Sudden Oak Death pathogen is evolving, says new study
Conditions favorable to the pathogen have led to rapid spread of SOD to areas distant from its sites of origin in Northern California
| 23 April 2008
The pathogen responsible for Sudden Oak Death (SOD) got its grip on California’s forests at two locations — outside a nursery in Santa Cruz and at Mt. Tamalpais in Marin County — before spreading out to kill millions of oaks and tanoaks along the Pacific Coast. So say the authors of a new study that provides, for the first time, evidence of how the epidemic unfolded in this state.
“In this paper, we actually reconstruct the Sudden Oak Death epidemic,” says Matteo Garbelotto, associate extension specialist and adjunct professor of ecosystem sciences, the study’s principal investigator. “We point to where the disease was introduced in the wild and where it spread from those introduction points.”
The study, scheduled to appear later this month in the online early edition of the journal Molecular Ecology, also shows that the pathogen is currently evolving in California, with mutant genotypes appearing as new areas are infested. These findings suggest that movement of infected plants between different regions where SOD is established should be minimized, says Garbelotto, who presented his findings last week at the annual meeting of the California Oak Mortality Task Force, of which he is a member.
The researchers analyzed genetic markers of nearly 300 samples of the fungus-like pathogen Phytophthora ramorum, taken from 14 forest stands in Humboldt, Sonoma, Marin, Santa Cruz, and Monterey counties. The sites, chosen to represent the geographic range of Sudden Oak Death infestation, included newly infected areas as well as regions that had relatively old infestations. Samples from the wild were compared with an additional 15 P. ramorum isolates collected from nurseries in 12 states.
From the samples, the researchers identified 35 unique strains of the pathogen; a computer analysis further revealed how those strains were related to each other. The study found that all strains were originally derived from three basal strains that were most prevalent in the samples and common in all sites.
Armed with that information, the researchers plotted out which regions were linked to the basal strains to create a history of the epidemic.
Two sites emerged as the origin of the basal strains: Bean Creek in Santa Cruz County, located just outside a nursery shut down because of its SOD infestation, and Bolinas Ridge in the Golden Gate National Recreation Area on Mt. Tamalpais, only 5 kilometers from the site where the disease was first observed in California. The basal strains also matched those found in the nursery samples.
Garbelotto notes that previous research has already pointed to the international plant trade as having introduced the pathogen to the United States. The basal strains from the Santa Cruz and Mt. Tamalpais sites also matched the strains from the nursery samples in the study, providing further support for the key role nurseries played in the spread of the epidemic, he says.
The most likely scenario is that the pathogen arrived in California through the nursery trade, then spread from the nursery in Santa Cruz to trees bordering the facility. While the site at Mt. Tamalpais is not adjacent to a nursery, there is anecdotal evidence of frequent use of ornamental plants from nurseries for landscaping in the area, says Garbelotto.
The disease could have then progressed to other parts of California’s coast, including Sonoma County and Big Sur, according to the study.
“Interestingly, areas where the infestation is particularly severe are not necessarily the first ones to have become infected,” says Garbelotto. “Big Sur was hit hard by Sudden Oak Death, with a proportionally larger amount of trees killed by the disease. That is why this historical reconstruction based upon genetic analysis is so important; it does not always match the picture of the epidemic one would develop based solely upon observations.”
What is SOD’s ‘X factor’?
The fact that there are more symptoms and higher mortality in areas where the pathogen didn’t originate suggests that some factor other than length of infestation, such as climate or environmental conditions, is needed for the pathogen to thrive, the researchers say.
The study also found that strains from areas of recent infestations are more genetically distant from current nursery strains, which suggests that regulations controlling the spread of the pathogen from the nursery to the wild are working. The bad news? “Unfortunately,” says Garbelotto, “evidence shows that the pathogen is spreading on its own in the wild. New strains are evolving.”
Previous research led by Garbelotto has shown that there was very little genetic variability of the pathogen in the forest, an indication that the pathogen was spreading by asexual, clonal reproduction in the wild. Samples from nurseries, however, revealed significantly greater genetic variation, suggesting that nurseries host a much broader representation of the pathogen.
Garbelotto notes that current regulations restrict the movement of known host-plant material from natural areas within quarantine counties to non-restricted areas, but moving plant material within the quarantined counties is allowed.
“The sites within the quarantined areas are at different points in the epidemic’s evolutionary history with different strains of the pathogen, so moving plants between those locations could be dangerous,” says Garbelotto. “What our study shows is that not every infected site is the same.”