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128<br />

ANTONY V. STURZ<br />

“...antagonistic potential resides in every soil microorganism...” (Baker and Cook,<br />

1974). Consequently, it is generally held that most soils possess the biological<br />

propensity to inhibit or reduce their soil microflora’s tendency toward disease, and so<br />

can be considered disease suppressive to some extent (Hornby, 1983). As a result,<br />

there exists in the literature a vast array of a terms used to describe soils that are<br />

inhospitable to plant pathogens. For example, i) soils where plant pathogens fail to<br />

become established have been referred to as resistant (Walker and Snyder, 1933),<br />

long-life, immune, intolerant, or antagonistic (Baker and Cook, 1974; Huber and<br />

Schneider, 1982), ii) soils where pathogens become established but fail to produce<br />

disease have also been termed suppressive (Schroth and Hancock, 1982); while iii)<br />

soils where disease incidence diminishes with continued monoculture have been termed<br />

decline soils (Shipton, 1975; Hornby, 1979, 1983).<br />

Attempts to simplify the biological basis for disease suppression in agricultural<br />

soils have reduced this concept to two broad mechanisms; namely that of i) a “general<br />

suppression” based upon the activity of the total microbial biomass that is not<br />

transferable between soils, and ii) a “specific suppression” that depends upon the<br />

activity of specific groups of microorganisms (Weller et al., 2002).<br />

Whether a bacterial population behaves pathogenically or not will be a function<br />

of that component species’ genetics, the restraints which other members in the<br />

community are able to impose, and the result of any overriding selection pressures<br />

dictated by environmental factors governing habitat type and host predisposition to<br />

disease.<br />

Environmentally mediated host predisposition to disease have been linked with<br />

obligate pathogen performance, and included exposure to cold (Schulz and Bateman,<br />

1969), low light intensity, or short day lengths (Foster and Walker, 1947), salinity<br />

stress (MacDonald, 1982), high temperature (Edmunds, 1964), and drought or moisture<br />

stress (Boyer, 1995; Duniway, 1977).<br />

In contrast, factors predisposing host plants to attack by rogue members of a<br />

commensal community, or protocooperative assemblage, are less well understood,<br />

though it appears likely that any dramatic change in the niche environment can provide<br />

an ecological advantage that benefits some community members at the expense of<br />

others. During the resulting population increase of the favoured community population,<br />

cell density dependent pathogenesis is triggered.<br />

3.2. Disease Suppression and Pathogen Evasion<br />

The wide array of nomenclature used to describe disease suppression in agricultural<br />

soils, is matched by an equally wide variety of individual microbial mechanisms<br />

postulated to explain these phenomena. However, it should be noted that these<br />

mechanisms are fairly presumptive, and, if they occur in vivo, are likely to operate in<br />

parallel with each other (Figure 1).<br />

In general, microbial biocontrol mechanisms have been classified according to<br />

effect (Baker, 1968) and have included such actions as parasitism/predation, niche<br />

competition, antibiosis and systemic induced resistance - the latter three falling

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