Insect Control: Biological and Synthetic Agents - Index of

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