As we slide into Memorial Day weekend, I thought it would be worthwhile to look back at an earlier forest disease epidemic that galvanized foresters and forest pathologists for half a century and changed the look, makeup, and function of forests in the eastern U.S. for perpetuity: chestnut blight.

This disease, caused by the fungus Cryphonectria parasitica, practically eliminated the American chestnut, Castanea dentata, from the eastern forests to which it is native. In these forests, the chestnut tree was a stately dominant that provided an important mast crop for wildlife and also durable, rot-resistant lumber. Its abundant tannins were used for tanning leather. Because of these qualities, you could think of chestnut trees as having been analogous in different ways to both the redwoods (stateliness, wood quality) and tanoaks (tannins, wildlife food) of our western forests. It was a very important tree that has now been replaced in dominance throughout much of its range by oak species.

Canker on chestnut stem caused by C. parasitica (photo courtesy of Linda Haugen, USDA Forest Service, bugwood.org)

Two particular features of chestnut blight are interesting to me in relation to Sudden Oak Death: (1) its spread was both fast and slow, and (2) it changed the ecological niche of the American chestnut tree without eliminating it entirely.

Chestnut blight was discovered in 1904 and had taken out most mature American chestnut trees by 1940. Looking back, this is swift work! But if we look at it from the perspective of someone learning about chestnut blight in, say, 1913, it might not command the same sense of urgency. At that point, one could not predict its ultimate effects on the east's hardwood forests. This is roughly the same point we are at today with P. ramorum and Sudden Oak Death. P. ramorum was named nine years ago, and we are trying to learn more about it, wondering what its ultimate effects will be. If it does eventually eliminate a majority of its primary host, tanoak, from western forests, this too could take several decades. This is slow according to a human perspective, but from a forest perspective, even a couple of centuries is the blink of an eye.

Above, I said that C. parasitica practically eliminated the American chestnut from its former range. I inserted that "practically" because plenty of American chestnut trees still exist. Their root collars and root systems are fairly resistant to the fungus, and the chestnut can resprout (again, like tanoaks). But before the sprouts can mature, the fungus kills them. Thus, chestnut is maintained as an understory plant rather than as the mature tree it once was. This bears interesting resemblances to the case of tanoak and P. ramorum, in which P. ramorum can kill the main stem and then somehow hang around and continue to cause problems to the new sprouts that re-emerge from the old root system. Whether it does this in every case, or even in a majority of cases, is yet to be seen. Perhaps this won't be as big a problem for tanoak as it was for chestnut. But if it is, tanoak, too, could be reduced to an understory plant that never grows large enough to produce the mast crop that so many wildlife species depend on.

There's a lot more that could be said about chestnut blight--for example, about hopeful efforts to breed resistant trees (this link has a great picture of a historic chestnut stand) and provide biological control of C. parasitica--but for this Memorial Day weekend, thinking about what it has done so far is enough for me. Looking at this historical case through the lens of our uncertainty about the possible future effects of P. ramorum is enough to inspire some thoughtfulness about the future of our coastal Western forests.