Antimicrobial Resistance in<I> Brachyspira pilosicoli</I> with Special Reference to Point Mutations in the 23S rRNA Gene Associated with Macrolide and Lincosamide Resistance

Abstract Background Neisseria gonorrhoeae (NG) isolates with high-level azithromycin resistance (HL-AziR) have emerged worldwide in recent decades, threatening the sustainability of current dual-antimicrobial therapy. Objectives This study aimed to characterize the first 16 NG isolates with HL-AziR in Barcelona between 2016 and 2018. Methods WGS was used to identify the mechanisms of antimicrobial resistance, to establish the MLST ST, NG multiantigen sequence typing (NG-MAST) ST and NG sequence typing for antimicrobial resistance (NG-STAR) ST and to identify the clonal relatedness of the isolates with other closely related NG previously described in other countries based on a whole-genome SNP analysis approach. The sociodemographic characteristics of the patients included in the study were collected by comprehensive review of their medical records. Results Twelve out of 16 HL-AziR isolates belonged to the MLST ST7823/NG-MAST ST5309 genotype and 4 to MLST ST9363/NG-MAST ST3935. All presented the A2059G mutation in all four alleles of the 23S rRNA gene. MLST ST7823/NG-MAST ST5309 isolates were only identified in men who have sex with women and MLST ST9363/NG-MAST ST3935 were found in MSM. Phylogenomic analysis revealed the presence of three transmission clusters of three different NG strains independently associated with sexual behaviour. Conclusions Our findings support the first appearance of three mild outbreaks of NG with HL-AziR in Spain. These results highlight the continuous capacity of NG to develop antimicrobial resistance and spread among sexual networks. The enhanced resolution of WGS provides valuable information for outbreak investigation, complementing the implementation of public health measures focused on the prevention and dissemination of MDR NG.

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Minimal inhibitory concentration (MIC) values and different point mutations in the 23S rRNA gene for clarithromycin resistance in Helicobacter pylori

Digestive and Liver Disease ◽

10.1016/j.dld.2009.01.001 ◽

2009 ◽

Vol 41 (8) ◽

pp. 610-611 ◽

Cited By ~ 15

Author(s):

Vincenzo De Francesco ◽

Angelo Zullo ◽

Enzo Ierardi ◽

Dino Vaira

Keyword(s):

Helicobacter Pylori ◽

Minimal Inhibitory Concentration ◽

Inhibitory Concentration ◽

Point Mutations ◽

23S Rrna ◽

Rrna Gene ◽

Clarithromycin Resistance ◽

23S Rrna Gene

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Point mutations in the 23S rRNA gene of Helicobacter pylori associated with different levels of clarithromycin resistance

Journal of Antimicrobial Chemotherapy ◽

10.1093/jac/40.2.283 ◽

1997 ◽

Vol 40 (2) ◽

pp. 283-286 ◽

Cited By ~ 124

Author(s):

J Versalovic

Keyword(s):

Helicobacter Pylori ◽

Point Mutations ◽

23S Rrna ◽

Rrna Gene ◽

Clarithromycin Resistance ◽

23S Rrna Gene ◽

Different Levels

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Two New Point Mutations at A2062 Associated with Resistance to 16-Membered Macrolide Antibiotics in Mutant Strains ofMycoplasma hominis

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.45.10.2958-2960.2001 ◽

2001 ◽

Vol 45 (10) ◽

pp. 2958-2960 ◽

Cited By ~ 26

Author(s):

Pio Maria Furneri ◽

Giancarlo Rappazzo ◽

Maria Pia Musumarra ◽

Patrizia Di Pietro ◽

Lucrezia S. Catania ◽

...

Keyword(s):

Escherichia Coli ◽

Point Mutations ◽

Mycoplasma Hominis ◽

23S Rrna ◽

Macrolide Antibiotics ◽

Rrna Gene ◽

In Vitro Exposure ◽

Mutant Strains ◽

23S Rrna Gene

ABSTRACT We describe two mutants of Mycoplasma hominis PG-21 which show resistance to 16-membered macrolides but susceptibility to lincosamides, obtained by in vitro exposure to increasing doses of josamycin. The 23S rRNA gene showed that each had a mutation (A2062G and A2062T) corresponding to nucleotide 2062 in Escherichia coli, which was associated with the acquired phenotype.

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Rapid Detection, by PCR and Reverse Hybridization, of Mutations in the Helicobacter pylori 23S rRNA Gene, Associated with Macrolide Resistance

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.43.7.1779 ◽

1999 ◽

Vol 43 (7) ◽

pp. 1779-1782 ◽

Cited By ~ 51

Author(s):

Leen-Jan van Doorn ◽

Yvette J. Debets-Ossenkopp ◽

Armelle Marais ◽

Ricardo Sanna ◽

Francis Mégraud ◽

...

