Control failure likelihood and spatial dependence of insecticide resistance in the tomato pinworm, Tuta absoluta

BACKGROUND: Insecticide resistance is a likely cause of field control failures of Tuta absoluta, but the subject has been little studied. Therefore, resistance to ten insecticides was surveyed in seven representative field populations of this species. The likelihood of control failures was assessed, as well as weather influence and the spatial dependence of insecticide resistance. RESULTS: No resistance or only low resistance levels were observed for pyrethroids (bifenthrin and permethrin), abamectin, spinosad, Bacillus thuringiensis and the mixture deltamethrin + triazophos (<12.5‐fold). In contrast, indoxacarb exhibited moderate levels of resistance (up to 27.5‐fold), and chitin synthesis inhibitors exhibited moderate to high levels of resistance (up to 222.3‐fold). Evidence of control failures was obtained for bifenthrin, permethrin, diflubenzuron, teflubenzuron, triflumuron and B. thuringiensis. Weather conditions favour resistance to some insecticides, and spatial dependence was observed only for bifenthrin and permethrin. CONCLUSION: Insecticide resistance in field populations of the tomato pinworm prevails for the insecticides nowadays most frequently used against them—the chitin synthesis inhibitors (diflubenzuron, triflumuron and teflubenzuron). Local selection favoured by weather conditions and dispersal seem important for pyrethroid resistance evolution among Brazilian populations of T. absoluta and should be considered in designing pest management programmes. Copyright © 2011 Society of Chemical Industry     

Cross‐resistance study and biochemical mechanisms of thiamethoxam resistance in B‐biotype Bemisia tabaci (Hemiptera: Aleyrodidae)

BACKGROUND: B‐biotype Bemisia tabaci (Gennadius) has invaded China over the past two decades. To understand the risks and to determine possible mechanisms of resistance to thiamethoxam in B. tabaci, a resistant strain was selected in the laboratory. Cross‐resistance and the biochemical mechanisms of thiamethoxam resistance were investigated in the present study. RESULTS: A 66.3‐fold thiamethoxam‐resistant B. tabaci strain (TH‐R) was established after selection for 36 generations. Compared with the susceptible strain (TH‐S), the selected TH‐R strain showed obvious cross‐resistance to imidacloprid (47.3‐fold), acetamiprid (35.8‐fold), nitenpyram (9.99‐fold), abamectin (5.33‐fold) and carbosulfan (4.43‐fold). No cross‐resistance to fipronil, chlorpyrifos or deltamethrin was seen. Piperonyl butoxide (PBO) and triphenyl phosphate (TPP) exhibited significant synergism on thiamethoxam effects in the TH‐R strain (3.14‐ and 2.37‐fold respectively). However, diethyl maleate (DEM) did not act synergistically with thiamethoxam. Biochemical assays showed that cytochrome P450 monooxygenase activities increased 1.21‐ and 1.68‐fold respectively, and carboxylesterase activity increased 2.96‐fold in the TH‐R strain. However, no difference was observed for glutathione S‐transferase between the two strains. CONCLUSION: B‐biotype B. tabaci develops resistance to thiamethoxam. Cytochrome P450 monooxygenase and carboxylesterase appear to be responsible for the resistance. Reasonable resistance management that avoids the use of cross‐resistance insecticides may delay the development of resistance to thiamethoxam in this species. Copyright © 2009 Society of Chemical Industry     

Pyrethroid tolerance in Culex pipiens pipiens var molestus from Marin County, California

