American chestnut (Castanea dentata), whose native range is shown at left, is highly susceptible to the disease. European chestnut (C. sativa) is also quite susceptible. Chinese chestnut (C. mollissima) is resistant; a small canker can occur. Some oak species (Quercus spp.) get minor bark infections that can produce inoculum.
If you could custom design the ideal tree species, you couldn’t come up with a better one than American chestnut. It was a huge, majestic tree, with a very straight stem. The wood was nearly ideal. As George Hepting  has written, “Not only was baby’s crib likely made of chestnut, but chances were, so was the old man’s coffin.” One of its good qualities was high durability. The heartwood could be used in situations where decay was a hazard. The tree was common. It made up about 50% of most eastern hardwood forests. It grew fast, and would regenerate itself by root sprouts vigorously. The nuts were edible, not only by wildlife but also by humans. It was an important food source for all. “The farmer’s hogs were fattened on chestnuts, and, to no small degree, his children were also” . Chestnut was also prized as a landscape tree.
The pathogen is Cryphonectria parasitica. It is an ascomycete, and produces perithecia in small stromata. They can appear at any time of year when conditions are suitable. The perithecial necks are very long and come together where they protrude through the bark. The ascospores are forcibly ejected and wind-dispersed.
Usually prior to perithecia, pycnidia are produced in the same small stroma or in other stromata. They also can appear any time of year. The conidia ooze out in a tendril after rains. They are quite small, as small as 4 x 1 µm wide. In that little conidium is all the information and machinery necessary to wipe out one of the most important tree species in North America. Conidia may be carried by rain splash or catch a ride on an insect or bird.
In 1913 a USDA plant explorer found the fungus in its native land of China . There, it was hardly a pathogen, colonizing dying twigs and small patches of bark.
Within the range of environmental conditions found in the geographic range of chestnut, there do not appear to be important differential effects of the environment. Environmental conditions are conducive to disease throughout the range of chestnut.
Conidia and ascospores can infect wounds, even very small ones that don’t go all the way to cambium. It is thought that insects of various kinds make most of the infection courts.
The fungus grows in the inner bark and cambium, producing small brownish mycelial fans. Even after the branch or stem is girdled and killed, the fungus continues to colonize it, producing ever more inoculum.
Chestnut blight is a canker disease. Perhaps it is called blight because infected branches and stems die quickly, as in a shoot blight. But it doesn’t just infect shoots; it infects branches and stems of any size.
The cankers are of the diffuse type. They grow rapidly and in most cases continue to develop until the stem is girdled and killed; then they continue to colonize the dead tree.
In North America, chestnut blight is present in the entire native range of the host and has moved to areas of planted chestnut far from the native range. It is also present in Europe, and the pathogen is native to China, where it causes an inconsequential disease of Chinese chestnut.
We will never have chestnut like we did in 1900, at least not in the next few hundred years. But there are two areas of hope for some form of recovery.
Breeding for resistance. Chinese chestnut is somewhat resistant. The fungus causes persistent perennial cankers rather than diffuse cankers. Resistance can slow the fungus down and limit its reproduction. But chinese chestnut is not such a great tree – it is short and spreading instead of tall and straight, with less desirable timber and fruit characteristics. So traditional breeding followed by backcrossing is underway, primarily by The American Chestnut Foundation (TACF). Although it is slow and a grope in the dark, there has been success in developing individuals with characteristics of American chestnut after hybridization and three successive generations of backcrossing . This yields a generation (BC3) that is 15/16 American chestnut, but has been selected at each stage for resistance and form. Then follows 2 generations of intercrosses among promising BC3 individuals to make them homozygous for blight-resistance alleles. TACF is now increasing seed production of blight-resistant lines for outplanting in test sites throughout the natural range of American chestnut . There are also plans to introduce resistance genes into chestnut directly.
