Abamectin Resistance Research Articles

Putative Polymerase Chain Reaction Markers for Insecticide Resistance in the Leafminer Liriomyza trifolii (Diptera: Agromyzidae) to Cyromazine and Abamectin

In this study, random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) was used to identify polymorphic genomic DNA that would discriminate among cyromazine-resistant, abamectin-resistant, and susceptible Liriomyza trifolii (Burgess) (Diptera: Agromyzidae) leafminers. Using a reference strain that was susceptible to both cyromazine and abamectin, and a cyromazine-resistant strain and an abamectin-resistant strain, 400 oligonucleotides were assayed using RAPD-PCR. We found that two oligonucleotides, B10 and G16, amplified unique bands in the cyromazine-resistant strain but not in the reference or abamectin-resistant strains. Three oligonucleotides, K04, J13, and I02, showed polymorphisms unique to the abamectin-resistant strain but not in the reference or cyromazine-resistant strain. Leaf dip bioassays and RAPD-PCR were performed on two additional reference strains, seven strains from commercial ornamental production greenhouses, and one field strain. The two reference strains were negative for the resistance-correlated oligonucleotides. Of the seven strains from ornamental greenhouses, leaf dip bioassays showed that five had some level of resistance to both abamectin and cyromazine, whereas two were susceptible. The field strain was susceptible to both cyromazine and abamectin. In RAPD-DNA analyses, the five strains with abamectin resistance were positive for the three abamectin resistance-correlated oligonucleotides K04, J13, and I02. In the cases of cyromazine resistance, the five strains with cyromazine resistance were positive for the two cyromazine resistance-correlated oligonucleotides B10 and G16. The field strain and two greenhouse strains that were susceptible in leaf dip bioassays were negative for all three abamectin resistance-correlated oligonucleotides. The field strain and one greenhouse strain were negative for the two cyromazine resistance-correlated oligonucleotides; however, one greenhouse strain that was susceptible to cyromazine in leaf dip bioassay tested positive for one of the cyromazine resistance-correlated oligonucleotides. This method can be used to quickly identify cyromazine resistance, abamectin resistance, or both in leafminers, enabling a grower to choose an effective insecticide for leafminer control in a timely manner.

High γ-aminobutyric acid content, a novel component associated with resistance to abamectin in Tetranychus cinnabarinus (Boisduval)

An abamectin-resistant strain of Tetranychus cinnabarinus (Boisduval) (Rf=25.3) was selected in laboratory. We compared the γ-aminobutyric acid (GABA) content in abamectin-susceptible T. cinnabarinus individuals with that in resistant individuals and investigated its relationship to abamectin resistance. High performance liquid chromatography (HPLC) was used to ascertain GABA content in abamectin-susceptible (SS) and resistant (AR) strains of T. cinnabarinus. The results indicate that GABA content in the AR was significantly higher than that in the SS (1.39-fold). AR individuals treated with a sublethal dose of abamectin did not show significant differences in GABA levels compared with AR individuals that were not treated with abamectin. However in the SS, abamectin treated individuals had a significantly higher GABA content than those that were untreated (1.52-fold). Individuals in the SS that survived from selection with LC95 of abamectin (SS–AR) showed significantly higher GABA levels compared to SS (1.41-fold). Similarly, progenies of the SS–AR parental generation (SS–ARF1) also showed increased GABA levels (1.51-fold) compared to SS. In addition, behavioral observations have shown that all individuals from the AR, SS–AR and SS–ARF1, which had more GABA content than the SS, demonstrated a significant decrease in crawling speed compared with SS individuals. This observation is consistent with excessive GABA levels had inhibitory effect on the central nervous system. Thus, we postulate that increasing GABA content in T. cinnabarinus is associated with resistance against abamectin.

A point mutation in a glutamate‐gated chloride channel confers abamectin resistance in the two‐spotted spider mite, Tetranychus urticae Koch

The molecular mechanisms and genetics of abamectin resistance mediated by target site insensitivity in the two-spotted spider mite, Tetranychus urticae, were investigated by comparing two isogenic abamectin-susceptible (AbaS) and abamectin-resistant (AbaR) strains. Cloning and sequencing of full-length cDNA fragments of gamma-amino butyric acid (GABA)-gated chloride channel genes revealed no polymorphisms between the two strains. However, sequence comparison of the full-length cDNA fragment of a T. urticae glutamate-gated chloride channel gene (TuGluCl) identified a G323D point mutation as being tentatively related with abamectin resistance. In individual F(2) progenies obtained by backcrossing, the G323D genotype was confirmed to correlate with abamectin resistance. Bioassays using progeny from reciprocal crossings revealed that the abamectin resistance trait resulting from TuGluCl insensitivity is incompletely recessive.

