Changes in cross-resistance patterns of houseflies selected with natural pyrethrins or resmethrin (5-benzyl-3-furylmethyl (±)-cis-trans-chrysanthemate)

A pyrethrins-resistant strain of houseflies, 213ab, previously selected with a 1:10 (by wt.) mixture of natural pyrethrins and piperonyl butoxide, was further selected either with natural pyrethrins alone (strain NPR) or with resmethrin (strain 104). After 50 generations the two populations differed in their resistance to the natural and synthetic esters. Both were resistant to all pyrethroids. Part of strain NPR was immune and very much more resistant than strain 104 to the natural pyrethrins and allethrin, but it was only 2–3 times more resistant than strain 104 against the new synthetic esters resmethrin (5-benzyl-3-furylmethyl (±)-cis-trans-chrysanthemate), bio-resmethrin (5-benzyl-3-furylmethyl (+)-trans-chrysanthemate), pyresmethrin (5-benzyl-3-furylmethyl pyrethrate) and 5B2Me3FC (5-benzyl-2-methyl-3-furylmethyl (±)-cis-trans-chrysanthemate). Pretreatment of both strains with sesamex diminished but did not eliminate resistance. Synergism was greater in strain NPR, especially with natural pyrethrins and allethrin. Both strains had great resistance to DDT indicating that resistance to DDT and pyrethroids is linked. Differences in resistance to different compounds suggest that at least three factors can confer resistance, one of which, pen, delays penetration and two others involve detoxication, one py a on the acid side of the ester linkage and the other, py b, on the alcohol side. Natural pyrethrins and resmethrin select for different groupings of these factors. Treatment with resmethrin does not select for py b presumably because this mechanism cannot attack the resmethrin molecule. Similarly when piperonyl butoxide is added to the natural pyrethrins py b is inhibited and so removed from selection pressure. Under these conditions, the strain produced contains the same factors as one selected by resmethrin and so shows the same small resistance to natural pyrethrins alone.     

The cross-resistance to pyrethrins and eight synthetic pyrethroids,of an organophosphorus-resistant strain of the rust-red flour beetle Tribolium castaneum (herbst)

Comparisons with standard susceptible insects showed that a strain of Tribolium castaneum, with a specific resistance to malathion and its carboxylic ester analogues, had no cross-resistance to topical applications of natural pyrethrins. Another strain of T. castaneum, showing resistance to many organophosphorus (OP) insecticides, was cross-resistant to pyrethrins ( × 34) and eight synthetic pyrethroids also applied topically; least cross-resistance occurred with resmethrin ( × 2.2), bioresmethrin ( × 3.3) and phenothrin ( × 4.0). Generally larger resistance factors were recorded with formulations synergised by piperonyl butoxide (PB). The greatest cross-resistance encountered was with unsynergised tetramethrin ( × 338). Apart from tetramethrin, factors of synergism did not exceed 5.7 with either the susceptible or multi-OP resistant strains. PB antagonised six of the nine pyrethroids against the multi-OP resistant strain. Antagonism also occurred with two of these six, permethrin (cis: trans ratio 1:3) and 5-prop-2-ynylfurfuryl ( 1RS)-cis,trans-chrysanthemate (‘Prothrin’), against the susceptible strain. Considering only formulations without the synergist, the most effective compounds against the susceptible strain, relative to pyrethrins, were bioresmethrin (2.7) and permethrin (2.4). Similarly with the multi-OP resistant strain the most effective compounds were bioresmethrin (28), resmethrin (14) and permethrin (6.6). Thus the LD₅₀ (the dose required to kill 50% of the test species) for bioresmethrin against the resistant strain (0.14 μg) only slightly exceeded the LD₅₀ for pyrethrins against the susceptible strain (0.12 μg).     

Effects of organic‐farming‐compatible insecticides on four aphid natural enemy species

