Abstract
There are concerns regarding the potential development of drug resistance in scabies. Recently, there has been a substantial increase in the global incidence of scabies, together with reports of treatment failure in parts of Europe. While it can be difficult to demonstrate cases of genuine resistance, there is now clinical evidence that permethrin resistance may indeed explain a proportion of these treatment failures. Permethrin resistance has been confirmed in a laboratory model of Sarcoptes scabiei var. canis and is associated with sodium channel mutations and increased detoxification activity. Ivermectin resistance has also been noted in cases of crusted scabies, with several other cases of ivermectin treatment failure likely linked to resistance. Resistance to ivermectin and other macrocyclic lactones is likely a polyfactorial trait. Increased transcription of a P-glycoprotein efflux pump and detoxifying Glutathione S- transferases was found in mites collected from patients after ivermectin treatment. Mutations in ligand-gated chloride channels have been associated with ivermectin resistance in other mites and lice and would be worthy of investigation in S. scabiei. Research efforts should focus on the collection of mites in cases of suspected resistance for molecular analysis. Further characterisation of the scabies mite ion channels would better develop understanding of the physiological targets of acaricides and help guide treatment strategies to avoid further development of resistance. This may include using synergised pyrethroids and/or combination therapies with different target effects in S. scabiei.