Structure-related effects of pyrethroid insecticides on the lateral-line sense organ and on peripheral nerves of the clawed frog, Xenopus laevis

The effects of seven different pyrethroid insecticides on the lateral-line sense organ and on peripheral nerves of the clawed frog, Xenopus laevis, were investigated by means of electrophysiological methods. The results show that two classes of pyrethroid can be clearly distinguished. (i) Pyrethroids without an α-cyano group (permethrin, cismethrin, and bioresmethrin). These noncyano pyrethroids induce short trains of nerve impulses in the lateral-line sense organ. In peripheral nerve branches they induce a depolarizing afterpotential and repetitive firing. These effects are very similar to those previously reported for allethrin. (ii) Pyrethroids with an α-cyano-3-phenoxybenzyl alcohol (cypermethrin, fenpropathrin, deltamethrin, and fenvalerate). In the lateral-line sense organ these α-cyano pyrethroids induce very long trains of nerve impulses which may last for seconds and may contain hundreds or even thousands of impulses. The α-cyano compounds do not cause repetitive activity in peripheral nerves. Instead they induce a quickly reversible, stimulus frequency-dependent suppression of the action potential. Since the chemical structure of cypermethrin differs from that of permethrin only in the α-cyano group and because all four α-cyano compounds act in a very similar way, it is concluded that the α-cyano substituent is responsible for the large differences in neurotoxic effects. In the lateral-line sense organ the duration of nerve impulse trains induced by the noncyano as well as the α-cyano pyrethroids increases dramatically when the temperature is lowered. Further, in sensory fibers the effects of both classes of pyrethroid on the nerve action potential are more pronounced compared to their effects on motor fibers. It is argued that the different neurotoxic effects reported here originate from a common mechanism of action of pyrethroids, which is a prolongation of the transient increase of sodium permeability of the nerve membrane associated with excitation.It is concluded that the sodium channel in the nerve membrane is the major target site of noncyano and α-cyano pyrethroids.     

Binary mixtures of pyrethroids produce differential effects on Ca influx and glutamate release at isolated presynaptic nerve terminals from rat brain

Isolated rat brain synaptosomes were used to evaluate the action of pyrethroid mixtures on Ca²⁺ influx and subsequent glutamate release under depolarizing conditions. In equipotent binary mixtures at their respective and/or estimated EC₅₀s with deltamethrin always as one of the two components, cismethrin, λ-cyhalothrin, cypermethrin, esfenvalerate and permethrin were additive and S-bioallethrin, fenpropathrin and tefluthrin were less-than-additive on Ca²⁺ influx. In binary mixtures with deltamethrin always as one of the two components, esfenvalerate, permethrin and tefluthrin were additive and λ-cyhalothrin was less-than-additive on glutamate release. Binary mixture of S-bioallethrin and cismethrin was additive for both Ca²⁺ influx and glutamate release. Only a subset of pyrethroids (S-bioallethrin, cismethrin, cypermethrin, and fenpropathrin) in binary mixtures with deltamethrin caused a more-than-additive effect on glutamate release. These binary mixtures were, however, only additive (cismethrin and cypermethrin) or less-than-additive (S-bioallethrin and fenpropathrin) on Ca²⁺ influx. Therefore, increased glutamate release evoked by this subset of pyrethroids in binary mixture with deltamethrin is not entirely occurring by Ca²⁺-dependent mechanisms via their action at voltage-sensitive calcium channels. These results suggest that pyrethroids do not share a common mode of toxicity at presynaptic nerve terminals from rat brain and appear to affect multiple target sites, including voltage-sensitive calcium, chloride and sodium channels.     

Deltamethrin: A neurophysiological study of the sites of action

Recent experiments on the mode of action of pyrethroids have indicated that those pyrethroids containing an α-cyano phenoxybenzyl group may act on GABA-mediated chloride channels. The crayfish stretch receptor neuron provides a useful preparation for examining the effects of pyrethroids on these channels and on sodium channels. The lowest concentration of deltamethrin to have an effect on sodium channels was 10⁻¹² M, but the response of the preparation to GABA appeared to be unaffected by concentrations of deltamethrin up to 10⁻⁷ M. Although 10⁻⁶ M deltamethrin had a slight effect on the GABA response of the dactyl abductor muscle, it appears that the majority of the effects of cyano pyrethroids in invertebrates could be accounted for solely by their action on sodium channels.     

