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

Abstract 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 .