In May 2001 a sample of Culex pipiens pipiens variety molestus Forskål from Marin County, California, collected as larvae and reared to adults, was found to show reduced resmethrin and permethrin knock‐down responses in bottle bioassays relative to a standard susceptible Cx pipiens quinquefasciatus Say colony (CQ1). Larval susceptibility tests, using CQ1 as standard susceptible, indicated that the Marin mosquitoes had LC₅₀ resistance ratios of 18.3 for permethrin, 12 for deltamethrin and 3.3 for pyrethrum. A colony of Marin was established and rapidly developed higher levels of resistance in a few generations after exposure to permethrin as larvae. These selected larvae were shown to cross‐resist to lambda‐cyhalothrin as well as to DDT. However, adult knock‐down time in the presence of permethrin, resmethrin and pyrethrum was not increased after increase in tolerance to pyrethroids as larvae. Partial and almost complete reversion to susceptibility as larvae was achieved with S, S, S‐tributylphosphorotrithioate and piperonyl butoxide (PBO), respectively, suggesting the presence of carboxylesterase and P450 monooxygenase mediated resistance. Insensitive target site resistance (kdr) was also detected in some Marin mosquitoes by use of an existing PCR‐based diagnostic assay designed for Cx p pipiens L mosquitoes. Carboxylesterase mediated resistance was supported by use of newly synthesized novel pyrethroid‐selective substrates in activity assays. Bottle bioassays gave underestimates of the levels of tolerance to pyrethroids of Marin mosquitoes when compared with mortality rates in field trials using registered pyrethroid adulticides with and without PBO. This study represents the first report of resistance to pyrethroids in a feral population of a mosquito species in the USA. Copyright © 2003 Society of Chemical Industry     

Various mechanisms responsible for permethrin metabolic resistance in seven field-collected strains of the German cockroach from Iran, Blattella germanica (L.) (Dictyoptera: Blattellidae)

Insecticide resistance in the German cockroach can be mediated by a number of mechanisms, the most common being enhanced enzymatic metabolism. Seven field-collected strains of German cockroach, Blattella germanica (L.) with various levels of resistance to pyrethroids, five out of which were also cross-resistant to DDT were used in this study. The investigation of possible mechanisms responsible for permethrin resistance was carried out using the synergists PBO, DEF and DMC and biochemical assays, including general esterases, glutathione S-transeferases and monooxygenases assays, using an automated microtitre plate reader. PBO and DEF, the inhibitors of cytochrome p450 monooxygenases and general esterases, respectively, affected permethrin resistance to varying degrees depending on the strain. DDT resistance in five strains were not completely eliminated by the synergist DMC, an inhibitor of glutathione S-transferase enzymes, suggesting that a further non-metabolic resistance mechanism such as kdr-type may be present. This suggestion was further supported by GST assay data, where a little elevation in GST activity was detected in only two strains. The synergist data supported by biochemical assays implicated that cytochrome p450 monooxygenases or hydrolases are involved in permethrin resistance in some strains. However, these results implicated both enhanced oxidative and hydrolytic metabolism of permethrin as resistance mechanism in the other strains. The results of synergist and biochemical studies implicated that all the field-collected permethrin resistant strains have developed diverse mechanisms of resistance, although these strains have been collected from the same geographic area. The change in resistance ratios of some strains by using PBO or DEF is discussed. It is of interest to note that because resistance to permethrin was not completely eliminated by DEF and PBO, it is likely that one or more additional mechanisms are involved in permethrin resistance in every strain studied.     

Nicotinoid and pyrethroid insecticide resistance in houseflies (Diptera: Muscidae) collected from Florida dairies

BACKGROUND: The housefly, Musca domestica L., continues to be a major pest of confined livestock operations. Houseflies have developed resistance to most chemical classes, and new chemistries for use in animal agriculture are increasingly slow to emerge. Five adult housefly strains from four Florida dairy farms were evaluated for resistance to four insecticides (beta‐cyfluthrin, permethrin, imidacloprid and nithiazine). RESULTS: Significant levels of tolerance were found in most field strains to all insecticides, and in some cases substantial resistance was apparent (as deduced from comparison with prior published results). At the LC₉₀ level, greater than 20‐fold resistance was found in two of the fly strains for permethrin and one fly strain for imidacloprid. Beta‐cyfluthrin LC₉₀ resistance ratios exceeded tenfold resistance in three fly strains. The relatively underutilized insecticide nithiazine had the lowest resistance ratios; however, fourfold LC₉₀ resistance was observed in one southern Florida fly strain. Farm insecticide use and its impact on resistance selection in Florida housefly populations are discussed. CONCLUSION: Housefly resistance to pyrethroids is widespread in Florida. Imidacloprid resistance is emerging, and tolerance was observed to both imidacloprid and nithiazine. If these insecticides are to retain efficacy, producer use must be restrained. Copyright © 2009 Society of Chemical Industry     

