Return to Prominence
Controlling Chestnut Blight Disease
By Grant Mortenson | Computer Science Major
The most common tree in America from which timber (lumber) was harvested prior to 1904 was the American chestnut tree. In 1904, the Chestnut Blight (Cryphonectria parasitica) was introduced in America and took its toll on American chestnut trees, which was among the dominant choices of timber prior to its functional extinction today.[1] Its qualities enabled it to be used for shipbuilding and furniture, among many other uses.[2] Today, few American chestnut trees are found along the Appalachian mountains where they used to thrive, and any remaining shoots are unable to grow to maturity before being infected with C. parasitica themselves. The loss of viability of highly profitable timber and chestnuts (the nuts themselves) wreaked havoc on the economy and the environment.[3] Today, few Americans have roasted chestnuts on an open fire, for there are so few mature, seed-bearing trees available to supply the nuts. The dramatic effect on the environment that C. parasitica brought has prompted scientists across the world to study the relationship between C. parasitica and its chestnut tree hosts, many for the sole purpose of determining a means of returning the American chestnuts and their European counterpart to their former prominence. The American chestnut tree may yet be able to return to its former status as a canopy tree in the eastern United States due to ongoing research to increase the natural resistance of the trees to C. parasitica, and to decrease the virulence of the fungus itself by infecting it with a virus known to induce passive behavior, reducing its ability to damage chestnut trees.
The symptoms were first discovered in America on an American chestnut tree in the New York Zoological Gardens.
C. parasitica is a fungal parasite native to East Asia, particularly China and Japan.[4] There are also chestnut trees in the East Asian ecosystem, and they have a natural resistance to the deadly effects of C. parasitica. This does not mean that the trees are impervious to infection, but rather that the trees and fungi are able to live together peaceably, without one ever completely destroying the other.[5] However, American and European chestnut trees do not have the same natural resistance for their own protection, so when C. parasitica arrived in America in 1904 and Europe in 1938, the fungus quickly spread across the indigenous chestnut tree population, wiping out millions.[6] The symptoms were first discovered in America on an American chestnut tree in the New York Zoological Gardens.[7] At first, it was identified as Diaporthe parasitica, but in 1912 it was reclassified as Endothia parasitica. Finally in 1978 it was reclassified to its current identification, Cryphonectria parasitica.[8] A wide range of literature has been published using any of these three names.
C. parasitica “is a bark pathogen, which only infects above-ground tree parts, i.e. stems, branches and, eventually, twigs.”[9] Fungal spores attach to the tree at the point of a wound, such as a crack in the bark like a branch joint or where a branch has been removed or grafted.[10]
The fungus takes root in the cambium — the layer of wood from which the tree actually grows, similar to how bone marrow generates blood cells — and relies on the cambium for its supply of nutrients.[11] This fungal growth is called a canker — which, like a canker sore that can develop in a person’s mouth, is akin to an ulcer or open sore on the tree. C. parasitica kills its host by girdling the tree — completely cutting off a ring of the cambium.[12] When the tree is girdled by the fungus, nutrients are unable to flow through the point of infection to parts of the tree beyond it, so any branches above the girdle will die for lack of nutrition.
Trees do have a built-in mechanism for suppressing infections, especially cankers.
After spore germination, the rate and extent of mycelial fan formation by C. parasitica appears to be a key process in canker enlargement. By building up physical pressure, the mycelial fans split the host cells and advance intercellularly in the bark and cambium of susceptible chestnut species. The host tree reacts against the infection by lignification of cell walls and subsequent wound periderm formation. Mycelial fans, however, are able to penetrate through zones of lignified host cells and developing wound periderm. Only fully developed wound periderm prevents further penetration of mycelial fans. Wound periderm formation is continuously inhibited in susceptible chestnut species because the advancing mycelial fans kill the host cells by means of toxins and cell wall-degrading enzymes.[13]
In other words, when a tree is infected, the mycelium — the vegetative part of a fungus[14] — grows in a fan-like formation, forcing its way between the bark and the cambium, splitting the bark away from the tree and damaging the cambium. The tree responds by attempting to wall off the infection with woody and corky material (lignin and periderm) around the wound. C. parasitica releases toxins and enzymes that prevent the full formation of these defenses. If the canker is not stopped before it surrounds the tree, the girdling process will complete, and the any part of the tree beyond the canker will die. This process may take several years on a fully-grown chestnut tree, but only one or two on a young chestnut tree.
