Inheritance of pyrethroid resistance and a sodium channel gene mutation in the cattle tick Boophilus microplus.

A substitution (Phe-->Ile) within the sodium channel gene sequence has been associated with pyrethroid resistance in Boophilus microplus. The aim of the present study was to analyze the inheritance of pyrethroid resistance and the mutant allele, on reciprocal crosses of a susceptible (SS) and a resistant (RR) strain. Bioassays and genotypes were determined to evaluate pyrethroid resistance. The resistance allele frequency of both parental strains were 100% and 2.27% for RR and SS, respectively. The reciprocal crosses show a predominance of the heterozygote genotype, in agreement with the significant decrease of the acaricide resistance to cypermethrin, deltamethrin, and flumethrin. However, the RS progeny showed a complete recessive survival (D (ML) = 0) for deltamethrin and flumethrin, suggesting a complete dominance of the susceptible allele and incomplete dominance for cypermethrin (D (ML) = 0.169). On the other hand, SR progeny showed a partially recessive survival for cypermethrin (D (ML) = 0.380), deltamethrin (D (ML) = 0.319), and flumethrin (D (ML) = 0.258), indicative of a partially dominant inheritance of the resistance. A possible maternal strain effect should be considered for practical purposes and prediction of acaricide resistance and further work needs to be done to elucidate the underlying inheritance of pyrethroid resistance and the sodium channel mutation in B. microplus.

Roles played by esterase activity and by a sodium channel mutation involved in pyrethroid resistance in populations of Boophilus microplus (Acari: Ixodidae) collected from Yucatan, Mexico.

Pyrethroid resistance in Boophilus microplus (Canestrini) (Acari: Ixodidae) was studied by correlating discriminating-dose (DD) bioassay results and esterase activity or the frequency of a sodium channel mutation known to be involved in pyrethroid resistance in nine field strains of B. microplus from Yucatan, Mexico. Two tick strains (P67 and B74) were identified as susceptible to cypermethrin, deltamethrin, and flumethrin by DD, one strain (P65) was susceptible to cypermethrin and resistant to deltamethrin and flumethrin, and six strains were resistant to cypermethrin, delta-methrin, and flumethrin (T11, M10, C54, R49, B71, and T66). By using polymerase chain reaction, only 6.0 and 6.2% of resistance allele (R) was found in the susceptible strains (P67 and B74, respectively). In the T66 strain, with 100% of larval survival to the DD of pyrethroids as measured by the larval packet test (LPT), 98.0% of the gene pool contained the R allele. Positive correlations between the larval survival and the percentage of the R allele were found (deltamethrin r2 = 0.8875, P < 0.01; cypermethrin r2 = 0.8563, P < 0.01; and flumethrin r2 = 0.8491, P < 0.01). There were no significant correlations between the level of larval survival and esterase-based hydrolytic activity. It was concluded that within the B. microplus populations studied, resistance to flumethrin, deltamethrin, or cypermethrin was because of the novel sodium channel mutation (Phe-->Ile amino acid substitution in the S6 transmembrane segment of domain III), and there was a correlation between tick mortality by pyrethroid exposure (larval survival) and the presence of R allele. It was not determined whether enhanced esterase-based hydrolytic activity was involved in pyrethroid resistance in the populations tested.