Michael Elliott's billion dollar crystals and other discoveries in insecticide chemistry

The crowning achievement for Michael Elliott came in 1973 when his most outstanding candidate insecticide from 25 years of research crystallized from hexane solution. The stereochemically pure crystalline compound was the most potent synthetic insecticide ever made until that time, and it was highly selective for insects compared with mammals. It was given the name deltamethrin. Sequential stereospecific crystallization to isolate the most potent epimer and base‐catalyzed racemization of the remaining less active isomer could be used to produce deltamethrin efficiently on a large scale; it became the billion dollar crystals. Elliott's discoveries at Rothamsted in England with Norman Janes and David Pulman of resmethrin, permethrin, cypermethrin and ultimately deltamethrin provided crop protection and malaria control for millions of people. Michael also laid the background for lipophilic amide, dithiane and other insecticides and nerve probes that are not involved in pyrethroid cross‐resistance. Some aspects of these investigations were best conducted at Berkeley, where Michael studied pyrethrins in 1969, synthetic pyrethroids in 1974 and alternative insecticides in 1986–1988. This review considers Michael's seminal discoveries in insecticide chemistry, with emphasis on his Berkeley years. Copyright © 2010 Society of Chemical Industry     

Voltage‐sensitive sodium channel mutations S989P + V1016G in Aedes aegypti confer variable resistance to pyrethroids,DDT and oxadiazines

BACKGROUND

Aedes aegypti is a vector of several important human pathogens. Control efforts rely primarily on pyrethroid insecticides for adult mosquito control, especially during disease outbreaks. A. aegypti has developed resistance nearly everywhere it occurs and insecticides are used. An important mechanism of resistance is due to mutations in the voltage‐sensitive sodium channel (Vssc) gene. Two mutations, in particular, S989P + V1016G, commonly occur together in parts of Asia.

RESULTS

We have created a strain (KDR:ROCK) that contains the Vssc mutations S989P + V1016G as the only mechanism of pyrethroid resistance within the genetic background of Rockefeller (ROCK), a susceptible lab strain. We created KDR:ROCK by crossing the pyrethroid‐resistant strain Singapore with ROCK followed by four backcrosses with ROCK and Vssc S989P + V1016G genotype selections. We determined the levels of resistance conferred to 17 structurally diverse pyrethroids, the organochloride DDT, and oxadiazines (VSSC blockers) indoxacarb (proinsecticide) and DCJW (the active metabolite of indoxacarb). Levels of resistance to the pyrethroids were variable, ranging from 21‐ to 107‐fold, but no clear pattern between resistance and chemical structure was observed. Resistance is inherited as an incompletely recessive trait. KDR:ROCK had a > 2000‐fold resistance to DDT, 37.5‐fold cross‐resistance to indoxacarb and 13.4‐fold cross‐resistance to DCJW.

CONCLUSION

Etofenprox (and DDT) should be avoided in areas where Vssc mutations S989P + V1016G exist at high frequencies. We found that pyrethroid structure cannot be used to predict the level of resistance conferred by kdr. These results provide useful information for resistance management and for better understanding pyrethroid interactions with VSSC. © 2017 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.     

