Mode of action of the anthelmintics morantel,pyrantel and levamisole on muscle cell membrane of the nematode Ascaris suum

Intracellular current and voltage clamp techniques were used to investigate the mode of action of the anthelmintics, morantel, pyrantel and levamisole applied to the bag region of Ascaris suum muscle cells. Microperfusion of the anthelmintics and of O-acetylcholine (ACh) increased the input conductance and depolarised the membrane potential of the muscle bags. The relative potencies of these drugs were determined from dose–conductance relationships and found to be: morantel = pyrantel > levamisole > ACh. High doses (>10μM) of morantel caused antagonism of ACh responses. ACh-induced currents were measured under voltage clamp (over the range ?80 to +10mV). At membrane potentials between ?80 and 0 mV, microperfusion of ACh induced a voltage-dependent inward current. The current–voltage relationship was linear for membrane potentials in the range ?30 to +10mV. The reversal potential was measured directly and found to be about +10mV. The relationship became non-linear at membrane potentials more negative than ?30 mV, and the degree of non-linearity was dependent upon the concentration of ACh. The current–voltage relationships for morantel, pyrantel and levamisole also possessed both linear (?30 to 0mV) and non-linear components. The reversal potential for each agonist, determined by extrapolation of the linear component of the current–voltage relationship, was approximately +10mV, indicating the same cation channels were activated both by ACh and the anthelmintics. Evidence for competition between ACh and pyrantel for the same membrane receptor was obtained using iontophoretic delivery of each agonist from a double-barrelled micropipette. It is concluded that the anthelmintics, morantel, pyrantel and levamisole act as potent agonists at ACh receptors on muscle bag membranes of A. suum.     

Cholinergic receptors of the central nervous system of insects

Concentrated particulate preparations were made from housefly heads and the nerve cords of the American and Madagascar cockroaches. Macromolecules present in these preparations bound ³H-nicotine reversibly and with high affinities (3, 1.1, and 1.5 μM, respectively). Binding of ACh to the macromolecules in the preparation of houseflies and Madagascar cockroach was determined by inhibition of ³H-nicotine binding, and was found to be of much lower affinity than that of nicotine.There was a 2 × purification of the nicotine-binding macromolecules in this particulate preparation of housefly heads as compared to an earlier preparation of supernatant of 100,000g. Nicotine binding to this particulate preparation was blocked also by d-tubocurarine and atropine demonstrating the nicotinic and muscarinic nature of these nicotine-binding macromolecules. Prior exposure of the preparation to trypsin and chymotrypsin reduced nicotine binding by 58 and 68%, respectively.The relationship of these nicotine and ACh binding macromolecules to ACh-receptors is discussed.     

Pharmacological differentiation of responses to dopamine,octopamine and noradrenaline recorded from a cockroach motoneurone

Recordings have been made from the soma of a cockroach common inhibitory motoneurone. Locally applied dopamine, octopamine or noradrenaline all depolarised the neurone and produced a modest increase in membrane conductance. Under voltage-clamp, currents evoked by these amines showed considerable voltage dependence. The current-voltage relationships for dopamine and octopamine responses were similar, but differed from that for noradrenaline. The unusual voltage-dependent characteristics of these responses suggest that these compounds may serve a modulatory function in the insect CNS. The effects of a range of pharmacological antagonists indicate that dopamine acts upon a class of receptors distinct from those mediating responses to octopamine, noradrenaline and acetylcholine (ACh). Dopamine currents were abolished by SCH 23390 or cis-(Z)-flupenthixol, which did not depress responses to the other agonists. Octopamine and noradrenaline currents were selectively blocked by metoclopramide and ergometrine respectively, while β-bungarotoxin and gallamine preferentially suppressed ACh responses. At the present time the ionic basis of dopamine responses is unclear. Dopamine-evoked currents were totally abolished by application of Cd2²⁺ or verapamil or when the preparation was bathed in Ca²⁺ free external solutions. Changes in the external concentrations of Na⁺, K⁺ or Cl^?, however, also had some effect upon dopamine currents.     

