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The strongest resistance of Staphylococcus aureus to erythromycin is caused by decreasing uptake of the antibiotic into the cells

Abstract

The consequence of excessive use of macrolides is a high occurrence of mechanisms responsible for resistance to these drugs. Of 97 erythromycin-resistant bacterial strains gathered in the Wrocław area in Poland, 60% exhibited very high resistance, and those with the inducible MLSB (macrolide-lincosamide-streptogramin B) resistance phenotype predominated. Direct genetic investigation revealed that the erm genes coding for ribosomal methylases are the most frequently occurring erythromycin resistance-determining genes. No genetic resistance determinant was detected in 13% of the erythromycin-resistant strains. The efflux mechanism occurs in strains isolated from the nasopharyngeal cavity twice as often as in those isolated from other material, where the mechanism connected with target site modification predominates. Measurements of radiolabelled antibiotic accumulation inside bacterial cells revealed that in highly resistant strains (MIC > 1024 μg/ml), an important factor responsible for the resistance is the permeability barrier at the cell wall level. This would be a hitherto unknown mechanism of resistance to erythromycin in Staphylococcus aureus.

Abbreviations

CCCP:

carbonyl cyanide m-chlorophenyl hydrazone

CPM:

counts of radioactive decay per minute

MIC:

minimum inhibitory concentration

MLSB CONST :

constitutive resistance to macrolides, lincosamides and streptogramin B

MLSB IND :

inducible resistance to macrolides, lincosamides and streptogramin B after induction by erythromycin

MS:

resistance to macrolides and streptogramin B

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Correspondence to Jerzy Piątkowski.

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Piątkowska, E., Piątkowski, J. & Przondo-Mordarska, A. The strongest resistance of Staphylococcus aureus to erythromycin is caused by decreasing uptake of the antibiotic into the cells. Cell Mol Biol Lett 17, 633–645 (2012). https://doi.org/10.2478/s11658-012-0034-3

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  • DOI: https://doi.org/10.2478/s11658-012-0034-3

Key words

  • Transmembrane transporters
  • Antibiotic efflux
  • Resistance to erythromycin
  • Drug accumulation
  • Staphylococcus aureus
  • Ribosomal methylases
  • ermA
  • ermC
  • msr(A)
  • MLSB