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and both could be much more durable if susceptible hosts were mixed into the
population and insects that had been selected on resistant and susceptible hosts
mated randomly (Gould, 1986b). Thus, fine-scale diversity slowed down adaptation.
When simulating the planting of resistant and susceptible hosts in adjacent fields
rather than in mixtures, Gould (1986a,b) found that the critical factors influencing
the effectiveness of these strategies were the insects' migration rates and field size.
The rotation of resistant and susceptible hosts over time was predicted to speed up
insect adaptation because it allowed for the build-up of half-adapted insects every
other year.
Natural enemies potentially also influence pest adaptation to resistance factors in
host plants. Depending on the kind of host resistance and the timing of attack by the
natural enemies, these can either increase or decrease the rate of pest adaptation.
Adaptation to a resistant plant type should be slower if the pest suppression is due to
a combination of natural enemies and resistance rather than to resistance alone
(Gould et al., 1991).
It is at the interface of analytical population genetics and epidemiological
simulation models where studies have provided insights into population dynamic
processes in pathogen populations. For example, Luo and Zadoks (1992) found that
maximum stabilising effects and maximum disease reduction could not be achieved
simultaneously. Lannou and Mundt (1995) explored different parameters and
showed that maximising control of disease means maximising control of simple
races which leads to maximisation of selection for the complex race. These results
indicate that, in a systems approach, one cannot and must not aim simply to
minimise disease but rather to consider short-term disease control in the context of
long-term effects on the system as a whole.
10.6.2 Results from small scale field experiments
In the field, attempts to follow changes in pathogen population structure on mixed
hosts relative to those on their pure components have produced inconclusive results.
For example, Chin and Wolfe (1984b) found that barley mixtures selected for more
complex powdery mildew races than did the pure stands, but, because of epidemic
delay in the mixtures, complex genotypes did not necessarily increase in absolute
number relative to the numbers on pure stands. Moreover, they found that disruptive
selection by different barley cultivars containing the same race-specific resistance,
split races of the pathogen into sub-races that were differentially adapted to the
genetic background of the cultivars. Villareal and Lannou (2000) also found that the
rate of progress towards complexity in a pathogen population being selected on a
cultivar mixture was significantly slower than that predicted from simple models.
Chuke and Bonman (1988) found little evidence for an increase in race complexity
in rice blast on rice among isolates from mixtures, relative to those from pure stands.
In other trials, complex pathogen genotypes increased in frequency on host mixtures
relative to pure stands (Wolfe, 1984; Wolfe et al. , 1984; Dileone and Mundt, 1994;
Huang et al. , 1994).
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