Open Access

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

  • Elżbieta Piątkowska1,
  • Jerzy Piątkowski2, 3Email author and
  • Anna Przondo-Mordarska1
Cellular & Molecular Biology LettersAn International Journal201217:34

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

Received: 6 February 2012

Accepted: 7 September 2012

Published: 20 September 2012

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.

Key words

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

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