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Infect Dis Clin North Am. 2016 Jun;30(2):523-537. doi: 10.1016/j.idc.2016.02.011.

Aminoglycoside Resistance: The Emergence of Acquired 16S Ribosomal RNA Methyltransferases.

Author information

1
Division of Infectious Diseases, University of Pittsburgh School of Medicine, S829 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261, USA. Electronic address: yod4@pitt.edu.
2
Department of Bacteriology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan.

Abstract

Aminoglycoside-producing Actinobacteria are known to protect themselves from their own aminoglycoside metabolites by producing 16S ribosomal RNA methyltransferase (16S-RMTase), which prevents them from binding to the 16S rRNA targets. Ten acquired 16S-RMTases have been reported from gram-negative pathogens. Most of them posttranscriptionally methylate residue G1405 of 16S rRNA resulting in high-level resistance to gentamicin, tobramycin, amikacin, and plazomicin. Strains that produce 16S-RMTase are frequently multidrug-resistant or even extensively drug-resistant. Although the direct clinical impact of high-level aminoglycoside resistance resulting from production of 16S-RMTase is yet to be determined, ongoing spread of this mechanism will further limit treatment options for multidrug-resistant and extensively drug-resistant gram-negative infections.

KEYWORDS:

16S ribosomal RNA; Aminoglycoside; Carbapenemease; Posttranscriptional methylation

PMID:
27208771
PMCID:
PMC4878400
DOI:
10.1016/j.idc.2016.02.011
[Indexed for MEDLINE]
Free PMC Article

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