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Updated: Sep 2, 2026

Biosensor for Detection of Antibiotic Resistant Staphylococcus Bacteria
Published on: May 8, 2013
Detection and Genotypic Characterization of Clindamycin Resistance Among Staphylococcus aureus Clinical Isolates
Raechal Sanjana Hans1, Suchitra Shenoy M1
1Department of Microbiology, Kasturba Medical College Mangalore, Manipal Academy of Higher Education, Manipal, India, manipal.edu.
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.
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