BACKGROUND: The toxicities of pyrethrins + rapeseed oil, pyrethrins + piperonyl butoxide (PBO), potassium salts of fatty acids and linseed oil were assessed in the laboratory on the parasitic wasp Aphidius rhopalosiphi (Destefani‐Perez), the ladybird Adalia bipunctata (L.), the rove beetle Aleochara bilineata (Gyll.) and the carabid beetle Bembidion lampros (Herbst.). The methods selected were residual contact toxicity tests on inert and natural substrates. RESULTS: Both the pyrethrin products led to 100% mortality in the adult parasitic wasps and ladybird larvae on glass plates and plants. The pyrethrins + PBO formulation was toxic for B. lampros on sand and natural soil, but the pyrethrins + rapeseed oil formulation was harmless for this species. Insecticidal soaps were harmless for all these beneficial species. None of the tested products significantly affected the parasitism of the onion fly pupae by A. bilineata. CONCLUSION: The results indicated the potentially high toxicity of natural pyrethrins for beneficial arthropods. Although this toxicity needs to be confirmed in field conditions, the toxicity levels obtained in the laboratory were similar to or higher than those of several synthetic insecticides known to be toxic in the field. Insecticidal soaps could be considered as an alternative for aphid control in organic farming in terms of selectivity. Copyright © 2010 Society of Chemical Industry     

Potential of piperonyl butoxide‐synergised pyrethrins against psocids (Psocoptera: Liposcelididae) for stored‐grain protection

BACKGROUND: Piperonyl butoxide (PB)‐synergised natural pyrethrins (pyrethrin:PB ratio 1:4) were evaluated both as a grain protectant and a disinfestant against four Liposcelidid psocids: Liposcelis bostrychophila Badonnel, L. entomophila (Enderlein), L. decolor (Pearman) and L. paeta Pearman. These are key storage pests in Australia that are difficult to control with the registered grain protectants and are increasingly being reported as pests of stored products in other countries. Firstly, mortality and reproduction of adults were determined in wheat freshly treated at 0.0, 0.75, 1.5, 3 and 6 mg kg^?1 of pyrethrins + PB (1:4) at 30 ± 1 °C and 70 ± 2% RH. Next, wheat treated at 0.0, 1.5, 3 and 6 mg kg^?1 of pyrethrins + PB (1:4) was stored at 30 ± 1 °C and 70 ± 2% RH and mortality and reproduction of psocids were assessed after 0, 1.5, 3 and 4.5 months of storage. Finally, the potential of synergised pyrethrins as a disinfestant was assessed by establishing time to endpoint mortality for adult psocids exposed to wheat treated at 3 and 6 mg kg^?1 of synergised pyrethrins after 0, 3, 6, 9 and 12 h of exposure. RESULTS: Synergised pyrethrins at 6 mg kg^?1 provided 3 months of protection against all four Liposcelis spp., and at this rate complete adult mortality of these psocids can be achieved within 6 h of exposure. CONCLUSION: Piperonyl butoxide‐synergised pyrethrins have excellent potential both as a grain protectant and as a disinfestant against Liposcelidid psocids. Copyright © State of Queensland, Department of Employment, Economic Development and Innovation, 2010. Published by John Wiley and Sons, Ltd.     

Mechanisms of DDT resistance in larvae of the mosquito Aedes aegypti L

Larvae of eight strains of Aedes aegypti were exposed to DDT and compared for resistance, DDT uptake, in-vivo breakdown of DDT and residual unmetabolised DDT. Resistance varied widely between strains, three being fully susceptible, two almost immune and three of intermediate resistance. Breakdown of DDT by dehydrochlorination to 1,1-dichloro-2,2-bis(4-chlorophenyl)ethylene (pp'-DDE) occurred in all strains and was greater in the five resistant types, but there was no significant correlation between the extent of breakdown in the resistant strains and the level of resistance. Moreover the overall difference between susceptible and resistant strains disappeared when they were compared at a low, almost sublethal, concentration of DDT. Larvae of resistant strains carried a greater absolute quantity of unmetabolised DDT in the body and were able to tolerate levels of DDT that were lethal to susceptible larvae. However the two most resistant strains (T8 and B51) contained significantly less DDT plus pp'-DDE than strains of intermediate resistance (T30 and BSJ) from which they had been derived. Addition of the synergist chlorfenethol to DDT increased its knockdown effect on all resistant strains, suggesting that dehydrochlorination was a factor in resistance. Three strains, two DDT-resistant and one DDT-susceptible, were tested with 1,1-bis(4-ethoxyphenyl)-2,2-dimethylpropane (I), an insecticide that cannot be dehydrochlorinated. All the strains were relatively tolerant to it although the DDT-susceptible strains were less tolerant. Addition of the synergist sesamex decreased the level of tolerance to I in all strains which suggested that microsomal oxidation made some contribution to it. It is concluded that three factors contribute to larval DDT resistance in A. aegypti; (a) increased metabolism to pp'-DDE; (b) increased tolerance to unmetabolised internal DDT; and (c) reduced content of DDT+pp'-DDE (only in the most resistant strains and due either to reduced absorption or increased excretion). These factors are discussed in relation to known larval resistance genes R^DDT1 and y.     

