New infections of American chestnut in the South occurred faster than government programs were able to eradicate infected stems. A legislative appropriation in North Carolina provided funds to cut a swath across the mountains to stop the spread. Before the cutting was well underway, E. parasitica infected chestnut trees throughout the species' range in the south.
Within 40 years, the disease had spread by wind, birds, and insects to all American chestnut-growing zones. There was one exception. In the late 1950s, a stand of a few healthy stems at elevations above 4500 feet in the southernmost Blue Ridge Mountains still persisted, perhaps separated for awhile by distance from forests of diseased trees.
The feet of a single downy woodpecker carried over 7,000 E. parasitica spores. When these minute unicellular reproductive organs land on the bark of trees, they produce spore horns that exude from bark pustules. Dissolved by rainwater, the small particles wash into bark wounds. Other
spores are "shot" from pustules into the air and carried on wind currents for great distances. Infected trees die as the fungal mycelia strands spread within the inner bark and sapwood.25
Sites left vacant by the death of chestnut trees have been captured by several other understory hardwoods, the crowns filling small openings. On mesic sites in the Great Smoky Mountains, eastern hemlock, yellow-poplar, basswood, sugar maple, hickories, and chestnut oak take over the land. Pure, vigorous yellow-poplar stands, mostly limited to the coves and lower slopes, make rapid growth. Above the coves on dry slopes and ridges, species more drought-hardy than chestnut now dominate. These include chestnut oak, scarlet oak, sourwood, and pitch pine. All oaks together compose about 40% of the replacement species in the Smoky Mountains. Composition of the post-
chestnut forest is similar for both the Blue Ridge Mountains and the Cumberland Plateau of the Appalachian chain.26
A prolific sprouter, coppice shoots of American chestnut stems often arise following death of above-ground stems. Thus, the species is not in danger of becoming extinct. Sprouts from roots of disease-killed stems escape the blight long enough to bear fruit. Seeds from the fruit germinate and young trees survive, in turn to produce nuts, before succumbing to the fungus. There appears little promise for blight-resistant trees to appear among the survivors of the species. Neither does the extensive research in hybridizing with resistant Chinese chestnut species from the mountains of the Peoples' Republic of China encourage optimism for the return to commercial status of this valuable broadleaf tree. American chestnut has responded to virus-induced hypovirulence, but only when hybridized with certain oriental chestnut species. The compatible hypovirulent isolates of E. parasitica applied to blight cankers reduces the dieback. Similar healing remains to be demonstrated for non-hybridized American chestnut trees.27
Even before the appearance of the chestnut blight, disease was an important factor in the evolution of upland forest composition. The ink rootrot, caused by the common Phytophthora cinnamomi, eliminated many chestnut stands between 1825 and 1875, according to dendrochrono-logical studies. A black liquid dye extracted from the wood by pioneers suggested P. cinnamomi as the causal agent of a tree's death.28
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