Oregon Forests

Sudden oak death caused by the oomycete Phytophthora ramorum was first discovered in California toward the end of the 20th century and subsequently emerged on tanoak forests in Oregon before its first detection in 2001 by aerial surveys. The Oregon Department of Forestry has since monitored the epidemic and sampled symptomatic tanoak trees from 2001 to the present. Populations sampled over this period were genotyped using microsatellites and studied to infer the population genetic history. To date, only the NA1 clonal lineage is established in this region, although three lineages exist on the North American west coast. The original introduction into the Joe Hall area eventually spread to several regions: mostly north but also east and southwest. A new introduction into Hunter Creek appears to correspond to a second introduction not clustering with the early introduction. Our data are best explained by both introductions originating from nursery populations in California or Oregon and resulting from two distinct introduction events. Continued vigilance and eradication of nursery populations of P. ramorum are important to avoid further emergence and potential introduction of other clonal lineages.

Temporal Epidemiology of Sudden Oak Death in Oregon.

An effort to eradicate Phytophthora ramorum, causal agent of sudden oak death, has been underway since its discovery in Oregon forests. Using an information-theoretical approach, we sought to model yearly variation in the size of newly infested areas and dispersal distance. Maximum dispersal distances were best modeled by spring and winter precipitation 2 years before detection, and infestation size the year prior. Infestation size was best modeled by infestation size and spring precipitation the year prior. In our interpretation, there is a 2-year delay between the introduction of inoculum and onset of mortality for a majority of sites. The year-long gap in between allows ample time for the production of inoculum contributing to the spread of P. ramorum. This is supported by epidemic development following changes in eradication protocols precipitated by an outbreak in 2011, attributable to a 2009 treatment delay and an uncharacteristically wet spring in 2010. Posteradication, we have observed an increase in the total area of new outbreaks and increased frequency in dispersal distances greater than 4 km. Although the eradication program has not eliminated P. ramorum from Oregon forests, it has likely moderated this epidemic, emphasizing the need for prompt treatment of future invasive forest pathogens.

First Report of the EU1 Clonal Lineage of Phytophthora ramorum on Tanoak in an Oregon Forest

Initially reported in California as the causal agent of sudden oak death (SOD), efforts to limit spread of Phytophthora ramorum in Oregon natural forests have concentrated on quarantine regulations and eradication of the pathogen from infested areas. P. ramorum has four clonal lineages: NA1; NA2; EU1; and EU2 (Grünwald et al. 2012; Van Poucke et al. 2012). Forest infestations in Oregon have been limited to the NA1 clonal lineage, whereas EU1, NA1, and NA2 clonal lineages have all been found in U.S. nurseries (Kamvar et al. 2015; Prospero et al. 2007). In February 2015, in response to an aerial survey, P. ramorum was isolated from a dying Notholithocarpus densiflorus tree in the South Fork Pistol River drainage of Curry Co., Oregon. The isolated strain was identified as P. ramorum based on presence of chlamydospores, characteristic hyphae, and sporangial morphology. Microsatellite genotyping at 14 loci (Vercauteren et al. 2011) and comparison with reference cultures revealed that these isolates belonged to the EU1 clonal lineage. Subsequently, five more isolates were obtained from the original tree stump and the EU1 lineage was confirmed. Microsatellite alleles of the forest EU1 isolates were nearly identical to EU1 isolates collected in 2012 from a nearby nursery during routine P. ramorum nursery monitoring, except for one allele at locus PrMS145a. Interestingly, several isolates differed at locus ILVOPrMS131a within both the 2015 forest and the 2012 nursery findings with identical allele frequencies in each population for this locus. These data provide inconclusive support for the introduction of EU1 into Curry Co. from the 2012 populations found in nurseries, given that no direct match was found probably owing to the paucity of EU1 samples from nurseries. These results provide further evidence that multiple distinct P. Quick Links Add to favorites

Alder Canopy Dieback and Damage in Western Oregon Riparian Ecosystems

Abstract 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.

Climatic influences on needle cohort survival mediated by Swiss needle cast in coastal Douglas-fir

Swiss needle cast (SNC) severity in Douglas-fir (Pseudotsuga menziesii) has been shown to vary spatially and temporally in response to climatic factors both within its native range and in regions where it has been planted as an exotic species. Survival models were developed for different Douglas-fir needle cohorts to enhance our understanding of how climatic influences on needle longevity are mediated by SNC in the Oregon Coast Range. The climate-based models were based on repeated measurement of 100 plots between 1998 and 2005 coupled with downscaled PRISM climate data. Potential predictors of needle survival by annual cohort were selected from numerous climatic variables at annual, seasonal, and monthly scales. Needle survival probability was positively associated with maximum summer temperature, and negatively associated with minimum winter temperature and spring precipitation. Seasonal climate variables associated with needle longevity are consistent with current epidemiological understanding of Phaeocyrptopus gaeumannii, as well as with previous analyses of climatic influences on SNC severity as measured by average years of foliage retention and frequency of fungal fruiting bodies, or pseudothecia, in stomates.