Journal
INFECTIOUS DISEASE CLINICS OF NORTH AMERICA
Volume 30, Issue 2, Pages 523-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.idc.2016.02.011
Keywords
Aminoglycoside; 16S ribosomal RNA; Posttranscriptional methylation; Carbapenemease
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Funding
- National Institutes of Health [R01AI104895, R21AI107302, R21AI123747]
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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.
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