Summary• California coastal woodlands are suffering severe disease and mortality as a result of infection from Phytophthora ramorum . Quercus agrifolia is one of the major woodland species at risk. This study investigated within-and among-population variation in host susceptibility to inoculation with P. ramorum and compared this with population genetic structure using molecular markers.• Susceptibility was assessed using a branch-cutting inoculation test. Trees were selected from seven natural populations in California. Amplified fragment length polymorphism molecular markers were analysed for all trees used in the trials.• Lesion sizes varied quantitatively among individuals within populations, with up to an eightfold difference. There was little support for population differences in susceptibility. Molecular structure also showed a strong within-population, and weaker among-population, pattern of variation.• Our data suggest that susceptibility of Q. agrifolia to P. ramorum is variable and is under the control of several gene loci. This variation exists within populations, so that less susceptible local genotypes may provide the gene pool for regeneration of woodlands where mortality is high.
Summary• Variations in synchronicity between colonization rate by the pathogen and host phenology may account for unexplained spatial distribution of canker disease. The hypothesis that synchronous pathogenicity and host development are necessary for incidence of sudden oak death disease was tested by correlating seasonal variations in host cambial phenology and response to inoculation with Phytophthora ramorum.• Response to infection was estimated by inoculating branch cuttings from coast live oak (Quercus agrifolia) trees at nine dates through a full annual cycle in [2003][2004]. Host phenology was estimated from measurements of bud burst and cambial activity in spring 2006.• Lesions were largest in the spring soon after the cambium resumed activity. A moderate genetic component to lesion size was detected. Variation among trees in date of largest lesions correlated with variation in timing of bud burst and cambial phenology.• The data support the hypothesis that active host cambial tissue is a necessary requisite for successful infection with the pathogen that causes sudden oak death canker disease. Genetic variation in host phenology will buffer coast live oak against epidemics of this disease.
Summary Sudden oak death is an emerging forest disease caused by the invasive pathogen Phytophthora ramorum. Genetic and environmental factors affecting susceptibility to P. ramorum in the key inoculum‐producing host tree Umbellularia californica (bay laurel) were examined across a heterogeneous landscape in California, USA. Laboratory susceptibility trials were conducted on detached leaves and assessed field disease levels for 97 host trees from 12 225‐m2 plots. Genotype and phenotype characteristics were assessed for each tree. Effects of plot‐level environmental conditions (understory microclimate, amount of solar radiation and topographic moisture potential) on disease expression were also evaluated. Susceptibility varied significantly among U. californica trees, with a fivefold difference in leaf lesion size. Lesion size was positively related to leaf area, but not to other phenotypic traits or to field disease level. Genetic diversity was structured at three spatial scales, but primarily among individuals within plots. Lesion size was significantly related to amplified fragment length polymorphism (AFLP) markers, but local environment explained most variation in field disease level. Thus, substantial genetic variation in susceptibility to P. ramorum occurs in its principal foliar host U. californica, but local environment mediates expression of susceptibility in nature.
The ability of metalaxyl-M, phosphonic acid in the form of phosphonate, and copper hydroxide to inhibit different stages in the life cycle of Phytophthora ramorum , the causal agent of sudden oak death (SOD), was tested in vitro using 12 isolates from the North American forest lineage. In addition, experiments were conducted in planta to study the ability of phosphonic acid injections and metalaxyl-M drenches to control pathogen growth on saplings of California coast live oak ( Quercus agrifolia ), and of copper hydroxide foliar sprays to control infection of California bay laurel ( Umbellularia californica ) leaves. Phytophthora ramorum was only moderately sensitive to phosphonic acid in vitro , but was highly sensitive to copper hydroxide. In planta experiments indicated the broad efficacy of phosphonic acid injections and of copper hydroxide sprays in preventing growth of P. ramorum in oaks and bay laurels, respectively. Finally, although metalaxyl-M was effective in vitro , drenches of potted oak trees using this active ingredient were largely ineffective in reducing the growth rate of the pathogen in planta .
Aims: To determine the effects of heat and composting treatments on the viability of the plant pathogen Phytophthora ramorum grown on both artificial and various natural substrates. Methods and Results: Phytophthora ramorum was grown on V8 agar, inoculated on bay laurel leaves (Umbellularia californica) and on woody tissues of coast live oak (Quercus agrifolia). Effects on growth, viability and survival were measured as a result of treatment in ovens and compost piles. Direct plating onto PARP medium and pear‐baiting techniques were used to determine post‐treatment viability. No P. ramorum was recovered at the end of the composting process, regardless of the isolation technique used. By using a PCR assay designed to detect the DNA of P. ramorum, we were able to conclude the pathogen was absent from mature compost and not merely suppressed or dormant. Conclusions: Some heat and composting treatments eliminate P. ramorum to lower than detectable levels on all substrates tested. Significance and Impact of the Study: Composting is an effective treatment option for sanitization of P. ramorum‐infected plant material. Assaying for pathogen viability in compost requires a direct test capable of differentiating between pathogen suppression and pathogen elimination.
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