Susceptibility to Fungal Pathogens of Forests Differing in Tree Diversity

Abstract

Plant communities commonly have both host diversity and biotic diseases (Kimmins 1997a; Roy and Kirchner 2000), but to differing degrees. Disease and diversity are classically connected in the literature by the co-evolutionary explanation of sex (Hamilton 1980): recombinations of the host genome may produce disease-resistant genotypes, while preserving or enhancing diversity (Clay and Kover 1996; Kirchner and Roy 2000; Lively 2001).We argue here that this concept of species interaction has to be viewed in the context of both individuals and populations in order to make sense from the evolutionary (Tokeshi 1999) and forest economy viewpoints (Perry and Amaranthus 1997; Perry 1998). The general importance of disease and parasites in the dynamics of plant populations is well recognized (Harper 1977, 1990; Burdon 1987; Dobson and Crawley 1994; Garrett and Mundt 1999), but studies on disease dynamics in natural multi-species plant communities remain rare (Kranz 1990; Burdon 1993; Roy et al. 2000; Thrall and Burdon 2002). Most forest ecosystems have been altered in their patterns and processes by human influences (Glatzel 1991; Edmonds et al. 2000; Wohlgemuth et al. 2002). Also biotic perturbations, including diseases, are increasingly perceived as an intrinsic part of the system (Ehrlich 1994; Schowalter et al. 1997; Spies and Turner 1999). Trees are an obvious structural component of ecosystems (Jones et al. 1997; Rao et al. 1997), but pathogenic and saprotrophic organisms also form an important part of biodiversity and contribute to the holistic functioning of forests (Ingram 1999; Courtecuisse 2001; Siitonen 2001). We refer here only to fungal pathogens of trees and thus do not focus on abiotic disturbances (Hansen and Rotella 1999; see Dhote, Chap. 14, this vol.), or viruses, bacteria, and insects (Haack and Byler 1993; see Jactel et al., Chap. 12, this vol.), although, in many cases, these may be intimately interrelated with fungal pathogenesis (Hatcher 1995; Lundquist 1995; Maloney and Rizzo 2002).