Linezolid Resistance in SequentialStaphylococcus aureusIsolates Associated with a T2500A Mutation in the 23S rRNA Gene and Loss of a Single Copy of rRNA

ABSTRACT Pyrosequencing was used to detect rapidly and estimate the number of 23S rRNA genes with a G2576T mutation in 43 linezolid-resistant and -susceptible clinical isolates of enterococci. The method showed 100% concordance with PCR-restriction fragment length polymorphism for detecting isolates homozygous for either G2576 or T2576 or heterozygous for this mutation. A good correlation was found between linezolid MICs and the number of 23S rRNA gene copies carrying the mutation.

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Linezolid Resistance in Staphylococcus aureus: Gene Dosage Effect, Stability, Fitness Costs, and Cross-Resistances

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01098-07 ◽

2008 ◽

Vol 52 (4) ◽

pp. 1570-1572 ◽

Cited By ~ 88

Author(s):

Silke Besier ◽

Albrecht Ludwig ◽

Johannes Zander ◽

Volker Brade ◽

Thomas A. Wichelhaus

Keyword(s):

Staphylococcus Aureus ◽

Gene Dosage ◽

Single Point ◽

23S Rrna ◽

Cross Resistance ◽

Single Point Mutation ◽

Rrna Gene ◽

Gene Dosage Effect ◽

Linezolid Resistance ◽

23S Rrna Gene

ABSTRACT Linezolid resistance in Staphylococcus aureus is typically associated with mutations in the 23S rRNA gene. Here we show that the accumulation of a single point mutation, G2576T, in the different copies of this gene causes stepwise increases in resistance, impairment of the biological fitness, and cross-resistance to quinupristin-dalfopristin and chloramphenicol.

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Deletion of One 23S rRNA Gene (rrl) Copy Contributes to the Development of Linezolid Resistance in Staphylococcus warneri

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01139-18 ◽

2018 ◽

Vol 62 (11) ◽

Author(s):

Caroline Rouard ◽

Florence Doucet-Populaire ◽

Christelle Guillet-Caruba ◽

Millie Villet ◽

Nadège Bourgeois-Nicolaos

Keyword(s):

23S Rrna ◽

Rrna Gene ◽

Staphylococcus Warneri ◽

Linezolid Resistance ◽

23S Rrna Gene

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Linezolid resistance in Staphylococcus epidermidis associated with a G2603T mutation in the 23S rRNA gene

International Journal of Antimicrobial Agents ◽

10.1016/j.ijantimicag.2009.02.023 ◽

2009 ◽

Vol 34 (3) ◽

pp. 281-282 ◽

Cited By ~ 14

Author(s):

Nilton Lincopan ◽

Lara M. de Almeida ◽

Maria R. Elmor de Araújo ◽

Elsa M. Mamizuka

Keyword(s):

Staphylococcus Epidermidis ◽

23S Rrna ◽

Rrna Gene ◽

Linezolid Resistance ◽

23S Rrna Gene

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Investigation of Linezolid Resistance in Staphylococci and Enterococci

Journal of Clinical Microbiology ◽

10.1128/jcm.01929-15 ◽

2016 ◽

Vol 54 (5) ◽

pp. 1289-1294 ◽

Cited By ~ 8

Author(s):

Christopher D. Doern ◽

Jason Y. Park ◽

Michael Gallegos ◽

Debbie Alspaugh ◽

Carey-Ann D. Burnham

Keyword(s):

Susceptibility Testing ◽

Gene Sequencing ◽

Disk Diffusion ◽

23S Rrna ◽

Poor Correlation ◽

Rrna Gene ◽

Broth Microdilution ◽

Linezolid Resistance ◽

23S Rrna Gene ◽

Rrna Gene Sequencing

The objective of this study was to investigate an apparent increase in linezolid-nonsusceptible staphylococci and enterococci following a laboratory change in antimicrobial susceptibility testing from disk diffusion to an automated susceptibility testing system. Isolates with nonsusceptible results (n= 27) from Vitek2 were subjected to a battery of confirmatory testing which included disk diffusion, Microscan broth microdilution, Clinical and Laboratory Standards Institute (CLSI) reference broth microdilution, gradient diffusion (Etest), 23S rRNA gene sequencing, andcfrPCR. Our results show that there is poor correlation between methods and that only 70 to 75% of isolates were confirmed as linezolid resistant with alternative phenotypic testing methods (disk diffusion, Microscan broth microdilution, CLSI broth microdilution, and Etest). 23S rRNA gene sequencing identified mutations previously associated with linezolid resistance in 16 (59.3%) isolates, and thecfrgene was detected in 3 (11.1%) isolates. Mutations located at positions 2576 and 2534 of the 23S rRNA gene were most common. In addition, two previously undescribed variants (at positions 2083 and 2345 of the 23S rRNA gene) were also identified and may contribute to linezolid resistance.

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Molecular pathways to high-level azithromycin resistance in Neisseria gonorrhoeae

Journal of Antimicrobial Chemotherapy ◽

10.1093/jac/dkab084 ◽

2021 ◽

Cited By ~ 1

Author(s):

J G E Laumen ◽

S S Manoharan-Basil ◽

E Verhoeven ◽

S Abdellati ◽

I De Baetselier ◽

...