Acute lethal and behavioral sublethal responses of two stored-product psocids to surface insecticides

BACKGROUND: The psocids Liposcelis bostrychophila Badonnel and L. entomophila (Enderlein) (Liposcelididae) are emerging pests of stored products. Although their behavior, particularly their high mobility, may contribute to the reported relatively low efficacy of insecticides against them, studies to investigate this have not been conducted. The present study aimed to assess the label rate efficacy of three commercial insecticides (β‐cyfluthrin, chlorfenapyr and pyrethrins) applied on concrete surfaces against L. bostrychophila and L. entomophila, and also their sublethal effect on the mobility of these species. RESULTS: The synthetic insecticides β‐cyfluthrin and chlorfenapyr showed high short‐term efficacy (LT₉₅≤15 h) against both psocid species, unlike the natural pyrethrins (LT₉₅ ≥ 4 days). Liposcelis bostrychophila was slightly more tolerant (≥1.2×) than L. entomophila to all three insecticides. Behavioral assays with fully sprayed and half‐sprayed concrete arenas indicated that the insecticides reduced the mobility of both species. Pyrethrins seem to elicit weak repellence in L. bostrychophila. CONCLUSION: β‐Cyfluthrin and chlorfenapyr were effective against both psocid species, but not pyrethrins. The mobility of both species does not seem to play a major role in the differential selectivity observed, but the lower mobility of L. bostrychophila may be a contributing factor to its higher insecticide tolerance. Published in 2008 by John Wiley & Sons, Ltd.     

Genetic and biochemical studies of resistance to permethrin in a pyrethroid-resistant strain of the housefly (Musca domestica L.)

One or more weak factors of resistance on autosome 2, and barely detectable resistance on autosome 3, confer moderate resistance to several pyrethroids (5–13-fold) in the field-collected Ipswich strain of houseflies. In these flies, which unlike other pyrethroid-resistant strains lack kdr or super-kdr, pyrethroid resistance probably developed in response to prolonged treatment of buildings for animals with pyrethrins synergised with piperonyl butoxide. Substrains, isolated genetically from Ipswich flies and with resistance only on autosome 2, degraded permethrin more rapidly than susceptible flies and produced larger amounts of very polar metabolites. In this, they differed from flies with kdr or super-kdr which resembled susceptible flies in their metabolism of permethrin. NIA 16388 (propyl prop-2-ynyl phenylphosphonate) was a better synergist and reduced the metabolism of permethrin more than piperonyl butoxide in both the susceptible and resistant insects. The slight increase in synergism and minimal decrease in metabolism when piperonyl butoxide was applied with NIA 16388 indicated that the latter also inhibited detoxication that was sensitive to piperonyl butoxide.     

Investigating the potential of selected natural compounds to increase the potency of pyrethrum against houseflies Muscadomestica (Diptera: Muscidae)

BACKGROUND: A study was undertaken to determine the efficacy of seven natural compounds compared with piperonyl butoxide (PBO) in synergising pyrethrum, with the intention of formulating an effective natural synergist with pyrethrum for use in the organic crop market. RESULTS: Discriminating dose bioassays showed PBO to be significantly more effective at synergising pyrethrum in houseflies than the seven natural compounds tested, causing 100% mortality in insecticide‐susceptible WHO and resistant 381zb strains of housefly. The most effective natural synergists against WHO houseflies were dillapiole oil, grapefruit oil and parsley seed oil, with 59, 50 and 41% mortality respectively, compared with 18% mortality with unsynergised pyrethrum. Against 381zb houseflies, the most effective natural synergists were parsley seed oil and dillapiole oil. Esterase inhibition by the natural compounds and PBO in vitro showed no correlation with pyrethrum synergism in vivo, whereas the inhibition of oxidases in vitro more closely correlated with pyrethrum synergism in vivo. CONCLUSION: Dillapiole oil and parsley seed oil showed the greatest potential as pyrethrum synergists. PBO remained the most effective synergist, possibly owing to its surfactant properties, enhancing penetration of pyrethrins. The results suggest the involvement of oxidases in pyrethroid resistance in houseflies, with the efficacy of synergists showing a high correlation with inhibition of oxidases. Copyright © 2011 Society of Chemical Industry     

