Abstract:
Global efforts to control Aedes mosquito-transmitted pathogens still rely heavily on insecticides. However, available information on vector resistance is mainly restricted to mosquito
populations located in residential and public areas, whereas commercial settings, such as
hotels are overlooked. This may obscure the real magnitude of the insecticide resistance
problem and lead to ineffective vector control and resistance management. We investigated
the profile of insecticide susceptibility of Aedes aegypti mosquitoes occurring at selected
hotel compounds on Zanzibar Island. At least 100 adults Ae. aegypti females from larvae
collected at four hotel compounds were exposed to papers impregnated with discriminant
concentrations of DDT (4%), permethrin (0.75%), 0.05 deltamethrin (0.05%), propoxur
(0.1%) and bendiocarb (0.1%) to determine their susceptibility profile. Allele-specific qPCR
and sequencing analysis were applied to determine the possible association between
observed resistance and presence of single nucleotide polymorphisms (SNPs) in the voltage-gated sodium channel gene (VGSC) linked to DDT/pyrethroid cross-resistance. Additionally, we explored the possible involvement of Glutathione-S-Transferase gene (GSTe2)
mutations for the observed resistance profile. In vivo resistance bioassay indicated that Ae.
aegypti at studied sites were highly resistant to DDT, mortality rate ranged from 26.3% to
55.3% and, moderately resistant to deltamethrin with a mortality rate between 79% to and 100%. However, genotyping of kdr mutations affecting the voltage-gated sodium channel
only showed a low frequency of the V1016G mutation (n = 5; 0.97%). Moreover, for GSTe2,
seven non-synonymous SNPs were detected (L111S, C115F, P117S, E132A, I150V,
E178A and A198E) across two distinct haplotypes, but none of these were significantly
associated with the observed resistance to DDT. Our findings suggest that cross-resistance
to DDT/deltamethrin at hotel compounds in Zanzibar is not primarily mediated by mutations
in VGSC. Moreover, the role of identified GSTe2 mutations in the resistance against DDT
remains inconclusive. We encourage further studies to investigate the role of other potential
insecticide resistance markers.
