The I936F mutation was identified at low levels in a survey of genetic resistance
markers of the pyrethroid-resistant bed bugs (Cimex lectularius) in Israel
[148]. I936F has also been associated with d-allethrin-resistant populations of
bedbugs in Australia, although the authors noted that its function in pyrethroid
resistance is tentative and requires further investigation [149]. In addition to the
identification of target site mutations in H. azteca, Weston et al. [57] used a
microarray to detect gene expression differences between sensitive laboratory and
a highly resistant pyrethroid- resistant population (Grayson Creek) at each
population’s no observable effects concentration (NOEC ¼ 0.4 ng L
À1 and
170 ng L
À1 , respectively). Differentially expressed genes in the sensitive laboratory
population were consistent with the mechanism of action of the pyrethroids – these
animals had differentially expressed genes related to neural function, while Grayson
Creek animals instead expressed stress response genes related to oxidation/reduction
(cytochrome P450s, glutathione S-transferases, other oxidases), heat shock proteins,
and metabolic enzymes. These results are consistent with a differential mode of toxic
action in sensitive versus resistant populations which can be explained by differential Vgsc amino acid sequences.
In contrast with the other cases of potential nontarget pyrethroid resistance in
aquatic invertebrates previously mentioned, H. azteca that have demonstrated pyrethroid resistance and high frequencies of the L925I mutation appear to be more
sensitive to toxicant challenges with DDT. Regardless, there is no indication that
pyrethroid-resistant animals confer any resistance to DDT [150, 151]. DDT has been
banned in the United States since the early 1970s and therefore would have been
unlikely to contribute to the selection and maintenance of resistance alleles measured
in H. azteca nearly four decades later. Because field-collected H. azteca were used to
screen for pyrethroid sensitivity, it is possible that some of the decreased sensitivity
to pyrethroids observed can be attributed to physiological acclimation and/or maternal effects instead of exclusively adaptive resistance. However, three populations of
resistant H. azteca have been maintained in a pyrethroid-free laboratory setting
between 9 and 16 months, with a maximum of a 35% loss in tolerance to cyfluthrin
[151]. A decrease in tolerance during that time could be attributed to nonadaptive
resistance mechanisms that have not been explored in H. azteca, but the high
frequencies and substantial (62-fold) increase in tolerance compared to sensitive
populations still support the presence of an adaptive resistance mutation (L925I).
Another study showed a 50% decrease in pyrethroid resistance between fieldcollected and laboratory-reared F1 animals in the absence of pyrethroids, but
again, that population still maintained a 40-fold greater tolerance than sensitive H.
azteca [150], supporting the existence of genetic, adaptive target site mutations in
the conferral of resistance in H. azteca.
130
K. M. Major and S. M. Brander
markers of the pyrethroid-resistant bed bugs (Cimex lectularius) in Israel
[148]. I936F has also been associated with d-allethrin-resistant populations of
bedbugs in Australia, although the authors noted that its function in pyrethroid
resistance is tentative and requires further investigation [149]. In addition to the
identification of target site mutations in H. azteca, Weston et al. [57] used a
microarray to detect gene expression differences between sensitive laboratory and
a highly resistant pyrethroid- resistant population (Grayson Creek) at each
population’s no observable effects concentration (NOEC ¼ 0.4 ng L
À1 and
170 ng L
À1 , respectively). Differentially expressed genes in the sensitive laboratory
population were consistent with the mechanism of action of the pyrethroids – these
animals had differentially expressed genes related to neural function, while Grayson
Creek animals instead expressed stress response genes related to oxidation/reduction
(cytochrome P450s, glutathione S-transferases, other oxidases), heat shock proteins,
and metabolic enzymes. These results are consistent with a differential mode of toxic
action in sensitive versus resistant populations which can be explained by differential Vgsc amino acid sequences.
In contrast with the other cases of potential nontarget pyrethroid resistance in
aquatic invertebrates previously mentioned, H. azteca that have demonstrated pyrethroid resistance and high frequencies of the L925I mutation appear to be more
sensitive to toxicant challenges with DDT. Regardless, there is no indication that
pyrethroid-resistant animals confer any resistance to DDT [150, 151]. DDT has been
banned in the United States since the early 1970s and therefore would have been
unlikely to contribute to the selection and maintenance of resistance alleles measured
in H. azteca nearly four decades later. Because field-collected H. azteca were used to
screen for pyrethroid sensitivity, it is possible that some of the decreased sensitivity
to pyrethroids observed can be attributed to physiological acclimation and/or maternal effects instead of exclusively adaptive resistance. However, three populations of
resistant H. azteca have been maintained in a pyrethroid-free laboratory setting
between 9 and 16 months, with a maximum of a 35% loss in tolerance to cyfluthrin
[151]. A decrease in tolerance during that time could be attributed to nonadaptive
resistance mechanisms that have not been explored in H. azteca, but the high
frequencies and substantial (62-fold) increase in tolerance compared to sensitive
populations still support the presence of an adaptive resistance mutation (L925I).
Another study showed a 50% decrease in pyrethroid resistance between fieldcollected and laboratory-reared F1 animals in the absence of pyrethroids, but
again, that population still maintained a 40-fold greater tolerance than sensitive H.
azteca [150], supporting the existence of genetic, adaptive target site mutations in
the conferral of resistance in H. azteca.
130
K. M. Major and S. M. Brander