German cockroach resistance: Propoxur selection induces the same resistance spectrum as diazinon selection

A resistant laboratory strain of the German cockroach, Blattella germanica, was developed from a normal laboratory strain by selection with propoxur. Resistance to all insecticides except chlordane began increasing after 15 generations of selection and reached a plateau for most insecticides by generation 27. The resistant colony, designated B-strain, developed significant resistance to carbamates, organophosphorus compounds, pyrethrins and DDT, developed low resistance to gamma-BHC and no resistance to chlordane. The resistance spectrum, effect of synergists and inheritance of resistance of this propoxur resistant strain are similar to a diazinon resistant strain. Therefore, diazinon and propoxur may select for the same resistance mechanism(s) in this species. The practical implications of this research are discussed.     

Diazinon poisoning in large white butterfly larvae and the influence of sesamex and piperonyl butoxide

The toxicity of diazinon and diazoxon to fourth instar Pieris brassicae larvae was determined, with or without modifying chemicals. Piperonyl butoxide and sesamex antagonised diazinon but synergised diazoxon. The penetration, excretion and internal concentration of diazinon were measured following topical application. Penetration of diazinon followed first order kinetics and was considerably slower after pretreatment with sesamex and piperonyl butoxide. Pretreatment with piperonyl butoxide increased the internal concentration of diazinon, but the onset of symptoms of poisoning was delayed, presumably because of inhibition of diazinon activation.     

Electrophysiological studies on the effect of sesamex upon the action of dieldrin in Blaberus discoidalis

Treatment of the metathoracic ganglion of the cockroach, Blaberus discoidalis, with dieldrin (HEOD) at a concentration of 10^?5M produced changes in spontaneous efferent activity and afterdischarge in efferent pathways. Pretreatment with sesamex markedly reduced the spontaneous activity caused by dieldrin and also reduced the latency of appearance of symptoms from 60 min to nearly 30 min. However, pretreatment with sesamex did not alter the intensity and duration of the dieldrin-induced synaptic afterdischarge. Pretreatment of cockroaches with sesamex did not measurably change the toxicity of dieldrin in vivo.     

The resistance to eighteen toxicants of a strain of Musca domestica L. collected from a farm in England

A sample of houseflies initially collected from a pig farm and found to be resistant to bendiocarb, DDT, gamma-HCH, pyrethrins + piperonyl butoxide (PB), tetrachlorvinphos and trichlorfon, was tested for resistance to knockdown by other toxicants. At the KD₅₀ response level, resistance factors were obtained for: permethrin (× 141), deltamethrin (×96), bioresmethrin + PB (×37), resmethrin + PB (×33), fenitrothion (×94), bromophos (×58), iodofenphos (×42), pirimiphos-methyl (×30), dichlorvos (×22), dimethoate (×9), diazinon (×8), methomyl (×4) and methomyl + PB (×4). The slopes of the dose–response lines were lower for the farm strain than for a susceptible strain. This resulted in an increase of resistance factors at the KD₉₅ level by an average of × 1.6. The houseflies on the farm could not be controlled using space sprays of pyrethrins + PB, although resistance to this toxicant was only ×12. However, control was achieved with a methomyl bait.     

Oxidative cleavage of a carboxyester bond as a mechanism of resistance to malaoxon in houseflies

The synergistic effect of triphenyl phosphate (a carboxyesterase inhibitor), sesamex (inhibitor of microsomal oxidation) and O,O-diethyl O-phenyl phosphorothioate on the toxicity of malathion and malaoxon for one susceptible and two resistant strains of housefly was studies. It was found that in the resistant strain G (characterized by high carboxyesterase activity) both malathion and malaoxon were synergized by triphenyl phosphate, but only malaoxon (and not malathion) by sesamex. The other resistant strain E 1, moderately tolerant for malathion but highly resistant to malaoxon, differed from strain G in that triphenyl phosphate had no effect; its response to sesamex was similar to that of strain G. The third synergist, O,O-diethyl O-phenyl phosphorothioate, combined the properties of triphenyl phosphate and sesamex. It was found to be the best of the three compounds used.Biochemical in vitro studies showed that both resistant strains could degrade malaoxon oxidatively at a rate at least 10 × higher than that of the susceptible strain. This oxidation could be inhibited by very low concentrations of the thiono analogue; a malaoxon to malathion ratio of 10:1 gave an inhibition of about 70% at a malaoxon concentration of 5 × 10^?6M. The product of this oxidation is malaoxon β-monocarboxylic acid. This metabolite was also found 1 hr after application of malaoxon in vivo.The results mentioned in this paper indicate that houseflies may become resistant to malaoxon by an increased rate of oxidative carboxyester bond cleavage.     