Actions of quinolizidine alkaloids on Periplaneta americana nicotinic acetylcholine receptors

BACKGROUND: Botanical insecticides do not play a major role as crop protectants, but they are beneficial in some applications. The authors investigated the actions of naturally occurring alkaloids on insect nicotinic acetylcholine (ACh) receptors (nAChRs) by evaluating their abilities to inhibit specific binding of [³H]imidacloprid (IMI) to nerve‐cord membranes from Periplaneta americana L. Two alkaloids were also tested for their actions on nAChRs expressed by cockroach neurons using patch‐clamp electrophysiology. RESULTS: Four natural quinolizidine alkaloids (matrine, sophocarpine, cytisine and aloperine) exhibited more than 50% inhibition of [³H]IMI binding at 10 µM , although other compounds were found to have no or low inhibitory activity. The rank order of potency based on concentration–inhibition curves was cytisine > sophocarpine ≥ aloperine ≥ matrine. Patch‐clamp analysis indicated that sophocarpine and aloperine were not agonists of nAChRs expressed in P. americana neurons, yet, at 10 µM , aloperine, but not sophocarpine, suppressed ACh‐induced inward currents significantly. CONCLUSION: Three of the four natural alkaloids tested possess structural moieties that are necessary for interaction with P. americana nAChRs. Aloperine, which possesses a unique structure and showed a distinctive dose–response curve, was found to act as an antagonist. Appropriate modifications of these alkaloids might result in novel insecticidal nAChR ligands. Copyright © 2008 Society of Chemical Industry     

Pharmacological evidence for a discrete neurotoxic action of dieldrin (HEOD) in the American cockroach,Periplaneta americana (L.)

The excitatory effects of HEOD poisoning on spontaneous activity, and synaptic function in the sixth abdominal ganglion of the American cockroach are described. These effects are shown to be antagonized by Mg²⁺, hemicholinium-3, atropine, and d-turbocurarine. HEOD poisoning did not alter the nicotine sensitivity of the ganglion. On the basis of the findings it is hypothesized that HEOD acts at presynaptic membranes of cholinergic junctions, causing excessive and spontaneous release of presynaptic stores of acetylcholine.     

Cartap activity on the cockroach nervous and neuromuscular transmission

By employing intracellular electrodes on the 6th abdominal ganglion, Cartap hydrochloride 10^?5M caused in all experiments a block of the provoked stimulus transmission and a decrease of the cell membrane resting potential; the giant fiber conduction was not affected. In the experiments with extracellular electrodes Cartap 10^?5M provoked a marked increase of the spontaneous activity followed by block which partially disappeared after washing. The same effects were obtained on spontaneous activity when Cartap 10^?5M was used on the denervated 6th abdominal ganglion and in experiments conducted at 0 Ca²⁺ or at 20 mM Mg²⁺. Cartap 10^?5M did not affect the response to direct or indirect stimulation of cockroach neuromuscular preparation. These results tend to confirm that Cartap affects the postsynaptic region of the ganglionic nervous junction. The possible cause of the resting potential decrease is also discussed.     

Dibromo addition products of (1R)-cis-permethrin and deltamethrin; evidence that debromination is an obligatory requirement for biological activity

3-Phenoxybenzyl (1R-)-cis-3-(1,2-dibromo-2, 2-dichloroethyl)-2, 2-dimethylcyclopropanecarboxylate [dibromo-(1R)-cis-permethrin] was >100 times less active than (1R)-cis-permethrin in causing repetitive firing in a cockroach cereal sensory nerve in vitro, although its toxicity, symptomology and nerve effects in vivo were comparable to the parent compound. Treatment of the in-vitro preparation with glutathione significantly increased the effectiveness of dibromo-(1R)-cis-permethrin in a concentration-dependent manner, while having no effect on the action of (1R)-cis-permethrin. Topical treatment of the cockroach with dibromo-(1R)-cispermethrin gave a similar time of onset of symptoms to that caused by (1R)-cis-permethrin (∼2 min). Pretreatment of the cockroach with N-ethylmaleimide (NEM) significantly (P<0.05) increased dose-dependently the latency of signs of poisoning caused by dibromo-(1R)-cis-permethrin, but had no significant effect on the latency following (1R)-cis-permethrin treatment. Deltamethrin and tralomethrin, applied to the cockroach at LD₉₅ doses of 0.03 and 0.07 m̈g g⁻¹ respectively, also had similar latencies for the development of symptoms. Moreover, pretreatment with NEM delayed the time of onset of symptoms for tralomethrin (P<0.02) but not for deltamethrin. The results strongly suggest that debromination is an obligatory requirement for the biological activity of dibromo-(1R)-cis-permethrin and tralomethrin.     

