Background: CA-MRSA has emerged as a leading cause of skin and soft tissue infections worldwide. Recently, a novel variant of the USA300 CA-MRSA strain (MRSA-ST8-IV) was documented in the Northern region of South America. Here, we aimed to evaluate the antimicrobial resistance mechanisms in South American CA-MRSA isolates.
Methods: The presence of the following genes was determined in a total of 174 CA-MRSA belonging to the USA300-variant clone: ermA, ermB, ermC, msrA (in 18 erythromycin-resistant isolates), tetK and tetM (in 74 tetracycline-resistant isolates), aac(6')/aph(2") (in 2 gentamicin-resistant isolates) and cfr (in 2 chloramphenicol-resistant isolates). Additionally, the D-test and population analysis profile (PAP-AUC) were performed in all erythromycin-resistant isolates and one CA-MRSA that had previously exhibited the vancomycin-intermediate (VISA) phenotype, respectively.
Results: The tetK gene was identified in all tetracycline-resistant CA-MRSA isolates from South-America belonging to the USA300-variant clone (all had been previously shown to be susceptible to minocycline). Among the macrolide-resistant isolates, the majority (8) exhibited the macrolide resistant (M) phenotype; the ermC and msrA were detected in 10 and 8 isolates, respectively. Both gentamicin-resistant CA-MRSA harbored the aac(6')/aph(2") gene and none of the chloramphenicol-resistant isolates had cfr. The CA-MRSA was did not exhibit the VISA phenotype by the PAP-AUC analysis (ratio ≤ 0.9).
Conclusion: The tetK gene is frequently present in resistant isolates belonging to the South American USA300, but minocycline retain activity against all tetK-harboring isolates. Due to the common presence of ermC, clindamycin may not be used to treat CA-MRSA severe infections with isolates reported as macrolide-resistant.