Molecular characterization and expression of a heat shock protein gene (HSP90) from the carmine spider mite, Tetranychus cinnabarinus (Boisduval).

In this study, the cDNA of Tetranychus cinnabarinus (Boisduval) (Acarina: Tetranychidae) HSP90 (designated TcHSP90) was cloned using a combination of the homology cloning and rapid amplification of cDNA ends (RACE) approaches. The full-length cDNA of TcHSP90 is 2595 bp, including a 5′-untranslated region (UTR) of 177 bp, 3′-UTR of 249 bp, and an open reading frame (ORF) of 2169 bp. The ORF encodes a polypeptide of 722 amino acids with a predicted molecular weight of 83.45 kDa and a theoretical isoelectric point of 4.81. There is an mRNA polyadenylation signal of ATTAAA at the positions 2558–2564. In addition, the expression pattern of TcHSP90 mRNA relative to that of β-actin gene in the three stains of T. cinnabarinus (AbR, abamectin-resistant strain; HR, heat-resistant strain; SS, the susceptible strain) were examined by using fluorescent real time quantitative PCR after the impact of abamectin, high and low temperature, respectively. The results showed that under the normal condition, the mRNA level of TcHSP90 was 1.64 and 1.29-fold higher in the AbR and HR than in SS, respectively. After 8 h treatment with abamectin, the TcHSP90 mRNA levels of SS, AbR, and HR were 1.25, 1.87, and 2.05-fold higher than those of their untreated controls, respectively. The TcHSP90 mRNA levels of SS, AbR, and HR were also significantly increased after being induced at 40° C for 1 h, and they were 3.76, 3.42, and 3.79-fold higher than those of their untreated controls, respectively. The mRNA level of TcHSP90 was also significantly increased after being induced at 4° C for 1 h. These results suggest that TcHSP90 might be involved in the abamectin and extreme temperature resistance or tolerance.

Residual contact vial bioassay for the on-site detection of acaricide resistance in the two-spotted spider mite

To develop a less technique-dependent bioassay technique that can be conveniently used by practitioners or farmers in the field for the monitoring of acaricide resistance of the two-spotted spider mite, Tetranychus urticae Koch, a residual contact vial (RCV) method was established using a 5-ml glass vial coated with acaricides. The RCV bioassay procedures were optimized by using abamectin and tebufenpyrad, two widely used acaricides. The diagnostic concentrations causing 100% mortality within 8 h post-treatment in a susceptible strain of T. urticae was set at 30 and 60 ppm for abamectin and tebufenpyrad, respectively. The vial-coated pesticides were stable at least one year when stored at − 20 °C as determined by HPLC. There was no significant difference in the bioassay results in repeated RCV bioassay by three different experimenters, indicating its high reproducibility and reliability. RCV-based resistance monitoring of 15 field populations of mites revealed that abamectin resistance begins to spread but tebufenpyrad resistance is already prevalent in Korea. The RCV diagnostic kit, when used by practitioners or farmers on site, should provide crucial information for the selection of most suitable acaricides for different field populations of T. urticae.

Multiple resistance mechanisms to abamectin in the two-spotted spider mite

The two-spotted spider mite, Tetranychus urticae, is one of the most destructive pests of various orchard trees and garden plants. Biochemical mechanisms of abamectin resistance in two T. urticae strains (PTF, 239-fold resistance; AbaR, ca. 4753-fold resistance) were investigated. The involvement of both esterase (Est) and mixed function oxidase (MFO) in abamectin resistance was suggested by synergistic bioassays, in which median lethal time (LT 50) values were significantly reduced by pretreatment with triphenyl phosphate (TPP) and piperonyl butoxide, respectively. Detoxification enzyme assays confirmed that Est and MFO were related to abamectin resistance as metabolic factors. Moreover, some Est bands on a native isoelectric focusing gel were specifically inhibited by TPP, implying their association with resistance. Pretreatment with verapamil in synergistic bioassays did not reduce the LT 50 to abamectin, suggesting that the ABC transporter is not likely involved in resistance. However, enhanced MFO and Est activities in the AbaR strain were not enough to account for the extremely high level of abamectin resistance, which suggests the involvement of additional resistance mechanisms, such as target site insensitivity.

