2.3.2S
PlHELLINUS WEIRII: CONIFER INTERACTIONS IN WESTERN NORTH AMERICA

EM HANSEN, J HOLAH and P. LATTIN

Department of Botany and Plant Pathology, Oregon State University, Corvallis, Oregon, USA

Background and objectives
Phellinus weirii, a native pathogen, causes laminated root rot of Douglas fir and other Pinaceae in the temperate coniferous forests of western North America and eastern Asia. The fungus imposes dramatic changes in structure, composition, and function on forests. We have studied several of the interactions between this widespread pathogen and forest ecosystems.

Results and conclusions
P. weirii is characterized by long periods of saprophytic survival in the roots of killed trees and slow spread through the forest, growing as ectotrophic mycelium from tree-to-tree across overlapping root systems. Spreading by spores has not been demonstrated. Most conifers of the region can be infected by the fungus, but species differ greatly in tolerance to infection. Susceptible trees are killed slowly, often collapsing from decay of supporting roots or attacked by bark beetles [1]. In stands of susceptible species, laminated root rot appears as more or less discrete mortality centre that slowly expand throughout the life of the stand. When the stand is replaced, whether by timber harvest or naturally by fire, the fungus persists for decades in residual roots and stumps of infected trees and starts to spread again when roots of regenerating susceptible species grow into contact with the old inoculum. Fungus individuals are thus much older than the trees they occupy, and often span large areas.

Local distribution is determined by stand history and topographic barriers to root-to-root spread. If stand successional history includes a prolonged period of occupancy by resistant angiosperm species, such as alder or maple, then the fungus may exhaust its resources in old conifer roots and die. If on the other hand, periods without susceptible conifers are relatively short, as when Douglas-fir is replanted after harvest or seeds naturally from scattered trees that survive wildfire, the fungus will persist and increase on the site. In many forests, it is the most important disturbance agent, affecting stand structure and composition in the long intervals between catastrophic stand-replacing fires or timber harvest. The consequences to the forest are determined by the abundance of the fungus and the existing and potential vegetation of the site [2].

In the vast Douglas fir dominated forests west of the Cascade Mountains in Oregon, P. weirii is common. Stand-replacing fires occur at 300- to 400-year intervals. The 'climax' species is shade-tolerant western hemlock, but without intermediate disturbance events to kill the Douglas fir, hemlock is confined to the understory. By killing Douglas fir, P. weirii allows the disease-tolerant hemlock to achieve dominance. Thus, root rot advances the succession in a patchy but slowly increasing manner in the forest. Because hemlock forms a very dense stand with little light penetration, the diversity of understory vegetation in infection centre occupied by this tree is often lower than in the surrounding Douglas-fir stand. In stands that lack hemlock, the slowly expanding mortality pockets may allow persistence of the diverse early successional vegetation.

At high elevations in the Cascade Mountains, the conifer forest grows under harsh conditions. In many places, on pumice soils, mountain hemlock is the dominant and climax species. It is very susceptible to laminated root rot, and the disease reaches its most dramatic expression in these forests. Individual genets of the fungus may span many hectares and be thousands of years old. The huge infection centre contain a younger, more diverse forest, with increased decomposition and nutrient cycling rates and hence greater productivity than the surrounding old growth. Although the specific consequences differ in different forest ecosystems, wherever it is found laminated root rot is a major factor in shaping forest structure, composition, and process.

References
1. Goheen D, Hansen E, 1993. In: T Schowalter, G Filip, eds. Beetle Pathogen Interactions in Conifer Forests. London: Academic Press, pp. 175-198.
[2] Holah J, Wilson M, Hansen E, 1994. Canadian Journal of Forest Research 23, 2473-2480.