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Cited by 263Antibiotic Resistance in BacteriaAntimicrobial Resistance in StaphylococcusBacterial Genetics and Biotechnology

An Enterococcus faecalis ABC Homologue (Lsa) Is Required for the Resistance of This Species to Clindamycin and Quinupristin-Dalfopristin

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Singh, Kavindra V., Weinstock, George M., Murray, Barbara E.·2002·Antimicrobial Agents and Chemotherapy
DOI 10.1128/aac.46.6.1845-1850.2002PMC PMC127256
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Abstract

Enterococcus faecalis isolates are resistant to clindamycin (CLI) and quinupristin-dalfopristin (Q-D), and this is thought to be a species characteristic. Disruption of a gene ( abc-23 , now designated lsa , for “lincosamide and streptogramin A resistance”) of E. faecalis was associated with a ≥40-fold decrease in MICs of Q-D (to 0.75 μg/ml), CLI (to 0.12 to 0.5 μg/ml), and dalfopristin (DAL) (to 4 to 8 μg/ml) for the wild-type E. faecalis parental strain (Q-D MIC, 32 μg/ml; CLI MIC, 32 to 48 μg/ml; DAL MIC, 512 μg/ml). Complementation of the disruption mutant with lsa on a shuttle plasmid resulted in restoration of the MICs of CLI, Q-D, and DAL to wild-type levels. Under high-stringency conditions, lsa was found in 180 of 180 isolates of E. faecalis but in none of 189 other enterococci. Among 19 erm (B)-lacking Enterococcus faecium strains, 9 (47%) were highly susceptible to CLI (MIC, 0.06 to 0.25 μg/ml) and had DAL MICs of 4 to 16 μg/ml; for the remaining erm (B)-lacking E. faecium strains, the CLI and DAL MICs were 4 to >256 and 2 to >128 μg/ml, respectively. In contrast, none of 32 erm (B)-lacking E. faecalis strains were susceptible (CLI MIC range, 16 to 32 μg/ml; DAL MIC range, ≥32 μg/ml). When lsa was introduced into an E. faecium strain initially susceptible to CLI, the MICs of CLI and DAL increased ≥60-fold and that of Q-D increased 6-fold (to 3 to 6 μg/ml). Introduction of lsa into two DAL-resistant (MICs, >128 μg/ml), Q-D-susceptible (MICs, 0.5 and 1.5 μg/ml) E. faecium strains (CLI MICs, 12 and >256 μg/ml) resulted in an increase in the Q-D MICs from 3- to 10-fold (to 8 and >32 μg/ml), respectively. Although efflux was not studied, the similarity (41 to 64%) of the predicted Lsa protein to ABC proteins such as Vga(A), Vga(B), and Msr(A) of Staphylococcus aureus and YjcA of Lactococcus lactis and the presence of Walker A and B ATP-binding motifs suggest that this resistance may be related to efflux of these antibiotics. In conclusion, lsa appears to be an intrinsic gene of E. faecalis that explains the characteristic resistance of this species to CLI and Q-D.

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  • Chromosomally encoded efflux pumps can explain the inherent resistance of some bacterial species to a particular antibiotic, such as E. faecalis intrinsic resistance to streptogramin A.

    “Importantly, chromosomally encoded pumps can explain the inherent resistance of some bacterial species to a particular antibiotic (e.g. E. faecalis intrinsic resistance to streptogramin A, see below) (45).”

    From Mechanisms of Antibiotic Resistance (2016) · cites this paper as [45]

  • Lsa is a predicted efflux pump encoded by the chromosomal gene lsa that is responsible for intrinsic resistance of E. faecalis to lincosamides and streptogramin A, the LSA phenotype.

    “Finally, another predicted efflux pump is Lsa (encoded by the chromosomal gene lsa), which is responsible for the intrinsic resistance of E. faecalis to lincosamides and streptogramin A (LSA phenotype) (44, 45).”

    From Mechanisms of Antibiotic Resistance (2016) · cites this paper as [45]

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  1. [42]Sambrook, J., E. F. Fritsch, and T. Maniatis. 1989. Molecular cloning: a laboratory manual, 2nd ed. Cold Spring Harbor Laboratory Press, Cold Spring Harbor, N.Y.
  2. [47]Wirth, R., F. An, and D. B. Clewell. 1987. Highly efficient cloning system for Streptococcus faecalis: protoplast transformation, shuttle vectors, and applications, p. 25-27. In J. J. Ferretti and R. Curtiss III (ed.), Streptococcal genetics. American Society for Microbiology, Washington, D.C.

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Authors
Singh, K. V., Weinstock, G. M., & Murray, B. E.
Affiliations
  • Center for the Study of Emerging and Reemerging Pathogens
  • Baylor College of Medicine (US)
  • The University of Texas Health Science Center at Houston (US)
Corresponding author
Murray, Barbara E.
ORCID
Venue
Antimicrobial Agents and Chemotherapy
Publisher
American Society for Microbiology
Published
2002-06
Volume
46
Issue
6
Pages
1845-1850
ISSN
  • 0066-4804 (ISSN-L)
  • 1098-6596
DOI
10.1128/aac.46.6.1845-1850.2002
PMC
PMC127256
OpenAlex
W1980535030
Cited by
263
References
45
Citations by year
2026: 11 · 2025: 9 · 2024: 16 · 2023: 17 · 2022: 19 · 2021: 15 · 2020: 15 · 2019: 7 · 2018: 10 · 2017: 6 · 2016: 16 · 2015: 9 · 2014: 10 · 2013: 10 · 2012: 4
FWCI
7.05
Type
journal article
Language
en
Open access
Licence
journals.asm.org/non-commercial-tdm-license (tdm)
Locations
  • Antimicrobial Agents and Chemotherapy (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • U.S. Public Health Service
  • National Institute of Allergy and Infectious Diseases (R37AI047923, AI 47923, R01AI047923)
  • Division of Microbiology and Infectious Diseases, National Institute of Allergy and Infectious Diseases
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
  • Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
Keywords
Enterococcus faecalis, ABC transporters, clindamycin resistance, quinupristin-dalfopristin resistance, Enterococcus faecium, ermB gene, antibiotic resistance genes
MeSH terms
Amino Acid Sequence, Anti-Bacterial Agents, Clindamycin, DNA, Bacterial, Drug Resistance, Drug Therapy, Combination, Genes, Bacterial, Genetic Complementation Test, Microbial Sensitivity Tests, Molecular Sequence Data, Enterococcus faecalis, Virginiamycin, Reverse Transcriptase Polymerase Chain Reaction

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