FEATURE ARTICLE (September/October 2004)

Here in the 100th Anniversary year of the first  detection of

the chestnut blight, the tree that has largely replaced it in the forests of the southern Appalachians is at risk for a similar fate. Though extinction of our oaks is neither certain nor necessarily imminent, the threat is real enough to
have mobilized experts in the region and to have garnered a $15.5 million infusion of federal funding to help make sure it does not become either.

“All words about the American Chestnut are now but an elegy for it. This once mighty tree, one of the grandest features of our sylva, has gone down like a slaughtered army before a foreign fungus disease, the Chestnut blight. In the youth of a man not yet old, native Chestnut was still to be seen in glorious array, from the upper slopes of Mount Mitchell, the great forest below waving with creamy white Chestnut blossoms in the crowns of the ancient trees, so that it looked like a sea with white combers plowing across its surface. Gone forever is that day; gone is one of our most valuable timber trees, gone the beauty of its shade, the spectacle of its enormous trunks, sometimes ten to twelve feet in diameter. And gone the harvest of the nuts, that stuffed our Thanksgiving turkey or warmed our hearts and fingers at the vendor’s street corner.… From the time the blight was first detected, in 1904 in the New York Zoological Park, it spread with a sickening rapidity. Crossing New Jersey, it entered the great Chestnut stands of Pennsylvania; that state, thoroughly alarmed, appropriated a large sum for the control of the malady, in which the federal government joined. But all in vain. Destruction of infected trees proved ineffectual; new infections broke out at distant points. For it was discovered that the spores are carried far by wind, and the disease was already scattered so far that quarantine lines were futile.…Never again will those proud forests rise.” —Donald Culross Peattie, “A Natural History of Trees of Eastern and Central North America”

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I am sitting in an office in the USDA Forest Service Southern Research Station in Asheville, talking to an affable man with curly gray hair and matching mustache whose name, all too appropriately, is Steve Oak. A USDA Forest Health Protection plant pathologist whose specialty is oak diseases, Oak’s life has been a blur of training sessions, conference calls and task force meetings since March 9. That was the day that the USDA’s Animal and Plant Health Inspection Service (APHIS) announced that  a huge Southern California wholesale nursery had shipped plants to customers all over the United States that might be infected with the pathogen that has caused tens of thousands of West Coast oaks and tanoaks to die. The pathogen, Phytophthora ramorum, causes three diseases, two of them relatively benign. The third is a killer known as Sudden Oak Death (SOD). If unleashed in eastern forests, SOD could cause an ecological disaster as devastating as the chestnut blight. Sudden Oak Death is something of a misnomer, as another SOD researcher has observed, since the pathogen or causal agent affects other species in addition to oaks, since disease expression is not always sudden, and since not every infected tree dies. But it has become a major killer of western oaks in less than a decade. P. ramorum is a “new” pathogen, first detected in the United States in California in 1995, and not identified until 1999. Until this spring, its range in the US – it is also present in Europe – was thought to be confined to 13 central coastal California counties and part of an Oregon county near the California line. Quarantines prohibited nurseries located in the infected counties from shipping the pathogen’s host plants, which include rhododendrons and other ornamental shrubs, out of state. But Southern California, the location of the Monrovia nursery that shipped the suspect stock, was outside the quarantined area. By the end of March, when APHIS expanded the quarantine to cover all California nurseries, P. ramorum had escaped its former bounds.

Within days of the March 9 announcement, laboratory tests showed that infected stock had indeed made its way to the East. By May 13, with testing still incomplete, stock shipped by Monrovia and Specialty Products (another Southern California mail order business) to 118 nurseries and garden centers in 14 states – including North Carolina, Tennessee, Maryland, Alabama, Virginia and Georgia – had tested positive for P. ramorum. By that time too, Oak, in his capacity as technical coordinator of the National SOD Detection Survey, had held three training sessions – one in New England, one in the Midwest and one in the Southeast – for state cooperators who are conducting surveys involving 11 host genera this summer, combing forests for SOD. The “soldiers in the SOD army,” as he calls them, are drawn from 35 states, most of them east of a line from Minnesota to Texas. APHIS is conducting a second national SOD survey – of nurseries – looking for SOD-infected stock. On May 18, Agriculture Secretary Ann Veneman transferred $15.5 million in emergency funding to APHIS for nursery inspection, sampling and testing, SOD education and outreach. “We’re operating in crisis mode now,” Oak acknowledges. But it’s too early to assume that SOD will devastate eastern forests, he says. Why? First, because “while the pathogen that causes SOD has arrived in the East, the killing disease has not expressed itself here.” At least not yet. Whether it will, no one knows – nor wants to run a field experiment to find out. “There are a range of possible outcomes in the East that run from a chestnut blight-type scenario to innocuous,” he says. “What’s hampering our finding out is that this is a quarantined pathogen that requires a ‘containment greenhouse’ to study it outside of the regulated areas on the West Coast.” A containment greenhouse is a hyper-controlled environment secure enough to ensure that not so much as a single spore accidentally escapes. There’s only one of these facilities in the East – at Ft. Detrick, Md.

 

Steve Oak. The aptly named expert
says "it's virtually certain that infected
plants have been planted in people's back yards."

