Electrophoresis was used to characterize the esterases in Lucilia cuprina (Wiedemann). Of the 16 esterase bands visualized, only one was associated with resistance to organophosphorus insecticides. In laboratory reference strains, the esterase E 3 was consistently found in both susceptible and heterozygously resistant flies, but was absent from homozygously resistant flies. It was postulated that resistant flies possessed a non-staining form of E 3 , designated E 3 null. Genetic analyses mapped the locus for E 3 null to a position in the same region as the gene for organophosphorus resistance. No recombinants between the genes for resistance and E 3 null were detected. In field populations of L. cuprina from several areas in Australia, a close association was found between the frequency of E 3 null (0-97) and the proportion of flies resistant to organophosphorus insecticide (0-967). This association suggests that E 3 null represents the product of a major resistance gene in terms of the 'mutant ali-esterase' theory. E 3 , as found in susceptible blowflies, represents the 'original' ali-esterase, the gene for which mutated to one coding for E 3 null. This mutant enzyme can hydrolyse organophosphates more efficiently than E 3 but has lost the ability to hydrolyse 1-and 2-naphthyl acetate (the substrates used to visualize the esterases after electrophoresis).

A treated surface technique to measure the response of the sheep body louse, Dumaliniu ovis to contact insecticides is described. The responses of 30 populations of D. ovis to the synthetic pyrethroid cypermethrin showed wide variation at LCs0 and LCPr. Half the populations sampled were considered as pyrethroid susceptible, based on 100% mortality at 5 ppm (or less) to cypermethrin. This suggests that factors other than pyrethroid resistance were responsible for inefficient lice control on the properties from which these populations were obtained. Lice surviving 5 ppm or greater were considered provisionally as resistant.

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