Clinical Correlation of the CLSI Susceptibility Breakpoint for Piperacillin- Tazobactam against Extended-Spectrum-β-Lactamase-Producing
            <i>Escherichia coli</i>
            and
            <i>Klebsiella</i>
            Species

Gavin, Patrick J.; Suseno, Mira; Thomson, Richard B.; Gaydos, J. Michael; Pierson, Carl L.; Halstead, Diane; Aslanzadeh, Jaber; Brecher, Stephen M.; Rotstein, Coleman; Brossette, Stephen E.; Peterson, Lance R.

doi:10.1128/aac.00381-05

Cited by 71 publications

(38 citation statements)

References 27 publications

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“…Among the K. pneumoniae isolates studied, the piperacillin-tazobactam regimen produced the most profound reduction in CFU (0.75 and Ͼ1-log-unit decreases) over the 24-h treatment period. The efficacy of piperacillin-tazobactam against ESBL-positive organisms has been demonstrated in several studies, with some studies showing that piperacillin-tazobactam was the most active agent studied (9,14,18). In these, efficacy was dependent not only on the actual MIC of the organism, but also on the % fT Ͼ MIC achieved by the piperacillin-tazobactam regimen, striving for a % fT Ͼ MIC of Ͼ30 to 35% (1,9).…”

Section: Discussionmentioning

confidence: 99%

In Vivo Comparison of CXA-101 (FR264205) with and without Tazobactam versus Piperacillin-Tazobactam Using Human Simulated Exposures against Phenotypically Diverse Gram-Negative Organisms

Bulik

Tessier

Keel

et al. 2012

Antimicrob Agents Chemother

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Section: Discussionmentioning

confidence: 99%

In Vivo Comparison of CXA-101 (FR264205) with and without Tazobactam versus Piperacillin-Tazobactam Using Human Simulated Exposures against Phenotypically Diverse Gram-Negative Organisms

Bulik

Tessier

Keel

et al. 2012

Antimicrob Agents Chemother

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“…Several recent retrospective studies of clinical outcomes from E. coli and K. pneumoniae ESBL-producing isolates argue for the efficacy of piperacillin-tazobactam in the treatment of these infections (135,336,370,420). Gavin et al showed that when in vitro testing revealed susceptibility to piperacillin-tazobactam (Յ16/4 g/ml), successful outcomes were seen in 10 out of 11 non-urinary tract infections (135).…”

Section: ␤-Lactamase Inhibitors In Clinical Practicementioning

confidence: 99%

“…Gavin et al showed that when in vitro testing revealed susceptibility to piperacillin-tazobactam (Յ16/4 g/ml), successful outcomes were seen in 10 out of 11 non-urinary tract infections (135). An examination of 43 bloodstream infections caused primarily by CTX-M ESBL-producing E. coli isolates revealed that piperacillin-tazobactam, amoxicillin-clavulanate (i.v.…”

Section: ␤-Lactamase Inhibitors In Clinical Practicementioning

confidence: 99%

Three Decades of β-Lactamase Inhibitors

Drawz¹,

2010

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SUMMARYSince the introduction of penicillin, β-lactam antibiotics have been the antimicrobial agents of choice. Unfortunately, the efficacy of these life-saving antibiotics is significantly threatened by bacterial β-lactamases. β-Lactamases are now responsible for resistance to penicillins, extended-spectrum cephalosporins, monobactams, and carbapenems. In order to overcome β-lactamase-mediated resistance, β-lactamase inhibitors (clavulanate, sulbactam, and tazobactam) were introduced into clinical practice. These inhibitors greatly enhance the efficacy of their partner β-lactams (amoxicillin, ampicillin, piperacillin, and ticarcillin) in the treatment of seriousEnterobacteriaceaeand penicillin-resistant staphylococcal infections. However, selective pressure from excess antibiotic use accelerated the emergence of resistance to β-lactam-β-lactamase inhibitor combinations. Furthermore, the prevalence of clinically relevant β-lactamases from other classes that are resistant to inhibition is rapidly increasing. There is an urgent need for effective inhibitors that can restore the activity of β-lactams. Here, we review the catalytic mechanisms of each β-lactamase class. We then discuss approaches for circumventing β-lactamase-mediated resistance, including properties and characteristics of mechanism-based inactivators. We next highlight the mechanisms of action and salient clinical and microbiological features of β-lactamase inhibitors. We also emphasize their therapeutic applications. We close by focusing on novel compounds and the chemical features of these agents that may contribute to a “second generation” of inhibitors. The goal for the next 3 decades will be to design inhibitors that will be effective for more than a single class of β-lactamases.

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“…Clinicians must keep in mind that presence of a chromosomal AmpC enzymes that is normally resistant to inactivation by a beta-lactamase inhibitor may be present [70]. Based on this and the data obtained from microbiological and clinical observations, we do not regard beta-lactam/beta-lactamases inhibitor combinations as a suitable option for serious infections due to ESBL-producing enterobacteria [87,88].…”

Section: Beta-lactam/beta-lactamases Inhibitor Combinationsmentioning

confidence: 99%

The continuing challenge of ESBLs

Pérez

Endimiani

Hujer

et al. 2007

Current Opinion in Pharmacology

262

209

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Summary of recent advancesSince their first description more than twenty years ago, Escherichia coli and Klebsiella pneumoniae possessing extended-spectrum class A beta-lactamases (ESBLs) continue to thwart our best clinical efforts. In the "early years" the most common beta-lactamases were of the TEM and SHV varieties. Now, CTX-M enzymes are being discovered though out the world and are becoming the most prevalent beta-lactamases found in clinical isolates. The Klebsiella pneumoniae carbapenemases (KPC) (ESBL type enzymes that confer resistance to extended spectrum cephalosporins and carbapenems) present the most significant challenge to date. Structural studies of ESBLs indicate that active site expansion and remodeling are responsible for this extended hydrolytic activity. Continuing questions still exist regarding the optimal detection method for ESBLs. Most relevant are the increasing concerns regarding the status of carbapenems as "best therapy" for ESBL producing bacteria in light of the emergence of carbapenemases.

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Clinical Correlation of the CLSI Susceptibility Breakpoint for Piperacillin- Tazobactam against Extended-Spectrum-β-Lactamase-Producing Escherichia coli and Klebsiella Species

Cited by 71 publications

References 27 publications

In Vivo Comparison of CXA-101 (FR264205) with and without Tazobactam versus Piperacillin-Tazobactam Using Human Simulated Exposures against Phenotypically Diverse Gram-Negative Organisms

In Vivo Comparison of CXA-101 (FR264205) with and without Tazobactam versus Piperacillin-Tazobactam Using Human Simulated Exposures against Phenotypically Diverse Gram-Negative Organisms

Three Decades of β-Lactamase Inhibitors

The continuing challenge of ESBLs

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