A patch—clamp study of the action of a nitromethylene heterocycle insecticide on cockroach neurones growing in vitro

The mode of action of a nitromethylene heterocycle (NMH) insecticide was studied by patch–clamp techniques using cockroach embryonic cultures as an experimental model. Under whole-cell recordings, this compound elicited inward currents resembling those induced by O-acetylcholine (ACh). The reversal potentials for both ACh and the NMH were similar, suggesting that the inward currents induced by both were carried by the same species of ion. Pharmacological investigations of NMH-induced responses revealed that the insecticidal action of this compound is exerted through agonistic action at the nicotinic acetylcholine receptor. Single-channel studies were also performed to study the interaction of NMH with the nicotinic-receptor-coupled ion channel.     

Enzymatic hydrolysis of diazoxon by rat tissue homogenates

The enzymatic hydrolysis of ³²P-labeled diazoxon was studied using tissue homogenates of rat and American cockroach. The order of the hydrolytic activities of rat tissues for diazoxon was as follows: liver > blood > lung > heart > kidney > brain. A liver enzyme hydrolyzing diazoxon to diethyl phosphoric acid and 2-isopropyl-4-methyl-6-hydroxypyrimidine was located in the microsomes. The activity of the microsomal enzyme was inhibited by EDTA, heavy and rare earth metal ions, and SH reagents. Ca²⁺ activated the enzyme and protected it from inactivation. Mitochondrial and soluble enzymes from liver and a serum enzyme also hydrolyzed diazoxon and they were also activated by Ca²⁺. The removal of calcium bound to the microsomal enzyme protein by dialysis against EDTA led to a partially irreversible change of the enzyme. The hydrolysis of diazoxon by the Ca²⁺-requiring microsomal and serum enzymes was more rapid than that of paraoxon. Hydrolysis of diazoxon did not occur in American cockroach homogenates. This difference in the capacity to hydrolyze diazoxon between mammals and insects is discussed in relation to the selective toxicity of diazinon.     

The mode of action and neurotoxicity of mirex,chlordecone, and four hydrogenated mirex analogs

The toxicity and neurological effects of mirex, chlordecone, and four hydrogenated mirex analogs were evaluated on the American cockroach. The severity of poisoning symptoms correlated with the ability of each compound to increase spontaneous activity and prolong synaptic afterdischarge in ganglia of the ventral nerve cord. Afterdischarge across the metathoracic ganglion was consistent with a characteristic wing splaying symptom in mirex-poisoned cockroaches. The actions of hemicholinium-3 and nicotine on nerve cords from mirex-poisoned cockroaches are described and are consistent with a hypothesis that the increased spontaneous activity and afterdischarge are the result of enhanced transmitter release in ganglia of poisoned animals.     

Myotoxic and neurotoxic activity of Bacillus thuringiensis var. israelensis crystal toxin

The mechanism of the entomocidal action of Bacillus thuringiensis var. israelensis (BTI) in Periplaneta americana has been studied. Cockroaches treated with the alkali-solubilized BTI crystal gradually became sluggish and immobile. A physiological examination of poisoned cockroaches indicated that BTI possessed both myotoxic and neurotoxic activity. Following hemocoel or foregut administration of BTI, myotoxic effects were observed within 10–20 min whereas the onset of neurotoxic effects was considerably delayed. The results of this study suggest that the myotoxic action of BTI is probably important for the initial manifestation of its toxicity. The neurotoxic effects of BTI were ascribed to its ability to interfere with transmitter release. BTI exerted a dual action on transmitter release in the cockroach sixth abdominal ganglion. At lower doses (2–4 μg/ml) BTI was found to suppress transmitter release by interfering with calcium uptake. At higher concentrations (12 μg/ml or higher), however, BTI caused blockage of synaptic transmission which was preceded by massive transmitter release. In either case, the synapse blocking action of BTI was probably due to its effects upon presynaptic terminals. Postsynaptic membranes and axons in the ventral nerve cord apparently remained unaffected.     

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.     