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

BACKGROUND: 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. RESULTS: Compared with a susceptible Roth strain, the field‐derived TH population showed ～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. CONCLUSION: 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. Copyright © 2009 Society of Chemical Industry     

Monooxygenase mediated pyrethroid detoxification in sea lice (Lepeophtheirus salmonis)

The role of monooxygenases in detoxification of the pyrethroids cypermethrin and deltamethrin was examined. Four strains of sea lice (Lepeophtheirus salmonis Krøyer) with normal or moderately reduced sensitivity towards the pyrethroids were tested in bioassays by exposure to the pyrethroid alone and in combination with an oxygenase inhibitor, piperonyl butoxide (PBO). The normal (baseline) sensitivity was considered as the sensitivity range for the two most sensitive strains. Pre‐treatment with PBO elevated the sensitivity (P < 0.01) compared with groups exposed to the pyrethroid only. A positive, but not statistically significant, correlation between the activity of haem peroxidases and the pyrethroid concentration immobilizing 50% of the parasites was demonstrated (ρ = 0.500 for deltamethrin and ρ = 0.310 for cypermethrin). The results indicate that cytochrome P450 monooxygenases are involved in detoxification of pyrethroids in sea lice. ¹⁴C‐Deltamethrin was absorbed in a lesser amount in a group of sea lice exposed to a mixture of the compound and PBO than in a group exposed to ¹⁴C‐deltamethrin alone. A significant difference could be demonstrated both immediately after exposure (P < 0.01) and 24 h after exposure (P < 0.05). No significant differences were found between groups pre‐treated with PBO and groups exposed to ¹⁴C‐deltamethrin only. ¹⁴C‐Deltamethrin was taken up mainly through the cuticle, especially the cuticle on the extremities of the ventral surface, and subsequently distributed throughout the body of the parasite. Copyright © 2005 Society of Chemical Industry     

Cross-Resistance to Imidacloprid in Strains of German Cockroach (Blattella germanica) and House Fly (Musca domestica)

The toxicity of a promising new insecticide, imidacloprid, was evaluated against several susceptible and resistant strains of German cockroach and house fly. Imidacloprid rapidly immobilized German cockroaches followed by a period of about 72 h during which some cockroaches recovered. After 72 h there was no further recovery. Imidacloprid-treated houseflies were immobilized more slowly than treated cockroaches, with the maximum effect observed after 72 h, and there was no recovery. Based upon 72-h LD₅₀ values imidacloprid was moderately toxic to German cockroaches (LD₅₀ values were 6–8 ng mg^-1) and had only low toxicity to house flies (LD₅₀ 140 ng mg^-1). Piperonyl butoxide (PBO) blocked the observed recovery in German cockroaches. PBO also greatly enhanced the 72-h LD₅₀ of imidacloprid from 43- to 59-fold in cockroaches and 86-fold in house flies. Two strains of German cockroach (Baygon-R and Pyr-R) showed >4-fold cross-resistance to imidacloprid. This cross-resistance could not be suppressed by PBO, suggesting that P450 monooxygenase-mediated detoxication is not responsible for this cross-resistance. Variation in the level of synergism observed with PBO (between strains) suggests the ‘basal’ level of monooxygenase-mediated detoxication of imidacloprid is quite variable between strains of German cockroach. The AVER and LPR strains of house fly showed significant cross-resistance to imidacloprid. PBO reduced the level of cross-resistance in AVER from >4·2-fold to 0·5-fold (i.e. the AVER strain LD₅₀ was half that of the susceptible strain when both were treated with PBO), but PBO did not suppress the cross-resistance in LPR. These data suggest monooxygenases are the mechanism responsible for cross-resistance to imidacloprid in AVER, but not in the LPR strain. © of SCI.     

