Insect Control: Biological and Synthetic Agents - Index of
Insect Control: Biological and Synthetic Agents - Index of
Insect Control: Biological and Synthetic Agents - Index of
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imidacloprid conferring a high level <strong>of</strong> crossresistance<br />
to thiamethoxam <strong>and</strong> acetamiprid was<br />
first demonstrated, <strong>and</strong> best studied in Q-type<br />
B. tabaci from greenhouses in the Almeria region<br />
<strong>of</strong> southern Spain, but was also detected in single<br />
populations from Italy <strong>and</strong> recently Germany as<br />
well (Nauen <strong>and</strong> Elbert, 2000; Nauen et al., 2002;<br />
Rauch <strong>and</strong> Nauen, 2003). Neonicotinoid resistance<br />
seem to remain stable in all field-collected Q-type<br />
strains maintained in the laboratory without further<br />
selection pressure (Nauen et al., 2002). Neonicotinoid<br />
cross-resistance was also reported in B-type<br />
whiteflies from cotton in Arizona but at lower<br />
levels (Li et al., 2000). More recently a high level<br />
<strong>of</strong> cross-resistance between neonicotinoids was also<br />
described in a B-type strain <strong>of</strong> B. tabaci from Israel,<br />
<strong>and</strong> resistance factors detected in a leaf-dip bioassay<br />
exceeded 1000-fold (Rauch <strong>and</strong> Nauen, 2003).<br />
The Colorado potato beetle, L. decemlineata has<br />
a history <strong>of</strong> developing resistance to virtually all<br />
insecticides used for its control. The first neonicotinoid,<br />
i.e., imidacloprid was introduced for controlling<br />
Colorado potato beetles in North America in<br />
1995. Concerns over resistance development were<br />
reinforced when extensive monitoring <strong>of</strong> populations<br />
from North America showed about a 30-fold<br />
variation in LC50 values from ingestion <strong>and</strong> contact<br />
bioassays against neonates (Olsen et al., 2000).<br />
Much <strong>of</strong> this variation appeared unconnected with<br />
imidacloprid use, <strong>and</strong> was probably a consequence<br />
<strong>of</strong> cross-resistance from chemicals used earlier.<br />
Lowest levels <strong>of</strong> susceptibility occurred in populations<br />
from Long Isl<strong>and</strong>, New York, an area that has<br />
experienced the most severe resistance problems<br />
<strong>of</strong> all with L. decemlineata. Zhao et al. (2000) <strong>and</strong><br />
Hollingworth et al. (2002) independently studied<br />
single strains collected from different areas in Long<br />
Isl<strong>and</strong>, both treated intensively with imidacloprid<br />
between 1995 <strong>and</strong> 1997. In the first study, grower’s<br />
observations <strong>of</strong> reduced control were supported by<br />
resistance ratios for imidacloprid <strong>of</strong> 100-fold <strong>and</strong><br />
13-fold in adults <strong>and</strong> larvae, respectively. The second<br />
study reported 150-fold resistance from topical<br />
application bioassays against adults. In this case<br />
the strain was also tested with thiamethoxam,<br />
which had not been used for beetle control at the<br />
time <strong>of</strong> collection. Interestingly, resistance to thiamethoxam<br />
(about threefold) was far lower than to<br />
imidacloprid.<br />
Other reports referring to resistance to neonicotinoid<br />
insecticides were on species <strong>of</strong> lesser importance,<br />
including species either from field-collected<br />
populations or artificially selected strains. Among<br />
these were the small brown planthopper, Laodelphax<br />
striatellus (Sone et al., 1997), western flower<br />
3: Neonicotinoid <strong>Insect</strong>icides 97<br />
thrips, Franklienella occidentalis (Zhao et al.,<br />
1995), houseflies, Musca domestica <strong>and</strong> German<br />
cockroach, Blattella germanica (Wen <strong>and</strong> Scott,<br />
1997), Drosophila melanogaster (Daborn et al.,<br />
2001), Lygus hesperus (Dennehy <strong>and</strong> Russell,<br />
1996), <strong>and</strong> brown planthoppers, Nilaparvata lugens<br />
(Zewen et al., 2003).<br />
3.9.2. Mechanisms <strong>of</strong> Resistance<br />
Many pest insects <strong>and</strong> spider mites have developed<br />
resistance to a broad variety <strong>of</strong> chemical classes <strong>of</strong><br />
insecticides <strong>and</strong> acaricides, respectively (Knowles,<br />
1997; Soderlund, 1997). One <strong>of</strong> the three major<br />
classes <strong>of</strong> mechanisms <strong>of</strong> resistance to insecticides<br />
in insects is allelic variation in the expression <strong>of</strong><br />
target proteins with modified insecticide binding<br />
sites, e.g., acetylcholinesterase insensitivity towards<br />
organophosphates <strong>and</strong> carbamates, voltage-gated<br />
sodium channel mutations responsible for knockdown<br />
resistance to pyrethroids, <strong>and</strong> a serine to alanine<br />
point mutation (rdl gene) in the g-aminobutyric<br />
acid (GABA)-gated chloride channel (GABA A-R) at<br />
the endosulfan/fipronil/dieldrin binding site (ffrench-<br />
Constant et al., 1993; Williamson et al., 1993, 1996;<br />
Mutero et al., 1994; Feyereisen, 1995; Dong, 1997;<br />
Soderlund, 1997; Zhu <strong>and</strong> Clark, 1997; Bloomquist,<br />
2001; Gunning <strong>and</strong> Moores, 2001; Siegfried <strong>and</strong><br />
Scharf, 2001). The second – <strong>and</strong> <strong>of</strong>ten most<br />
important – class <strong>of</strong> resistance mechanisms in insect<br />
pest species is metabolic degradation involving detoxification<br />
enzymes suchas microsomalcytochrome<br />
P-450dependentmonooxygenases,esterases,<strong>and</strong>glutathione<br />
S-transferases (Hodgson, 1983; Armstrong,<br />
1991; Hemingway <strong>and</strong> Karunarantne, 1998; Bergé<br />
et al., 1999; Devonshire et al., 1999; Feyereisen,<br />
1999; Hemingway, 2000; Field et al., 2001; Scott,<br />
2001; Siegfried <strong>and</strong> Scharf, 2001). The third, least<br />
important mechanism is an altered composition<br />
<strong>of</strong> cuticular waxes which affects penetration <strong>of</strong><br />
toxicants. Reduced penetration <strong>of</strong> insecticides<br />
through the insect cuticle has <strong>of</strong>ten been described<br />
as a contributing factor, in combination with target<br />
site insensitivity or metabolic detoxification<br />
(or both), rather than functioning as a major mechanism<br />
on its own (Oppenoorth, 1985). Most <strong>of</strong><br />
the mechanisms mentioned above affect in many<br />
cases the efficacy <strong>of</strong> more than one class <strong>of</strong> insecticides,<br />
i.e., constant selection pressure to one chemical<br />
class could to a greater or lesser extent confer crossresistance<br />
to compounds from other chemical<br />
classes (Oppenoorth, 1985; Soderlund, 1997).<br />
When the first neonicotinoid insecticide was<br />
introduced to the market in 1991, aphids were<br />
considered to be high risk pests with regard to<br />
their potential to develop resistance to this class <strong>of</strong>