Actions of pyrethroid insecticides on insect axonal sodium channels

The actions of pyrethroid insecticides were tested on isolated giant axons of the cockroach Periplaneta americana, using oil-gap, single-fibre recording techniques. Current-clamp and voltage-clamp experiments were used to determine the actions of pyrethroids on axonal membrane potentials and ionic currents. Treatment with deltamethrin at micromolar concentrations caused gradual depolarisation of the axon accompanied by a reduction in amplitude of the action potential. This depolarisation was enhanced by an increase in stimulation frequency. Other synthetic pyrethroids: 3,4,5,6-tetrahydrophthalimidomethyl (1RS)-cis-3-[(RS)-2,2-dimethylcyclopropyl]-2,2-dimethylcyclopropanecarboxylate, biopermethrin and its (1S)-enantiomer, (1R)-tetramethrin, S-bioallethrin, bioresmethrin and its (1S)-enantiomer, cismethrin, and 5-benzyl-3-furylmethyl (E)-(1R)-cis-2,2-dimethyl-3-(2-oxothiolan-3-ylidenemethyl)cyclopropanecarboxylate (RU-15525, ‘Kadethrin’) were investigated. The (1S)-enantiomers were inactive, but all the other pyrethroids tested, apart from deltamethrin, induced prolonged negative (depolarising) after-potentials. All the treatments with the active pyrethroids resulted in the appearance of a voltage and time-dependent ‘maintained’ sodium conductance. The duration of this ‘slow’ conductance varied considerably depending on the pyrethroid under test. Clearly, the effectiveness of pyrethroids on whole insects is not determined only by the degree to which they directly modify the properties of sodium channels. Nevertheless, voltage-clamp experiments on isolated axons readily permit direct comparison of the actions of different pyrethroids on the sodium channels of insect neurones.     

Characterization of 11 commercial pyrethroids on the functional attributes of rat brain synaptosomes

The action of 11 commercial pyrethroids on Ca²⁺ influx and glutamate release was assessed using high-throughput functional assays with rat brain synaptosomes to better understand the mechanistic nature of pyrethroid-induced neurotoxicity and aid in the reassessment of pyrethroids in vivo. Concentration-dependent response curves for each of the non-cyano and α-cyano containing pyrethroids were determined and the data used in a cluster analysis. The previously characterized α-cyano pyrethroids that induce the CS-syndrome (cypermethrin, deltamethrin, and esfenvalerate) increased Ca²⁺ influx and glutamate release, and clustered with two other α-cyano pyrethroids (β-cyfluthrin and λ-cyhalothrin) that shared these same actions. Previously characterized T-syndrome pyrethroids (bioallethrin, cismethrin, and fenpropathrin) did not share these actions and clustered with two other non-cyano pyrethroids (tefluthrin and bifenthrin) that likewise did not elicit these actions. Our current findings indicate that pyrethroids that have an α-cyano group (with the exception of fenpropathrin) were more potent enhancers of Ca²⁺ influx and glutamate release under depolarizing conditions than pyrethroids that did not possess this functional group. The collective data set does not support the hypothesis that pyrethroids, as a class, act in a similar fashion at presynaptic nerve terminals.     

Interaction of tralomethrin,tralocythrin, and related pyrethroids in Na+ channels of insect and mammalian neuronal cells

The neurotoxic activity of the tetrahalogenated pyrethroids, tralomethrin and tralocythrin, which are dibromo adducts of deltamethrin and RU 24501, respectively, and RU 27218, which is a dichloro adduct of RU 24501, have been studied on two different excitable membranes using in vitro methods: insect axonal membranes and mammalian neuroblastoma cells in culture. The results show that molecules whose chrysanthemic acid chain at C₃ is saturated by halogen addition have intrinsic toxicity on the sodium channels of nerve membranes. They increase the amplitude of negative after-potential, depolarize the cockroach axonal membrane, and stabilize an open conformation of voltage-dependent Na⁺ channels in mouse neuroblastoma cells, thereby producing a massive uptakeof Na⁺ by the cells. All effects were observed in the absence of metabolic transformation of the compounds tested. In light of these experiments, it is concluded that tralomethrin and tralocythrin cannot be considered as propyrethroids.     