哈氏啮小蜂的繁殖和利用

用人工培养液饲养的哈氏啮小蜂,羽化后将成蜂释放至159户住户的碗橱中,40天和80天后第一代和第二代寄生蜂在蜚蠊卵荚内最高寄生率分别为93.8％和95.1％,放蜂户的烟色大蠊的密度明显地下降,放蜂后一年内,蜚蠊密度稳定地保持在较低水平。     

Comparative molluscicidal action of extract of Ginko biloba sarcotesta,arecoline and niclosamide on snail hosts of Schistosoma japonicum

In search for new local plant molluscicides for the control of the vectors of schistosomiasis, we compared the molluscicidal action of the extract of Ginkgo biloba sarcotesta by benzinum (EGSB) to that of arecoline (ARE) and niclosamide (NIC) against Oncomelania hupensis snails. NIC showed the highest toxicity on snails with 24 h LC₅₀ vales of 0.12 mg/L and LC₉₀ of 0.98 mg/L, while the LC₅₀ and LC₉₀ of EGSB were much lower than that of ARE. Sublethal in vivo 24 h exposure to 40% and 80% LC₅₀ of NIC, EGSB and ARE altered the activities of different enzymes in different body tissues of snails. EGSB could significantly inhibit Choline esterase (ChE), Alanine aminotransferase (ALT), Alkaline phosphatase (ALP) and Malic dehydrogenase (MDH) activities both in the cephalopodium and liver. ARE could significantly cause a reduction in ChE, ALP activities in the cephalopodium and ChE, ALT, ALP, Succinodehydrogenase (SDH), MDH activities in the liver. NIC significantly altered activities of ChE, ALT, ALP, SDH, and MDH in the cephalopodium and ChE, ALT, ALP, SDH activities in the liver. All molluscicides could not affect Lactate dehydrogenase (LDH) activity in the cephalopodium and the liver. Maximum inhibition of ALT and MDH activities was found in the cephalopodium and liver of snails treated with 80% of 24 h LC₅₀ of EGSB. However, NIC and ARE caused maximum reduction in ALP and SDH activities, respectively. The results indicated that molluscicidal action of EGSB was different to that of ARE and NIC in some extent.     

Effects of diazepam and chlordimeform analogs on the German and the American cockroaches

Twenty-one diazepam- and chlordimeform (CDM)-related compounds were synthesized by mimicking some parts of the 1,4-benzodiazepine tranquilizing drugs, and were tested for their insecticidal activity against the German cockroach. Some of these compounds showed knockdown effects and some were insecticidal. Against the German cockroach the most toxic CDM analog was N-propargyl CDM (compound 6), and that with a potent knockdown potency was compound 13 which has a structural resemblance to diazepam. Ligand-receptor binding assay was carried out, using [³H]diazepam as a ligand to examine the relation between CDM-related compounds and the 1,4-benzodiazepines. The [³H]diazepam binding to a specific site in the American cockroach brain was inhibited by the insecticidal compounds. Among these compounds a correlation exists between their inhibitory potency on specific [³H]diazepam binding and their insecticidal activity, suggesting a possible significance of such an interaction with the diazepam binding site for the toxicity of these compounds against cockroaches.     

Comparative molluscicidal action of extract of Ginko biloba sarcotesta, arecoline and niclosamide on snail hosts of Schistosoma japonicum

In search for new local plant molluscicides for the control of the vectors of schistosomiasis, we compared the molluscicidal action of the extract of Ginkgo biloba sarcotesta by benzinum (EGSB) to that of arecoline (ARE) and niclosamide (NIC) against Oncomelania hupensis snails. NIC showed the highest toxicity on snails with 24 h LC₅₀ vales of 0.12 mg/L and LC₉₀ of 0.98 mg/L, while the LC₅₀ and LC₉₀ of EGSB were much lower than that of ARE. Sublethal in vivo 24 h exposure to 40% and 80% LC₅₀ of NIC, EGSB and ARE altered the activities of different enzymes in different body tissues of snails. EGSB could significantly inhibit Choline esterase (ChE), Alanine aminotransferase (ALT), Alkaline phosphatase (ALP) and Malic dehydrogenase (MDH) activities both in the cephalopodium and liver. ARE could significantly cause a reduction in ChE, ALP activities in the cephalopodium and ChE, ALT, ALP, Succinodehydrogenase (SDH), MDH activities in the liver. NIC significantly altered activities of ChE, ALT, ALP, SDH, and MDH in the cephalopodium and ChE, ALT, ALP, SDH activities in the liver. All molluscicides could not affect Lactate dehydrogenase (LDH) activity in the cephalopodium and the liver. Maximum inhibition of ALT and MDH activities was found in the cephalopodium and liver of snails treated with 80% of 24 h LC₅₀ of EGSB. However, NIC and ARE caused maximum reduction in ALP and SDH activities, respectively. The results indicated that molluscicidal action of EGSB was different to that of ARE and NIC in some extent.     

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.     

