Raechal Sanjana Hans, Suchitra Shenoy M
ermC-mediated MLSB resistance was present in 30.5% of isolates, with cMLSB (23.2%) being more common than iMLSB (12.0%). Routine D-testing is essential to avoid clinical failure when using clindamycin for erythromycin-resistant, clindamycin-susceptible S. aureus. Also, 8 isolates were clindamycin resistant and susceptible to erythromycin, showcasing the diversity of the resistance profile of S. aureus toward MLSB.
PURPOSE: Resistance to macrolide, lincosamide, and streptogramin B (MLSB) antibiotics in Staphylococcus aureus has emerged as a significant therapeutic challenge. erm gene-encoded ribosomal methylation is expressed either constitutively or inducibly, causing resistance to erythromycin and clindamycin with possible induction of clindamycin resistance during therapy. msrA-mediated active drug efflux confers resistance to macrolides and streptogramin B while preserving clindamycin susceptibility. This study aimed to determine the antimicrobial susceptibility pattern of S. aureus isolates and correlate between the phenotypic and genotypic patterns of clindamycin resistance.
METHODS: This cross-sectional study was conducted from October 2022 to September 2023 at a tertiary care hospital laboratory. A total of 233 clinical isolates of S. aureus were included from exudate, blood, and bodily fluids. Antimicrobial susceptibility testing was performed using the Vitek 2 Compact system and interpreted according to CLSI 2022 and 2023 guidelines. Inducible clindamycin resistance was detected using the D-test. Multiplex and uniplex PCR assays were performed for the detection of ermA, ermB, ermC, and msrA genes.
RESULTS: Among 233 S. aureus isolates, methicillin resistance was identified in 45.9% (107/233) isolates. The prevalence of constitutive MLSB (cMLSB), inducible MLSB (iMLSB), and MS phenotypes was 23.17%, 12.01%, and 10.3%, respectively. Overall clindamycin resistance was observed in 38.6% (90/233; 95% CI: 32.6%-45.0%). The ermC gene was detected in 30.47% (71/233) isolates, while msrA was identified in 9.44% (22/233), including 91.7% of isolates of the MS phenotype. Neither ermA nor ermB genes were detected. All isolates were susceptible to vancomycin, daptomycin, and tigecycline.
CONCLUSION: ermC-mediated MLSB resistance was present in 30.5% of isolates, with cMLSB (23.2%) being more common than iMLSB (12.0%). Routine D-testing is essential to avoid clinical failure when using clindamycin for erythromycin-resistant, clindamycin-susceptible S. aureus. Also, 8 isolates were clindamycin resistant and susceptible to erythromycin, showcasing the diversity of the resistance profile of S. aureus toward MLSB.