Insecticide resistance is sometimes exacerbated by the development of cross and multiple resistance. Cross-resistance occurs when development of resistance to one insecticide automatically confers resistance to one or more others insecticides to which the insect has not been previously exposed. This phenomenon usually arises, but not necessarily among insecticides that inhibit the same target. However cross-resistance can also result from the large number of detoxification enzymes or from their broad spectrum activity, targeting functional groups of a wide variety of insecticides. Selection of housefly strain ALHF to permethrin resulted in increased resistance from an initial 260-fold to 1,800-fold. This strain also showed cross-resistance to beta-cypermethrin, cypermethrin, deltamethrin and propoxyr (Liu and Yue,2000). In another study an azinphosmethyl-resistant codling moth Cydia pomonella (L),was also found to be relatively resistant to several other insecticides including two organophosphates (diazinon, Phosmet), one carbamate (carbaryl), DDT and two pyrethroids (esfenvalerate and fenpropathrin) (Dunley et al. 2000). Sometimes increasing resistance to one insecticide leads to increased suscptibilty to another insecticide, phenomenon known as negative cross-resistance. Yamamoto et al. (1983) found that in the green rice leafhopper resistance to N-methyl carbamate had led to higher susceptibility to N-propyl carbamate to which the insect was previously resistant. Additionally, negatively correlated cross-resistance was identified in the coddling moth for resistance to azinphosmethyl that become susceptible to chlorpyrifos and methyl parathion Dunley et al., 2000). Multiple resistance occurs when insects develop resistance simultaneously to many insecticides by developing multiple resistance mechanisms. This phenomenon has been documented in various insects species and involves nearly all classes of insecticides. Inhibition of P450 enzymes and hydrolases respectively by piperonyl butoxide (PBO) and s,s,s,s-tributylphosphorotrithioate(DEF) lead to partial reduction of permethrin resistance in a highly resistant housefly, suggesting the existence of others mechanisms contributing to the resistance (Liu and Yue, 2000). A population of Anopheles arabiensis from Ethiopia has developed resistance to DDT, permethrin, deltamethrin and malathion but not to propoxyr (Yewhalaw et al., 2011). Molecular investigation of the underlaying mechanisms of these resistances revealed a kdr and ace-1 mutations respectively on sodium channel and acetylcholinesterase genes. Similarly, Koekemoer et al. (2011) have detected multiple insecticide resistance in Anopheles gambiae from Congo. In this study a population of mosquito previously known to be resistant only to organophosphates, was also found resistant to dieldrin, DDT and pyrethroids. Target site mutations Rdl and kdr (L1014F/L1014S) were respectively responsible for resistance to dieldrin and DDT, while pyrethroids resistance was essentially due elevated P450 enzymes and kdr mutation.
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