There are three types of fungal wood rot: brown, white, and soft rot . Further terms are either older names (e.g., destruction rot = brown rot), specifications (red rot = white rot by Heterobasidion annosum) or terms used in practice ( marble rot = white rot with black demarcation lines) or false names (blue rot = blue stain).
According to the classical school of thought a fungal species causes only one type of decay, and species causing different rots shall not be grouped in the same genus [e.g.: Lentinus lepideus: brown rot; Lentinula (in former times Lentinus) edodes: white rot].
Regarding the delineation between the three decay types, there are, however, exceptions: The brown-rot fungus Coniophora puteana produced cavities to be typical of soft-rot fungi and erosion and thinning of the cell wall to be charac-teristic of white-rot fungi (Kleist and Schmitt 2001; Lee et al. 2004).
Fistulina hepatica revealed the soft-rot mode in cell walls rich in syringyl lignin, whereas brown rot was associated with cells rich in guaiacyllignin (Schwarze et al. 2000). Several white-rot Basidiomycetes like Phellinus pini (Liese and Schmid 1966) as well as Inonotus hispidus and Meripilus giganteus caused cavities (Schwarze and Fink 1998; Schwarze et al. I995a), which differed between the host trees, cell type, and location in the annual ring.
Cavities in the secondary wall of fibers and tracheids were also found to be caused by two Armillaria species as well as by Stereum sanguinolenturn, Ganoderma applanatum, and Grifola fron-dosa (Schwarze and Engels 1998). It was hypothesized that soft-rotting activity of white-rot Basidiomycetes may commonly precede white rotting when the fungus invades previously uninfected zones in the xylem, in which moisture content is high. Delignification of Norway spruce tracheids by Stereum san-guinolentum associated with the presence of radial and concentric clefts containing cell wall entities in the secondary wall (Schwarze and Fink 1999) supporting observations of a radial and concentric arrangement of cell wall constituents within the S2 (Sell and Zimmermann 1993).