GENOTYPIC CHARACTERISATION OF MLS (MACROLIDE–LINCOSAMIDE–STREPTOGRAMIN B) RESISTANCE IN CLINICAL ISOLATES OF STAPHYLOCOCCUS AUREUS
Main Article Content
Keywords
Staphylococcus aureus, MLSB resistance, ermA, ermC, inducible clindamycin resistance, PCR.
Abstract
Background:
Resistance to macrolide–lincosamide–streptogramin B (MLSB) antibiotics in Staphylococcus aureus is primarily mediated by erm genes encoding rRNA methyltransferases. Among these, ermA and ermC are the major determinants conferring inducible or constitutive resistance. Phenotypic identification of inducible clindamycin resistance using D-test has clinical relevance, but genotypic detection provides confirmatory insights into resistance mechanisms.
Methods:
A cross-sectional study was conducted at Index Medical College Hospital & Research Centre (IMCHRC), Indore (2021–2024). A total of 250 S. aureus isolates from various clinical specimens were processed. Phenotypic detection of MLSB resistance was performed using D-test and VITEK-2 system. Genotypic characterization for ermA and ermC genes was carried out using PCR.
Results:
Among 250 isolates, 59 % were MRSA and 41 % MSSA. iMLSB phenotype was observed in 26 % MRSA and 11 % MSSA isolates, while cMLSB was seen in 40 % MRSA and 11 % MSSA. ermC was the predominant gene, followed by ermA. D-test sensitivity and specificity were 57.6 % and 100 %, respectively, compared to VITEK-2.
Conclusion:
The predominance of ermC among iMLSB isolates suggests plasmid-mediated dissemination. Routine molecular surveillance of erm genes is essential to prevent clindamycin treatment failure and guide antibiotic stewardship.
References
2. Chambers HF, Deleo FR. Waves of resistance: S. aureus in the antibiotic era. Nat Rev Microbiol. 2009;7(9):629–41.
3. Daurel C, et al. Inducible MLSB resistance in S. aureus. J Clin Microbiol. 2008;46(2):547–9.
4. Leclercq R. Mechanisms of resistance to macrolides and lincosamides. Int J Antimicrob Agents. 2002;19(1):1–7.
5. Roberts MC. Update on acquired macrolide–lincosamide–streptogramin resistance. Front Microbiol. 2019;10:1502.
6. Kuroda M, et al. Whole genome sequencing of MRSA. Lancet. 2001;357(9264):1225–40.
7. CLSI. Performance Standards for Antimicrobial Susceptibility Testing. 34th ed. Wayne, PA: CLSI; 2024.
8. Fiebelkorn KR et al. D-test for inducible clindamycin resistance. J Clin Microbiol. 2003;41(12):4740–4.
9. Baron EJ, et al. Manual of Clinical Microbiology. 11th ed. ASM Press; 2022.
10. Magiorakos AP, et al. Multidrug resistance definitions. Clin Microbiol Infect. 2012;18(3):268–81.
11. Regha V, et al. Inducible clindamycin resistance in South India. J Lab Physicians. 2021;13(2):112–7.
12. Filipin M, et al. Evaluation of VITEK-2 for MLS resistance. J Clin Microbiol. 2014;52(12):4404–8.
13. Timsina B, et al. PCR detection of erm genes. BMC Microbiol. 2018;18(1):199.
14. Hori S, et al. ermA and ermC prevalence in MRSA. Microb Drug Resist. 2017;23(3):305–12.
15. Goudarzi M, et al. Prevalence and genetic diversity of iMLSB Staphylococcus aureus in Iran. Front Microbiol. 2019;10:940.
16. Chopra I, Roberts M. Mechanisms of antibiotic resistance. Microbiol Mol Biol Rev. 2001;65(2):232–60.
17. Baral R, et al. iMLSB phenotypes among MRSA isolates. J Nepal Health Res Counc. 2017;15(2):117–21.
18. Adhikari R, et al. MLSB phenotypes in S. aureus. Indian J Med Microbiol. 2018;36(3):396–400.
19. Alekshun MN, Levy SB. Molecular basis of multidrug resistance. Cell. 2007;128(6):1037–50.
20. Sasirekha B, et al. Incidence of iMLSB resistance among S. aureus. Indian J Pathol Microbiol. 2012;55(4):478–82.
21. Yadav R, et al. Correlation of erm genes and iMLSB resistance. Indian J Med Res. 2023;157(5):432–9.
22. Memariani H, et al. Global meta-analysis of MLSB resistance. Infect Drug Resist. 2021;14:1357–69.
23. Tiwari A, Malviya S. Genotypic–phenotypic correlation in MRSA. J Glob Antimicrob Resist. 2024;42:51–9.
24. Loeffelholz M, et al. Performance of VITEK-2 for iMLSB detection. Diagn Microbiol Infect Dis. 2022;103(3):1155–60.
25. WHO. Global Antimicrobial Resistance and Use Surveillance Report 2025. Geneva: WHO; 2025.