昆虫对拟除虫菊酯类杀虫剂的代谢抗性机制研究进展

随着拟除虫菊酯类杀虫剂在卫生和农业害虫防治中的广泛应用,昆虫对此类杀虫剂产生抗性的报道越来越多。目前已明确昆虫对拟除虫菊酯类杀虫剂的抗性机制包括表皮穿透率下降、靶标抗性以及代谢抗性,其中代谢抗性机制较为普遍,而且其与昆虫对多种杀虫剂的交互抗性关系密切。目前,随着基因组、转录组以及蛋白质组学等新技术的发展及应用,昆虫对拟除虫菊酯类杀虫剂的代谢抗性机制研究也取得了很多新进展。昆虫体内细胞色素P450酶（P450s）、羧酸酯酶（CarE）及谷胱甘肽S-转移酶（GSTs）等重要解毒酶系的改变均与昆虫对拟除虫菊酯类杀虫剂的代谢抗性有关,其中这3类解毒酶的活性及相关基因表达量的变化是昆虫对此类杀虫剂产生代谢抗性的主要原因。明确昆虫对拟除虫菊酯类杀虫剂的代谢抗性机制,对合理使用此类杀虫剂及延缓抗药性的产生均具有重要意义。本文在总结拟除虫菊酯类杀虫剂代谢路径及相关生物酶研究概况的基础上,综述了近年来有关昆虫对此类杀虫剂代谢抗性机制研究的主要进展。     

Resistance of Pakistani field populations of spotted bollworm Earias vittella (Lepidoptera: Noctuidae) to pyrethroid,organophosphorus and new chemical insecticides

BACKGROUND: The spotted bollworm Earias vittella (Fab.) is a serious pest of cotton and okra in Pakistan. Owing to persistent use of insecticides, this pest has developed resistance, especially to pyrethroids. The present studies aimed at determining the extent of resistance to pyrethroid, organophosphorus and new chemical insecticides in Pakistani populations of E. vittella. RESULTS: Field populations of E. vittella were monitored at Multan, Pakistan, from 1999 to 2007 for their resistance against six pyrethroid, four organophosphorus and six new chemical insecticides using a leaf‐dip bioassay. Of the pyrethroids, resistance was generally low to zeta‐cypermethrin and moderate to high or very high to cypermethrin, deltamethrin, esfenvalerate, bifenthrin and lambda‐cyhalothrin. Resistance to organophosphates chlorpyrifos, profenofos, triazophos and phoxim was recorded at very low to low levels. Among new chemicals, E. vittella had no or a very low resistance to spinosad, emamectin benzoate and methoxyfenozide, a very low to low resistance to abamectin, a very low to moderate resistance to indoxacarb and a moderate resistance to chlorfenapyr. CONCLUSION: The results indicate a lack of cross‐resistance between pyrethroid and organophosphorus insecticides in E. vittella. Rotation of insecticides showing no, very low or low resistance, but belonging to different insecticide classes with unrelated modes of action, may prevent or mitigate insecticide resistance in E. vittella. Copyright © 2009 Society of Chemical Industry     

Insecticide resistance compromises the control of Aedes aegypti in Bangladesh

BACKGROUND

With no effective drugs or widely available vaccines, dengue control in Bangladesh is dependent on targeting the primary vector Aedes aegypti with insecticides and larval source management. Despite these interventions, the dengue burden is increasing in Bangladesh, and the country experienced its worst outbreak in 2019 with 101 354 hospitalized cases. This may be partially facilitated by the presence of intense insecticide resistance in vector populations. Here, we describe the intensity and mechanisms of resistance to insecticides commonly deployed against Ae. aegypti in Dhaka, Bangladesh.

RESULTS

Dhaka Ae. aegypti colonies exhibited high-intensity resistance to pyrethroids. Using CDC bottle assays, we recorded 2–24% mortality (recorded at 24 h) to permethrin and 48–94% mortality to deltamethrin, at 10× the diagnostic dose. Bioassays conducted using insecticide–synergist combinations suggested that metabolic mechanisms were contributing to pyrethroid resistance, specifically multi-function oxidases, esterases, and glutathione S-transferases. In addition, kdr alleles were detected, with a high frequency (78–98%) of homozygotes for the V1016G mutation. A large proportion (≤ 74%) of free-flying and resting mosquitoes from Dhaka colonies survived exposure to standard applications of pyrethroid aerosols in an experimental free-flight room. Although that exposure affected the immediate host-seeking behavior of Ae. aegypti, the effect was transient in surviving mosquitoes.

