Common Name: American Chestnut – The common name is a derivative of the scientific name Castanea which gradually was Anglicized to ‘chesten’; subsequently ‘chesten-nut’ was
American Chestnut Trees grow from the roots until killed by a fungal blight after several years
concatenated to chestnut. American distinguishes it from the European, Chinese, and Japanese chestnut trees.

Scientific Name: Castanea dentataThe generic name is thought to have originated from association with Kastanea, a city in the region of modern day Turkey on the Black Sea known by the Greeks as Pontus. It is hypothesized that the European chestnut, which likely originated in southern Russia, was first grown and the nuts harvested there. In spreading throughout the Roman Empire, the Greek name for the chestnut tree Kastanea became the Latin Castanea. Dentata is the Latin word for ‘toothed’ and refers to the dentate leaf margin.

Potpourri: The American chestnut tree was a key indicator species of the Appalachian uplands from Maine to Georgia for two thousand years as it migrated north with arboreal steadfastness at the end of the last ice age of glaciation. Its heritage extends to the first glimmers of the Holocene Epoch; pollen in New York confirms its presence there about 40,000 years ago. At the turn of the 20th century, and perhaps marking the beginning of the Anthropocene Epoch, the trees slowly but inexorably succumbed to an Asian fungus in what is considered by many to be the most devastating environmental onslaught by an invasive species in recorded history (discounting the literal decimation of North American natives by the European invasion – mostly by diseases - that preceded it by four centuries). The mighty chestnuts once ranged in dense ranks along the mountain ridges and comprised about one quarter of all trees in the 200 million acres of woodlands – the toponym Oak-Chestnut Forest referred. Shortly after his Walden Pond sojourn, Henry David Thoreau wrote “Now is the time for chestnuts. A stone cast against the trees shakes them down in showers upon one’s head and shoulders.”

All that changed in 1876 when a New York horticulturalist named Samuel Parsons received a shipment of Japanese chestnut seeds which he planted in order to sell the exotic Asian trees as a business venture to his orchard customers in several states. Unbeknownst to him, the Japanese seeds were a horticultural Trojan horse; a fungal pathogen lurked in their midst. Unlike its related Chinese and Japanese chestnut trees, the American chestnut lacked immunity to the Asian invader and antibiosis ensued. The devastation began with little fanfare; blight was first discovered almost thirty years later on chestnut trees growing in the New York Zoological Garden by Herman Merkel, the chief forester. Working with the noted mycologist of the New York Botanical Garden, William Murrill, the fungal culprit was identified and named Endothia parasitica. By 1906, almost all the chestnut trees in the Bronx were infected, a harbinger of the disaster to follow. With a touch of irony, Parsons became the landscape architect of New York City in 1895 and served in that capacity until 1911.

The fungus, having been renamed Cryphonectria parasitica by Murrill, is commonly known as either Chestnut blight fungus or Chestnut bark disease. It is one of a family of pathogens in the Division Ascomycota that includes Ophiostoma ulmi which causes Dutch elm disease, and Ceratocystis fagacearum responsible for oak wilt. They occupy a niche of the Kingdom Fungi whose parasitism stands in stark contrast to the beneficent mycorrhizal fungi without which many trees could not survive; both groups of fungi are subject to the same trophic needs they share with animals as only plants make food directly. Chestnut blight begins with spores that land in a crack that bypasses the tree’s protective bark armor. The spores germinate to form the growing hyphal filament of fungal physiology that ultimately evolves to a rust-colored canker, or visible tree wound. The canker can grow outward, in which case it is called swollen, or inward which is called sunken; the latter gradually kills the tree by girdling. Trees are the vascular masters of all botany in the movement of water and dissolved minerals upward in the xylem at the center of the bole to feed the photosynthetic engine of individual leaves. Their product sugars are returned to the roots through the annular phloem that surrounds the xylem just beneath the bark. In disrupting this flow circumferentially, which is called girdling, the canker kills the epigeal tree in a matter of years – but it does not entirely kill the tree below the encircling canker. American chestnut tree relicts resprout from their immortal roots, surviving for several years before the process of canker and demise repeats. Like the chained Prometheus, whose liver is consumed by an eagle only to grow back so that the agony can be prolonged indefinitely, the Greek version of eternal damnation is played out in the truncated chestnut life cycle with its revenant stunted trees. Recrudescent chestnut trees are encountered with some regularity on the trails of the Appalachians, their rebirth an inspiration for those who seek to restore their former grandeur.

