School of Engineering and Science - Jacobs University

Introduction
2.1.2 Host, pathogen and antagonist – more than a “ménage à trois”
The first step to understand complexity of biological control is the determination
of crucial features of the individual relationships; the virulence determinants of
the pathogen, defense mechanisms of the host plant, and mode of action of the
control agent. If these basics are known, the impact of environmental conditions
and competing organisms can be assessed.
The best characterized part of the biological control complex is the interaction
between plant and pathogen. Since the discovery of microbes as causal agents
of infectious plant disease in 1878, numerous plant diseases have been studied
for virulence determinants of the pathogens and defense mechanisms of host
plants (Burrill, 1878; Montesinos, 2000). The following principles have been
determined as common themes in plant disease: Prior to disease development,
most pathogens undergo an epiphytic growth phase. The pathogen attaches to
the plant surface and proliferates in this environment until it finds an entry site,
for example wounds or stomata where the pathogen can overcome structural
defense barriers provided by cuticula, cell wall etc. (Agrios, 2005; Montesinos
et al., 2002). The next step during disease formation would be the induction of
virulence determinants. This genetic switch to the pathogenic life style is tightly
regulated. Virulence factors of a pathogen could be perceived by the host and
lead to defense induction, thus they are only expressed under disease-favoring
conditions after the pathogen has reached a certain threshold population size.
Quorum sensing is considered an important regulation mechanism for many
virulence factors (Lugtenberg et al., 2002; Montesinos, 2000; Staskawicz et al.,
2001). Most pathogen attacks do not result in disease formation. In case the
host plant recognizes the pathogen, it starts an immediate defense reaction, the
so-called “hypersensitive response” (HR). HR is a localized reaction of the
infected tissue. The affected areas undergo programmed cell death consisting
of cellular electrolyte leakage and “oxidative burst” i.e. the rapid formation of
reactive oxygen species (ROS). Apart from the direct damage to the pathogen,
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