Characterisation of abamectin resistance in a field‐evolved multiresistant population of Plutella xylostella

Plutella xylostella (L.) has evolved resistance to various kinds of insecticide in the field. Reversion and selection, cross-resistance, inheritance and mechanisms of abamectin resistance were characterised in a field-derived multiresistant population of P. xylostella from China. Compared with a susceptible Roth strain, the field-derived TH population showed approximately 5000-fold resistance to abamectin. Rapid reversion of abamectin resistance was observed in the TH population when kept without insecticide selection. The TH-Abm strain, selected from the TH population with abamectin, developed 23 670-fold resistance to abamectin, a high level of cross-resistance to emamectin benzoate and low levels of cross-resistance to spinosad and fipronil. Genetic analyses indicated that abamectin resistance in the TH-Abm strain was autosomal, incompletely dominant and polygenic. P450 monooxygenase activities in the TH-Abm strain were significantly elevated compared with the TH strain. Piperonyl butoxide (PBO) inhibited a small part of abamectin resistance in the TH-Abm strain. Field-evolved high-level resistance to abamectin in the TH population was not stable. Selection of the TH population with abamectin resulted in an extremely high level of cross-resistance to emamectin benzoate and low levels of cross-resistance to spinosad and fipronil. Enhanced oxidative metabolism was involved in, but may not be the major mechanism of, polygenic abamectin resistance in the TH-Abm strain.

Milbemectin resistance in Tetranychus urticae (Acari: Tetranychidae): selection, stability and cross-resistance to abamectin

Studies on artificial laboratory selections with milbemectin, stability of milbemectin resistance and possible cross-resistance with abamectin were carried out with Tetranychus urticae Koch to provide basic information for a milbemectin resistance management program. Selections for resistance and susceptibility to milbemectin were performed in a population of T. urticae, collected from a commercial chrysanthemum field in the State of São Paulo, Brazil. After six selections for resistance and five selections for susceptibility, susceptible (S) and resistant (R) strains of T. urticae to milbemectin were obtained. The resistance ratio (R/S) at the LC(50) reached 409-fold value. The stability of milbemectin resistance was also studied under laboratory conditions, using a population with initial frequency of 75% of resistant mites. The frequencies of milbemectin resistance were evaluated monthly for a period of 7 months. In order to observe possible correlation between milbemectin and abamectin resistance, the frequencies of abamectin resistance were also evaluated for that population, during the same period. The frequency of milbemectin resistance decreased from 75 to 14.5%, while the percentage of abamectin resistant mites decreased from 57 to 9.1%, in 7 months. The frequencies of milbemectin and abamectin resistance were also evaluated in 25 field populations of T. urticae, collected from several crops in the State of São Paulo. The frequencies of milbemectin resistance varied from 4.1 to 89.5%, and of abamectin, from 7.0 to 90.5%. A positive and significant correlation was observed between the frequencies of milbemectin and abamectin resistance, indicating positive cross-resistance between these acaricides. The results indicate that abamectin should be avoided for managing milbemectin resistance in T. urticae. This is the first report on milbemectin resistance in T. urticae in Brazil.