Three years ago, Oak provided specimens of 10 different Eastern forest trees, 8 of them oaks, to a researcher there named Dr. Paul Tooley, who inoculated their stems and foliage with P. ramorum. The results were bad news for eastern species: all 10 developed symptoms of the disease, though some were more susceptible to the pathogen than others. Especially ominous were results that showed that chestnut oak – a member of the white oak group – was the most highly susceptible of all the tested species. “The implications are that, unlike Western white oak species which have been unaffected by SOD, Eastern species in the white oak group can be infected,” Oak says. “In greenhouse inoculations, chestnut and white oak were the most susceptible, followed by northern red oak.” Still, Oak cautions, what happens in the laboratory may not occur in the field. Lab conditions are tilted in favor of the pathogen – the goal, after all, is to discover whether it is capable of infecting a potential host. Tooley directly introduced P. ramorum into stem wounds; he sealed leaves into plastic bags containing P. ramorum sporangia and shook them up. In the field, conditions are more haphazard. Spores of P. ramorum may land on the leaves of a foliar host, where they produce blotchy brown spots on the leaves’ surfaces. Those spots are spore factories, producing more inoculum, which a puff of wind may – or may not – lift to a nearby oak. Some foliar hosts produce more spores than others. “Apparently, it takes a lot of spores to infect an oak,” he says, “We don’t know whether we have the foliar hosts – the big inoculum producers – in the East that will create enough inoculum to infect our oaks. That’s the big unknown in the East.” But we do know that we have two of the three necessary ingredients to produce SOD: an abundance of host plants susceptible to ramorum leaf blight and ramorum shoot dieback, the two less-threatening diseases. In addition to the tests he conducted on the 10 tree species, Tooley tested many varieties of woody ornamentals that are native – and common – to the Southern Appalachians and Blue Ridge: mountain and sheep laurel; flame, pinkshell and smooth azalea; Carolina, Catawba and Rosebay rhododendron; and dog hobble. All proved susceptible to P. ramorum. And, for most of the year, we have precisely the kind of environment – cool and moist – that P. ramorum requires to thrive.

Mabry Mill. Rhododendron, azalea and oak's
susceptibility to P. ramorum could change the look of one
of the most-photographed spots on the Blue Ridge Parkway.

And now we have the pathogen – thanks to interstate commerce and the
nursery trade. Since it’s airborne, and since there are oaks and other hosts pretty much all over the United States (though deserts and the Great Plains are formidable natural hurdles between California to the East), P. ramorum might have reached us on its own eventually. Ever since it was identified as the killer of California’s oaks, its potential for wreaking havoc in the East has been a concern. In the fall of 2002, SOD began dominating Oak’s work. Since March, it’s occupied 95 percent of his time. Last summer he headed up a seven-state pilot survey designed to develop survey methods for early detection of P. ramorum. Using USFS funds, state foresters in Georgia, North and South Carolina, Tennessee, West Virginia, Virginia and Pennsylvania collected 10,000 leaf and oak bark samples from host plants with P. ramorum-like symptoms. A third of the samples came from the perimeters of nurseries, two-thirds from the general forest area concentrated in high risk areas. The samples were tested; all came up negative. Simultaneously, five of the seven states conducted a nursery survey, inspecting hundreds of thousands of plants and collecting thousands of leaf samples. Again, no positives turned up. “The good news was that the techniques used were good enough to detect other Phytophthora pathogens common on plants, but no ramorum,” he says. “The bad news was that it wasn’t a very robust survey – only 10-15 nurseries per state were sampled. Those surveys were preparing us for the day that has now arrived.”
Once the discovery was made that infected plants had been shipped outside California, the wholesalers who shipped them were required to provide a list of their customers dating back to March 2003. Those lists went to state agriculture departments who notified nurseries and garden centers who might have received infected stock, and directed them to stop selling the plants. Agricultural personnel visited each of the nurseries, isolated the suspect stock and took samples. If tests came back negative, sales could resume. But a lot of them didn’t. By early May, plants from 13 nurseries in Georgia and eight in North Carolina alone had turned up positive. (The numbers were lower for other eastern states.) And those were from plants that hadn’t already been sold before the halt sale order was  issued.
“It’s virtually certain,” Oak says, “that infected plants have been planted in people’s back yards.”
He hastens to add that “introduction doesn’t mean establishment” of P. ramorum in the wild. “We think we have an excellent strategy for dealing with the situation inside nurseries that have received infected or potentially infected stock,” he says. “And we have a good strategy for looking in places where the pathogen might have moved, in the immediate vicinity of those nurseries. But we’re working feverishly now to try to reach the back yards.” Cooperative efforts are being launched by state departments of agriculture, state universities and county agricultural extension services to address that problem.
“We have to get people trained, get materials printed and into homeowners’ hands, come up with sampling kits and a way to handle collected samples,” Oak says. “Our strategy in the east will be twofold: early detection, followed by aggressive eradication.” A document to  guide the eradication effort is being developed, based on the approach Oregon – where SOD is present, but in a limited area – has followed.

Why so much effort to prevent a disease that may not materialize? Or – conversely – whose pathogen may already be incubating spores, inoculating host plants, insidiously building to critical mass in this yard and that one, may already have spilled over into the tangle of rhododendron, mountain laurel and oak in nearby woods? The die may already be cast for the trees whose name Steve Oak bears. Trees that – in the 100th anniversary year of the first detection of the chestnut blight – occupy the niche vacated by those vanished giants whose creamy, blossom-studded crowns churned in the wind like ocean waves. Not to make an effort – which may be futile – can’t be an option. As timber trees, as ecosystem components, as providers of mast for wildlife that once relied on burnished nuts hidden within spiky green burrs to make it through the winter, oaks are too vital to eastern forests not to put up a fight, if there’s a fighting chance, to protect them from SOD. The losses, if SOD gains a foothold in our forests, will be staggering. “In the West,” Oak says, “oaks are islands in a sea of conifers. In the East, oaks are the sea."

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