scholarly journals Heterogeneous Macrolide Resistance and Gene Conversion in the Pneumococcus

2006 ◽  
Vol 50 (1) ◽  
pp. 359-361 ◽  
Author(s):  
Nicole Wolter ◽  
Anthony M. Smith ◽  
David J. Farrell ◽  
Keith P. Klugman

ABSTRACT A macrolide-resistant clinical isolate of Streptococcus pneumoniae with 23S rRNA mutations showed a heterogeneous phenotype and genotype. The mutant 23S rRNA genes from this isolate transformed susceptible strain R6 to resistance. Culture of resistant strain R6 in the absence of antibiotic pressure showed gene conversion to occur between the four 23S rRNA alleles, resulting in reversion to susceptibility with the resistant phenotype showing a fitness cost. These data explain the disappearance on subculture of heterogeneous macrolide resistance in the pneumococcus.

2007 ◽  
Vol 30 (4) ◽  
pp. 341-344 ◽  
Author(s):  
Ana-Belén Flórez ◽  
Víctor Ladero ◽  
Pablo Álvarez-Martín ◽  
Mohammed-Salim Ammor ◽  
Miguel-Ángel Álvarez ◽  
...  

2004 ◽  
Vol 48 (3) ◽  
pp. 1021-1023 ◽  
Author(s):  
B. Helen Jost ◽  
Hien T. Trinh ◽  
J. Glenn Songer ◽  
Stephen J. Billington

ABSTRACT Four macrolide-resistant Arcanobacterium pyogenes isolates contained A2058T, A2058G, or C2611G (Escherichia coli numbering) mutations in their 23S rRNA genes. While these mutations conferred resistance to erythromycin, oleandomycin, and spiramycin, they did not confer resistance to tylosin.


2020 ◽  
Vol 9 (6) ◽  
pp. 1930
Author(s):  
Eun Jeong Gong ◽  
Ji Yong Ahn ◽  
Jung Mogg Kim ◽  
Sun Mi Lee ◽  
Hee Kyong Na ◽  
...  

Background: The increasing prevalence of antimicrobial resistance, together with the lack of novel treatment options, negatively affects successful eradication of Helicobacter pylori. The aim of this study was to investigate genetic mutations in the 23S rRNA genes, which is associated with clarithromycin resistance, and to determine the clinical impact of genotype on phenotypic antimicrobial resistance. Methods: A total of 46 H. pylori strains were obtained from 13 patients, before and after unsuccessful eradication with clarithromycin-based triple therapy. The phenotypic resistance of each H. pylori strain was determined by minimum inhibitory concentration against clarithromycin using the serial two-fold agar dilution method. The genomic sequences of 23S rRNA genes were identified through next-generation sequencing, and nucleotide variants were determined based on comparison with genome sequences of the reference strain H. pylori 26695. Results: Clarithromycin resistance was found in 9 of 13 subjects before treatment and all subjects after unsuccessful eradication. Whole-genome sequencing of the 23S rRNA genes detected 42 mutations on 40 nonidentical loci, including 2147A>G (formerly 2143A>G) and 2146A>G (formerly 2142A>G). All strains with clarithromycin-resistant phenotype had either 2147A>G or 2146A>G mutation. When comparing genotype and phenotype for clarithromycin resistance, there was a significant association between 2147A>G mutation and clarithromycin-resistant phenotype. Conclusions: All clarithromycin-resistant strains had either 2146A>G or 2147A>G mutation, suggesting that tests targeting these two mutations may be enough for the prediction of clarithromycin resistance in this population.


2009 ◽  
Vol 49 (4) ◽  
pp. 386-394 ◽  
Author(s):  
Akihiro Tazumi ◽  
Yuki Kakinuma ◽  
John E. Moore ◽  
Cherie B. Millar ◽  
Ikue Taneike ◽  
...  

1982 ◽  
Vol 10 (5) ◽  
pp. 1607-1624 ◽  
Author(s):  
Kate Loughney ◽  
Elsebet Lund ◽  
James E. Dahlberg

1997 ◽  
Vol 41 (12) ◽  
pp. 2724-2728 ◽  
Author(s):  
A Occhialini ◽  
M Urdaci ◽  
F Doucet-Populaire ◽  
C M Bébéar ◽  
H Lamouliatte ◽  
...  

Resistance of Helicobacter pylori to macrolides is a major cause of failure of eradication therapies. Single base substitutions in the H. pylori 23S rRNA genes have been associated with macrolide resistance in the United States. Our goal was to extend this work to European strains, to determine the consequence of this mutation on erythromycin binding to H. pylori ribosomes, and to find a quick method to detect the mutation. Seven pairs of H. pylori strains were used, the parent strain being naturally susceptible to macrolides and the second strain having acquired an in vivo resistance during a treatment regimen that included clarithromycin. The identity of the strains was confirmed by random amplified polymorphic DNA testing with two different primers, indicating that resistance was the result of the selection of variants of the infecting strain. All resistant strains were found to have point mutations at position 2143 (three cases) or 2144 (four cases) but never on the opposite DNA fragment of domain V of the 23S rRNA gene. The mutation was A-->G in all cases except one (A-->C) at position 2143. Using BsaI and BbsI restriction enzymes on the amplified products, we confirmed the mutations of A-->G at positions 2144 and 2143, respectively. Macrolide binding was tested on purified ribosomes isolated from four pairs of strains with [14C]erythromycin. Erythromycin binding increased in a dose-dependent manner for the susceptible strain but not for the resistant one. In conclusion we suggest that the limited disruption of the peptidyltransferase loop conformation, caused by a point mutation, reduces drug binding and consequently confers resistance to macrolides. Finally, the macrolide resistance could be detected without sequencing by performing restriction fragment length polymorphism with appropriate restriction enzymes.


2005 ◽  
Vol 102 (14) ◽  
pp. 5180-5185 ◽  
Author(s):  
P. Pfister ◽  
N. Corti ◽  
S. Hobbie ◽  
C. Bruell ◽  
R. Zarivach ◽  
...  

2001 ◽  
Vol 183 (14) ◽  
pp. 4382-4385 ◽  
Author(s):  
Steven T. Gregory ◽  
Jamie H. D. Cate ◽  
Albert E. Dahlberg

ABSTRACT Spontaneous, erythromycin-resistant mutants of Thermus thermophilus IB-21 were isolated and found to carry the mutation A2058G in one of two 23S rRNA operons. The heterozygosity of these mutants indicates that A2058G confers a dominant or codominant phenotype in this organism. This mutation provides a valuable tool for the genetic manipulation of the 23S rRNA genes ofThermus.


2011 ◽  
Vol 34 (6) ◽  
pp. 462-469 ◽  
Author(s):  
Pelin Yilmaz ◽  
Renzo Kottmann ◽  
Elmar Pruesse ◽  
Christian Quast ◽  
Frank Oliver Glöckner

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