Potentiation/antagonism of deltamethrin and cypermethrins with organophosphate insecticides in the cotton bollworm, Helicoverpa armigera (Lepidoptera: Noctuidae)

The joint action of pyrethroids deltamethrin and cypermethrins in combination with organophosphates ethion, profenofos, chlorpyrifos, quinalphos, and triazophos was studied on putatively resistant field populations of Helicoverpa armigera from Pakistan by using a leaf-dip method. Ethion produced a good potentiation with deltamethrin, cypermethrin, alphacypermethrin, and zetacypermethrin, whereas profenofos, chlorpyrifos, quinalphos, and triazophos exhibited an antagonism with deltamethrin as well as cypermethrins. Implications of using mixtures for counteracting insecticide resistance are discussed.     

Effects of pyrethroids on neuronal excitability of adult honeybees Apis mellifera

Pyrethroids act on the nervous system as a primary target organ and exert their neurotoxic effects primarily by altering the conductance of sodium channel, leading to hyperexcitation. However, few studies investigated the effects of pyrethroids on neuronal excitability of honeybee brain neurons. In this study, a whole-cell patch-clamp technique was used to record current threshold, the minimum current to induce an action potential, and peak sodium current in the dissociated honeybee brain neurons treated with bifenthrin, deltamethrin and fluvalinate in vitro & in vivo. The study showed that these pyrethroids greatly suppressed the neuronal excitability as revealed by increasing current injected and inhibited the peak sodium current in honeybees. The three pyrethroids also inhibited steady-state inactivation in addition to reduction of sodium peak current.     

Pyrethroid resistance in a strain of Spodoptera littoralis is correlated with decreased sensitivity of the CNS in vitro

The effects of permethrin and cypermethrin on the isolated abdominal nerve cord of insecticide-resistant [R] and -susceptible [S] strains of Spodoptera littoralis larvae have been studied. Above ca. 19°C, permethrin at 10^?7M caused a prolonged spike train to follow electrical stimulation of the nerve cord. The time of onset of this repetitive firing was significantly greater for the [R] strain. Moreover, cypermethrin, to which this strain shows negligible resistance, did not cause such repetitive discharges. Thus, resistance to permethrin but not to cypermethrin appears to be based on a qualitative difference between the pyrethroids. Nerve blockage by the two pyrethroids was also investigated, with particular reference to temperature. Once again, differences were apparent: when considered relative to untreated controls, permethrin caused quicker nerve blockage as temperature was reduced whereas the blocking action of cypermethrin was not affected by temperature. However, the times taken to cause nerve blockage by permethrin in [R] and [S] larvae were not significantly different, making it unlikely that nerve blockage plays a major role in this resistance. Two methods were employed to reduce the resistance factor in vitro. The synergist dodecyl imidazole failed to significantly reduce the time taken for permethrin to cause either repetitive firing or nerve blockage. However, reducing the calcium concentration in the saline did significantly reduce the latency of repetitive firing caused by permethrin in [R] larvae, thus increasing the nerve sensitivity to approximately the same level as normal calcium, [S] insects.     

Neurotoxic implications of the agonistic action of CS-syndrome pyrethroids on the N-type Ca(v)2.2 calcium channel

BACKGROUND: Cismethrin (T-syndrome) and deltamethrin (CS-syndrome) pyrethroids have been previously shown to increase membrane depolarization and calcium influx, but only deltamethrin increased Ca(2+)-dependent neurotransmitter release from rat brain synaptosomes. Deltamethrin's action was blocked by omega-conotoxin GVIA, delineating a separate action at N-type Ca(v)2.2 channels that is consistent with the in vivo release of neurotransmitter. It is hypothesized that other CS-syndrome pyrethroids will elicit similar actions at presynaptic nerve terminals.RESULTS: Nine additional pyrethroids were similarly examined, and these data were used in a cluster analysis. CS-syndrome pyrethroids that possessed alpha-cyano groups, cypermethrin, deltamethrin and esfenvalerate, all caused Ca(2+) influx and neurotransmitter release and clustered with two other alpha-cyano pyrethroids, cyfluthrin and cyhalothrin, that shared these same actions. T-syndrome pyrethroids, bioallethrin, cismethrin and fenpropathrin, did not share these actions and clustered with two non-alpha-cyano pyrethroids, tefluthin and bifenthrin, which likewise did not elicit these actions. Deltamethrin reduced peak current of heterologously expressed wild-type Ca(v)2.2, increased peak current of T422E Ca(v)2.2 and was 20-fold more potent on T422E Ca(v)2.2 than on wild-type channels, indicating that the permanently phosphorylated form of Ca(v)2.2 is the preferred target.CONCLUSIONS: Ca(v)2.2 is directly modified by deltamethrin, but the resulting perturbation is dependent upon its phosphorylation state. The present findings may provide a partial explanation for the different toxic syndromes produced by these structurally distinct pyrethroids.     