CONCLUSION

The intense resistance characterized in this study is likely compromising the operational effectiveness of pyrethroids against Ae. aegypti in Dhaka. Switching to alternative chemical classes may offer a medium-term solution, but ultimately a more sustainable and effective approach to controlling dengue vectors is required. © 2023 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.     

Cross‐resistance,inheritance and biochemical mechanisms of imidacloprid resistance in B‐biotype Bemisia tabaci

BACKGROUND: The B‐type Bemisia tabaci (Gennadius) has become established in many regions in China, and neonicotinoids are extensively used to control this pest. Imidacloprid resistance in a laboratory‐selected strain of B‐type B. tabaci was characterised in order to provide the basis for recommending resistance management tactics. RESULTS: The NJ‐Imi strain of B‐type B. tabaci was selected from the NJ strain with imidacloprid for 30 generations. The NJ‐Imi strain exhibited 490‐fold resistance to imidacloprid, high levels of cross‐resistance to three other neonicotinoids, low levels of cross‐resistance to monosultap, cartap and spinosad, but no cross‐resistance to abamectin and cypermethrin. Imidacloprid resistance in the NJ‐Imi strain was autosomal and semi‐dominant. It is shown that enhanced detoxification mediated by cytochrome‐P450‐dependent monooxygenases contributes to imidacloprid resistance to some extent in the NJ‐Imi strain. Results from synergist bioassays and cross‐resistance patterns indicated that target‐site insensitivity may be involved in imidacloprid resistance in the NJ‐Imi strain of B. tabaci. CONCLUSION: Although oxidative detoxification mediated by P450 monooxygenases is involved in imidacloprid resistance in the NJ‐Imi strain of B‐type B. tabaci, target‐site modification as an additional resistance mechanism cannot be ruled out. Considering the high risk of cross‐resistance, neonicotinoids should be regarded as a single group when implementing an insecticide rotation scheme in B. tabaci control. Copyright © 2009 Society of Chemical Industry     

灰飞虱对杀虫剂抗药性的研究进展

灰飞虱对杀虫剂产生抗药性是其近年来暴发频繁的重要原因。本文综述了国内外关于灰飞虱抗药性的研究成果,包括灰飞虱抗药性的发展、交互抗性、抗性机理、抗性遗传及生物适合度等。田间灰飞虱种群对多种药剂产生了不同程度的抗药性,其中对新烟碱类药剂吡虫啉和昆虫生长调节剂噻嗪酮产生了高水平到极高水平抗性(抗药性倍数分别为44.6～108.8倍和超过200倍),对有机磷类药剂毒死蜱和乙酰甲胺磷(抗药性倍数分别为10～12.6倍和9～13倍)、氨基甲酸酯类药剂甲萘威和残杀威(抗药性倍数分别为29.8～45.3倍和40.1～131.5倍)和拟除虫菊酯类药剂高效氯氰菊酯和溴氰菊酯(抗药性倍数分别为7.8～108.8倍和12～21倍)产生了中等水平到高水平的抗药性,对氟虫腈、阿维菌素和噻虫嗪没有产生抗药性(抗性倍数5倍)。长期大面积使用化学药剂是灰飞虱产生抗药性的重要原因。因此,必须加强灰飞虱的抗性治理,以延缓其抗药性进一步发展。     

Resistance to spinosad in the western flower thrips, Frankliniella occidentalis (Pergande), in greenhouses of south-eastern Spain

