Abstract

Head lice infestations remain an important public health problem, albeit poorly defined in most endemic countries. Reports of increasing resistance to first-line treatment have renewed scientific research into this neglected ectoparasitosis. Mapping and understanding resistance mechanisms are essential for the development of more effective treatments, as well as for prolonging the life of existing pediculicides. This review aims to synthetize recent data on the type, frequency, and distribution of genetic mutations associated with head lice resistance to chemical treatments. Head lice resistance is reported in all continents. The most studied mechanism of resistance is through Knockdown resistance (kdr) mutations, with biomarkers M815I, T917I, and L920F, most commonly reported. Other reported mechanisms such as cytochrome P450 enzyme inhibition, altered acetylcholinesterase binding, and GluCl mutations are still being investigated. Allele mutations linked to pyrethroid resistance differ between regions and countries, which highlights the need for monitoring resistance through region-specific genetic markers. In geographic areas where resistance is well-established, louse populations are predominantly homozygous. In regions where heterozygosity still prevails, selective pressure through the use of chemical pediculicides will cause resistance to increase. Continuous surveillance of resistance is needed to monitor the frequency of resistance alleles, which is expected to increase as lice populations move into fixation. Further research should be conducted on new treatments with physical mechanisms of action.

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