Frank S C Tenywa, Silvan Hälg, Haji Makame, Jason Moore, Osward Dogan, Harubu Mapipi, Pie Müller, Sarah J Moore
Aedes aegypti populations from Dar es Salaam show widespread resistance to pyrethroids, and organochlorines. There was evidence of metabolic involvement suggested by partial restoration of susceptibility to pyrethroids through pre-exposure to PBO. A twofold increase in LD90 relative to the susceptible reference strain for Bti and temephos indicates no evidence of resistance, although continued monitoring is warranted to detect potential shifts in susceptibility.
BACKGROUND: Dengue, Zika and chikungunya are Aedes-borne arboviruses that pose a major global public health threat. In the absence of effective treatments or universally available vaccines, disease control in sub-Saharan Africa relies primarily on insecticidal vector control. However, sustained insecticide application imposes selection pressure for insecticide resistance that compromises intervention effectiveness. This study assessed the insecticide resistance profile and knockdown resistance of Aedes aegypti populations in Dar es Salaam, Tanzania.
METHODS: Phenotypic resistance of Ae. aegypti was evaluated using WHO-recommended adulticide and larvicide susceptibility bioassays at discriminating concentrations. F1 progeny derived from wild Ae. aegypti larvae were used for the tests. In adulticide bioassays, groups of 25 female Ae. aegypti were exposed for 1 h to insecticide-treated WHO susceptibility test papers. Larvicide bioassays exposed 25 third- and fourth-instar larvae to a larvicide based on Bacillus thuringiensis israelensis (Bti) or temephos for 24 h in 200 ml of water. Mosquito mortality was recorded 24 h post-exposure. Genotypic resistance was assessed using DNA extracted from phenotyped mosquitoes. The extracted DNA was screened for knockdown resistance (Kdr) mutations using diagnostic quantitative polymerase chain reaction (qPCR) assays.
RESULTS: Aedes aegypti populations from Ilala and Temeke districts of Dar es Salaam demonstrated phenotypic resistance to Pyrethroid: permethrin, deltamethrin, alpha-cypermethrin, lambda-cyhalothrin, and organochlorine, with adult mortality rates below 20% and 5%, respectively, while remaining susceptible to organophosphates and carbamates. In Kinondoni, resistance was observed across all classes except carbamates, and pre-exposure to piperonyl butoxide (PBO) increased pyrethroids mortality to an average of 40%. The LD50 and LD90 values for Bti and temephos showed resistance ratios (RR) below 5. The F1534C mutation was detected across all study districts; Ilala (77%, n = 77), Kinondoni (90%, n = 90) and Temeke (83%, n = 83), while low frequencies were observed for V1016I mutation.
CONCLUSIONS: Aedes aegypti populations from Dar es Salaam show widespread resistance to pyrethroids, and organochlorines. There was evidence of metabolic involvement suggested by partial restoration of susceptibility to pyrethroids through pre-exposure to PBO. A twofold increase in LD90 relative to the susceptible reference strain for Bti and temephos indicates no evidence of resistance, although continued monitoring is warranted to detect potential shifts in susceptibility.