Susceptibility to spinosad of western flower thrips (WFT), Frankliniella occidentalis (Pergande), from south-eastern Spain was determined. LC(50) values of the field populations without previous exposure to spinosad collected in Murcia in 2001 and 2002 ranged from 0.005 to 0.077 mg L(-1). The populations collected in Almeria in 2003 in greenhouses were resistant to spinosad (LC(50) > 54 mg L(-1)) compared with the authors' highly susceptible laboratory strain. The highly sensitive laboratory strain leads to very high resistance ratios for the field populations (>13 500), but these ratios do not necessarily mean resistance problems and control failures (spinosad field rate 90-120 mg L(-1)). The populations collected in Murcia from some greenhouses in 2004 were also resistant to spinosad (RF > 3682). Spinosad overuse, with more than ten applications per crop, produced these resistant populations in some greenhouses. Spinosad showed no cross-resistance to acrinathrin, formetanate or methiocarb in laboratory strains selected for resistance towards each insecticide. Correlation analysis indicated no cross-resistance among spinosad and the other three insecticides in 13 field populations and in nine laboratory strains. The synergists piperonyl butoxide (PBO), S,S,S-tributyl phosphorotrithioate (DEF) and diethyl maleate (DEM) did not enhance the toxicity of spinosad to the resistant strains, indicating that metabolic-mediated detoxification was not responsible for the spinosad resistance. These findings suggest that rotation with spinosad may be an effective resistance management strategy.     

Genetics of Pyrethroid Resistance in a Strain (ALHF) of House Flies (Diptera: Muscidae)

Five house fly lines were derived from crosses of the pyrethroid-resistant ALHF (wildtype) and the susceptible aabys (bearing recessive morphological markers on each of five autosomes) strains. Each line was homozygous for one mutant-type marker from aabys. The level of resistance to permethrin was measured for each line to determine the genetic linkage of pyrethroid resistance in ALHF. Permethrin resistance in ALHF was 6600-fold compared with that in aabys. Resistance in flies bearing a mutant-type marker on autosome 4 was similar to that in ALHF. Flies with mutant-type markers on autosomes 1 and 2 had relatively lower resistance than ALHF; flies with mutant-type markers on autosomes 3 and 5 had much lower levels of resistance. These results demonstrated that factors on autosomes 3 and 5 play very important roles in pyrethroid resistance, whereas factors on autosomes 1 and 2 may have relatively small roles in resistance. Piperonyl butoxide (PBO) increased toxicity of permethrin in strains with mutant-type markers on autosomes 3 and 4 similar to that in ALHF. Slightly decreased synergism ratios in strains with autosomes 1 and 2 mutant-type markers compared with ALHF indicated that factors on autosomes 1 and 2 might make a small contribution in P450 monooxygenase-mediated resistance. However, when the autosome 5 mutant-type marker was present, PBO did not substantially decrease resistance, suggesting that the factor(s) on autosome 5 plays the most important role in P450 monooxygenase-mediated resistance. The resistance ratios of permethrin + PBO in strains with mutant-type markers on autosomes 1, 2, and 5 were significantly lower than those in ALHF, suggesting that factors on autosomes 1, 2, and 5 might be involved in pyrethroid resistance mechanisms other than P450-mediated detoxication. Injection did not change levels of resistance in the house flies tested, revealing that decreased rate of cuticular penetration (pen) probably does not play an important role in pyrethroid resistance in ALHF. The interaction and regulation of different mechanisms and/or factors involved in pyrethroid resistance in house flies are discussed.     

