Insect Control: Biological and Synthetic Agents - Index of

22 1: Pyrethroids
used. Organophosphates and carbamates were used in
Stage III and also if required for additional sprays
during Stages I and II.
The use of a ‘‘softer’’ insecticide (endosulfan) in
the early season was deliberate to minimize disruption
of beneficial parasitoids and predators and to
avoid a potential upsurge of secondary pests such as
mites, aphids, and whiteflies, which were not controlled
by the pyrethroids available at the time.
Examples of nonchemical countermeasures incorporated
in the strategy to reduce selection pressure
included the use of early-maturing crops, avoiding
early-growing crops (e.g., maize) in adjacent fields,
which may act as early-season nurseries for resistant
H. armigera, and utilization of host plants in refugia
to maintain a large pool of susceptible individuals,
which would continually dilute the resistant
population in the crop. Resistance was monitored
on a weekly basis using a discriminating dose of
fenvalerate with and without the synergist PBO.
Later monitoring showed a rise in metabolic resistance
attributed to MFOs and this resulted in the
inclusion of PBO in the last of the maximum of three
pyrethroid sprays. This strategy was successful for
many years but the underlying trend of upward
increase in the proportion of resistant insects continued
and finally led to a complete reorganization of
the strategy in the mid 1990s with a shift away from
reliance on pyrethroids.
Initial resistance to pyrethroids was thought to be
due to the presence of the knockdown site-insensivity
resistance (kdr) mechanism probably as a direct
result of cross-resistance to DDT. Over the years of
the IRM strategy, metabolic resistance mechanisms
appear to have taken over. However, there is still
controversy over whether it is primarily due to elevated
levels of esterases or mixed-function oxidases
(MFOs). The main reason for the uncertainty concerns
the role of synergists used in the studies. For
example, PBO is now thought to inhibit both these
types of enzymes. Furthermore, it has been suggested
that such inhibitors may themselves have
become resisted in the field over time (McCaffery,
1998), thus obscuring the mechanism of resistance.
The second IRM strategy involved the whitefly,
B. tabaci, a representative sucking pest on a wide
range of crops (Denholm et al., 1998). In 1995, overreliance
on a limited range of pyrethroids in Arizona
had led to a classic treadmill scenario, with farmers
responding to rising levels of resistance by increasing
the number of sprays (as many as 8–12 applications
per season). In this pest, the haplodiploid
breeding system encourages rapid selection and
fixation of resistance genes. Males are produced
uniparentally from unfertilized, haploid eggs, and
females are produced biparentally from fertilized
diploid eggs. In addition, for this (and other) highly
polyphagous species, the interaction between pest
ecology and resistance is complex and generally
not well understood, making formulation of IRM
strategies even more difficult. The strategy of
Dennehy and Williams (1997) implemented in
1996 had several features in common with that for
H. armigera. It too relies on the continuous availability
of a pool of susceptible whiteflies in refugia
(e.g., Brassica crops) throughout the year and alteration
of agronomic practices (e.g., timing of planting)
in crops to minimize whitefly numbers whilst
still maintaining the level of natural enemies. The
first of the three-stage IRM strategy involved use of
a single spray each of pyriproxyfen and buprofezin
(then newly available insect-growth regulators) with
a 14- or a 21-day gap. The second stage allowed
nonpyrethroid conventional insecticides and the
third used pyrethroids synergized with acephate as
late as possible in the season. A threshold of infestation
was defined to initiate insecticide applications.
Mixtures were limited to no more than two compounds
and any one active ingredient was restricted
to no more than two applications in one season.
This strategy has been extremely successful in reducing
the number of sprays required and regaining
susceptibility both to synergized pyrethroids and
key nonpyrethroid insecticides.
As for H. armigera, the need for monitoring,
establishing threshold levels to trigger spray applications,
and cooperation of the growers was key to
the strategy. Long-term success of any IRM strategy
depends on many factors because, even when an
IRM strategy has been successful (McCaffery,
1998), effectiveness of synergized pyrethroids can
be lost after just two applications in areas with a
history of resistance to pyrethroids.
In conclusion, the key requirement for the development
and sustainability of an IRM strategy is
diagnosis of the resistance mechanism(s) in field
populations. This is especially important when
assessing the relative importance of individual
mechanisms when several are present, which influences
changes to the strategy with time. As alluded
to earlier, there is still much uncertainty in the diagnosis
of mechanisms. The use of established inhibitors
or just in vitro bioassay data has been shown
to be unreliable in this regard. For example in
M. persicae, elevated esterase was considered for
many years to be the main resistance mechanism. It
was only recently shown (Devonshire et al., 1998) that
this mechanism made only a minor contribution to the