Effects of chlordimeform and lindane on monoamine levels in the central nervous system of the american cockroach, Periplaneta americana L

The effects of chlordimeform and lindane on levels of 5-hydroxytryptamine, tryptophan, and N-acetyl dopamine were studied in the cerebral ganglia of the american cockroach, Periplaneta americana. The effects of chlordimeform on nerve cord levels of 5-hydroxytryptamine, tryptophan, dopamine, and octopamine, and the effect of lindane on cerebral ganglia levels of dopamine were also investigated in this species. Topical applications of chlordimeform deplete 5-hydroxytryptamine and tryptophan from the cerebral ganglia whereas levels of n-acetyl dopamine are elevated. The effect of chlordimeform on these compounds is dose-dependent. Similar chlordimeform-induced effects are observed in the nerve cord, and octopamine levels are also depleted in this tissue following treatment with chlordimeform. A biphasic response to chlordimeform is observed in the nerve cord for dopamine levels with a 40% decrease evident after 2 hr and a 30% increase apparent after 6 hr. In contrast to chlordimeform, lindane does not affect 5-hydroxytryptamine and tryptophan levels in the cebral ganglion but low doses of this insecticide effect increases in brain levels of dopamine and n-acetyl dopamine.     

Passive heat treatment of sweet basil crops suppresses white mould and grey mould

Sweet basil white mould (BWM, Sclerotinia sclerotiorum) and grey mould (BGM, Botrytis cinerea) are important diseases in Israel and other basil‐growing regions. The impact of microclimate on BWM and BGM and on plant sensitivity to these diseases was studied. Disease incidence was evaluated in three field experiments, each consisting of 10–12 polyethylene‐covered tunnels. BWM and BGM incidences were correlated with air temperature, relative humidity (RH) and soil temperature data. The incidence of BWM was negatively correlated with high (above >25 or >30 °C) air temperatures, RH > 50% and RH > 75% and high (>21 or >24 °C) soil temperatures. BGM incidence was negatively correlated with high (>25 °C) air temperatures and high (>21 or >24 °C) soil temperatures, and positively correlated with RH >65% or >75%. Shoots harvested from plants grown in the walk‐in tunnels were inoculated with S. sclerotiorum or B. cinerea under controlled conditions. Severity of BWM and BGM on those shoots was negatively correlated with tunnel air temperatures of >25 and >30 °C and soil temperatures >18 °C. Thus, high temperatures were related to reduced disease incidence and to reduced sensitivity to the pathogens. Experiments involving potted plants revealed that heating only the root zone suppresses canopy susceptibility to BWM and BGM. These findings indicate that the effect of high greenhouse temperatures involves an indirect systemic effect that renders the host less susceptible to disease. This effect was also observed in harvested shoots that were no longer at the high temperatures, and the effect was systemic.     

Secondary transmission of fipronil toxicity between Oriental cockroaches Blatta orientalis L in arenas

Mixed colonies of adult male and female Oriental cockroaches were conditioned to a 12:12 h photocycle in arenas (0.23 m²) with a harbourage, food and water and then exposed to deposits (30 mg or 2 × 30 mg) of 0.5 g kg⁻¹ fipronil gel bait at the beginning of a dark phase. The bait was rapidly consumed by the first sub‐group of insects to emerge from the harbourage; any residual bait was removed from the arenas 4 h into the following light phase. Third‐instar nymphs were then introduced and mortality was monitored over the subsequent 14 days with all cadavers left in situ. Death of cockroaches under these conditions was due to direct poisoning of the sub‐group of the adults that consumed the bait and to secondary transfer of toxicity to the remainder of the adult and to the nymphal populations. Mean mortality in the adult populations increased to > 96% (females) and > 53% (males) with consistently higher mortality of females than males; that in the third‐instar nymph (unexposed) populations increased to 25–50%. Some cadavers were wholly or partially eaten by other cockroaches during this period, and this was interpreted as the major mechanism of secondary transfer of toxicity. Individual adult females were fed weighed bait deposits (10 mg) and, following death (24 h), the cadavers were transferred to closed containers held at 33%, 52% or 76% relative humidity /28 °C for periods of up to 7 weeks. They were then added individually to groups of five adult females provided with water but no alternative food source. Mean mortalities (>64% at 1 week and > 96% at 7 weeks) were not significantly lower than mean mortalities produced by freshly poisoned cockroaches, showing that no loss in the insecticidal activity of the cadavers occurred under these storage conditions. The potential of necrophagy to supplement the primary action of fipronil bait treatment of Oriental cockroach infestations by inhibiting colony redevelopment is discussed. © 2000 Society of Chemical Industry