Keyword(s):

Helicobacter Pylori ◽

Fragment Length Polymorphism ◽

Simultaneous Detection ◽

Point Mutations ◽

Macrolide Resistance ◽

23S Rrna ◽

Rrna Gene ◽

Reverse Hybridization ◽

23S Rrna Gene ◽

H Pylori

ABSTRACT A PCR-based reverse hybridization system (research prototype kit INNO-LiPA for H. pylori resistance) was developed and evaluated for simultaneous detection of 23S ribosomal DNA point mutations, associated with macrolide resistance in Helicobacter pylori. Fifty-seven H. pylori strains (51 natural, 6 laboratory-derived artificial, 52 resistant, and 5 susceptible strains) were tested by PCR-LiPA (detecting mutations A2115→G, G2141→A, A2142→G, A2142→C, A2143→G, A2143→C, and A2143→T), DNA sequencing, restriction fragment length polymorphism, and/or hybridization to oligonucleotide probes. Results were highly concordant, but PCR-LiPA appears to be more sensitive for the simultaneous detection of multiple mutants.

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Atypical Mutation in Neisseria gonorrhoeae 23S rRNA Associated with High-Level Azithromycin Resistance.

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00885-20 ◽

2020 ◽

Author(s):

Cau D. Pham ◽

Evelyn Nash ◽

Hsi Liu ◽

Matthew W. Schmerer ◽

Samera Sharpe ◽

...

Keyword(s):

Antimicrobial Resistance ◽

Genetic Analysis ◽

Neisseria Gonorrhoeae ◽

23S Rrna ◽

Rrna Gene ◽

Neisseria Gonorrhoea ◽

23S Rrna Gene ◽

High Level ◽

Azithromycin Resistance

A2059G mutation in the 23S rRNA gene is the only reported mechanism conferring high-level azithromycin resistance (HL-AZMR) in Neisseria gonorrhoea. Through U.S. gonococcal antimicrobial resistance surveillance projects, we identified four HL-AZMR gonococcal isolates lacking this mutational genotype. Genetic analysis revealed an A2058G mutation of 23S rRNA alleles in all four isolates. In vitro selected gonococcal strains with homozygous A2058G recapitulated the HL-AZMR phenotype. Taken together, we postulate that A2058G mutation confers HL-AZMR in N. gonorrhoeae.

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PCR-Based Rapid Identification System Using Bridged Nucleic Acids for Detection of Clarithromycin-Resistant Mycobacterium avium-M. intracellulare Complex Isolates

Journal of Clinical Microbiology ◽

10.1128/jcm.02954-15 ◽

2016 ◽

Vol 54 (3) ◽

pp. 699-704 ◽

Cited By ~ 3

Author(s):

Takashi Hirama ◽

Ayako Shiono ◽

Hiroshi Egashira ◽

Etsuko Kishi ◽

Koichi Hagiwara ◽

...

Keyword(s):

Mycobacterium Avium ◽

Detection System ◽

Point Mutations ◽

23S Rrna ◽

Clinical Samples ◽

Identification System ◽

Rrna Gene ◽

Clarithromycin Resistance ◽

23S Rrna Gene ◽

Resistant Mutants

The nontuberculous mycobacteria (NTM) cause miscellaneous disorders in humans, especially in the lungs, which present with a variety of radiological features. To date, knowledge of the pathogenic role of theMycobacterium avium-intracellularecomplex (MAC) in the human lung and the definitive criteria for initiating multidrug therapy are still lacking. However, there is little doubt that clarithromycin is the most efficacious drug among the various treatment regimens for lung NTM. In this study, with the use of a bridged nucleic acid (BNA) probe a detection system based on a real-time PCR (BNA-PCR) for the identification of the point mutations at position 2058 or 2059 in domain V of the 23S rRNA gene responsible for clarithromycin resistance was developed and has been assessed using MAC isolates from clinical samples. Out of 199 respiratory specimens, the drug susceptibility test demonstrated 12 strains resistant to clarithromycin, while the BNA-PCR showed 8 strains carrying the point mutation at position 2058 or 2059 of the 23S rRNA gene. This system revealed that there were mycobacterial strains resistant to clarithromycin which do not carry previously identified resistance genes. This paper documents a novel system for detecting clarithromycin-resistant strains and demonstrates that although these mutations are tacitly assumed to account for >90% of the reported resistant mutants, there is a significant fraction of resistant mutants that do not harbor these mutations. Therefore, unknown mechanisms affecting clarithromycin resistance remain to be elucidated.

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