Keyword(s):

Neisseria Gonorrhoeae ◽

Ribosomal Proteins ◽

Efflux Pump ◽

23S Rrna ◽

Rrna Gene ◽

23S Rrna Gene ◽

Evolution Of Resistance ◽

High Level ◽

Azithromycin Resistance ◽

Level Resistance

Abstract Background The prevalence of azithromycin resistance in Neisseria gonorrhoeae is increasing in numerous populations worldwide. Objectives To characterize the genetic pathways leading to high-level azithromycin resistance. Methods A customized morbidostat was used to subject two N. gonorrhoeae reference strains (WHO-F and WHO-X) to dynamically sustained azithromycin pressure. We tracked stepwise evolution of resistance by whole genome sequencing. Results Within 26 days, all cultures evolved high-level azithromycin resistance. Typically, the first step towards resistance was found in transitory mutations in genes rplD, rplV and rpmH (encoding the ribosomal proteins L4, L22 and L34 respectively), followed by mutations in the MtrCDE-encoded efflux pump and the 23S rRNA gene. Low- to high-level resistance was associated with mutations in the ribosomal proteins and MtrCDE efflux pump. However, high-level resistance was consistently associated with mutations in the 23S ribosomal RNA, mainly the well-known A2059G and C2611T mutations, but also at position A2058G. Conclusions This study enabled us to track previously reported mutations and identify novel mutations in ribosomal proteins (L4, L22 and L34) that may play a role in the genesis of azithromycin resistance in N. gonorrhoeae.

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Molecular characterization of a ceftriaxone-resistant Neisseria gonorrhoeae strain found in Switzerland: a case report

Annals of Clinical Microbiology and Antimicrobials ◽

10.1186/s12941-021-00456-5 ◽

2021 ◽

Vol 20 (1) ◽

Author(s):

Konrad Egli ◽

Anna Roditscheff ◽

Ursula Flückiger ◽

Martin Risch ◽

Lorenz Risch ◽

...

Keyword(s):

Neisseria Gonorrhoeae ◽

23S Rrna ◽

Rrna Gene ◽

Limited Information ◽

Specific Pcr ◽

Appropriate Treatment ◽

23S Rrna Gene ◽

Allele Type ◽

Ciprofloxacin Resistance

Abstract Background The resistance of Neisseria gonorrhoeae to ceftriaxone is unusual in Switzerland. The underlying genotype responsible for resistance is suspected to be novel. Generally, resistance in Neisseria gonorrhoeae (Ng) involves a comprehensive set of genes with many different mutations leading to resistance to different β-lactams and fluoroquinolones. Case presentation A patient had a positive result from specific PCR for Ng. We routinely culture all clinical specimens with a positive NG-PCR. In this particular case, we isolated a strain with resistance to ceftriaxone in Switzerland. A total of seven different genes (penA, ponA, porinB, mtr, gyrA, parC, 23S rRNA gene) in this strain were partially sequenced for comparison with phenotypic susceptibility testing. Interestingly, two different mutations in the porinB gene were observed, and data on this gene are limited. Information on the identified allele type of the penA gene is very limited as well. Three different mutations of parC and gyrA that correlate with ciprofloxacin resistance were found. The combination of ceftriaxone and ciprofloxacin resistance makes an appropriate treatment difficult to obtain due to multidrug resistance. Conclusion The combined results for all genes show the appearance of new mutations in central Europe either due to worldwide spread or the emergence of new genetic combinations of mutations.

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Molecular Basis of Macrolide Resistance inCampylobacterStrains Isolated from Poultry in South Korea

BioMed Research International ◽

10.1155/2018/4526576 ◽

2018 ◽

Vol 2018 ◽

pp. 1-9 ◽

Cited By ~ 3

Author(s):

Bai Wei ◽

Min Kang

Keyword(s):

Molecular Mechanisms ◽

Macrolide Resistance ◽

23S Rrna ◽

Rrna Gene ◽

Campylobacter Coli ◽

Erythromycin Resistance ◽

23S Rrna Gene ◽

Ribosomal Protein L22 ◽

Resistant Strains ◽

Azithromycin Resistance

We investigated the molecular mechanisms underlying macrolide resistance in 38 strains ofCampylobacterisolated from poultry. Twenty-seven strains were resistant to azithromycin and erythromycin, five showed intermediate azithromycin resistance and erythromycin susceptibility, and six showed azithromycin resistance and erythromycin susceptibility. FourCampylobacter jejuniand sixCampylobacter colistrains had azithromycin MICs which were 8–16 and 2–8-fold greater than those of erythromycin, respectively. The A2075G mutation in the 23S rRNA gene was detected in 11 resistant strains with MICs ranging from 64 to ≥ 512μg/mL. Mutations including V137A, V137S, and a six-amino acid insertion (114-VAKKAP-115) in ribosomal protein L22 were detected in theC. jejunistrains. Erythromycin ribosome methylase B-erm(B) was not detected in any strain. All strains except three showed increased susceptibility to erythromycin with twofold to 256-fold MIC change in the presence of phenylalanine arginine ß-naphthylamide (PAßN); the effects of PAßN on azithromycin MICs were limited in comparison to those on erythromycin MICs, and 13 strains showed no azithromycin MIC change in the presence of PAßN. Differences between azithromycin and erythromycin resistance and macrolide resistance phenotypes and genotypes were observed even in highly resistant strains. Further studies are required to better understand macrolide resistance inCampylobacter.

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