C. parasitica has not been nearly so destructive in Europe as it is in America, which some researchers think shows that European chestnut has a greater resistance to C. parasitica than American chestnut.[15] Researchers also discovered the existence of a mycovirus — the technical name for a virus that infects fungi — in Europe known as CHV-1. Research quickly commenced to determine if CHV-1 could be used as a biological means of controlling the spread and symptoms of C. parasitica. When infected with CHV-1, C. parasitica itself exhibits a range of symptoms, including reduced growth and altered reproduction capabilities, enabling its host tree to fight back and prevent its own demise. Some cankers, after being manually infected with a strain of CHV-1 slowed its growth one year after the inoculation, a result that was counted a success.[16]
Researchers have successfully identified five strains of CHV-1, two found in France, one in Italy, one in Germany, and one in Spain. There is a balancing act that must be performed when dealing with biological methods of control. In order for the hypovirus to spread naturally — negating the need for manual intervention on each tree — the fungus must remain capable of distributing its spores, with the goal of infecting other cankers with the hypovirus. However, in order for the tree to heal, the fungus needs to stop growing and reproducing. Currently scientists are trying to determine the most effective balance between a natural spread of the hypovirus and a hypovirus that is truly effective at controlling C. parasitica. The following passage illustrates the varying effectiveness of the current CHV-1 subtypes.
The fitness of three CHV-1 subtypes (F[rance]1 and F[rance]2 and subtype I[taly]) were analysed in a French study, revealing that the Italian CHV-1 subtype I grew at similar rates and displayed similar sporulation levels as virus-free strains, in contrast to CHV1 [sic] subtypes F1 and F2, which greatly reduced the growth and sporulation of C. parasitica (Robin et al., 2010). The higher level of sporulation of subtype I make this sub- type more invasive than subtypes F1 and F2. The first biological control assay with the Italian CHV-1 subtype I in Cataluña (Spain) yielded good results as regards reducing tree mortality. Almost all inoculated trees healed, and dispersion of the hypovirus was very high in both treated and untreated areas.[17]
The French subtypes are more effective at decreasing the growth of C. parasitica, but the Italian subtype is more contagious. Research is ongoing to determine the best method of balancing the transmission and effectiveness of CHV-1 to keep C. parasitica under control. Manual introduction of CHV-1 to cankers has proven successful at inducing hypovirulence in Serbian and Spanish chestnut orchards, but a means of natural transmission of effective CHV-1 has yet to be discovered.
While the exact mechanism by which CHV-1 induces hypovirulence in C. parasitica is still under research,[18] we do know that the vegetative incompatibility across the varying types of C. parasitica increases the difficulty of transmitting the hypovirus from one canker to another.[19] See the note for further explanation.[20] The range of vegetative incompatibility is far greater in America than it is in Europe, which has inhibited the success of hypovirus treatment in America. Consequently, research in America has primarily focused on creating a crossbreed between Asian chestnut tree species, which have a natural resistance to C. parasitica, and American chestnut trees, which produce higher-quality timber. The nut quality is similar, and Asian trees are commonly used in orchards in China and Japan, but the timber is the true prize of American chestnut trees.[21] Researchers are attempting to backcross the specific genes that control genetic resistance in Chinese chestnut trees and the genes that provide high-quality timber production in American chestnut trees into a breed that will thrive even in the presence of C. parasitica.[22]
It is worth noting that the value of a tree does not end the moment an infection is discovered.
It is worth noting that the value of a tree does not end the moment an infection is discovered. Research has shown that the timber will still be usable even if infection and death by C. parasitica occurs. Gunduz, et al. compared the cellular structure of diseased wood with disease-free wood from the same tree and concluded that the only extra action recommended is to heat treat the wood so as to kill any remaining fungus,[23] with the goal being to prevent further spread of the fungus. The disease did not significantly affect the capabilities of the harvested timber. This is important, because it lowers the minimum requirements for managing C. parasitica. Instead of requiring the total eradication of the blight, the trees may retain a canker during its life and still produce high-quality timber. Diseased wood will be rougher,[24] denser,[25] and absorb less water[26] than disease-free wood, but if a hybrid tree is able to sustain growth and resist canker growth, we may begin the process of reviving the chestnut population in the United States with these hybrid trees.