Genetic analysis of abamectin resistance in Tetranychus cinnabarinus

The carmine spider mite is the most serious crop mite pests in China. Abamectin has been used to control insects and mites worldwide but carmine spider mites, Tetranychus cinnabarinus, had developed resistance to it. Genetic research on insecticide resistance has been fundamental for understanding the resistance development, studying resistance mechanisms, and designing appropriate resistance management strategies to control insect pests. A resistant colony of T. cinnabarinus, RRG42 , was established to examine the inheritance of abamectin resistance in T. cinnabarinus. The females of T. cinnabarinus were selected for bioassay using a slide dip method. After 42 generations of selection, the RRG42 strain was 8.7-fold resistant to abamectin compared with the susceptible strain (SS). The logarithm (log) concentration–probit response curve for F 1s from reciprocal crosses, of F 1RS and F 1SR, were inclined to that for SS and the degree of dominance ( D) values for F 1s were −0.81 and −0.17. There was a significant difference in values of LC 50 and slope of log concentration–probit lines between F 1RS and F 1SR. The observed mortalities of BC1 (F 1RS♀ × RRG42♂) and BC1′ (F 1SR♀ × SS♂) were significantly different from the expected mortalities based on a monogenic resistance in the chi-square tests. The inheritance of abamectin resistance in T. cinnabarinus is incompletely recessive and may be controlled by more than one gene. The maternal or cytoplasmic effect may exist in the inheritance of resistance to abamectin in T. cinnabarinus.

Unreliable Real-Time PCR Analysis of Human Endogenous Retrovirus-W (HERV-W) RNA Expression and DNA Copy Number in Multiple Sclerosis

Unreliable Real-Time PCR Analysis of Human Endogenous Retrovirus-W (HERV-W) RNA Expression and DNA Copy Number in Multiple Sclerosis

Multiple resistance, detoxifying enzyme activity, and inheritance of abamectin resistance in Tetranychus urticae Koch (Acarina: Tetranychidae)

The present study investigated the biochemical mechanism of abamectin resistance in a Tetranychus urticae Koch population collected from a bean greenhouse (BEYO 2) in Beyobası village in Gazipaşa district, Antalya province, and maintained in the laboratory. LC_{50, 60, 90} levels of BEYO 2 population of T. urticae were determined using a dry film method. The LC50 level of the BEYO 2 strain with abamectin was selected 15 times and was increased from 2.42 µL 100 mL^{-1} water to 38.67 µL 100 mL^{-1} water. A selected strain showing 35.05-fold resistance was named ABA 15 strain. It was investigated whether the resistant strain developed multiple resistance to different pesticide groups. The ABA 15 strain with abamectin resistance developed multiple resistance to chlorpyrifos, propargite, clofentezine, and fenpyroximate. The synergistic activity between abamectin and piperonyl butoxide (PBO), triphenyl phosphate (TPP), and S-benzyl-O,O-diisopropyl phosphorothioate (IBP) was studied in the resistant strain. Application of abamectin with synergists PBO, IBP, and TPP resulted in 1.76-, 2.43-, and 1.73-fold synergistic ratios, respectively, in the ABA 15 strain. The inheritance of resistance to abamectin of F1 females after reciprocal crosses between resistant and susceptible strains was maternal and paternal incompletely dominant. GSS (susceptible strain), BEYO 2, and ABA 15 strains were investigated in terms of the enzyme activities of esterase, glutathione S-transferase (GST), and monooxygenase (P450). No significant change was determined in esterase enzyme activities of the ABA 15 resistance strain to abamectin. The band density of esterase enzyme increased in the electrophoretic method. GST enzyme activity increased from 10.23 mOD min^{-1} mg^{-1} protein to 12.36 mOD min^{-1} mg^{-1} protein. The P450 enzyme activity was raised from 0.0017 mOD min^{-1} mg^{-1} protein to 0.0039 mOD min^{-1} mg^{-1} protein.

Resistance selection and biochemical mechanism of resistance to two Acaricides in Tetranychus cinnabarinus (Boiduval)

A Tetranychus cinnabarinus strain was collected from Chongqing, China. After 42 generations of selection with abamectin and 20 generations of selection with fenpropathrin in the laboratory, this T. cinnabarinus strain developed 8.7- and 28.7-fold resistance, respectively. Resistance to abamectin in AbR (abamectin resistant strain) and to fenpropathrin in FeR (fenpropathrin resistant strain) was partially suppressed by piperonyl butoxide (PBO), diethyl maleate (DEM) and triphenyl phosphate (TPP), inhibitors of mixed function oxidase (MFO), glutathione S-transferases (GST), and hydrolases, respectively, suggesting that these three enzyme families are important in conferring abamectin and fenpropathrin resistance in T. cinnabarinus. The major resistant mechanism to abamectin was the increasing activities of carboxylesterases (CarE), glutathione- S-transferase (GST) and mixed function oxidase (MFO), and the activity in resistant strain developed 2.7-, 3.4- and 1.4-fold contrasted to that in susceptible strain, respectively. The activity of glutathione- S-transferase (GST) in the FeR strain developed 2.8-fold when compared with the susceptible strain, which meant the resistance to fenpropathrin was related with the activity increase of glutathione- S-transferase (GST) in T. cinnabarinus. The result of the kinetic mensuration of carboxylesterases (CarE) showed that the structure of CarE in the AbR has been changed.

