{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T20:29:39Z","timestamp":1788985779693,"version":"build-2803163510"},"reference-count":37,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2023,7,10]],"date-time":"2023-07-10T00:00:00Z","timestamp":1688947200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acad Dermatol Venereol"],"published-print":{"date-parts":[[2023,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Increasing evidence has sparked a debate on the loss of sensitivity of scabies mites to conventional permethrin therapy. Mutations in the voltage\u2010sensitive sodium channels (VSSC) were associated with knockdown resistance (kdr) in many arthropods, but have never been identified in\n                      <jats:italic>Sarcoptes scabiei<\/jats:italic>\n                      variatio (var.)\n                      <jats:italic>hominis<\/jats:italic>\n                      mites.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To identify factors contributing to therapy failure.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Sixty\u2010seven mites were collected from 64 scabies\u2010infested patients in Vienna, Austria, of whom 85.9% were refractory to prior permethrin\u2010based treatments, and genotyped for the presence of nucleotide polymorphisms in Domain II of the\n                      <jats:italic>VSSC<\/jats:italic>\n                      , known to be associated with kdr. Information regarding previous antiscabietic therapies, decontamination procedures and possible re\u2010infestations by contacts as well as the response to re\u2010imposed therapies were obtained.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Sequence alignment comparisons revealed previously unidentified mutations in the coding region of Domain II of the\n                      <jats:italic>VSSC<\/jats:italic>\n                      . A novel A1663T transversion was detected in 97.0% of the mites, resulting in a non\u2010synonymous substitution from methionine to leucine, M918L, a mutation known to confer kdr in other arthropods. In addition, a synonymous G1659A transition was identified in one mite, which otherwise showed a nucleotide sequence identical to the wild\u2010type reference. No major inconsistencies were observed within the previous therapeutic and decontamination procedures, which could have accounted for the observed non\u2010responsiveness to permethrin\u2010based therapies. Subsequent cure of infestation was achieved in 65.6% of the participants, predominantly by combination therapies with topical permethrin and systemic ivermectin. However, in 14.6% of the cured cases, permethrin monotherapy sufficed for eradication of scabies, albeit in some cases prolonged exposure was necessary.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      The kdr\u2010associated M918L mutation in the\n                      <jats:italic>VSSC<\/jats:italic>\n                      gene has now emerged in\n                      <jats:italic>S.\u2009scabiei<\/jats:italic>\n                      var.\n                      <jats:italic>hominis<\/jats:italic>\n                      mites. Hence, loss of sensitivity to permethrin due to kdr\u2010type resistance may be more prevalent than anticipated and may be decisive for the therapy responsiveness of scabies\u2010infested patients.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jdv.19288","type":"journal-article","created":{"date-parts":[[2023,6,25]],"date-time":"2023-06-25T13:20:35Z","timestamp":1687699235000},"page":"2355-2361","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":33,"title":["Detection of a knockdown mutation in the voltage\u2010sensitive sodium channel associated with permethrin tolerance in\n                    <i>Sarcoptes scabiei<\/i>\n                    var.\n                    <i>hominis<\/i>\n                    mites"],"prefix":"10.1111","volume":"37","author":[{"given":"K.","family":"Riebenbauer","sequence":"first","affiliation":[{"name":"Department of Dermatology Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"K.","family":"Purkhauser","sequence":"additional","affiliation":[{"name":"Department of Dermatology Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J.","family":"Walochnik","sequence":"additional","affiliation":[{"name":"Institute of Specific Prophylaxis and Tropical Medicine, Center for Pathophysiology, Infectiology and Immunology Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N.","family":"Urban","sequence":"additional","affiliation":[{"name":"Department of Dermatology Medical University of Vienna  Vienna Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. 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