By Sarah Yang
The pathogen responsible for Sudden Oak Death first got its grip in
California's forests outside a nursery in Santa Cruz and at Mt. Tamalpais in
Marin County before spreading out to eventually kill millions of oaks and
tanoaks along the Pacific Coast, according to a new study led by researchers
at the University of California, Berkeley. It 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," said Matteo Garbelotto, UC Berkeley associate extension
specialist and adjunct professor, and principal investigator of the study.
"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 Sudden Oak Death is established should be
minimized, said Garbelotto.

Garbelotto will presented these findings yesterday at the annual
meeting of the California Oak Mortality Task Force, a coalition of research
institutions, public agencies, non-profit organizations and private industry
formed to coordinate management, research, outreach and policy efforts
surrounding Sudden Oak Death disease in California. Garbelotto is a member
of the task force.


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 were
chosen to represent the geographic range of Sudden Oak Death infestation and
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 then 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 that had been shut down
because of its Sudden Oak Death infestation, and the Bolinas Ridge site in
Marin County's 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.

"Although our study identified two locations from which the Sudden Oak
Death pathogen spread to other parts of California, the close proximity of
the site in Santa Cruz to a nursery makes it highly probable that the
epidemic began there rather than at Mt. Tam," said Garbelotto.

Garbelotto noted 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
said.

The most likely scenario, said Garbelotto, is that the pathogen
arrived in California through the nursery trade, and that it 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 in landscaping
projects in the area, said Garbelotto.

Based upon the genetic analysis of this study, 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 Sudden Oak Death infestation are
particularly severe are not necessarily the first ones to have become
infected," said Garbelotto. "Big Sur was hit particularly 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."

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 said.

To better understand how different areas ended up with matching
strains, the researchers analyzed how far the pathogen can spread naturally,
such as through airborne spores and wind gusts. To do this, GPS coordinates
were recorded for every plant sampled, and the distance between plants with
identical strains was calculated.

The researchers found that the vast majority of movement occurred
within 200 to 300 meters. However, spores were occasionally found moving 1
to 5 kilometers, possibly aided by strong winds, they said.

"That means if we find a perfect match in strains at sites more than
10 kilometers apart, we can safely assume that the spread did not happen
naturally, and that the pathogen was introduced to the site by some other
means," said Garbelotto. "The Santa Cruz site is about 100 kilometers away
from Mt. Tam, so it's clear that natural spread did not occur between the
sites."

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, said Garbelotto. "Nurseries do not seem to be the
source of current outbreaks of Sudden Oak Death in the wild," he said.
"Unfortunately, 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.

But as the epidemic continues, strains of P. ramorum found in wild
sites are beginning to show greater diversity, the researchers said.

Garbelotto noted 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," said Garbelotto.
"What our study shows is that not every infected site is the same."

Other UC Berkeley members of the research team are Silvia Mascheretti
and Peter J. Croucher, both post-doctoral researchers in the Department of
Environmental Science, Policy and Management.


[www.berkeley.edu]