Chestnut Blight

Chestnut blight canker in Pennsylvania, USA. Note that canker callus grew for a time, but then the fungus overgrew the callus and continued its invasion.
The spread of chestnut blight was very fast.


Native range of American chestnut. From Little (1977).

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. American chinquapins (C. pumila, C. ozarkensis) are also aggressively attacked and killed ​[1, 2]​. 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 ​[7]​ 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” ​[7]​. 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.

Perithecia of Cryphonectria parasitica in a stroma. The perithecia contain many asci (left) with 8 ascospores each. The ascospores are forcibly ejected and carried in air currents.

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 ​[7]​. 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.

Disease Cycle

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.


Quarantine and eradication are two management approaches that are often attempted with non-native diseases. Quarantines, unfortunately, were applied after the invasion of Europe and North America. Although the disease is well established and widespread, Europe has maintained the quarantine ​[14]​. This may account for the lower diversity of vegetative compatibility types in Europe than in America, facilitating spread of hypovirulence (see below). Oregon continues to quarantine all chestnuts and chinquapins from eastern states; the last report of the disease in the state was 1934 ​[13]​. Eradication was often attempted, but is unlikely to be successful except where the infestation is very limited and the host is well isolated from more general disease occurrence ​[14]​.

We will never have chestnut like we did in 1900, at least not in the next few hundred years. But there are some 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 of the two species and three successive generations of backcrossing to American chestnut ​[6]​. 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 ​[8, 15]​. TACF is now creating seed orchards of intercrossed lines and selecting them for blight resistance.

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.
Hypovirulence is often transmissible. If a hypovirulent and normal isolate grow together, the normal isolate becomes hypovirulent. When an active canker produced by a virulent isolate is inoculated with the hypovirulent isolate, the canker slows and starts to heal in many cases.
Dr. Bill MacDonald presenting data on stem mortality of young chestnut in clearcut and partially cut stands.

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 this is the replicating form of a virus in the family Hypoviridae. It causes a disease in the fungus, making the fungus less virulent ​[3]​. CHV1 is the most common virus used in studies, but other hypoviruses and unrelated viruses can also cause hypovirulence and have biocontrol potential ​[16]​.

Hypovirulence has been moderately effective in Europe, mostly due to natural infection by CHV1. Where the disease is more recently established, hypovirulence is often lacking and requires inoculation of cankers with virus-infected isolates to transfer the virus to the resident pathogen ​[4, 14]​. It also shows some promise in Michigan in the United States. However, it has failed almost completely in eastern North America. ​[9, 14]​. Therapeutic treatment of individual cankers is successful in most cases, but infected individuals must reproduce and propagate the virus in the population to manage the disease. 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 mycelia can fuse and exchange material, they are said to be vegetatively (somatically) compatible, and in the same vegetative compatibility group. North America has more VC groups than Europe, so natural spread of the virus is more limited. But there is hope that it may yet succeed.

Genetic engineering. One of the principle virulence factors of C. parasitica is production of oxalic acid, which kills host cells in advance of colonization. Many plants produce oxalate oxidase, which detoxifies oxalic acid and confers resistance against pathogens that use that strategy. Newhouse et al. transferred an oxalate oxidase gene from wheat to American chestnut ​[10]​. Plants from transformed cell lines and their sexual progeny produce the enzyme and have enhanced resistance to the disease. Some tests suggest they may be even more resistant than Chinese chestnut ​[12, 15]​.

Using high light in a growth chamber, pollen can be produced quickly from these transformed plants. Then wild chestnut can be control-pollinated to produce 50% seed with the gene. Screening for oxalate oxidase is easy and fast. Another generation of controlled pollination results in some progeny being homozygous for the gene, the holy grail. When progeny of transformed trees are planted in the wild, any seed produced with wild trees will be quickly selected because those without the gene will be killed. The gene should propagate in local populations in time.

A major hurdle is regulatory review of planting genetically modified organisms (GMOs, here sometimes called Frankentrees) in the wild. Three agencies are involved, US Department of Agriculture (Animal and Plant Health Inspection Service), US Environmental Protection Agency, and US Food and Drug Administration. USDA is taking the lead in preparing an environmental impact statement. The pre-EIS comment period is closed, but there will be another after a draft EIS is presented to the public. There is significant opposition from the anti-GMO crowd ​[11]​. That’s sad to see, because the ecological damage of obliterating this keystone species was a tragedy, while the damage caused by this gene, which could bring the species back, will be nil.

This petition to deregulate the transgenic trees does a great job of assembling detailed information about American chestnut, its history, the blight, past attempts to bring it back, and this research. Of course it also presents great arguments for deregulation. See the blog post on this work.

Other Issues

American chestnut was a very important tree species to people in Appalachia. The perfect tree.

Most forest pathologists like tree diseases. Generally, I like to see a diseased tree; it’s more interesting than a healthy one. Although human society often 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 the greatest tragedy in American forest history. No one 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 ​[7]​ 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, generations 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 ​[7]​. 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 ​[5]​. 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.


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