Biochemical mechanisms conferring cross-resistance between tebufenozide and abamectin in Plutella xylostella

Experiments have been carried out to confirm the cross-resistance between abamectin and tebufenozide in Plutella xylostella and demonstrate its mechanism. The results showed that the resistant strain of P. xylostella selected by tebufenozide (RF 99.38) really showed high cross-resistance to abamectin (RF 29.25). When this strain was subjected to resistance decaying treatment, breeding without contacting any insecticides, and abamectin resistance selection for 20 generations, the former resulted in decrease of its resistance to both tebufenozide and abamectin to about one third of the original (RF 35.03 and 11.67, respectively), and the later enhanced its resistance to abamectin dramatically (RF 303.77), but not to tebufenozide(RF 50.04). PBO showed high synergism to abamectin (SR 2.11–12.23), and the synergism ratio positively related to the resistance level among different strains. Enzyme analysis also proved that the activity of cytochrome P450 monooxygenase (MFO) was notable enhanced in the strains resistant to both tebufenozide and abamectin (1.71- to 3.01-fold). Based on discussion, it was concluded that tebufenozide selection could resulted in significant cross-resistance of P. xylostella to abamectin. The major mechanism for the cross-resistance should be the enhancement of MFO activity. For resistance management, tebufenozide and abamectin would not recommend for rotational use.

Cross‐resistance and biochemical mechanisms of abamectin resistance in the B‐type Bemisia tabaci

Abstract: To understand the risk of resistance and the possible mechanisms of resistance to abamectin in B‐type Bemisia tabaci (Gennadius) better, a resistant strain of B. tabaci was selected in the laboratory and cross‐resistance pattern and resistance mechanisms to abamectin were investigated. The NJ‐Abm strain of B. tabaci was derived from a field population (NJ) collected in Nanjing, China in 2002 with 18 generations of selection with abamectin in the laboratory. Compared with the unselected NJ strain, the selected NJ‐Abm strain developed 14.5‐fold resistance to abamectin and showed significant cross‐resistance to emamectin benzoate (4.4‐fold) and imidacloprid (3.4‐fold), but no cross‐resistance to fipronil. The oxidase inhibitor piperonyl butoxide (PBO) and glutathione S‐transferase inhibitor diethyl maleate (DEM) produced significant synergism on abamectin in the NJ‐Abm strain (with synergistic ratios of 3.9‐ and 4.1‐fold respectively); however, the esterase inhibitor triphenyl phosphate (TPP) did not act synergistically with abamectin. Biochemical analysis confirmed that P450 monooxygenase activity and glutathione S‐transferase activity of the NJ‐Abm strain were elevated to 2.1‐ and 2.0‐fold, respectively, compared with that of the NJ strain. This indicated that enhanced metabolism mediated by P450 monooxygenase and glutathione S‐transferase is likely to be involved in abamectin resistance and cross‐resistance to imidacloprid and emamectin benzoate in the NJ‐Abm strain.

Abamectin resistance in Tetranychus urticae Koch (Acari: Tetranychidae): selection, cross-resistance and stability of resistance

Studies on artificial laboratory selections with abamectin, cross-resistance relationships, and stability of resistance were carried out with Tetranychus urticae Koch to provide basic information for an abamectin resistance management program. Selections for resistance and susceptibility to abamectin were performed in a population of T. urticae, collected from a commercial strawberry field in the State of São Paulo, Brazil. After five selections for resistance and five selections for susceptibility, susceptible (S) and resistant (R) strains of T. urticae to abamectin were obtained. The resistance ratio (R/S) at the LC50 reached 342-fold values. The toxicity of eight acaricides was evaluated in the R and S strains, observing significant differences (at LC50) between R and S strains for milbemectin, fenpropathrin and chlorfenapyr. Significant correlation was detected between the LC50s of abamectin and milbemectin, indicating cross-resistance between these acaricides. No cross-resistance was detected for the acaricides fenpyroximate, cyhexatin, propargite and dimethoate. The stability of abamectin resistance was also studied under laboratory conditions. Abamectin resistance was unstable in the absence of selection pressure. For all studied populations (with 75, 50 and 25% of initial frequency of resistant mites), the percentage of resistant mites decreased to levels equal or lower than 15% in six months. The results indicate that milbemectin should be avoided for managing abamectin resistance in T. urticae.