While neither a universally successful hypovirus treatment nor a replacement breed have been created, progress continues. The blight has been in America since 1904, but it is conceivable that we may see a successful treatment discovered within our lifetime. However, it will take another lifetime for those treatments to have any economic effect, since the trees will still need time to grow to their full stature. Our children or grandchildren may yet be able to roast chestnuts on an open fire, thanks to the work of a multitude of researchers across the Atlantic.
Notes
[1] Ana Eusebio-Cope et al., “The chestnut blight fungus for studies on virus/host and virus/virus interactions: From a natural to a model host,” Virology 477 (2015): 164, accessed April 4, 2018, doi:10.1016/j.virol.2014.09.024.
[2] Gokhan Gunduz et al., “Physical, morphological properties and raman spectroscopy of chestnut blight diseased castanea sativa mill. wood,” Cerne 22, no. 1 (2016): 44, accessed April 4, 2018, doi:10.1590/01047760201622012101.
[3] Ibid.
[4] Ana Eusebio-Cope et al., “The chestnut blight fungus for studies on virus/host and virus/virus interactions: From a natural to a model host,” Virology 477 (2015): 164–165, accessed April 4, 2018, doi:10.1016/j.virol.2014.09.024.
[5] Daniel Rigling and Simone Prospero, “Cryphonectria parasitica, the causal agent of chestnut blight: invasion history, population biology and disease control,” Molecular Plant Pathology 19, no. 1 (2018): 7, accessed April 4, 2018, doi:10.1111/mpp.12542.
[6] Katie Burke, Niche contraction of American chestnut in response to chestnut blight,” Canadian Journal of Forest Research 42, no. 3 (2012): 615, accessed April 4, 2018. doi:10.1139/X2012–002.
[7] Daniel Rigling and Simone Prospero, “Cryphonectria parasitica, the causal agent of chestnut blight: invasion history, population biology and disease control,” Molecular Plant Pathology 19, no. 1 (2018): 7, accessed April 4, 2018, doi:10.1111/mpp.12542.
[8] Ibid.
[9] Ibid., 8.
[10] Anita Davelos and Andrew Jarosz. “Demography of American chestnut Populations: Effects of a Pathogen and a Hyperparasite.” Journal of Ecology 92, no. 4 (2004): 677. Accessed April 9, 2018. http://www.jstor.org/stable/3599727.
[11] Gokhan Gunduz et al., “Physical, morphological properties and raman spectroscopy of chestnut blight diseased castanea sativa mill. wood,” Cerne 22, no. 1 (2016): 44, accessed April 4, 2018, doi:10.1590/01047760201622012101.
[12] Ibid., 44.
[13] Daniel Rigling and Simone Prospero, “Cryphonectria parasitica, the causal agent of chestnut blight: invasion history, population biology and disease control,” Molecular Plant Pathology 19, no. 1 (2018): 11, accessed April 4, 2018, doi:10.1111/mpp.12542.
[14] New Oxford American Dictionary.
[15] Centre for Agriculture and Biosciences International, “Cryphonectria parasitica (blight of chestnut),” Invasive Species Compendium, March 28, 2018, accessed April 14, 2018, https://www.cabi.org/isc/datasheet/21108.
[16] P. Zamora et al., “Control of chestnut blight by the use of hypovirulent strains of the fungus Cryphonectria parasitica in northwestern Spain,” Biological Control 79 (2014): 64, accessed April 4, 2018, doi:10.1016/j.biocontrol.2014.08.005.
[17] Ibid., 59.
[18] Eusebio-Cope, e.g. has spent time addressing the role of DsRNA in the hypovirus. CHV-1 contains DsRNA, which has been identified as the causal agent for the transmission of hypovirulence from one canker to the other by means of sexual spores generated by the canker.
[19] P. Zamora et al., “Control of chestnut blight by the use of hypovirulent strains of the fungus Cryphonectria parasitica in northwestern Spain,” Biological Control 79 (2014): 59, accessed April 4, 2018, doi:10.1016/j.biocontrol.2014.08.005.
