One or more of the features that are needed to show you the maps functionality are not available in the web browser that you are using.
Please consider upgrading your browser to the latest version or installing a new browser.
More information about modern web browsers can be found at http://browsehappy.com/
Initial infestation by C. fagisuga appears as small patches of felted, white wax filaments in cracks in the bark and under bark flakes on the trunk. Heavy infestations appear as coatings of felted, white wax filaments on the rough bark of the trunk, branches and exposed roots (Kosztarab and Kozár, 1988; McCulloch, 2000).
If the scale insect infestation leads to infection of the tree by Nectria fungus, the tree develops beech bark disease, with cankers beneath the bark on the trunk and large branches. The scale insects fall off after the fungus kills the underlying tissues (Toronto Parks and Recreation, 2001). The dead bark may crack further and brown slime flux may form tarry spots on the outer surface. Leaves on dying trees do not reach their full size; they turn yellow and later brown, remaining on the tree through autumn. Branches die back (Kosztarab, 1996), and on some infected trees, may break off in high winds - a condition known as "beech snap" (McCulloch, 2000). The fungus may produce small, reddish fruiting bodies on the surface of the bark in autumn (ODNR, 2004).
Unfavourable site conditions such as shallow soil, steep slopes and south to east exposures were found to have some influence on the occurrence of beech bark disease in Slovakia (Kunca et al., 2000).
Regular thinning measures have been found to be very important in the control of beech bark disease in Germany (Lunderstadt, 2002). Removal of susceptible trees heavily infested by beech scale reduces the spread of beech bark disease considerably, especially if done in the early stages of the outbreak. Heavily infested trees should be cut in winter, when the crawlers are inactive, to avoid spreading the infestation further (NRC, 2004).
Due to the variable regulations around (de-)registration of pesticides, we are for the moment not including any specific chemical control recommendations. For further information, we recommend you visit the following resources:
C. fagisuga is the first of two causal agents of beech bark disease, a devastating disease of beech trees (Houston, 1994a; Toronto Parks and Recreation, 2001). It feeds on parenchyma cell contents in the bark (Dubeler et al., 1997), using long, fine mouthparts (stylets). Attack by beech scale on its own does not seriously damage beech trees; however, the feeding punctures it makes in the bark enable access to the cambium and phloem tissues by one or more species of Nectria fungus, the second causative agent of the complex (Houston, 1994a; Kosztarab, 1996). Beech bark disease is caused by both agents acting together; neither agent can produce beech bark disease symptoms on its own (Perrin, 1977).
Nectria spores are carried by the wind (McCulloch, 2000) but these are unable to infect beech trees unless there is a wound present in the bark (Kunca and Leontovic, 2000). It is the fungus that is responsible for the serious damage to beech trees associated with beech bark disease. Nectria fungus kills the cambial tissues, and blocks the tree's vascular tissues, sometimes ring-barking the tree (Kosztarab, 1996), with cumulative effects on tree vigour (Gavin and Peart, 1993). In North America, mortality may occur 2 to 5 years after initial scale infestation (Stimmel, 1993). In Europe, N. coccinea var. fagiata is the main native fungus involved (although N. ditissima also occurs in Germany (Lunderstadt, 2002)); in North America, the native N. galligena and the exotic N. coccinea var. fagiata are both present.
Beech bark disease has become a serious threat to the timber industry in Europe and in North America (Perrin, 1977). In Europe, C. fagisuga is an occasional pest (Kosztarab and Kozár, 1988) because the native beech trees have co-evolved with the scale, so some are resistant to it. In Normandy, France, Malphettes and Perrin (1974) estimated that beech bark disease was responsible for the loss of 25% of beech timber. In Europe, Malphettes (1977) recommended that beech trees heavily infested with C. fagisuga should be felled and removed without delay because infested timber quickly loses its value.
In eastern North America the American beech, F. grandifolia, did not co-evolve with beech scale and the level of resistance to beech bark disease is much lower than in Europe; resultant mortality frequently approaches 90-100% in individual stands (Morris et al., 2002). It is anticipated that perhaps 50% of large American beech trees in North America will be killed by beech bark disease over the next 20 years; a further 25% will be damaged by the disease, while the remaining 25% should escape scale infestation or Nectria infection during the first wave of the disease (McCulloch, 2000). Evidence suggests that N. galligena will eventually be replaced by the exotic N. coccinea var. faginata as the dominant pathogen in North America (Houston, 1994b).
In aftermath forests (after the first wave of infection has passed), the causal agents of beech bark disease are established on root sprouts and seedlings, which often develop into dense stands. Most of the new and surviving trees become cankered and highly defective (Houston, 1996). Mortality levels can be influenced by the species composition of the forest, with higher levels of mortality being recorded in stands dominated by Tsuga canadensis (Twery and Patterson, 1984).
A sawmill study of beech bark disease-affected lumber in Vermont, USA, showed that most bark defects were removed with the slab and that, where the lumber was affected, the defects reduced grade rather than volume. When the cambium was damaged, however, defects led to losses in lumber yield or quality (Burns and Houston, 1987). In Canada, losses due to beach bark disease varied from region to region; in 1969 1.4 million m³ of timber were lost in the Maritime Provinces (Lavallee, 1976).