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from birds, there was clear evidence for declines in populations of honeybees and
wild bees due to the application of fenitrothion.
10.2.5.3 Population genetics
There have been many reports of insect pest species developing resistance to OP
insecticides, to the extent that control of the pest has been lost. A detailed account
of resistance lies outside the scope of the present topic, and readers are referred to
specialized texts by Georghiou and Saito (1983), Brown (1971), and Otto and Weber
(1992). A few examples will now be considered that illustrate the mechanisms by
which insects become resistant to OP insecticides.
In Europe, one of the most widely studied cases of resistance was that developed
to OP insecticides in general by cereal aphids (Devonshire 1991). Existing OP insec-
ticides became ineffective for aphid control in some areas, and there was a need
to find suitable alternatives, for example, carbamates or pyrethroids, which were
not susceptible to the same resistance mechanism. It was found that there were a
number of different clones of the peach potato aphid (
Myzus persicae
) with differ-
ing levels of resistance to OPs. The level of resistance was related to the number of
copies of a gene for a carboxylesterase (see earlier discussion under Section 10.2.2).
In general, the larger the number of copies of the gene, the greater the activity of the
carboxylesterase and the greater the level of OP resistance (in certain instances, tran-
scriptional control was also found to be important). Resistance had evidently been
acquired through gene duplication, not through the appearance of a novel esterase
gene absent from susceptible aphids. Some strains of mosquitoes have also been
shown to develop OP resistance by this mechanism.
A number of other examples are known in which genetically based resistance was
due to enhanced detoxication of OPs. These include malathion resistance in some
stored product pests owing to high carboxylesterase activity, and resistance of strains
of the housefly to diazinon due to detoxication by specific forms of a glutathione-S-
transferase and monooxygenase (Brooks 1972).
In some strains of insects, resistance has been related to the presence of genes that
code for insensitive “aberrant” forms of the AChE. Interestingly, it has been shown
that resistance may be the consequence of the change of a single amino acid residue
in AChE. Sequence analysis of the AChE gene from resistant strains of
Drosophila
melanogaster
and the housefly has identified six point mutations that are associated
with resistance (Salgado 1999; Devonshire et al. 2000). All these mutations bring
changes in amino acid residues located near the active site of AChE, according to the
Torpedo enzyme model described earlier (Section 10.2.4). According to the model,
all the changes would cause steric hindrance of the relatively bulky insecticides,
but not to any important extent of acetylcholine itself. Thus, the insensitive enzyme
could continue to function as AChE. The existence of more than one of these point
mutations brings a higher level of resistance than does a single-point mutation.
Apart from the importance of OP resistance in pest control, ecotoxicologists have
become interested in the development of resistance as an indication of the environ-
mental impact of insecticides. Thus, the development of esteratic resistance mecha-
nisms by aquatic invertebrates may provide a measure of the environmental impact
of OPs in freshwater (Parker and Callaghan 1997).
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