The epic struggle to contain the chestnut pandemic blight began as soon as the devastation became manifest; federal funding for chestnut blight investigation was appropriated by Congress in 1911. A USDA study concluded in 1913 that the canker disease was also found in both Chinese and Japanese chestnut trees in mostly mountainous areas, which ultimately resolved the provenance of the fungus. However, due to the immature state of knowledge concerning fungal propagation (fungi were considered to be plants), remediation measures were limited to the standard tree disease methods employed by arborists. Chemical sprays, tree surgery - which amounted to selected removal of infected trees and branches - and the application of primitive fungicides did nothing to stop the die-off. When the cankers appeared in Pennsylvania’s vast forests, even quarantine was attempted by cutting a swath across the Appalachian Mountains as a physical barrier to the advance; ignis fatuus is evident in the lack of adequate scientific knowledge of the long range transport of nearly weightless spores. When it was discovered that chestnut blight had extended to the southern terminus of the Appalachian chestnut forests in Georgia the government funded effort was deemed futile and curtailed. The American chestnut began its slow but inexorable decline; by 1940, the dystopia of acres of dead trees became reality.

American Chestnut Mission Workers House Pocosin Hollow 160611.jpg
Chestnut Siding on the 1904 Pocosin Mission House in Shenandoah National Park
The American chestnut tree was the linchpin of the economy of the southern Appalachian Mountains – the nuts, bark and wood literally provided food, clothing money, and shelter respectively to its denizens. The decay resistant wood was strong, easy to split, and ideally suited to construction of houses, fences and furniture. The tannin-rich bark was stripped from the trees to sell to tanneries for the treatment of leather. According to Reeder’s Shenandoah Secrets, “Generations of mountain men, sometimes aided by wives and children, cut bark ….peeling it all off with a metal tool called a spudder. The bark was stacked to dry … and delivered to the tannery.” American chestnut bark comprised more than half of the tannin for the 21 tanneries in the southern Appalachian region, which were so successful that they operated complementary lumber companies to maintain the chestnut bark resource. The nuts of the American chestnut were prodigious – a large tree produced about 10 bushels of nuts that fell in prickly piles that blanketed the ground so thickly that they could be shoveled into collecting buckets. And, unlike the other nut-bearing oak and hickory trees that produce nuts every 3 to 5 years (a phenomenon known as masting), chestnuts produced an annual crop. Beyond the practicalities of food, clothing and shelter, chestnut leaves were steeped in water to make a tisane tea as a palliative for coughs and an ointment to quell the maddening itch of insect bites and poison ivy, practices adopted from the local Native American Cherokee. The American chestnut “essence,” called somewhat whimsically extractum castanea fluidum was in the U. S. Pharmacopoeia from 1873 to 1905.

While the impact of the loss of the American chestnut tree on the people was serious, it may well be that the less obvious damage to the forest ecosystem was even more profound. The nut crop, while important to the people as a supplement, was vital to the other forest fauna who were likely more highly dependent on its nutrition. It is likely that their numbers declined in consequence. Chestnut leaves have higher levels of nitrogen, phosphorous, magnesium and potassium than other hardwoods and they decay relatively rapidly. The end result is that the forest soil is richer under chestnut forests, a fact confirmed by direct analysis in 2002 by the U. S. Forest Service. Decay resistant chestnut wood in the form of fallen trees and branches provides a more permanent habitat for birds and den-building mammals. The observations of a hiker in 1926 hiking in what is now Shenandoah National Park capture the essence the ecological disaster “I passed through a scene impressive for its desolation, and also a tribute to the destructive powers of the chestnut blight. This section must have been entirely a pure chestnut grove. Now every tree was dead. The rains and snow had washed away the dead bark and bleached the trees a grayish white … A graveyard of giant trees.”

The restoration of the American chestnut forest has been the holy grail of prelapsarian arborists for almost a century; it has proven to be a tough nut to crack. The fundamental precept has been to develop a blight resistant chestnut tree variant. The USDA initiated the first hybridization effort in 1922 by crossbreeding American chestnut trees with resistant Chinese chestnut trees at the Connecticut Agricultural Experimental Station. While there was some success, the hybrids were generally stunted and rarely survived beyond a few years after planting in an open forest; the record tree, named Clapper after one of the breeders, survived blight-free for 19 years but succumbed at the age of 25. By the 1960’s, the dubious success of the chestnut program fell victim to the budget cutting ax and the federal government program funding was terminated. But the aspirational goal of restoring the chestnut to its former glory endured, the flame of hope fanned in part by the eternal growth of the tree, emerging from its living roots even after death; a leafy Lazarus. In the words of Robert Frost in the 1936 poem Evil Tendencies Cancel:

Will the blight end the chestnut?
The farmers rather guess not.
It keeps smoldering at the roots
And sending up new shoots
Till another parasite
Shall come to end the blight.

