Wood dowels sterilely overgrown with test mycelia of pathogenic and saprophytic basidiomycetous wood-decay fungi, respectively, were inserted into drill holes in the stems of 3 hardwood (Fagus sylvaticu, Betula irerrucosa, Sorbus aucupariu) and 1 softwood tree species (Picen abies). The host trees 40 -120 m m in diameter were part of the light-starved understory of a timber forest. Eighteen to 52 months after inoculation the trees were dissected and the colonized stemwood was microbiologically examined. Extension growth and survival of the test mycelia in trees of known vitality were taken as a basis for fungal pathovirulence rating. Basidiomycetous wood-decay fungi reach at best the status of physiologically facultative pathogens. They only colonized trees of the. lowest vitality classes in the understory. For the expected range of pathovirulence, an appropriate host tree to be chosen had a proper range of vitality which expressed itself in a crown volume of 5 to 70% that of the crown of a free-standing tree and a width of the current annual growth ring from 0.5 to 2.5 mm in dependence of the tree species. Increasingly moribund trees with low crown volumes and narrow growth rings favoured an unlimited mycelial expansion and survival, while in vital trees fungal expansion gradually came to a standstill within 18 to 52 months, frequently combined with an active killing of both the pathogenic and saprophytic mycelia. Development of pathogenic test mycelia much more depended on the choice of a n appropriate host tree species than did development of saprophytic test mycelia. The stem colonization by several late saprophytes was nearly as extensive and durable as the stem colonization by notorious tree pathogens. Pathosism in wood-decay basidiomycetes appeared thus to be a quantitative rather than a qualitative feature. For the dieback of the basidiomycetous test mycelia in the live stem reasons such as wood substrate depletion or antagonistic microbial activities could be excluded. The dieback rate of the test mycelia however was clearly enhanced in trees of increasing vitality, and it was enhanced with prolonged host-fungus interaction times. In comparison with sound dominant trees, the endophyte incidence in the sapwood of moribund P. abies trees was not increased. At the instant of tree death or crown decapitation however a severe colonization with blue stain and soft rot fungi was observed that exerted considerable antagonism on test mycelia low in kratovirulence. The implication of this antagonistic action for the colonization of dying trees by pathogenic decay fungi are discussed.
Pathogenic microorganisms can grow on host plants as they may tolerate (TEGTMEIER and VAN ETTEN 1982), suppress (BUSHNELL and ROWELL 1981, HEATH 1981), or detoxify (SMITH et al. 1982, VAN ETTEN and BARZ 1981) the chemical defence agents of their hosts that are determined to control microbial infection. Pathogen produced metabolites such as plant growth hormones (HOQUE 1982), enzymes (HOQUE 1982, JOHANSSON and STENLID 1985) and phytotoxins (YODER 1980) may in addition interfere with the regulatory, defensive, and structural life processes of the host plant. These many aspects of host-pathogen interactions to the disadvantage of the plant however cannot help establish why finally the parasitized plant falls ill and disease develops (BASHAN 1987). A comparatively simple host-pathogen interaction is the stem and butt rot syndrome of forest trees. The approximately 10% of living and widely uniform cells in standing timber, the cambial and ray parenchyma cells, have been shown to be the sole carrier of resistance against intruding microorganisms in Fagus sylvatica L. wood (GRAMSS 1989a). This fact is of almost unique 6*