西花蓟马抗甲氨基阿维菌素苯甲酸盐种群的交互抗性与生化抗性机制

为了解西花蓟马Frankliniella occidentalis(Pergande)对甲氨基阿维菌素苯甲酸盐的抗性风险,采用生物和生化测定方法研究了西花蓟马甲维盐抗性种群与其它杀虫剂的交互抗性和生化抗性机制。西花蓟马甲维盐抗性种群对阿维菌素有高水平交互抗性,抗性倍数为31.656,对啶虫脒有中等水平交互抗性,为12.182,对吡虫啉、溴虫腈、氯氟氰菊酯、毒死蜱和灭多威有低水平交互抗性,为5.517~8.568,而对多杀菌素无明显交互抗性。增效剂胡椒基丁醚(PBO)、马来酸二乙酯(DEM)、三丁基三硫磷酸酯(DEF)和磷酸三苯酯(TPP)对甲维盐抗性种群和田间种群均有显著增效作用。甲维盐抗性种群多功能氧化酶细胞色素P₄₅₀和b₅含量、O-脱甲基酶、谷胱甘肽S-转移酶和羧酸酯酶活性均显著提高,分别为敏感种群的3.89、3.61、5.32、4.42和1.30倍,表明多功能氧化酶、谷胱甘肽S-转移酶和羧酸酯酶等解毒代谢酶活性的提高是西花蓟马对甲维盐产生抗性的重要机制。     

Insecticide resistance status of Aedes aegypti (L.) from Colombia

BACKGROUND: To evaluate the insecticide susceptibility status of Aedes aegypti (L.) in Colombia, and as part of the National Network of Insecticide Resistance Surveillance, 12 mosquito populations were assessed for resistance to pyrethroids, organophosphates and DDT. Bioassays were performed using WHO and CDC methodologies. The underlying resistance mechanisms were investigated through biochemical assays and RT‐PCR. RESULTS: All mosquito populations were susceptible to malathion, deltamethrin and cyfluthrin, and highly resistant to DDT and etofenprox. Resistance to lambda‐cyhalothrin, permethrin and fenitrothion ranged from moderate to high in some populations from Chocó and Putumayo states. In Antioquia state, the Santa Fe population was resistant to fenitrothion. Biochemical assays showed high levels of both cytochrome P450 monooxygenases (CYP) and non‐specific esterases (NSE) in some of the fenitrothion‐ and pyrethroid‐resistant populations. All populations showed high levels of glutathione‐S‐transferase (GST) activity. GSTe2 gene was found overexpressed in DDT‐resistant populations compared with Rockefeller susceptible strain. CONCLUSIONS: Differences in insecticide resistance status were observed between insecticides and localities. Although the biochemical assay results suggest that CYP and NSE could play an important role in the pyrethroid and fenitrothion resistance detected, other mechanisms remain to be investigated, including knockdown resistance. Resistance to DDT was high in all populations, and GST activity is probably the main enzymatic mechanism associated with this resistance. The results of this study provide baseline data on insecticide resistance in Colombian A. aegypti populations, and will allow comparison of changes in susceptibility status in this vector over time. Copyright © 2011 Society of Chemical Industry     

Metabolic mechanisms of insecticide resistance in the western flower thrips, Frankliniella occidentalis (Pergande)

The interactions between six insecticides (methiocarb, formetanate, acrinathrin, deltamethrin, methamidophos and endosulfan) and three potential synergists (piperonyl butoxide (PBO), S,S,S-tributyl phosphorotrithioate (DEF) and diethyl maleate (DEM)) were studied by topical exposure in strains selected for resistance to each insecticide, and in a susceptible strain of Frankliniella occidentalis (Pergande). In the susceptible strain PBO produced appreciable synergism only of formetanate, methiocarb and methamidophos. Except for endosulfan, PBO synergized all the insecticides to varying degrees in the resistant strains. A very high level of synergism by PBO was found with acrinathrin, which reduced the resistance level from 3344- to 36-fold. PBO slightly synergized the carbamates formetanate (4.6-fold) and methiocarb (3.3-fold). PBO also produced a high synergism of deltamethrin (12.5-fold) and methamidophos (14.3-fold) and completely restored susceptibility to both insecticides. DEF did not produce synergism with any insecticide in the resistant strains and DEM was slightly synergistic to endosulfan (3-fold). These studies indicate that an enhanced detoxification, mediated by cytochrome P-450 monooxygenases, is the major mechanism imparting resistance to different insecticides in F occidentalis. Implications of different mechanisms in insecticide resistance in F occidentalis are discussed.