Relationship between the strength of biofilm production and the presence of pvl and mecA genes in Staphylococcus aureus isolated from skin and soft tissue infections

This research sought to investigate the association between the occurrence of the <i>pvl</i> and <i>mecA</i> genes and the strength of biofilm formation, as well as to assess the efficacy of vancomycin and ceftaroline against <i>Staphylococcus aureus</i> strains obtained from skin and soft tissue infections (SSTIs). A total of 134 <i>S. aureus</i> isolates were collected from SSTI patients and identified through standard microbiological techniques. Vancomycin and ceftaroline susceptibility testing were performed using the agar dilution and disc diffusion methods, respectively. PCR analysis was conducted to identify the <i>nuc</i>, <i>mecA</i>, and <i>pvl</i> genes. Biofilm production was measured using the tissue culture plate method. Methicillin-resistant <i>S. aureus</i> (MRSA) represented 58.2 % of the isolates. All isolates displayed biofilm-forming capability, with 10.4 % classified as high-grade biofilm producers, 85.7 % of which were positive for the <i>mecA</i> gene (<i>P</i> = 0.02). 16.4 % of the isolates had <i>pvl</i> gene and 59 % of PVL-positive strains identified as MRSA. Most of the low-grade biofilm producers had the <i>pvl</i> gene (P = 0.03). Vancomycin susceptibility was observed in 98.5 % of isolates, with an MIC₅₀ of 1 μg/mL in 51.4 % of cases. Among MRSA strains, 1.4 % exhibited intermediate resistance to vancomycin, with MICs between 4 and 8 μg/mL. No resistance to ceftaroline was found. The results demonstrate a significant association between biofilm production strength and the occurrence of the <i>mecA</i> and <i>pvl</i> genes; <i>mecA</i> correlated with increased biofilm production, while <i>pvl</i> was associated with lower biofilm levels. These findings offer valuable insights for future studies, suggesting that ceftaroline could be an effective alternative to vancomycin for treating MRSA-related SSTIs, particularly given the increasing resistance to vancomycin.