Fomitopsis pinicola (brown crumbly rot)

Basidiocarps (fruiting bodies) of F. pinicola constitute the most prominent external symptom of attack. They usually appear on wounds at stem bases (Holsten et al., 2001) and, due to their very conspicuous appearance, can be easily recognized during field surveys. Fruiting of the fungus also means that the decay inside a stem is already at an advanced stage. Following extensive deterioration, brown-rot might emerge on a wound surface, thus constituting another external symptom in cases when the fruiting is absent. The rot caused by F. pinicola develops in both sapwood and heartwood, and may vary in colour from yellow brown to slightly reddish. Cubical cracking is common, and the shrinkage cracks are usually filled with white fungus felts (Wright and Isaac, 1956; Scharpf, 1993). In the advanced stages, wood of dead trees is reduced to a residue of amorphous, crumbly, brown cubical chunks composed largely of slightly modified lignin (Ryvarden and Gilbertson, 1993).The period between infection and the exhibition of external symptoms lasts years or even decades, indicating latent presence of F. pinicola inside living stems. Moreover, in cases when younger trees are wounded and infected by F. pinicola, they usually maintain vigorous growth. Thus, F. pinicola has occasionally been isolated from wounded 30- to 50-year-old stems of Picea abies, but the trees were of healthy appearance and good radial increment (Vasiliauskas and Stenlid, 1998; Vasiliauskas et al., 2001). It is generally believed that, even in the absence of wounding, the fungus is able to enter young trees through twigs and other pathways and remains quiescent until a later wound triggers growth, wood decay and fruiting (Sinclair et al., 1993; Norden, 1997).

Management of F. pinicola in forestry could be achieved by limiting tree age (short timber rotations), reducing the incidence and size of wounds on residual trees left after selective wood harvesting, and the prompt salvaging of dead trees (Wright and Isaac, 1956; Hunt and Krueger, 1962; Hennon and DeMars, 1997; Holsten et al., 2001).

In Eurasia, F. pinicola cannot be regarded as a serious forest or tree pathogen of economic importance because of its low incidence in living trees. In fact, in a number of European studies, it has been proposed as a possible biological control agent against the root rot pathogens Heterobasidion spp. and Armillaria spp. by application of mycelial preparations to tree stumps (Orlos, 1957; Fedorov and Poleshchuk, 1978, 1981; Fedorov and Bobko, 1989; Hagle and Shaw, 1991; Anselmi and Nicolotti, 1998; Holdenrieder and Greig, 1998). Those fragmented areas of Eurasia in which the fungus was commonly observed on living trees, consist of old-growth protected forest reserves excluded from any form of wood harvesting (Kotiranta and Niemelä, 1981; Renvall et al., 1991; Dai, 1996). In forests of North America, however, the fungus seems to be an important disease agent, particularly on wounded trees in Oregon, Washington, British Columbia and Alaska. To date, no economic estimates are available for the damage caused exclusively by F. pinicola. Instead, losses of wood production in the region are generally attributed to 'wound decay' (e.g. Wright and Isaac, 1956; Hennon and DeMars, 1997). Consequently, at present, we can make only indirect estimations of economic loss caused by F. pinicola. It is known, for example, that heart rot fungi contribute to a loss of about 30% of the gross wood volume in old-growth forests of southeast Alaska, USA (Farr et al., 1976). Also in southeast Alaska, F. pinicola has been reported to cause more decay in live Picea sitchensis than all other fungi combined, and is the third leading decay agent for Tsuga heterophylla (Holsten et al., 2001). As another example, Shea (1961) states that in wounded P. menziesii, the volume of decay in the 10 years after logging comprised 86% of the volume increment at the same time, and the principal cause of decay was F. pinicola. F. pinicola was also reported to be major heartrot fungus in Prunus serotina (Davidson and Campbell, 1943).F. pinicola has occasionally been reported to affect horticultural crops: causing stem decay in apple orchards of central Washington, USA (Dilley and Covey, 1980), branch necroses in pome and stone fruit orchards of Idaho, USA (Helton et al., 1988), and decay and death of grapevine cuttings in Egypt (Mourad, 1986).F. pinicola has been reported as a possible decay agent of stored timber and buildings (Bondartsev, 1953; Parmasto, 1959; Stepanova-Kartavenko, 1967; Lyubarskyi and Vasilyeva, 1975; Holsten et al., 2001) and, in the Ural Mountains, it has been associated with timber decay in buildings (Demidova, 1963). However, it is not regarded as an important decayer of timber. Although there is no large-scale practical application of F. pinicola, it has been utilized for a variety of purposes. Wood decomposed by F. pinicola can be used as a lignified substrate additive for seedling growth in forest nurseries. Such substrates were shown to hold capillary water well which resulted in the formation of extensive seedling root systems (Penka and Cervena, 1984; Podracka and Cervena, 1991). In the wood industry, F. pinicola has been tested as a fungal pre-treatment of wood chips for fibreboard manufacture (Körner et al., 1992). Several investigations have demonstrated antitumour and antibacterial activities of extracts of F. pinicola fruit bodies (Mizuno et al., 1981, 1982; Keller et al., 1996; Rösecke and König, 1999). Furthermore, the fungus produces enzymes that catalyse the biosynthesis of the hormone prostaglandin (Kapich et al., 1992). In Japan, it was discovered that cultures of F. pinicola produce a milk-clotting enzyme, which can be used as a substitute for commercial rennet in cheese manufacture (Nakanishi and Itoh, 1968, 1970; Kawai and Mukai, 1970; Kawai, 1970; Mukai and Kawai, 1971).