Sudden Oak Death
Perspective1
Presented below is a condensed version of an August 15, 2004 editorial by
Richard A. Lovett that appeared in the Sacramento Bee. Lovett is a science
writer who lives in Portland, Ore.
California Environment: How sudden oak death is transforming the state
California's oaks are dying. Not all of them and not the ones around
Sacramento, but enough to raise questions about whether the Golden State's
ecology is about to be wildly altered.
The problem is a blight called sudden oak death, which started cropping up in
1995 and has since killed tens of thousands of trees, mostly in the coastal
mountains between Big Sur and northern Sonoma County. In places, the blight is
so extensive that entire hillsides have been devastated, says David Rizzo, a
plant pathologist at the University of California, Davis. The disease has also
shown up in nursery trees shipped to at least 17 other states and in Europe,
raising concerns that it may rapidly spread across the globe.
Sudden oak death is caused by a fungus called Phytophthora ramorum, which
invades the trunks of tanoaks and coast live oaks. Tanoaks are common in redwood
forests; coast live oaks are the dominant species in much of the rest of the
Coast Ranges.
The name "sudden oak death" is a bit of a misnomer. The disease actually infects
trees for several years, invading their trunks and causing them to ooze reddish
sap that looks disturbingly like blood. Eventually, the infection spreads
completely around the trunk, girdling the tree and preventing the flow of sap.
That's when the tree dies. From a distance, it does appear to be sudden because
until the infection cuts off the sap, the tree looks green and healthy. Then,
its branches die, all at once.
One of the problems with controlling Phytophthora is that the fungus infects
many plants other than oaks. Some it kills there are indications that
California's madrones may also be at risk but others simply develop a grayblack
mold on their foliage. These "foliar" infections don't kill the plant, but they
produce vast numbers of spores that may carry the disease to more susceptible
species.
To date, the infection has been patchy hitting some areas strongly and others
not at all. Rizzo believes it became established during the wet El Niņo years of
the early 1990s and continues to spread whenever the state gets an unusually wet
winter. Thus, after the wet April of 2003, it invaded numerous new areas,
including San Francisco's Angel Island State Park. But the dry spring of 2004
may have temporarily put the brakes on additional spread.
Meanwhile, scientists are scrambling to understand the disease and find ways to
control it. So far, much of the news is bleak. Early this month, at a meeting of
the Ecological Society of America in Portland, Ore., Letty Brown, an
environmental science graduate student at UC Berkeley, reported that the
infection might be even more destructive than had previously been thought.
Prior studies had found that Phytophthora infected from 4 percent to 30 percent
of the coast live oak in any given patch, and from 20 percent to 70 percent of
tanoak. But Brown found that up to 27 percent of the coast live oak within her
study plots died in the two-year interval from 2002 to '04. (Her research
focused only on coast live oak, and not the even-more-susceptible tanoak.) If
you add in recently dead trees that were probably killed by sudden oak death,
plus living trees showing symptoms of Phytophthora infection, the death rate in
her most heavily infected plots may soon exceed 60 percent. And that's not
counting any still-healthy trees that might yet succumb to the disease.
UC Berkeley ecologist Max Moritz believes that the future may not be completely
bleak. In yet another study presented at the ecology meeting in Portland, he
argued that controlled burns might someday play a role in preventing the spread
of the disease.
Ecologists have long believed that fire suppression may play a role in making
ecosystems vulnerable to disease outbreaks. The argument is that the buildup of
excess vegetation forces plants to compete too strongly for light, water and
nutrients, reducing their ability to fight off infection.
In seeing whether this applies to sudden oak death, Moritz compared the
locations of known infected zones to those where fires have occurred since 1950.
He found that infections were strongly concentrated in regions where fire had
been absent.
Remarkably, he says, fires that occurred 20, 30, 40 or 50 years ago decades
before the first case of sudden oak death was observed are affecting the
current resistance to it.
Moritz has several hypotheses for why this might be the case. One is simply the
weakening effect of dense vegetation on plants' disease resistance. But another
factor is that California bay laurels (whose leaves can play host to the
nonfatal form of the mold) change their chemistry as trees age. Young trees have
leaves that produce large amounts of aromatic chemicals called phenols, which
serve as natural antibiotics. But as the trees age, the amounts of phenols go
down. Fire resets the cycle by burning out the old bay laurel and allowing
disease-resistant young plants to grow in its place.
Another factor is that soil chemistry changes with the length of time since the
last fire. In particular, fire increases the amount of calcium in the soil, and
calcium, Moritz says, is an important factor in disease resistance.
Rizzo agrees that fire is probably an important part of the sudden oak death
story, and he applauds Moritz's efforts to figure out the link. He's concerned,
though, that the full story might prove to be quite complicated. His own
studies, he says, have indicated that the healthiest trees are the most
susceptible to infection.
"It may turn out that areas that burned 30 years ago are more resistant to
invasion," he says, "but once the cat's out of the bag (i.e., the disease has
become established), fire may or may not help."
People concerned about the future of California oaks point to other blights that
have devastated American forests. A few decades ago, Dutch elm disease swept
across the East and Midwest, demolishing trees that once shaded small-town lawns
throughout the American heartland. Earlier, chestnut blight wiped out the
American chestnut, previously a dominant species in the Eastern hardwood
forests.
It's easy to look at these prior examples and become depressed. Who wants to
lose yet another tree species? But even as he doubts that Moritz has found an
easy way to control sudden oak death, Rizzo doesn't paint a totally bleak
future. To begin with, he says, oaks won't go extinct. Fungicides exist that can
effectively protect individual trees in backyards, nurseries and parks.
Nor will large chunks of California be denuded. Wild tanoaks might be in
trouble, but coast live oak appears to be quite variable in its susceptibility
to the disease: Some stands quickly sicken and die, others don't. Why the
difference? "That's the $10,000 question," says Brown. Even if Moritz is right
and fire plays a role, it's likely that a host of other factors are at work, as
well.
The woodlands themselves will persist. Eastern forests are still green, despite
the loss of elms and chestnuts. People who don't know that those trees once
existed don't notice that anything is absent.
And yet, those of us who remember the elm, and who've read about the chestnut,
do miss them. Let us hope that California's oaks one of the signature species of
the Coast Ranges never join the elm and the chestnut on the list of things that
future generations don't even know they're missing.
1 Reprinted from California Oak Foundation Newsletter December
2004
