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Permethrin and malathion resistance in head lice: Results of ex vivo and molecular assays

      Background

      Treatment of head lice infestation relies on the application of topical insecticides. Overuse of these products has led to the emergence of resistance to pyrethroids and malathion worldwide. Permethrin resistance in head lice is mostly conferred by the knockdown resistance (kdr) trait.

      Objective

      To evaluate the occurrence of permethrin- and malathion-resistant head lice in Paris.

      Methods

      A prospective survey was conducted in 74 elementary schools. Live lice collected on schoolchildren were randomly selected and submitted to ex vivo bioassays or underwent individual DNA extraction. A fragment of kdr-like gene was amplified and compared with wild-type sequences.

      Results

      Live head lice were detected in 574 children. Ex vivo assays showed no surviving lice after a 1-hour contact with malathion while most lice died after a 1-hour exposure to permethrin and piperonyl butoxide (85.7%, 95% confidence interval [CI]: 83.9-87.5). Among the 670 lice with workable DNA sequences, 661 lice (98.7%, 95% CI 97.7-99.3) had homozygous kdr mutations.

      Limitations

      The findings of this large-scale survey of the occurrence of insecticide-resistant head lice indicated a major insecticide pressure in the study population, but it was not sufficient to draw conclusions about other populations. The presence of T917I-L920F mutations in kdr gene may not correlate with treatment failure in prospective studies.

      Conclusion

      The high occurrence of kdr mutant allele suggests that insecticide resistance was already strongly established in the studied population. This finding must be interpreted with caution as it may not be predictive of treatment failure.

      Key words

      Abbreviations used:

      CI (confidence interval), DASES (“Direction de l’Action Sociale, de l’Enfance et de la Santé”), kdr (knockdown resistance), PB (piperonyl butoxide), VGSC (voltage-gated sodium channel)
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