Serial invasive signal amplification reaction for genotyping permethrin-resistant (kdr-like) human head lice, Pediculus capitis

Permethrin resistance in the human head louse, Pediculus capitis De Geer (Anopulura: Pediculidae), has been reported worldwide, is associated with the knockdown phenotype, and elicits cross-resistance to DDT and the pyrethrins. Two point mutations, T929I and L932F, in the voltage-sensitive sodium channel α-subunit gene are responsible for permethrin resistance as a resistant haplotype (kdr-like). We have optimized a serial invasive signal amplification reaction (SISAR) protocol for the detection of these mutations using PCR amplified DNA fragments. SISAR distinguished all genotypes with high accuracy in a head louse population from Texas that was heterogeneous in terms of permethrin sensitivity. Using SISAR, resistance-conferring mutations are detected in a high throughput format, facilitating the efficient monitoring of permethrin resistance allele frequency in field populations.     

Cross resistance to juvenile hormone analogues in insecticide-resistant strains of Musca domestica L

Five juvenile hormone analogues (JHAs) were tested by topical application to prepupae of a susceptible (S) and 8 insecticide-resistant (R) strains of the housefly. Activity was measured by the inability to completely emerge from the puparium. Aitosid (isopropyl 11-methoxy-3,7,1l-trimethyldodeca-2,4-dienoate) was the most active compound against the S strain (ED₅₀ 0.0033 μg/prepupa) followed by Ro 7-9767 [6,7-epoxy-3,7-diethyl-(3,4-(methylenedioxy)phenoxy)-2-cis/trans-octene], R-20458 [trans l-(4-ethylphenoxy)-6,7-epoxy-3,7-dimethyl-2-octene], sesamex, and NIA 23509 (10,11 -epoxy-N-ethyl-3,7,11-trimethyI-2,6-dodecadienamide). The R strains, designated by the name of the selecting insecticide, have been under pressure for over 10 years and are considered maximally resistant. The dimethoate-R and OMS-15-R (carbamate-resistant) strains exhibited high levels of cross resistance to all JHAs often exceeding 100x at the ED₉₅ The fenthion-R strain showed high cross resistance toward all JHAs except Altosid, toward which it manifested an intermediate level (17.5x). The DDT/lindane-R demonstrated only negligible tolerance to Aitosid but an intermediate response to all the other JHAs. The OMS-12-R strain (phosphoramidothioate-R) exhibited intermediate to high levels of cross resistance toward all JHAs, whereas the parathion-R, Chlorthion-R and a multi-resistant field-collected strain showed only low to intermediate levels of cross resistance. On the basis of known degradative mechanisms of the OMS-15-R strain, mixed function oxidases apparently play an important role in deactivating JHAs.     

Pyrethroid action on the nicotinic acetylcholine receptor/channel

The interactions of natural pyrethrins and nine pyrethroids with the nicotinic acetylcholine (ACh) receptor/channel complex of Torpedo electric organ membranes were studied. None caused significant reduction in [³H]ACh binding to the receptor sites, but all inhibited [³H]perhydrohistrionicotoxin ([³H]H₁₂-HTX) binding to the channel sites in presence of carbamylcholine. Allethrin inhibited [³H]H₁₂-HTX binding noncompetitively, but [³H]imipramine binding competitively, suggesting that allethrin binds to the receptor's channel sites that bind imipramine. The pyrethroids were divided into two types according to their actions: type I, which included pyrethrins, allethrin, bioallethrin, resmethrin, and tetramethrin, was more potent in inhibiting [³H]H₁₂-HTX binding and acted more rapidly (i.e., in <30 sec). Type II, which included permethrin, fluvalinate, cypermethrin and fenvalerate, was less potent and their potency increased slowly with time. Also, inhibition of the initial rate of [³H]H₁₂-HTX binding by type I compounds increased greatly by the presence of the agonist carbamylcholine, but this was not so with type II compounds. The receptor-regulated ⁴⁵Ca²⁺ flux into Torpedo microsacs was inhibited by pyrethrins and pyrethroids, suggesting that their action on this receptor function is inhibitory. There was very poor correlation between the potencies of pyrethrins and pyrethroids in inhibiting [³H]H₁₂-HTX binding and their toxicities to house flies, mosquitoes, and the American cockroach. However, the high affinities that several pyrethroids have for this nicotinic ACh receptor suggest that pyrethroids may have a synaptic site of action in addition to their well known effects on the axonal channels.     