Insecticide resistance in Argentine populations of Tuta absoluta (Meyrick) (Lepidoptera: Gelechiidae)

The tomato leafminer, Tuta absoluta (Meyrick), is one of the key pests of tomato in Argentina. Since its dispersal in the 1970s, chemical control has been the main method of controlling it. However, reduced efficacy of some of the recommended insecticides has been observed since the 1980s. The aim of this work was to study the toxicity of three insecticides widely used in chemical control of T. absoluta (abamectin, deltamethrin and methamidophos) on larvae from a laboratory susceptible population (CASTELAR) and two greenhouse populations (ROSARIO and BELLA VISTA). Insecticides were dissolved in acetone and topically applied to the mid-dorsal abdominal region of two-day old 4th instar larvae. LD50 values were estimated and the Resistance Ratio (RR) for each insecticide was calculated (RR = LD50 value of each greenhouse population/LD50 value of the susceptible population). ROSARIO and BELLA VISTA populations showed the following RRs values: > 68.38 for deltamethrin; 2.48 and 3.49 for abamectin, respectively; and 0.79 and 0.86 for metamidophos, respectively. Deltamethrin resistance observed in ROSARIO could be due to the high selective pressure exerted by pyrethroids in this location. Deltamethrin resistance in BELLA VISTA is more difficult to explain, because pyrethroids were scarcely used in the greenhouse where the insects were sampled. The incipient abamectin resistance detected in the BELLA VISTA population could result from the frequent use of this insecticide in this location, although natural variation can not be discarded.

Resistance and cross-resistance to insecticides in human head lice from Florida and California

Head lice from Florida (SF-HL) and California (SC-HL) were resistant to permethrin compared with colonized susceptible lice from Panama (PA-HL) (5.5- and 3.4-fold, respectively) and Ecuador (EC-HL) (8.5- and 5.3-fold, respectively). Permethrin-resistant lice were cross-resistant to pyrethrum and DDT. DNA sequencing validated presence of kdr-type mutations (T929I and L932F). Permethrin resistance was synergized by piperonyl butoxide (PBO) in SC-HL. Resistance to malathion in SF-HL (1.4–2.2-fold) and SC-HL (2.1–3.6-fold) was detected. Malathion resistance in SF-HL was synergized by S, S, S-tributylphosphorotrithioate (DEF) and by PBO in SC-HL. Malathion/permethrin-resistant lice from the UK (BR-HL) were synergized by DEF but not synerziged by PBO. PBO protected BR-HL from malathion, indicating suppressed desulfuration. Abamectin resistance in SF-HL (1.7–2.5-fold) and SC-HL (1.8–2.3-fold) was detected. No resistance to lindane was found. Thus, multiple resistance mechanisms against commonly available and widely used pediculicides and insecticides are apparently occurring.

Development and stability of insecticide resistance in the leafminer Liriomyza trifolii (Diptera: Agromyzidae) to cyromazine, abamectin, and spinosad.

Three populations of the leafminer, Liriomyza trifolii (Burgess), were collected from commercial ornamental production greenhouses in the United States and tested for susceptibility to three commercial insecticides. A leaf dip bioassay of leaves containing young (1-2-d-old) larvae was used. Based on larval mortality and compared with a susceptible laboratory reference colony, the three strains varied in spectrum and level of resistance to the insecticides. CA-1, collected from Gerbera daisy, was moderately resistant to cyromazine (18.1-fold) and abamectin (22.0-fold), but highly resistant to spinosad (> 188-fold). CA-2, collected from chrysanthemums, was not resistant to abamectin, had a low level of resistance to cyromazine (8.2-fold), but was extremely resistant to spinosad (1,192-fold). GA-1, collected from chrysanthemums, had very low levels of resistance to cyromazine (5.4-fold) and spinosad (1.9-fold) but was moderately resistant to abamectin (30.6-fold). When reared in the absence of insecticide selection pressure, all three strains reverted to approximately the level of the reference strain. The CA-1 strain reverted in nine generations to cyromazine; however, the lowest levels of abamectin and spinosad resistance reverted to was 3.1-fold at F8 and 3.2 at the F10, respectively. The CA-2 strain reverted in five generations to both cyromazine and spinosad. GA-1 reverted in five generations to abamectin. Based on the results, resistance to these three insecticides was unstable. Additionally, there was no cross-resistance among these three insecticides.

