Detection of erythromycin-resistant determinants by PCR

Sutcliffe, Joyce A.; Grebe, Thorsten; Tait-Kamradt, Amelia; Wondrack, L

doi:10.1128/aac.40.11.2562

Cited by 891 publications

(368 citation statements)

References 51 publications

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“…We used a PCR technique derived from that described by Sutcliffe et al [11], which allowed amplification of the major erm genes and efflux genes found in streptococci, enterococci and staphylococci. This technique was modified to include the detection of a new ermTR gene recently described in b-hemolytic streptococci [12].…”

Section: Methodsmentioning

confidence: 99%

Macrolide Resistance Phenotypes and Genotypes in French Clinical Isolates of Streptococcus pneumoniae

Angot

Vergnaud

Auzou

et al. 2000

EJCMID

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The aim of this study was to analyze the mechanisms of macrolide resistance in French clinical isolates of Streptococcus pneumoniae. A total of 838 strains of pneumococci were isolated in 1997 in Normandy, a region of western France, by 19 microbiology laboratories. Fifty-three percent had displayed diminished susceptibility to penicillin G and 50% were resistant to erythromycin. From this collection, 92 penicillin-intermediate or -resistant and 18 penicillin-susceptible strains resistant to erythromycin were studied. The presence of erm genes coding for ribosomal methylases and of mefE-like genes responsible for macrolide efflux was screened by a multiplex polymerase chain reaction and confirmed by DNA/DNA hybridization. Of the 110 strains studied, 108 were cross-resistant to erythromycin, spiramycin and clindamycin, including 105 strains containing ermB-related genes and three strains that contained a combination of ermB-and mefE-related genes. Two strains apparently susceptible to clindamycin but resistant to spiramycin also contained ermBrelated genes. No strain was resistant to erythromycin alone or contained only a mef-like gene. Therefore, resistance to erythromycin is mostly related to ribosomal methylation in this region of France.

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Section: Methodsmentioning

confidence: 99%

Macrolide Resistance Phenotypes and Genotypes in French Clinical Isolates of Streptococcus pneumoniae

Angot

Vergnaud

Auzou

et al. 2000

EJCMID

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“…The samples were then centrifuged at 14,000 rpm for 5 min and the supernatant was used as target DNA. Specific ermA, ermB, ermC, ermTR and mefA gene sequences that were used to investigate resistance genes are listed in Table 1 [4]. A 25 ll polymerase chain reaction (PCR) mixture containing 2.5 ll Taq buffer, 1U Taq polymerase, 0.2 mM dNTP mix, 2 mM MgCl 2 , 0.4 pmol primers and 5 ll DNA was prepared for each strain.…”

Section: Macrolide Resistance Phenotypes and Macrolide Resistance Genesmentioning

confidence: 99%

“…The ermB gene is located on conjugative transposon Tn1545 together with other resistance genes such as the tetracycline resistance gene (tetM) [1,3]. Efflux system-mediated resistance results in the M phenotype (14-, 15-membered macrolide resistant, lincosamide sensitive), and the mefA gene is responsible for this resistance [1,4]. Another rare macrolide resistance mechanism of S. pneumoniae is associated with the changes resulting from mutations in domains V and II and ribosomal proteins L4 and L22 of 23S rRNA, which plays a key role in the binding of macrolides [5,6].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of resistance mechanisms and serotype and genotype distributions of macrolide-resistant strains in clinical isolates of Streptococcus pneumonia in Aydın, Turkey

Telli

Eyigör

Gültekin

et al. 2011

Journal of Infection and Chemotherapy

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“…The ribosomes of E. coli K12 strain expressing mefA display no evidence of methylated 23S rRNA and are more sensitive to macrolides that macrolide-susceptible strains [123], confirming a novel gene unrelated to erm genes [120]. Erythromycin inactivation and msrA-encoded efflux have been ruled out as potential candidates for the M-R phenotype seen in streptococci [123].…”

Section: Macrolidesmentioning

confidence: 91%

“…Erythromycin inactivation and msrA-encoded efflux have been ruled out as potential candidates for the M-R phenotype seen in streptococci [123]. Moreover, discernible regions of MefA show no homology to the Walker motifs A and B which characterize ABC transporters.…”

Section: Macrolidesmentioning

confidence: 99%

Molecular Mechanisms of Antibiotic Resistance: The Need for Novel Antimicrobial Therapies

Dale‐Skinner

Bonev

2008

New Strategies Combating Bacterial Infection

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Despite the enormous success of antibiotics as chemotherapeutic agents, infectious diseases remain a leading cause of mortality worldwide. Bacteria coevolving with infectious microorganisms have been driven to develop protection against environmental bioactive chemicals, and to resist their own antibiotics and defense compounds. Such resistance in pathogenic microorganisms provides protection against chemotherapeutic intervention and can lead to infections that are notoriously difficult to manage. Here, we introduce briefly the molecular mechanisms of action for common antibiotic classes and the structural determinants of bacterial resistance to antibiotics. Bacterial resistance to antibiotics interfering with cell wall biosynthesis is discussed with examples from b-lactams and glycopeptides. The molecular determinants of bacterial tolerance to protein biosynthesis inhibitors are analyzed with examples from aminoglycosides, marcolides and tetracyclines. Fluoroquinolone tolerance is described in connection with DNA regulation in the presence of inhibitors. The action of b-lactam and glycopeptides antibiotics, which target cell wall biosynthesis, is evaded through target modifications and antibiotic deactivation. bLactamases can be deployed to deactivate b-lactam antibiotics, while penicillinbinding proteins with altered binding sites provide an example of modification of the antibiotic target. Alteration of peptidoglycan peptide termini helps protect cell wall synthesis from glycopeptides, while reduced cross-linking and thickened cell wall obstruct glycopeptides access at the cell wall periphery. Specific molecular changes within ribosomal structures can foil aminoglycoside, tetracycline or macrolide attack. Further protection can be achieved by positioning proteins to protect protein synthesizing machinery from the action of tetracyclines. Important resistance mechanisms protecting bacterial protein synthesis include enzymatic deactivation of aminoglycosides and efflux systems expelling incoming macrolides, aminoglycosides and tetracyclines. Renewed efforts to explore alternative strategies for infection management have brought to the top of scientific agenda defense peptides, lanthionine antibiotics, phage therapies and other antimicrobial techniNew Strategies Combating Bacterial Infection. Edited by Iqbal Ahmad and Farrukh Aqil

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Detection of erythromycin-resistant determinants by PCR

Cited by 891 publications

References 51 publications

Macrolide Resistance Phenotypes and Genotypes in French Clinical Isolates of Streptococcus pneumoniae

Macrolide Resistance Phenotypes and Genotypes in French Clinical Isolates of Streptococcus pneumoniae

Evaluation of resistance mechanisms and serotype and genotype distributions of macrolide-resistant strains in clinical isolates of Streptococcus pneumonia in Aydın, Turkey

Molecular Mechanisms of Antibiotic Resistance: The Need for Novel Antimicrobial Therapies

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