[20] Many fungi do not have “male” and “female” reproductive systems, but are isogamous or “gender-neutral”. Some gametes are similar enough to be compatible and form a fertilized seed, but if two gametes are too dissimilar from each other, the two will not be able to produce a fertilized seed. This is known as vegetative incompatibility, when the two gametes produced by the reproductive organs of a fungus are incapable of combining to form a “baby” fungus.
[21]Julia Rellou, “Introduced Species Summary Project: Chestnut Blight Fungus (Cryphonectria parasitica),” Introduced Species Summary Project, Cornell University, March 15, 2002, accessed April 19, 2018, http://www.columbia.edu/itc/cerc/danoff-burg/invasion_bio/inv_spp_summ/Cryphonectria_parasitica.htm.
[22] Centre for Agriculture and Biosciences International, “Cryphonectria parasitica (blight of chestnut),” Invasive Species Compendium, March 28, 2018, accessed April 14, 2018, https://www.cabi.org/isc/datasheet/21108.
[23] Gokhan Gunduz et al., “Physical, morphological properties and raman spectroscopy of chestnut blight diseased castanea sativa mill. wood,” Cerne 22, no. 1 (2016): 55, accessed April 4, 2018, doi:10.1590/01047760201622012101.
[24] Ibid., 49
[25] Ibid., 47.
[26] Ibid., 47.
Bibliography
Burke, Katie, “Niche contraction of American chestnut in response to chestnut blight.” Canadian Journal of Forest Research 42, no. 3 (2012): 614–620. Accessed April 4, 2018. doi:10.1139/X2012–002.
Centre for Agriculture and Biosciences International. “Cryphonectria parasitica (blight of chestnut).” Invasive Species Compendium. March 28, 2018. Accessed April 14, 2018. https://www.cabi.org/isc/datasheet/21108.
Davelos, Anita and Andrew Jarosz. “Demography of American Chestnut Populations: Effects of a Pathogen and a Hyperparasite.” Journal of Ecology 92, no. 4 (2004): 675–685. Accessed April 9, 2018. http://www.jstor.org/stable/3599727.
Eusebio-Cope, Ana, Liying Sun, Toru Tanaka, Sotaro Chiba, Shin Kasahara, and Nobuhiro Suzuki. “The chestnut blight fungus for studies on virus/host and virus/virus interactions: From a natural to a model host.” Virology 477 (2015): 164–175. Accessed April 4, 2018. https://doi.org/10.1016/j.virol.2014.09.024.
Gunduz, Gokhan, Mehmet Ali Oral, Mehmet Akyuz, Deniz Aydemir, Barbaros Yaman, Nejla Asik, Ali Savas Bulbul, and Surhay Allahverdiyev. “Physical, morphological properties and raman spectroscopy of chestnut blight diseased castanea sativa mill. wood.” Cerne 22, no. 1 (2016): 43–58. Accessed April 4, 2018. doi:10.1590/01047760201622012101.
Rellou, Julia. “Introduced Species Summary Project: Chestnut Blight Fungus (Cryphonectria parasitica).” Introduced Species Summary Project. Cornell University. March 15, 2002. Accessed April 19, 2018. http://www.columbia.edu/itc/cerc/danoff-burg/invasion_bio
/inv_spp_summ/Cryphonectria_parasitica.htm.
Rigling, Daniel, and Simone Prospero. “Cryphonectria parasitica, the causal agent of chestnut blight: invasion history, population biology and disease control.” Molecular Plant Pathology 19, no. 1 (2018): 7–20. Accessed April 4, 2018. doi:10.1111/mpp.12542.
Zamora, P., A.B. Martín, R. San Martín, P. Martínez-Álvarez, and J.J. Diez. “Control of chestnut blight by the use of hypovirulent strains of the fungus Cryphonectria parasitica in northwestern Spain.” Biological Control 79 (2014): 58–66. Accessed April 4, 2018. doi:10.1016/j.biocontrol.2014.08.005.
ABOUT THE AUTHOR:
Grant Mortenson, a Junior at Bethel University in Saint Paul, MN, grew up in rural South Dakota. He is studying for a degree in computer science to become an IT administrator. He was born with profound hearing loss, but enjoys listening to theology podcasts, reading, and mathematics.
