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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Activity of aminoglycosides, including ACHN-490, against carbapenem-resistant Enterobacteriaceae isolates
David M. Livermore,Shazad Mushtaq,Marina Warner,Jiancheng Zhang,Sunil Maharjan,Michel Doumith,Neil Woodford +6 more
TL;DR: ACHn-490 has potent activity versus carbapenem-resistant isolates, except those also harbouring 16S rRNA methylases; isepamicin is also widely active, though less potent than ACHN-490.
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Evaluation of genetic mutations associated with Mycobacterium tuberculosis resistance to amikacin, kanamycin and capreomycin: a systematic review.
Sophia B. Georghiou,Marisa Magaña,Richard S. Garfein,Donald G. Catanzaro,Antonino Catanzaro,Timothy C. Rodwell +5 more
TL;DR: In this article, the authors conducted a systematic review of all published studies evaluating Mtb mutations associated with resistance to AMK, KAN, CAP in order to characterize the diversity and frequency of mutations as well as describe the strength of the association between specific mutations and phenotypic resistance in global populations.
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Coexistence of blaOXA-23 with blaNDM-1 and armA in clinical isolates of Acinetobacter baumannii from India.
TL;DR: Susceptibility testing showed increased MICs of carbapenems and an unusual phenotype of broad-spectrum high-level resistance to aminoglycosides, including amikacin, gentamicin, netilmicin and tobramycin (MICs), with susceptibility to tigecycline (MIC1⁄40.5–1 mg/L).
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AcrD of Escherichia coli Is an Aminoglycoside Efflux Pump
TL;DR: Deletion of the acrD gene decreased the MICs of amikacin, gentamicin, neomycin, kanamycin, and tobramycin by a factor of two to eight, and DeltaacrD cells accumulated higher levels of [(3]H]dihydrostreptomycin and [(3)H]gentamicin than did the parent strain.
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Structural basis for the inhibition of bacterial multidrug exporters
Ryosuke Nakashima,Keisuke Sakurai,Seiji Yamasaki,Katsuhiko Hayashi,Chikahiro Nagata,Kazuki Hoshino,Yoshikuni Onodera,Kunihiko Nishino,Akihito Yamaguchi +8 more
TL;DR: The first inhibitor-bound structures of AcrB and MexB are described, in which these proteins are bound by a pyridopyrimidine derivative that binds tightly to a narrow pit composed of a phenylalanine cluster located in the distal pocket and sterically hinders the functional rotation.