With the prescience of the poet, Frost predicted a parasite to end the blight, taking advantage of the alliteration. It was recently discovered that a fungal virus from the family Hypoviridae protected the European chestnut tree from the blight fungus, the virus is the parasite. While this is still quite tenuous, it is possible that hypovirulence, at it is now known, may at least play some future role. It is, however, only the latest of decades of effort by legions of dedicated foresters.

There have been four melioristic programs to restore the American chestnut to its erstwhile glory ranging from cross breeding American chestnut trees with each other to retain in totality the original genetic heritage to a GMO chestnut tree, taking advantage of the scientific breakthroughs of modern biology. The first of these programs, which in essence continued the government hybrid program with Asian chestnuts, started in 1983 as the American Chestnut Foundation (ACF). Using improved cross-breeding techniques known as backcrossing to take advantage of generational stepped improvements, a hybrid “Amerasian” chestnut tree was developed; there are now more than 100,000 in about 20 states. In June of 2011, thousands were intentionally inoculated with chestnut blight; a fifth were strongly resistant. A second program was independently organized at about the same time to attempt to achieve blight resistance using only the American chestnut, C. dentata – an All-American tree. For reasons that are obscure, the name American Chestnut Cooperator’s Foundation (ACCF) was selected; the two entities are often confused. A joint venture of Virginia Tech and Concord College, West Virginia, the ACCF took chestnut trees with demonstrable blight resistance and intercrossed them by literally placing a bag over the female flowers and manually pollinating them from male flowers of similarly promising trees, a meticulous process of moistening the stigmas and dragging the catkin anthers across them to ensure pedigreed parentage. According to their 2015 newsletter, the ACCF hybrid chestnut tree population of 2,609 extends across 29 states and Canada. The ACF and ACCF programs constitute classic cross-breeding, a trial and error process in use for millennia for everything from dogs to maize. However, extensive turnover times extend the theoretical construct to decades according to tree time. It takes about 7 years for a hybridized tree to produce nut-seeds and another 5 years of sapling growth to evaluate blight resistance. With the concomitant 12 year test cycle, it is not surprising that there has been marginal progress, as only three to four iterations of the test sequence have been completed since the mid 1980’s. While promising, the ultimate success of American chestnut cross breeding programs is not settled.

Modern genetic methods offer new promise to the restoration of the American chestnut forest. Ironically, the first attempt to genetically modify the American chestnut used the sledgehammer method - gamma and/or neutron radiation to randomly induce genetic mutations – the same thing that gene insertion does according to the new improved method except that in the latter it is carried out with full knowledge of cause and effect. In 1955, a University of Virginia genetics professor named Singleton sent some chestnut seeds to Brookhaven National Laboratory to be bombarded. A decade later, private funding was obtained to establish plantings at Accokeek, Maryland and at Lesesne State Forest in Virginia; the Stronghold Foundation of Maryland independently established a third radiated chestnut plantation at their Sugarloaf Mountain location. It didn’t work – the random mutations were randomly ineffective; the irradiated trees succumbed to blight in the 1980’s. Transgenic experiments were subsequently initiated at the State University of New York at Syracuse in1990. Experimentation revealed that the blight fungus killed the chestnut tree by secreting oxalic acid to lower the pH to a level necessary for the fungal enzymes to extract nutrients. A wheat gene called OxO was identified that catalyzes the oxalic acid to harmless carbon dioxide and hydrogen peroxide and thus renders the blight harmless to the tree. After fifteen years of dedicated effort, the first GMO American chestnut trees were planted in 2006. The transgenic tree is currently pending government approval for reforesting. It is worth noting that the transgenic trees created by irradiation required no approval, they were simply planted. Times have changed. As a symbolic measure, a transgenic tree was planted with some ceremony in 2014 at the New York Botanical Garden, the site of the original blight detection in 1906. We may yet see an American chestnut forest in our time, the restorative powers of science and technology having been fully brought to bear.