Mechanisms of resistance to aminoglycoside antibiotics: overview and perspectives
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TLDR
By far the most widespread mechanism of resistance to AGs is the inactivation of these antibiotics by AG-modifying enzymes, and an overview of these mechanisms is provided.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.read more
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References
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Structural asymmetry of AcrB trimer suggests a peristaltic pump mechanism.
TL;DR: A crystallographic structure of trimeric AcrB determined at 2.9 and 3.0 angstrom resolution in space groups reveals three different monomer conformations representing consecutive states in a transport cycle, implying an alternating access mechanism and a novel peristaltic mode of drug transport by this type of transporter.
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Mechanisms of antibiotic resistance in Pseudomonas aeruginosa.
TL;DR: The current position in which the resistance rates of P. aeruginosa strains from CF patients are all significantly higher than those from non-CF patients is summarized.
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Bacterial uptake of aminoglycoside antibiotics.
TL;DR: A critical overview of the process of aminoglycoside uptake is presented and a number of unresolved issues about the overall process are addressed to suggest directions for future research.
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Mistranslation of membrane proteins and two-component system activation trigger antibiotic-mediated cell death.
Michael A. Kohanski,Daniel J. Dwyer,Jamey Wierzbowski,Guillaume Cottarel,James J. Collins,James J. Collins +5 more
TL;DR: It is shown, by disabling systems that facilitate membrane protein traffic, that mistranslation and misfolding of membrane proteins are central to aminoglycoside-induced oxidative stress and cell death.
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New Plasmid-Mediated Fluoroquinolone Efflux Pump, QepA, Found in an Escherichia coli Clinical Isolate
Kunikazu Yamane,Jun-ichi Wachino,Satowa Suzuki,Kouji Kimura,Naohiro Shibata,Haru Kato,Keigo Shibayama,Toshifumi Konda,Yoshichika Arakawa +8 more
TL;DR: The augmented FQ resistance level acquired by the probable intergeneric transfer of a gene encoding a major facilitator superfamily-type efflux pump from some environmental microbes to E. coli was first identified.