Novel Introductions and Epidemic Dynamics of the Sudden Oak Death Pathogen Phytophthora ramorum in Oregon Forests.

Sudden oak death caused by Phytophthora ramorum has been actively managed in Oregon since the early 2000s. To date, this epidemic has been driven mostly by the NA1 clonal lineage of P. ramorum, but an outbreak of the EU1 lineage has recently emerged. Here, we contrast the population dynamics of the NA1 outbreak first reported in 2001 to the outbreak of the EU1 lineage first detected in 2015. We performed tests to determine whether any of the lineages were introduced more than once. Infested regions of the forest were sampled between 2013 and 2018 (n = 903), and strains were genotyped at 15 microsatellite loci. Most genotypes observed were transient, with 272 of 358 unique genotypes emerging during one year and disappearing the next year. The diversity of EU1 was very low and isolates were spatially clustered (less than 8 km apart), suggesting a single EU1 introduction. Some forest isolates are genetically similar to isolates collected from a local nursery in 2012, suggesting the introduction of EU1 from this nursery or simultaneous introduction to both the nursery and latently into the forest. In contrast, the older NA1 populations were more polymorphic and spread more than 30 km2. A principal component analysis supported two to four independent NA1 introductions. The NA1 and EU1 epidemics infest the same area but show disparate demographics because of the initial introductions of the lineages spaced 10 years apart. Comparing these epidemics provides novel insight regarding patterns of emergence of clonal pathogens in forest ecosystems.

Variation in Susceptibility of Tanoak to the NA1 and EU1 Lineages of Phytophthora ramorum, the Cause of Sudden Oak Death.

Phytophthora ramorum, the cause of sudden oak death (SOD), kills tanoak (Notholithocarpus densiflorus) trees in southwestern Oregon and California. Two lineages of P. ramorum are now found in wildland forests of Oregon (NA1 and EU1). In addition to the management of SOD in forest ecosystems, disease resistance could be used as a way to mitigate the impact of P. ramorum. The objectives of this study were to (i) characterize the variability in resistance of N. densiflorus among families using lesion length; (ii) determine whether lineage, isolate, family, or their interactions significantly affect variation in lesion length; and (iii) determine whether there are differences among isolates and among families in terms of lesion length. The parameters isolate nested within lineage (isolate[lineage]) and family × isolate(lineage) interaction explained the majority of the variation in lesion length. There was no significant difference between the NA1 and EU1 lineages in terms of mean lesion length; however, there were differences among the six isolates. Lesions on seedlings collected from surviving trees at infested sites were smaller, on average, than lesions of seedlings collected from trees at noninfested sites (P = 0.0064). The results indicate that there is potential to establish a breeding program for tanoak resistance to SOD and that several isolates of P. ramorum should be used in an artificial inoculation assay.

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.

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.