Evidence map›Paper›PMID 21245447›Full record

ArticleAntimicrobial agents and chemotherapy2011

Cross-resistance to lincosamides, streptogramins A, and pleuromutilins due to the lsa(C) gene in Streptococcus agalactiae UCN70.

Brigitte Malbruny, Anja M Werno, David R Murdoch, Roland Leclercq, Vincent Cattoir

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Antimicrobial agents and chemotherapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Veterinary macrolides againstFrontiers in veterinary science · 2026
    Pooled it
  2. Comparative Genomic Analysis of Bovine and Publicly Available HumanAnimals : an open access journal from MDPI · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Antimicrobial Resistance ofMicroorganisms · 2024
    Article
  10. Review
  11. Article
  12. Article
  13. Microbial genomics · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Mobile Antimicrobial Resistance Genes in Probiotics.Antibiotics (Basel, Switzerland) · 2021
    Article
  18. Article
  19. Review
  20. Observational
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Brigitte MalbrunyService de Microbiologie and EA 2128, Relations Hôte et Microorganismes des Epithéliums, Hôpital Côte de Nacre, Université de Caen Basse-Normandie, Caen, France.
Anja M Werno
David R Murdoch
Roland Leclercq
Vincent Cattoir
Université de Caen Normandie · FRCanterbury Health Laboratories · NZUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Streptococcus agalactiae UCN70, isolated from a vaginal swab obtained in New Zealand, is resistant to lincosamides and streptogramins A (LS(A) phenotype) and also to tiamulin (a pleuromutilin). By whole-genome sequencing, we identified a 5,224-bp chromosomal extra-element that comprised a 1,479-bp open reading frame coding for an ABC protein (492 amino acids) 45% identical to Lsa(A), a protein related to intrinsic LS(A) resistance in Enterococcus faecalis. Expression of this novel gene, named lsa(C), in S. agalactiae BM132 after cloning led to an increase in MICs of lincomycin (0.06 to 4 μg/ml), clindamycin (0.03 to 2 μg/ml), dalfopristin (2 to >32 μg/ml), and tiamulin (0.12 to 32 μg/ml), whereas no change in MICs of erythromycin (0.06 μg/ml), azithromycin (0.03 μg/ml), spiramycin (0.25 μg/ml), telithromycin (0.03 μg/ml), and quinupristin (8 μg/ml) was observed. The phenotype was renamed the LS(A)P phenotype on the basis of cross-resistance to lincosamides, streptogramins A, and pleuromutilins. This gene was also identified in similar genetic environments in 17 other S. agalactiae clinical isolates from New Zealand exhibiting the same LS(A)P phenotype, whereas it was absent in susceptible S. agalactiae strains. Interestingly, this extra-element was bracketed by a 7-bp duplication of a target site (ATTAGAA), suggesting that this structure was likely a mobile genetic element. In conclusion, we identified a novel gene, lsa(C), responsible for the acquired LS(A)P resistance phenotype in S. agalactiae. Dissection of the biochemical basis of resistance, as well as demonstration of in vitro mobilization of lsa(C), remains to be performed.

Indexed as

Amino Acid SequenceAnti-Bacterial AgentsBacterial ProteinsDiterpenesDrug Resistance, Multiple, BacterialLincosamidesMicrobial Sensitivity TestsMolecular Sequence DataOpen Reading FramesPleuromutilinsPolycyclic CompoundsPolymerase Chain ReactionSequence Homology, Amino AcidStreptococcus agalactiaeStreptograminsAnti-Bacterial AgentsBacterial ProteinsDiterpenesLincosamidesPleuromutilinsPolycyclic CompoundsStreptogramins

Identifiers

PMID21245447
PMCPMC3067124
OpenAlexW2129410020

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.