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Beta-Lactamase Inhibitors
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Pascalis Vergidis, Matthew E. Falagas
Imipenem and cefoxitin demonstrate variable rates of susceptibility against Mycobacterium abscessus (Lavollay et al., 2014). The production of BlaMab, a class A beta-lactamase, contributes to beta-lactam resistance. Avibactam inhibits BlaMab via the reversible formation of a covalent adduct (Dubee et al., 2015a). Ceftaroline is also hydrolyzed by BlaMab. However, the addition of avibactam potentiates the in vitro activity of ceftaroline and the combination requires further evaluation in the treatment of M. abscessus infections (Dubee et al., 2015b).
Combination Antimicrobial Therapy for Gram-Negative Infections: What Is the Evidence?
Published in Robert C. Owens, Lautenbach Ebbing, Antimicrobial Resistance, 2007
P. aeruginosa is intrinsically resistant to many antibiotics at concentrations achievable in vivo. Moreover, under selective antibiotic pressure, P. aeruginosa has been shown to rapidly acquire antibiotic resistance, by a number of different mechanisms (145). Beta-lactam resistance is mediated by production of beta-lactamases, permeability alterations, and penicillin-binding protein modifications. P. aeruginosa also contains inducible chromosomal beta-lactamases that confer resistance to cephalosporins. Resistance to fluoroquinolones continues to increase; both mutations in DNA gyrase and efflux pumps have been described.
A 2018–2019 patent review of metallo beta-lactamase inhibitors
Published in Expert Opinion on Therapeutic Patents, 2020
Nakita Reddy, Mbongeni Shungube, Per I Arvidsson, Sooraj Baijnath, Hendrik G Kruger, Thavendran Govender, Tricia Naicker
Beta-lactam antibiotics are the most widely prescribed class of antimicrobial drugs around the world [1]. The therapeutic benefits offered by this class of antimicrobials include accessibility, safety, and a unique mechanism of action against specific prokaryotic cell structures [2], making it the ideal antimicrobial drug of choice. However, with increased consumption, inappropriate prescribing practices, and misuse of beta-lactams to treat minor infections, beta-lactam resistance has escalated to uncontrollable rates [3]. Gram-negative bacteria are the main protagonists responsible for the rise in resistance, facilitated by genes carried on plasmids or other mobile genetic elements, which confer resistance to beta-lactam drugs [4]. Carbapenems are beta-lactam drugs that are often referred to as the last line of defense in the treatment of bacterial infections [4]. However, the emergence of carbapenem-resistant Enterobacteriaceae (CRE), along with carbapenem-resistant Acinetobacter baumannii (CRAB) and carbapenem-resistant Pseudomonas aeruginosa (CRPA) have emerged as urgent threats, requiring immediate intervention, as stated by the World Health Organization [5].
Overview of mechanisms of antibiotic resistance in Pseudomonas aeruginosa: an ocular perspective
Published in Clinical and Experimental Optometry, 2018
Dinesh Subedi, Ajay Kumar Vijay, Mark Willcox
Beta‐lactam antibiotics are the most widely used therapeutic choice for treatment of bacterial infections, accounting for 60 per cent of total antibiotics used by weight.2006 Their high effectivity, chemical diversity, comparatively low cost with minimum side‐effects make this class of antibiotics popular in treatment of microbial infections.2005 Cephalosporins such as cephazolin are commonly used beta‐lactams in the treatment of eye infections.2011 They are often prescribed in combination with aminoglycosides as fortified preparations.2008 However, increased beta‐lactam resistance in clinical isolates has threatened their therapeutic value.2006 Bacteria become resistant to beta‐lactams by producing heterogeneous enzymes commonly called beta‐lactamases.2006 These hydrolyse the beta‐lactam bond (Figure 3), which is vital for antimicrobial activity, and render the antibiotics ineffective.1991 The genes encoding beta‐lactamase can reside on the chromosome or on MGEs (for example, plasmids). Plasmid‐encoded enzymes are often expressed constitutively.1991 However, for chromosomally mediated resistance, expression is inducible.1991
Molecular diagnosis of antimicrobial resistance in Escherichia coli
Published in Expert Review of Molecular Diagnostics, 2018
Molly E Fleece, Suporn Pholwat, Amy J Mathers, Eric R Houpt
The major mechanism of beta-lactam resistance is via antibiotic-modifying beta-lactamases. Chromosomal beta-lactamases are intrinsic to E. coli; however, wild-type strains express these at low levels that are not phenotypically significant. Other beta-lactamases can be transferred via mobile genetic elements from one bacterium to another and can confer high levels of drug resistance [28]. Hundreds of beta-lactamases have been described [34]. There are two classification schemes for beta-lactamases. The Ambler system classifies enzymes based on their amino acid sequence into four major groups [35]. The Bush–Jacoby system classifies enzymes based on their functionality into three major groups and multiple subgroups [36].