Action of cismethrin and deltamethrin on functional attributes of isolated presynaptic nerve terminals from rat brain

Isolated presynaptic nerve terminals (synaptosomes) prepared from rat brain were used to evaluate the actions of a tremor (T)-syndrome (cismethrin) and a choreoathetosis-salivation (CS)-syndrome (deltamethrin) pyrethroid on the functional attributes of synaptosomes by measuring calcium influx and endogenous neurotransmitter (l-glutamate) release with fluorescent assays. Both cismethrin and deltamethrin stimulated calcium influx, however, only deltamethrin enhanced Ca²⁺-dependent neurotransmitter release and its action was stereospecific, concentration-dependent, stimulated by depolarization, unaltered by tetrodotoxin, and blocked by ω-conotoxin GVIA. Our results delineate a separate action of deltamethrin on presynaptic nerve terminals from that elicited by cismethrin and implicate Ca_v2.2 calcium channels as target sites for deltamethrin that is consistent with the observed in vivo release of neurotransmitter at the onset of convulsive symptom caused by CS-syndrome pyrethroids. This information will allow a more complete understanding of the molecular and cellular nature of pyrethroid-induced neurotoxicity and expands our knowledge of the structure–activity relationships of pyrethroids in regards to their action on voltage-sensitive calcium channels.     

Effects of the pyrethroids bioallethrin,deltamethrin and RU-15525 on the electrical activity of a cuticular mechanoreceptor of the cockroach Periplaneta americana

A study has been made of the effects of bioallethrin, RU-15525 [5-benzyl-3-furylmethyl (1R)-cis-2,2-dimethyl-3-(tetrahydro-2-oxo-3-thienylidenemethyl)-cyclopropanecarboxylate, ‘Kadethrin’], and deltamethrin on the electrical activity, measured in vivo, of a cuticular mechanoreceptor of Periplaneta americana. The modifications induced by these pyrethroids on the membrane excitability can be classified into two groups: Type I effects (bioallethrin) are characterised by a substantial increase in the number of action potentials triggered at the initiation site by a given mechanical stimulation, by an electrical activity persisting after mechanical stimulus has been stopped (repetitive activity), and possibly, by an inhibition of excitability of the cell membrane. Type II effects (RU-15525 and deltamethrin), are characterised by an inhibition of the excitability of the initiation site. In the case of RU-15525, there was a transient spontaneous electrical activity. Both types of effects have been linked to an action on the sodium channel, particularly at the initiation site. The preparation studied, which possessed no synapses, was shown to be more sensitive to deltamethrin (which is also the most insecticidal of the three pyrethroids) than to either allethrin or RU-15525. These results suggest that it is unnecessary to envisage a main target (sodium channel) that is different for the two types of pyrethroid.     

Mutated sodium channel genes and elevated monooxygenases are found in pyrethroid resistant populations of Sri Lankan malaria vectors

The present status of pyrethroid resistance in vectors of malaria; Anopheles culicifacies and Anopheles subpictus, was tested in two malarious Districts, Anuradhapura and Trincomalee, of Sri Lanka. Both species were resistant to permethrin and susceptible to cypermethrin and cyfluthrin. An. subpictus were resistant to deltamethrin. λ-Cyhalothrin and etofenprox resistance was shown only by Anuradhapura An. subpictus. Although there were no differences among the populations for esterase and glutathione S-transferase activities, increased monooxygenase levels were found among Trincomalee populations. The voltage-gated sodium channel gene, the target site gene of pyrethroids, was partially sequenced to screen for mutations previously associated with insecticide resistance. The classic leucine to phenylalanine substitution, TTA to TTT, was detected in An. subpictus. It appears that both kdr type and monooxygenase resistance underlie pyrethroid resistance in these two malaria vectors of Sri Lanka.     

