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Invasive aspergillosis (IA) is a potentially lethal infection that affects mostly immunocompromised patients caused by  Aspergillus fumigatus . Echinocandins are a second-line therapy against IA, used as a salvage therapy as well as for empirical or prophylactic therapy. Although they cause lysis of growing hyphal tips, they are considered fungistatic against molds. In vivo echinocandins resistance is uncommon; however, its wide clinical use could shortly lead to the emergence of  A. fumigatus  resistance. The aims of the present work was to assess the development of reduced echinocandins susceptibility phenotype by a  A. fumigatus  strain and to unveil the molecular mechanism underlying such phenotype. We induced in vitro cross-resistance to echinocandins following exposure of  A. fumigatus  to anidulafungin. Stability of the resistant phenotype was confirmed after removal of anidulafungin pressure. The  FKS1  gene was partially sequenced and a E671Q mutation was found. A computational approach suggests that it can play an important role in echinocandin resistance. Given the emerging importance of this mechanism for clinical resistance in pathogenic fungi, it would be prudent to be alert to the potential evolution of this resistant mechanism in  Aspergillus  spp infecting patients under echinocandins therapeutics.

FKS1 mutation associated with decreased echinocandin susceptibility of Aspergillus fumigatus following anidulafungin exposure