Antagonism of iprodione toxicity to Botrytis cinerea by mixed function oxidase inhibitors

The fungitoxicity of iprodione to a sensitive strain of Botrytis cinerea was antagonised by a variety of cytochrome P-450 mixed function oxidase inhibitors. Piperonyl butoxide, metyrapone and N-(2-ethylhexyl)-8,9,10-trinorborn-5-ene-2,3-dicarboximide (MGK-264) at non-fungitoxic concentrations were strongly antagonistic, whereas sesamex, nuarimol, fenarimol, etaconazole and 6-nitro or 6-methoxy 1,2,3-benzothiadiazole were moderately antagonistic. Phenobarbital and 2-diethylaminoethyl 2,2-diphenylvalerate (SKF 525-A) were slightly antagonistic. The results suggest that fungitoxicity of iprodione may be dependent on an activation catalysed by a cytochrome P-450 mixed function oxidase.     

Resynthesis of multiple resistance to organophosphorus insecticides from strains with factors of resistance isolated from the SKA strain of house flies

Individual factors of resistance to insecticides attributable to chromosomes II, III and ^V of the SKA strain of houseflies (Musca domestica L) were combined in pairs to determine how their presence affects resistance. The re-synthesised strains with resistance factors on chromosomes II and V, and on chromosomes III and V, were tested with several organophosphorus insecticides and DDT. The penetration delaying mechanism Pen on chromosome III, which alone gives little or no resistance, slightly increased the resistance of flies with the microsomal detoxifying factor Ses on chromosome V to diazinon and malaoxon-ethyl (c. × 1.5), but was more effective in increasing resistance to DDT (× 6). There was no effect on the response to other insecticides tested. The combined effect of the mechanisms of resistance on chromosome II (glutathione S-ethyl transferase and phosphatase) and on chromosome V (microsomal detoxication) approximated to the product of the resistance conferred by each of these mechanisms singly, suggesting that the mechanisms of resistance on the two chromosomes act independently. Therefore, most of the strong resistance to organophosphorus insecticides in the SKA strain results from the interaction between delayed penetration (chromosome III) and the factors of resistance on chromosome II, and the independent action of the resistance factors on chromosomes II and V.     

Synthetic Pyrethroids: Their possible Role in the Control of Locusts and Leafworms

Abstract

The toxicity of a number of topically applied pyrethroids has been tested in the laboratory against three species of locusts and parathion-resistant and susceptible strains of the Egyptian cotton leafworm. Bioresmethrin, resmethrin and 5-benzyl-3-furylmethyl (+)-cis-chrysanthemate (NRDC 119) proved to be extremely active against one or more of these pests and there were small but noteworthy improvements with the synergists sesamex and TBTP. The field potential of the pyrethroids is discussed against the background of environmental problems associated with some of the insecticides in current use.     

The current status of insecticide resistance in Musca domestica in England and Wales and the implications for housefly control in intensive animal units

Following the 1984–85 housefly (Musca domestica L.) resistance survey, a similar survey was carried out between January 1990 and April 1992 in order to monitor changes in UK housefly resistance. Samples of fly populations were collected from 35 farms throughout England and Wales. Dose-response data were obtained by topical application and feeding test methods. For both methods the knockdown (KD) after 48 h was used for all the dose-response comparisons. The ranges of resistance factors for the topical application method were for methomyl, 1·6–20·0 at KD₅₀ and 4·5–34·4 at KD₉₅; for azamethiphos, 2·5–58·5 at KD₅₀ and 5·0–2604 at KD₉₅; for pyrethrins+piperonyl butoxide, 1·2–9·6 at KD₅₀ and 1·6–14·7 at KD₉₅; and for permethrin, 2·2–118·8 at KD₅₀ and 4·3–200·0 at KD₉₅. The ranges of the resistance factors for the feeding tests were for methomyl, 1·2–56·1 at KD₅₀ and 3·1–80·0 at KD₉₅, and for azamethiphos, 3·9–125·0 at KD₅₀ and 4·4–380·0 at KD₉₅. The means of resistance factors for all of the insecticides showed increases over those obtained in a previous survey carried out in 1984–85. The significance of the results for housefly control in intensive animal units in the UK is discussed.