Emergence of a Staphylococcus aureus Clone Resistant to Mupirocin and Fusidic Acid Carrying Exotoxin Genes and Causing Mainly Skin Infections

Abstract

Skin and soft tissue infections (SSTIs) caused by mupirocin-resistant <i>Staphylococcus aureus</i> strains have recently increased in number in our settings. We sought to evaluate the characteristics of these cases over a 43-month period. Data for all community-acquired staphylococcal infections caused by mupirocin-resistant strains were retrospectively reviewed. Genes encoding products producing high-level resistance (HLR) to mupirocin (<i>mupA</i>), fusidic acid resistance (<i>fusB</i>), resistance to macrolides and lincosamides (<i>ermC</i> and <i>ermA</i>), Panton-Valentine leukocidin (PVL) (<i>lukS/lukF</i>-PV), exfoliative toxins (<i>eta</i> and <i>etb</i>), and fibronectin binding protein A (<i>fnbA</i>) were investigated by PCRs in 102 selected preserved strains. Genotyping was performed by SCC<i>mec</i> and <i>agr</i> typing, whereas clonality was determined by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). A total of 437 cases among 2,137 staphylococcal infections were recorded in 2013 to 2016; they were all SSTIs with the exception of 1 case of primary bacteremia. Impetigo was the predominant clinical entity (371 cases [84.9%]), followed by staphylococcal scalded skin syndrome (21 cases [4.8%]), and there were no abscesses. The number of infections detected annually increased during the study years. All except 3 isolates were methicillin susceptible. The rates of HLR to mupirocin and constitutive resistance to clindamycin were 99% and 20.1%, respectively. Among the 102 tested strains, 100 (98%) were <i>mupA</i> positive and 97 (95%) were <i>fusB</i> positive, 26/27 clindamycin-resistant strains (96.3%) were <i>ermA</i> positive, 83 strains (81.4%) were <i>lukS/lukF</i> positive, 95 (93%) carried both <i>eta</i> and <i>etb</i> genes, and 99 (97%) were <i>fnbA</i> positive. Genotyping of methicillin-sensitive <i>S. aureus</i> (MSSA) strains revealed that 96/99 (96.7%) belonged to one main pulsotype, pulsotype 1, classified as sequence type 121 (ST121). The emergence of a single MSSA clone (ST121) causing impetigo was documented. Resistance to topical antimicrobials and a rich toxinogenic profile confer to this clone adaptability for spread in the community.