Effects of deltamethrin and its commercial formulation DECIS on different cell types in vitro: Cytotoxicity,cellular binding,and intracellular localization

To investigate the effect of deltamethrin and other pyrethroids on nonexcitable cells, we tested these molecules on animal (fibroblasts) and plant (algae) cells in culture. The effects of pyrethroids on cellular proliferation vary according to their structure. Deltamethrin (from 5 × 10⁻⁵ M) affected the growth of fibroblasts, but was inactive on other cells. Commercial formulations (DECIS EC and DECIS FLO) were more active to cells, but this effect was due mostly to the matrix. However, these matrices facilitated the penetration of deltamethrin into cells. Studies of [³H]deltamethrin uptake indicated the labeling of macromolecules, but labeling was reduced significantly after treatment with organic solvents. Autoradiographic studies with [³H]deltamethrin showed labeling of cells at the cytpolasmic level.     

Two classes of pyrethroid action in the cockroach

Pyrethroids are divided into two classes (Types I and II) based on their effects on the cercal sensory nerves recorded in vivo and in vitro and on the symptomology they produce in dosed cockroaches, Periplaneta americana. Type I compounds include pyrethrins, S-bioallethrin, [1R,cis]resmethrin, kadethrin, the 1R,trans and 1R,cis isomers of tetramethrin, phenothrin, and permethrin, and an oxime O-phenoxybenzyl ether. Electrophysiological recordings from dosed individuals reveal trains of cercal sensory spikes and sometimes also spike trains from the cercal motor nerves and in the CNS. Low concentrations of these pyrethroids act in vitro to induce repetitive firing in a cercal sensory nerve following a single electrical stimulus. This in vitro measurement, standardized for evaluating structure-activity relationships, shows that only 1R, insecticidal isomers are highly effective neurotoxins. The most potent compounds on the isolated nerve are [1R,trans]- and [1R,cis]tetramethrin, each active at 3 × 10^?13M. The poisoning symptoms of Type I compounds are restlessness, incoordination, hyperactivity, prostration, and paralysis. Type II compounds include [1R,cis,αS]- and [1R,trans,αS]cypermethrin, deltamethrin, and [S,S]fenvalerate. These α-cyanophenoxybenzyl pyrethroids do not induce repetitive firing in the cercal sensory nerves either in vivo or in vitro; moreover, they cause different symptoms, including a pronounced convulsive phase. Two other pyrethroids with an α-cyano substituent, i.e., fenpropathrin and an oxime O-α-cyanophenoxybenzyl ether, are classified as Type I based on their action on a cercal sensory nerve but the symptoms with these compounds resemble Type II. The two classes of pyrethroid action evident with the cockroach are discussed relative to their neurophysiological effects and symptomology in other organisms.     

In vitro and in vivo effects of some pesticides on carbonic anhydrase enzyme from rainbow trout (Oncorhynchus mykiss) gills

Here we investigated the in vitro and in vivo effects of the pesticides, deltamethrin, diazinon, propoxur and cypermethrin, on the activity of rainbow trout (rt) gill carbonic anhydrase (CA). The enzyme was purified from rainbow trout gills using Sepharose 4B-aniline-sulfanilamide affinity chromatography method. The overall purification was approx. 214-fold. SDS-polyacrylamide gel electrophoresis showed a single band corresponding to a molecular weight of approx. 29 kDa. The four pesticides dose-dependently inhibited in vitro CA activity. IC₅₀ values for deltamethrin, diazinon, propoxur and cypermethrin were 0.137, 0.267, 0.420 and 0.460 μM, respectively. In vitro results showed that pesticides inhibit rtCA activity with rank order of deltamethrin > diazinon > propoxur > cypermethrin. Besides, in vivo studies of deltamethrin were performed on CA activity of rainbow trout gill. rtCA was significantly inhibited at three concentrations (0.25, 1.0 and 2.5 μg/L) at 24 and 48 h.     

DDT and pyrethroids: Receptor binding and mode of action in the house fly

The mode of action of DDT and pyrethroids was investigated in the house fly, Musca domestica L, using drug:receptor binding techniques. Both in vivo and in vitro binding studies demonstrated the existence of membrane receptors which bind specifically to [¹⁴C]DDT and [¹⁴C]cis-permethrin. The receptors show properties to be expected of a critical target site of these insecticides. These include negative temperature correlation with binding, relatively nonsensitivity to DDE, and sensitivity to Ca²⁺. The receptor sites are readily saturated at 45–90 nM [¹⁴C]DDT and have an apparent disassociation constant (K_d) of 12.2 nM. The maximum number of binding sites was estimated to be 17 pmol DDT/mg membrane protein (0.34 pmol/house fly head). Competition studies showed DDT, cis-permethrin, and cypermethrin bind to the same receptor but not at precisely the same site. The addition of Ca²⁺ to the incubation buffer significantly inhibited the binding of both [¹⁴C]DDT and [¹⁴C]cis-permethrin, suggesting the receptor binding is Ca²⁺ sensitive and may have a role in ion conductance.     

