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blight of chestnut

Cryphonectria parasitica
This information is part of a full datasheet available in the Crop Protection Compendium (CPC);www.cabi.org/cpc. For information on how to access the CPC, click here.
©CAB International. Published under a CC-BY-NC-SA 4.0 licence.

Distribution

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Host plants / species affected

Main hosts

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Castanea (chestnuts)
Castanea dentata (American chestnut)
Castanea sativa (chestnut)

List of symptoms / signs

Leaves - wilting
Stems - canker on woody stem
Stems - dieback
Stems - gummosis or resinosis
Whole plant - plant dead; dieback

Symptoms

The first evidence of infection on blight-susceptible chestnut trees may be a small, flat, orange-brown area on the smooth bark tissues of the main stem or branches. These small lesions may be associated with a small, shade-killed branch. The lesions develop into sunken cankers as buff-colored mycelial fans develop in the bark, at one or more bark depths in the phloem to the vascular cambium. The margin of the cankers may slight slightly and the bark may crack. Small, yellowish to orange stromata containing conidiomata break through the bark and become larger and more numerous as the canker grows. Distinctive yellow tendrils (cirrhi) of conidia extrude from the stroma in wet weather. In the later months of the first year, papillae and/or the black necks of the perithecia become apparent on the stromata. Stromata may reach densities of 50 or more per cm² and over 1000 per canker on American chestnuts. Cankers or stromata on European chestnuts may contain no, few, or many perithecia. Soon after, depending on the diameter of the stem, the canker expands around the circumference of the stem and the vascular cambium is girdled and killed on susceptible chestnuts. Wilting and death of the foliage above the branch or stem canker follows. On older and rougher bark with rhytidome, or on blight-resistant chestnuts or oaks, cankers may not be as obvious, and stromata may be infrequent. Blight-resistant trees infected with virulent strains may have superficial and swollen cankers with thick rhytidome, due to the wound periderm formation, or callused and swollen cankers, which develop after a small area of the vascular cambium has been killed. Intermediate cankers may be formed also with irregularly swollen and sunken areas within a canker. Killing of the vascular cambium and stem death can occur in normally blight-resistant Chinese chestnuts after severe spring frosts or at high altitude, but it is uncommon. Blight-susceptible chestnuts infected with hypovirulent strains may exhibit the same canker types exhibited by blight-resistant chestnuts and oaks infected with virulent strains. In the case of the former, only stromata with conidiomata may be formed by the hypovirulent strains. For further information, see Shear et al. (1917); Heald (1926); Sivanesan and Holliday (1981); Roane et al. (1986); Heineger and Rigling (1994); Guérin et al. (2000); Hogan and Griffin (2002).

Prevention and control

Research on the control of C. parasitica centres around breeding for blight resistance using the high levels of blight resistance found in Asian chestnut species; breeding using the lower levels of blight resistance in some European and large, surviving American chestnuts; the use of hypovirulent strains of C. parasitica that are infected with dsRNA hypoviruses; forest management practices; and application of soil and microbe compresses to cankers. After early efforts to hybridize Chinese and Japanese chestnut with American chestnut did not produce blight-resistant trees with forest-tree form, the backcross method of breeding was suggested and adopted (Burnham, 1981). With this approach, blight-resistance genes from Chinese chestnut are transferred to American chestnut by backcrossing the most resistant Chinese x American hybrids to American chestnut three or more times. Then, the most blight-resistant progeny are intercrossed to obtain the level of blight resistance of Chinese chestnut with the forest-tree form of American chestnut. Good progress with the aid of molecular mapping is being made in this approach (Anagnostakis, 1992; Kubisiak et al., 1997; Hebard, 2002). Selected trees of European chestnut (Bazzigher, 1981) and some large, surviving American chestnut trees (Griffin et al., 1983) have been shown to have useful levels of blight resistance. The American chestnuts have been intercrossed to increase the level of blight resistance (Griffin, 2000).

