This story is taken from Opinion at sacbee.com.

California Environment: How sudden oak death is transforming the state

By Richard A. Lovett -- Special To The Bee - (Published August 15, 2004)

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.

Sacramento's white oaks appear to be immune, possibly because Phytophthora is a "water mold" that needs moister climates - and the trees adapted to them - in order to spread.

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 gray-black 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.

Ecologically, the death of that many oaks is an immense change to California's coastal woodlands. To start with, all of that dead wood will provide fuel for potentially intense fires. In addition, sick, dead and dying trees open the door for the spread of other diseases. That's already happening in some areas, where Rizzo says that a native pathogen, oak root fungus, is already taking hold.

This doesn't mean that California's coastal woodlands are on the verge of turning into deserts. Eventually, some other species will move into the gaps - most likely California bay laurel, Brown says.

Unfortunately, Brown's colleague Kyle Apigian, also of UC Berkeley, says that this may be bad news for birds. Such species as oak titmice and chestnut-backed chickadees, which forage heavily on coast live oak, keep away from bay laurels, Apigian reported.

Nobody's really sure where sudden oak death originated, although some scientists speculate that it was the Himalayas. Wherever it came from, most ecologists believe that it is an exotic species for which California's trees have no native resistance.

Preventing such diseases from spreading is extremely difficult. Other Phytophthora species have been truly catastrophic: One caused the potato blight that led to famine in 19th century Ireland; another is currently devastating entire forests in Australia.

The closest relative to sudden oak death is a type of Phytophthora that causes root rot on Port Orford cedars in Northern California and Southern Oregon. When scientists learned that the disease's spores can be transported on muddy truck tires and hiking boots, the U.S. Forest Service began instituting wet-season road closures. It also began thinning trees from the most at-risk stands, and started requiring logging trucks to wash mud from their tires. The disease continues to spread, although the rate appears to have slowed.

Similar factors might slow the spread of sudden oak death. In another paper presented at the Ecological Society meeting in Portland, J. Hall Cushman of Sonoma State University found that hikers and mountain bikers may be spreading the disease around California parks. Examining soil samples from a nature preserve north of San Francisco, Cushman found that trails were heavily laced with Phytophthora spores, even in regions far way from infected trees. In a separate study of 100 square miles of woodlands between Sonoma and Santa Rosa, he found that heavily used areas were more likely to be infected.

The options for controlling human spread of the fungus aren't good, Cushman says, because they'll provoke conflict between park managers and outdoor enthusiasts. One choice is to do nothing - a choice that will be popular in the short run with hikers and mountain bikers, but which might contribute to the spread of the disease. Alternatively, park managers could shut down trails during the wet season, when the disease most easily spreads: a solution that's guaranteed to be unpopular with park users.

A less draconian solution would be to require hikers and bikers to clean shoes and tires when leaving infected areas. But that would take education, outreach, vigilance - and tax dollars.

Worse, it's possible that none of these will work. Cushman's team has yet to address the question of whether deer, rodents, birds and other animals might be even more effective at spreading disease spores than are people.

UC Berkley ecologist Max Moritz, however, 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 build-up 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 non-fatal 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.


About the Writer
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Richard A. Lovett, a longtime Forum contributor, is a science writer who lives in Portland, Ore.