TL;DR: The high susceptibility of tanoak to infection and death suggests that P ramorum is an exotic pathogen, but its origins, and most details of its biology and ecology, remain unknown.
Abstract: Sudden oak death is a new disease affecting tanoak (Lithocarpus densiflora) and oaks (Quercus spp) in California and Oregon, caused by the recently described pathogen Phytophthora ramorum. It has reached epidemic proportions in several counties in central California, leading to the death of tens of thousands of trees. In addition to oaks and tanoak, P ramorum has been found in nearly all woody plant species in mixed evergreen and redwood forests from central California to southern Oregon. Plant species that are not killed appear to serve as a reservoir for the pathogen. The high susceptibility of tanoak to infection and death suggests that P ramorum is an exotic pathogen, but its origins, and most details of its biology and ecology, remain unknown. Our limited knowledge only compounds our concern over the long-term implications of this epidemic for the ecology of coastal forests.
TL;DR: In this paper, the authors present a landscape-scale study of the spatio-temporal of native oak trees in California and demonstrate the utility of integrating remotely sensed imagery analysis with geographic information systems and spatial modeling for spatially clustered.
Abstract: plant community structure (Ristaino and Gumpertz, 2000; Sudden Oak Death is caused by a newly discovered virulent Lundquist and Klopfenstein, 2001). pathogen (Phytophthora ramorum) that is killing thousands We present a landscape-scale study of the spatio-temporal of native oak trees in California. We present a landscape-scale dynamics of SuddenOak Death (SOD), analarming disease that study on the spatio-temporal dynamics of oak mortality. is killing thousands of native oak trees and tanoaks in the Coast Second-order spatial point-pattern analysis techniques Ranges of California and southwestern Oregon (McPherson et (Ripley’s K) were applied to the distribution of dead tree al., 2000; Garbelotto et al., 2001). Considerable progress has crowns (derived from high-resolution imagery) in Marin been made in the past year identifying host species and underCounty, California to determine the existence and scale of standing how this disease is related to other tree-killing dismortality clustering in two years (2000 and 2001). Both years showed clustering patterns between 100 and 300 m. A eases (Davidson et al., 2001; Davidson et al., 2002; Rizzo et al., classification tree model was developed to predict spatial 2002). However, we still do not know how the disease extends patterns of risk for oak mortality based on several landscape- its range across California’s landscape, and we have no ability scale variables. Proximity to forest edge was the most important to predictwhich stands of treesare at highrisk of infection.The explanatory factor, followed by topographic moisture index, objectives of this research are to proximity to trails, abundance of Umbellularia californica, and ● Determine the distribution and rate of oak mortality in the potential summer solar radiation. This research demonstrates study area; the utility of integrating remotely sensed imagery analysis with ● Determine the scale and extent to which the oak mortality is geographic information systems and spatial modeling for spatially clustered;
TL;DR: This article found that nearly all of the state's main tree species in mixed-evergreen and redwood-tanoak forests, including the coniferous timber species coast redwood and Douglas fir, may be hosts for P. ramorum.
Abstract: The finding of Phytophthora ramorum — the pathogen that causes sudden oak death in four California native trees — on rhododendron in Europe led us to hypothesize that its host range in California's natural forests was much greater than previously suspected. In addition to the affected oak species, we have now identified an additional 13 species from 10 plant families that act as hosts for P. ramorum in California. Our data indicates that nearly all of the state's main tree species in mixed-evergreen and redwood-tanoak forests — including the coniferous timber species coast redwood and Douglas fir — may be hosts for P. ramorum. The broad host range of P. ramorum, the variability of symptoms among different hosts and the ability of the pathogen to disperse by air suggests that it may have the potential to cause long-term, landscape-level changes in California forests.
TL;DR: The degree to which invasive, generalist pathogens can cause rapid changes in forest canopy composition is demonstrated and that differences in transmission can be more important than susceptibility in driving patterns of apparent competition is demonstrated.
Abstract: Epidemiological theory predicts that asymmetric transmission, susceptibility, and mortality within a community will drive pathogen and disease dynamics. These epidemiological asymmetries can result in apparent competition, where a highly infectious host reduces the abundance of less infectious or more susceptible members in a community via a shared pathogen. We show that the exotic pathogen Phytophthora ramorum and resulting disease, sudden oak death, cause apparent competition among canopy trees and that transmission differences among canopy trees drives patterns of disease severity in California coast redwood forests. P. ramorum ranges in its ability to infect, sporulate on, and cause mortality of infected hosts. A path analysis showed that the most prolific inoculum producer, California bay laurel (Umbellularia californica), had a greater impact on the mortality rate of tanoak (Lithocarpus densiflorus) than did other inoculum-supporting species. In stands experiencing high tanoak mortality, lack of negative impacts by P. ramorum on bay laurel may increase bay laurel density and subsequently result in positive feedback on pathogen populations. This study demonstrates the degree to which invasive, generalist pathogens can cause rapid changes in forest canopy composition and that differences in transmission can be more important than susceptibility in driving patterns of apparent competition.
TL;DR: Examination of the influence of land-cover changes between 1942 and 2000 on the establishment of an invasive pathogen, Phytophthora ramorum, concludes that enlargement of woodlands and closure of canopy gaps facilitated establishment of P. ramorum by increasing the area occupied by inoculum-production foliar hosts and enhancing forest microclimate conditions.
Abstract: Human-caused changes in land use and land cover have dramatically altered ecosystems worldwide and may facilitate the spread of infectious diseases. To address this issue, we examined the influence of land-cover changes between 1942 and 2000 on the establishment of an invasive pathogen, Phytophthora ramorum, which causes the forest disease known as Sudden Oak Death. We assessed effects of land-cover change, forest structure, and understory microclimate on measures of inoculum load and disease prevalence in 102 15 x 15 m plots within a 275-km2 region in northern California. Within a 150 m radius area around each plot, we mapped types of land cover (oak woodland, chaparral, grassland, vineyard, and development) in 1942 and 2000 using detailed aerial photos. During this 58-year period, oak woodlands significantly increased in area by 25%, while grassland and chaparral decreased by 34% and 51%, respectively. Analysis of covariance revealed that vegetation type in 1942 and woodland expansion were significant predictors of pathogen inoculum load in bay laurel (Umbellularia californica), the primary inoculum-producing host for P. ramorum in mixed evergreen forests. Path analysis showed that woodland expansion resulted in larger forests with higher densities of the primary host trees (U. californica, Quercus agrifolia, Q. kelloggii) and cooler understory temperatures. Together, the positive effects of woodland size and negative effects of understory temperature explained significant variation in inoculum load and disease prevalence in bay laurel; host stem density had additional positive effects on inoculum load. We conclude that enlargement of woodlands and closure of canopy gaps, likely due largely to years of fire suppression, facilitated establishment of P. ramorum by increasing the area occupied by inoculum-production foliar hosts and enhancing forest microclimate conditions. Epidemiological studies that incorporate land-use change are rare but may increase understanding of disease dynamics and improve our ability to manage invasive forest pathogens.