Hypovirulent strains of C. parasitica, infected with Cryphonectria hypovirus 1 (CHV1), have spread naturally on European chestnut in Italy, southern Switzerland, and surrounding countries (Alleman et al., 1999). The spread of CHV1 and the hypovirulent strain have been associated with natural chestnut blight control on European chestnut, even though C. parasitica strains in different vegetative compatibility types potentially limit hypovirus transmission (Heiniger and Rigling, 1994). In addition, artificial inoculation of cankers with hypovirulent strains has been used successfully to control blight on European chestnut infected with a few vegetative compatiblity types of C. parasitica (Grente, 1981;Turchetti and Maresi, 1988). In contrast, cork-borer hole inoculations around cankers with mixtures of CHV1-infected C. parasitica and other hypovirulent strains of American origin have not generally resulted in blight control on blight-susceptible American chestnuts. Vegetative incompatibility among the many strains of C. parasitica present on American chestnut has been identified as an important barrier to transmission of hypoviruses and conversion of virulent strains to hypovirulence (Anagnostakis and Day, 1979; Liu and Milgoom, 1996). In addition, the abundance of virulent inoculum in American chestnut stands, the high blight susceptibility of American chestnut, and stressful site factors may result in rapid tree death and insufficient time for CHV1 and other hypoviruses to spread (Griffin, 2000). Inoculation of CHV1-infected C. parasitica strains around cankers on grafted American chestnut trees, derived from large survivors, has resulted in a high level and a long period (20 years) of blight control; spread of CHV1 into a large number of C. parasitica vegetative compatibility types on these trees has occurred (Hogan and Griffin, 2002). In this integrated management approach, low levels of blight resistance in the chestnut grafts, spread of CHV1, favorable spatial patterns of hypovirulent strains and vegetative compatibility types on the trees, and favorable forest management factors (low attitude, mesic site with control of competing hardwoods) have been associated with blight control.

Application of soil, compost, or sphagnum peat compresses, or antagonistic microbes (Roane et al., 1986; Tattar et al., 1996) to individual cankers has resulted in some blight control, but is limited to accessible parts of a tree, such as the lower stem or branches. Each canker must be treated separately. Soil compresses should be applied early in canker development to be effective. Graft unions can be protected from C. parasitica using soil from the base of the tree in a similar manner. Chemical control has not been effective except for the protection of graft unions with fungicides (Turchetti et al., 1981; Canciani et al., 1995).

Impact

The American chestnut was the most important tree species in the former oak-chestnut forest and a dominant species in the mixed mesophytic forest of eastern North America. It was very important economically for timber, edible nuts, and tannins. Within 40 years following discovery in 1904 of the chestnut blight disease in New York City, almost all canopy or 3.5 billion American chestnut trees were killed by C. parasitica in these regions. The area affected ranged from Maine in the north to Alabama in the south to southeastern Michigan, Indiana, and Ontario in the west. The American chestnut survives presently as mostly non-flowering, small understory trees on which C. parasitica is endemic. In Europe, the chestnut blight disease was discovered in 1938, and has been less destructive there, killing fewer trees than in North America. The lower level of disease may result in part from a higher level of blight resistance in the European chestnut; also, the recovery of chestnut stands and coppice stems in Italy, southern Switzerland, and surrounding countries has been associated with the natural occurrence of hypovirulent strains of C. parasitica (Anagnostakis, 1982; Heineger and Rigling, 1994; Roane et al., 1986). Although Chinese chestnut is considered to be highly blight resistant, variation in resistance has been found among Chinese chestnut cultivars and wild chestnut trees, and C. parasitica presently is considered to be the most important pathogen affecting the genus Castanea in China (Qin et al., 2002). The pathogen is also sometimes destructive in Japan on the relatively blight-resistant Japanese chestnut (Uchida, 1977). On oaks, the pathogen has been an important pathogen on live oak and post oak in the USA (Roane et al., 1986).