Genetic basis of resistance and studies on cross-resistance in a population of diamondback moth, Plutella xylostella (Lepidoptera: Plutellidae).

The genetic basis of abamectin resistance was studied in a strain of the diamondback moth, Plutella xylostella (L), following laboratory selection of a field population collected at Xuanhua, Hebei Province, China. Data from the testing of F1 progeny from reciprocal crosses between abamectin-resistant and abamectin-susceptible strains indicated that resistance might be autosomal and incompletely recessive with a degree of dominance of -0.13. Chi-squared analyses from the response of a backcross of crossed F1 progeny and the resistant strain and F2 progeny were highly significant, suggesting that the resistance was probably controlled by more than one gene. The results of cross-resistance studies showed that there was little cross-resistance between abamectin and four pyrethroid insecticides (deltamethrin, beta-cypermethrin, fenvalerate and bifenthrin) and no cross-resistance between abamectin and the acylureas chlorfluazuron or flufenoxuron.

Differential susceptibility to abamectin and two bioactive avermectin analogs in abamectin-resistant and -susceptible strains of Colorado potato beetle, Leptinotarsa decemlineata (Say) (Coleoptera: Chrysomelidae)

As resistance to currently used insecticides increases in the Colorado potato beetle (CPB), Leptinotarsa decemlineata (Say), abamectin and its 4″-epi and 8,9-oxide analogs may serve as likely replacements if proven effective. We previously selected an abamectin-resistant strain of CPB (AB-F) that is suitable for the determination of cross-resistance to these two bioactive avermectin analogs. Using bioassay and logit analysis, the present work shows that, on average and following normalization by weight, the larval stages of the insecticide-susceptible SS strain are equally sensitive to the toxic action of abamectin and its 4″-epi and 8,9-oxide analogs, indicating that all three compounds retain high bioactivity towards the susceptible larval stages. Abamectin and the two analogs also are similar in toxicity to the larval stages of the AB-F strain. However, the AB-F larval stages are significantly less sensitive on average to these insecticides than the SS larval stages, indicating resistance to abamectin and cross-resistance to both the two analogs tested. Likewise, adults of the AB-F strain are significantly less sensitive to the toxic action of abamectin and the two analogs compared to SS adults, also indicative of resistance and cross-resistance. Abamectin is significantly more toxic, however, to both SS and AB-F adults, respectively, than either of the two analogs. The reduction in sensitivity was particularly evident in SS adults to both the 4″-epi and 8,9-oxide analogs. Additionally, adults of the SS strain are significantly less sensitive to the toxic action of abamectin and the two analogs when compared to SS larval stages. There is no significant differences, however, in the toxicity of these three insecticides, respectively, between larval and adults stages of the AB-F strain. This phenomenon results in lower resistance ratio (RR) values calculated for the two avermectin analogs compared to those calculated for abamectin regardless of the insect stage examined but is particularly evident and significant in the adult stage. This relative decrease in resistance levels is primarily associated with SS adults that are less sensitive to the toxic action of these insecticides. The decrease in abamectin toxicity is apparently due to significantly increased levels of P450 associated with SS adults versus forth instars and to similar levels in adults of the SS and AB-F strains. Because abamectin resistance in CPB is due in large part to enhanced oxidative metabolism of abamectin, it is likely that the SS adults are more tolerant to abamectin due to an enhanced level of oxidative detoxification. Finally, neither abamectin nor the two analogs are structurally protected at the specific molecular locations, C 3″, C 24, and C 26 carbons, which leads to enhanced oxidative metabolism, resistance and cross-resistance. Structurally-protected avermectin analogs at these vulnerable intramolecular sites are likely to be more effective insecticides in suppressing the development of oxidative detoxification-based resistance to abamectin, as would the use of oxidative synergists.