Potentiation of Super-kdr resistance to deltamethrin and other pyrethroids by an intensifier (factor 161) on autosome 2 in the housefly (Musca domestica L.)

An intensifier (factor 161) identified on the second autosome in a pyrethroid-resistant strain of houseflies (Musca domestica L.) was isolated and introduced into a strain with super-kdr. Unlike E_0.39, which on its own also confers very weak (< × 3) resistance to pyrethroids, factor 161 very strongly intensified super-kdr resistance to pyrethroids. Together, factor 161 and super-kdr conferred immunity to deltamethrin in female houseflies (LD₅₀ > 20 μg fly^?1) but produced much less intensification of resistance to WL 48281, the (1R)cis (αS) isomer of cypermethrin, which differs from deltamethrin only in having chlorine instead of bromine substituents in the acid side-chain. Intensification was strongly decreased by piperonyl butoxide and propyl prop-2-ynylphenylphosphonate (NIA) but was unaffected by S,S,S-tributyl phosphorotrithioate (DEF). This synergism suggests involvement of oxidative rather than esteratic metabolism in the intensification of super-kdr by factor 161.     

Synergism of pyrethroid — organophosphorus insecticide mixtures in insects and their toxicity againstspodoptera littoralis larvae

Synergism of mixtures of pyrethroids with organophosphorus (OP) compounds in insects is reviewed, and the toxicity of such combinations againstSpodoptera littoralis (Boisd.) larvae is reported. Mixtures of one of the pyrethroids cypermethrin, fenvalerate or deltamethrin with one of the OP compounds monocrotophos, profenofos, azinphos-methyl or acephate were assayed at different ratios as 24-h-old dipping residues on alfalfa, which was fed toS. littoralis larvae for 48 h. With most of the binary mixtures containing various OP concentrations in excess of those of the pyrethroids, synergism was demonstrated. In the pairs fenvalerate — azinphos-methyl, deltamethrin — azinphos-methyl and deltamethrin — profenofos, however, no synergism was found. In a detailed investigation with pyrethroid concentrations causing 20% mortality and OP concentrations giving a kill of no higher than ;10%, the above findings on synergism were amply confirmed. A cypermethrinmonocrotophos mixture showed synergism also on cotton leaves sprayed in the field. Synergism could not be demonstrated by topical application of pyrethroid — OP mixtures.     

Assessment of field evolved resistance to some broad-spectrum insecticides in cotton jassid, <Emphasis Type="Italic">Amrasca devastans</Emphasis> from southern Punjab,Pakistan

Resistance management, targeting insect pests is one of the key components in developing integrated pest management strategies. Arguably, resistance monitoring is a scientific undertaking that can support and inform resistance management tactics and strategies. To monitor the current resistance status in Amrasca devastans against conventional insecticides (deltamethrin, bifenthrin, cypermethrin, chlorpyrifos, profenofos, acephate, and methomyl) which are used by the farming community as the predominant means to control this pest. Field populations of A. devastans were collected from six different districts: Multan, Bahawalpur, Khanewal, Lahore, Dera Ghazi Khan and Muzaffargarh from Punjab in Pakistan. The adult populations tested were 11.10–92.87 times more resistant to deltamethrin, 5.87–14.11 times more to bifenthrin, 3.16–17.5 times more to cypermethrin, 2.65–36.42 times more to chlorpyrifos, 7.28–57.71 times more to profenofos, 1.65–11.13 times more to acephate and 2.55–43.31 times more to methomyl as compared to control (lab population). In our study, no to high levels of resistance were observed against pyrethroids and organophosphates. Development of resistance to these pyrethroids and organophosphates might be due to the injudicious use of these types of insecticides in field crops. This study suggests that use of these insecticides should be minimized to avoid development of resistance in A. devastans. Future studies are also recommended to use new chemistry insecticides with novel modes of action and/or insecticide mixtures that may reduce the reliance of the farming communities on these insecticides.