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. 2023 Sep 7;13(1):14711.
doi: 10.1038/s41598-023-41952-2.

Evidence of intensification of pyrethroid resistance in the major malaria vectors in Kinshasa, Democratic Republic of Congo

Daniel Nguiffo-Nguete  1 , Leon M J Mugenzi  2 , Emile Zola Manzambi  3 , Magellan Tchouakui  2 , Murielle Wondji  2   4 , Theofelix Tekoh  2   5 , Francis Watsenga  3 , Fiacre Agossa  3 , Charles S Wondji  6   7   8
Affiliations

Evidence of intensification of pyrethroid resistance in the major malaria vectors in Kinshasa, Democratic Republic of Congo

Daniel Nguiffo-Nguete et al. Sci Rep. .

Abstract

Assessing patterns and evolution of insecticide resistance in malaria vectors is a prerequisite to design suitable control strategies. Here, we characterised resistance profile in Anopheles gambiae and Anopheles funestus in Kinshasa and assess the level of aggravation by comparing to previous 2015 estimates. Both species collected in July 2021 were highly resistant to pyrethroids at 1×, 5× and 10× concentrations (mortality < 90%) and remain fully susceptible to bendiocarb and pirimiphos methyl. Compared to 2015, Partial recovery of susceptibility was observed in A. gambiae after PBO synergist assays for both permethrin and α-cypermethrin and total recovery of susceptibility was observed for deltamethrin in 2021. In addition, the efficacy of most bednets decreased significantly in 2021. Genotyping of resistance markers revealed a near fixation of the L1014-Kdr mutation (98.3%) in A. gambiae in 2021. The frequency of the 119F-GSTe2 resistant significantly increased between 2015 and 2021 (19.6% vs 33.3%; P = 0.02) in A. funestus. Transcriptomic analysis also revealed a significant increased expression (P < 0.001) of key cytochrome P450s in A. funestus notably CYP6P9a. The escalation of pyrethroid resistance observed in Anopheles populations from Kinshasa coupled with increased frequency/expression level of resistance genes highlights an urgent need to implement tools to improve malaria vector control.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Figure 1
Figure 1
Susceptibility profile of Anopheles gambiae (a) and Anopheles funestus (b) population in Kinshasa in 2015 and 2021 using World Health Organization insecticide susceptibility tube assays. NM, no mortality.
Figure 2
Figure 2
Susceptibility profile of Anopheles gambiae (a) and Anopheles funestus (b) population in Kinshasa using resistance intensity with 1×, 5× and 10× the diagnostic concentrations of permethrin (0.75%) and deltamethrin (0.05%) World Health Organization insecticide susceptibility tube assays.
Figure 3
Figure 3
Bioefficacy of Anopheles gambiae (a) and Anopheles funestus (b) from Kinshasa in 2015 and 2021 using different long-lasting insecticidal nets; NM, No Mortality; N/A, not applicable.
Figure 4
Figure 4
Genotype distribution for key resistance markers (a) and genotype comparison between Anopheles funestus F0 females collected in 2015 and 2021 (b).
Figure 5
Figure 5
Genotype distribution for key resistance markers (a) and genotype comparison between Anopheles gambiae F0 female collected 2015 and 2021 (b).
Figure 6
Figure 6
Differential gene expression of the P450 genes CYP6P9a, CYP6P9b, CYP9K1, CYP6M7 and CYP6P5 and the Gluthatione S-tranferase GSTe2 in Anopheles funestus from Ndjili brasserie (a) and Comparison of gene expression between mosquitoes collected in 2015 and 2021 (b). Error bars represent standard error of the mean.
Figure 7
Figure 7
Differential gene expression in Anopheles gambiae from Ndjili brasserie. Error bars represent standard error of the mean.
See this image and copyright information in PMC

References

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