Prevalence of mecA Gene in Methicillin-resistant Staphylococcus aureus Strains Isolated at the National Public Health Laboratory of Brazzaville, Congo

Aims: The study aims to assess the prevalence of the mecA gene in Methicillin-resistant Staphylococcus aureus (MRSA) strains. Background: MRSA is currently a serious global public health problem, responsible for both nosocomial and community-acquired infections. This resistance is due to the acquisition of the mecA gene, carried by a mobile gene cassette. Methods: This study examined 120 Staphylococcus aureus isolates collected from urine samples, suppurations, and vaginal swabs between January and June 2021 at the the National Public Health Laboratory of Brazzaville's bacteriology department. The cefoxitin disk diffusion test was used to detect MRSA phenotypes, while PCR was used to amplify the mecA gene. Results: The results revealed that 54.2 % of the strains were resistant to cefoxitin, a phenotypic marker for MRSA. The interpretation of the antibiogram showed that these strains were also highly resistant to several other antibiotics, such as kanamycin (69.7%), tobramycin (65.2%), gentamicin (65.2%) and erythromycin (62.1%). Pristinamycin, rifampicin and lincomycin proved to be potential therapeutic alternatives because isolated-strains presented low resistance to these antibiotic molecules with respective rates of 4.6%, 13.7% and 15.2%. The PCR results showed that 47.0% of these isolated strains carried the mecA gene, revealing a discordance with the phenotypic detection. Conclusion: Although there is this discrepancy between the phenotypic and genotypic detection of MRSA, the high percentage of MRSA and the detection of the mecA gene could represent a serious public health concern that requires increased surveillance and refined diagnostic strategies. Therefore, the acquisition of the mecA gene, which confers resistance to methicillin, enables Staphylococcus aureus (MRSA) to persist and potentially facilitates the spread of MRSA epidemics through the accumulation of additional virulence factors.