Hypovirulence literally means “lesser virulence.” Soon after epidemics began in European chestnuts, it was observed in Italy and France that some cankers spontaneously slowed down or stopped. Experiments and observations showed that the trees involved were no more resistant than other trees:
|Isolations from normal cankers gave fast-growing isolates. When they were inoculated into new trees, normal, lethal cankers resulted.|
|Isolates from the cankers that slowed or stopped growth looked different from isolates from normal cankers. They grew more slowly and didn't fruit well. These isolates didn't cause much of a canker when reinoculated, so are called hypovirulent.|
|It was found that hypovirulence was in some cases transmissible. If they allowed a hypovirulent and normal isolate to grow together, the normal isolate became hypovirulent in many cases. When they had an active canker produced by a virulent isolate, and inoculated with the hypovirulent isolate, the canker slowed down and started to heal in some cases.|
It was later found that hypovirulent isolates have a piece of double-stranded RNA, which doesn’t normally occur in fungi. It is now known that the dsRNA is a virus in the family Hypoviridae, and essentially causes a disease in the fungus, making it less virulent .
Hypovirulence has had limited success against chestnut blight . It shows promise in some locations in Europe and in Michigan in the United States. However, it has failed almost completely in eastern North America. Therapeutic treatment of individual cankers is successful in most cases, but the success of hypovirulence at the population level depends on the natural spread of viruses. It is not clear how well the hypovirulent strains can reproduce, disperse, and make contact with virulent strains in nature. Factors limiting spread of the virus are not well understood.
One natural barrier to virus spread is hyphal fusion among individuals of the fungus. Hyphal fusion is necessary to transmit the virus. When hyphae can fuse and exchange material, they are said to be vegetatively compatible, and in the same vegetative compatibility group. In North America, we have more VC groups than they do in Europe, so getting the virus to spread around in nature is going to be difficult. But there is a lot of hope that it may yet succeed.
Most forest pathologists like tree diseases. Generally, I would like to see a diseased tree more than a healthy one. Although human society generally has a goal of reducing such diseases, if the truth be told, sometimes we root for the pathogen, just because it’s such fun to see a disease really do a job.
But chestnut blight is a different story. What it did to American forests is no joking matter. It’s a tragedy. Noone who loves forests can think about the decimation of such a fantastic and abundant tree species as anything else. An informal article by George Hepting  gives some insight into the role of chestnut in American life as well as the chaos that ensued in scientific and political circles as society struggled to deal with the new disease.
There is an emotional hook there that other diseases just don’t have. Even today, many years after the American chestnut was essentially wiped out as a forest tree, there are many ordinary citizens deeply interested in doing something to bring it back.
The reason there is little resistance in American Chestnut is that the pathogen was introduced. In 1904, the disease was observed in the New York Zoo killing chestnuts, but there is reason to suspect it was here as early as 1893 . The pathogen was later found to be native to China and was apparently introduced on nursery stock. In Asia the fungus was a weak parasite. In America, it spread very quickly and never met a tree it couldn’t kill. It spread up to 50 miles per year over the natural range of chestnut.
By 1940, chestnut was destroyed as a commercial species. The equivalent of 9 million acres of American chestnut had been destroyed . Today, incredibly, chestnut still survives in much of its former range, but only as sprouts from the old root systems. The roots and root collar are resistant. In many places, various oaks have replaced it. In dense oak stands, you can hardly find chestnut. But when the oaks are cut, fairly dense sprouts of chestnut pop up, trying to do their thing. But before they can get big enough to sexually reproduce, the damn disease cuts them down. They don’t seem to stand much chance of adapting.
- 1.Choi GH, Nuss DL. 1992. Hypovirulence of chestnut blight fungus conferred by an infectious viral cDNA. Science 257(5071):800–803.
- 2.Diller JD. 1965. Chestnut Blight. Forest Pest Leaflet 94., Vol. 94 Washington, D.C.: USDA Forest Service <https://www.fs.usda.gov/Internet/FSE_DOCUMENTS/fsbdev2_043617.pdf>.
- 3.Diskin M, Steiner KC, Hebard FV. 2006. Recovery of American chestnut characteristics following hybridization and backcross breeding to restore blight-ravaged Castanea dentata. Forest Ecology and Management 223(1):439–447 <10.1016/j.foreco.2005.12.022>.
- 4.Hepting GH. 1974. Death of the American chestnut. Journal of Forest History 18(3):61–67.
- 5.Horton T. 2010. The continuing saga of the American chestnut. American Forests 115(4):32–37 <https://www.americanforests.org/magazine/article/revival-of-the-american-chestnut/>.
- 6.Milgroom MG, Cortesi P. 2004. Biological control of chestnut blight with hypovirulence: a critical analysis. Annual Review of Phytopathology 42:311–338.