Mechanisms of resistance to aminoglycoside antibiotics: Overview and perspectives

Sylvie Garneau-Tsodikova, Kristin J. Labby

Research output: Contribution to journalReview articlepeer-review

240 Scopus citations

Abstract

Aminoglycoside (AG) antibiotics are used to treat many Gram-negative and some Gram-positive infections and, importantly, multidrug-resistant tuberculosis. Among various bacterial species, resistance to AGs arises through a variety of intrinsic and acquired mechanisms. The bacterial cell wall serves as a natural barrier for small molecules such as AGs and may be further fortified via acquired mutations. Efflux pumps work to expel AGs from bacterial cells, and modifications here too may cause further resistance to AGs. Mutations in the ribosomal target of AGs, while rare, also contribute to resistance. Of growing clinical prominence is resistance caused by ribosome methyltransferases. By far the most widespread mechanism of resistance to AGs is the inactivation of these antibiotics by AG-modifying enzymes. We provide here an overview of these mechanisms by which bacteria become resistant to AGs and discuss their prevalence and potential for clinical relevance.

Original languageEnglish
Pages (from-to)11-27
Number of pages17
JournalMedChemComm
Volume7
Issue number1
DOIs
StatePublished - 2016

Bibliographical note

Publisher Copyright:
© The Royal Society of Chemistry 2016.

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Pharmacology
  • Pharmaceutical Science
  • Drug Discovery
  • Organic Chemistry

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