Abstract
Aminoglycosides are a class of antibiotics that play a key role in antimicrobial treatment of Multidrug resistant (MDR) Gram-negative bacilli, typically in combination with β-lactams. Ribosomal 16S RNA modification by methyltransferases (e.g. RmtG) is an aminoglycoside resistance mechanism that, along with the occurrence carbapenem-resistant Enterobacteriaceae (CRE), has become a clinical concern. In Brazil, rmtG genes were initially reported in Klebsiella pneumoniae, and monitoring isolates from other species carrying this gene is critical for epidemiological studies and to prevent dissemination. Here we report the presence of rmtG in Klebisella aerogenes D3 and characterize its genetic context in comparison to isolates from other species. Further, we performed a phylogenetic reconstruction of 900 16S rRNA methyltransferases (16S-RMTases) and methyltransferase-related proteins. We show that, in K. aerogenes D3, rmtG co-occurs with sul2, near a transposon with an IS91-like insertion sequence. Resistome analysis revealed the co-production of RmtG and CTX-M-59. Ongoing surveillance of 16S-RMTases is crucial to delay the dissemination of such multiresistant isolates. Our results also highlight the reduction in treatment options for CRE infections, as well as the need of expanding prevention measures of these pathogens worldwide.
Highlights
Aminoglycosides are broad-spectrum and highly potent antibiotics that bind to the 30S ribosomal subunit and compromise translation
K. aerogenes D3 was isolated from bronchoalveolar lavage (BAL) from an elderly male patient under medical care at a tertiary teaching hospital located in Curitiba, Paraná, Brazil, in December 2006 (Grazziotin et al 2016)
Because the release of K. aerogenes MULTILOCUS SEQUENCE TYPING (MLST) profile is very recent, there is no sufficient information about lineage global distribution and clonal characteristics
Summary
Aminoglycosides are broad-spectrum and highly potent antibiotics that bind to the 30S ribosomal subunit and compromise translation. The resistance to aminoglycosides can be mediated by different mechanisms, such as: (i) the expression of enzymes that modify and inactivate the antibiotic and; (ii) modification of the ribosomal binding sites by 16S ribosomal RNA methyltransferases (16S-RMTases) (Ramirez and Tolmasky 2010, Wachino and Arakawa 2012). In addition to AMEs, new acquired 16S-RMTases have been shown to confer high levels of resistance against clinically important aminoglycosides (e.g. amikacin, gentamicin and tobramycin), increasing their minimal inhibitory concentration (MIC).
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