The development of pyrethroid resistance in Aedes aegypti (L) (Diptera: Culicidae) is a serious concern because major A. aegypti control programs are predominantly based on pyrethroid use during epidemic disease outbreaks. Research about the genetic basis for pyrethroid resistance and how it is transmitted among mosquito populations is needed. The objective of this study was to determine how deltamethrin resistance is inherited in the Cuban A. aegypti-resistant reference strain. Here, a field population of A. aegypti from Santiago de Cuba (SAN-F14), subjected to 14 generations of selection for high deltamethrin resistance level (91.25×), was used to prepare reciprocal F1 and backcross progeny with the insecticide-susceptible Rockefeller strain. Bioassays with larvae were performed according to World Health Organization guidelines. The activities of metabolic enzymes were assayed through synergist and biochemical tests. The null hypothesis of the parallelism test between the two probit regression lines of the reciprocal F1 (susceptible females × resistant males and vice versa) was not rejected at the 5% significance level (P = 0.42), indicating autosomal inheritance. The LC50 response of both F1 progenies to deltamethrin was elevated but less than the highly resistant SAN-F14 strain. DLC values for the F1 progenies were 0.91 and 0.87, respectively, suggesting that deltamethrin resistance in the SAN-F14 strain is inherited as an autosomal incompletely dominant trait, involving at least two factors, which implies a faster development of deltamethrin resistance in larvae and lost product effectiveness. Metabolic enzymes including esterases and cytochrome P-450 monooxygenases but not glutathione-S-transferases were involved in deltamethrin resistance in larvae.
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Vol. 51 • No. 6