scholarly journals Pharmacodynamic activity of ertapenem versus genotypically characterized extended-spectrum  -lactamase (ESBL)-, KPC- or NDM-producing Escherichia coli with reduced susceptibility or resistance to ertapenem using an in vitro model

2014 ◽  
Vol 69 (9) ◽  
pp. 2448-2452 ◽  
Author(s):  
G. G. Zhanel ◽  
A. Denisuik ◽  
S. Vashisht ◽  
C. Yachison ◽  
H. J. Adam ◽  
...  
2017 ◽  
Vol 118 ◽  
pp. 64-69 ◽  
Author(s):  
Andreia S. Azevedo ◽  
Carina Almeida ◽  
Luciana C. Gomes ◽  
Carla Ferreira ◽  
Filipe J. Mergulhão ◽  
...  

1996 ◽  
Vol 40 (3) ◽  
pp. 734-738 ◽  
Author(s):  
A A Firsov ◽  
D Saverino ◽  
D Savarino ◽  
M Ruble ◽  
D Gilbert ◽  
...  

The clinical outcome in patients treated with ampicillin-sulbactam may not always be predictable by disc susceptibility testing or with the MIC as determined with a constant level (4 micrograms/ml) of the beta-lactamase inhibitor (MIC1). The enzyme activities (EA) and the MICs estimated at a constant ratio of ampicillin to sulbactam of 2:1 (MIC2) for 15 TEM-1 beta-lactamase-producing strains of Escherichia coli were examined as alternatives to MIC1 as predictors of the antibacterial effects of this combined drug as studied in an in vitro model which simulates ampicillin-sulbactam pharmacokinetic profiles observed in human peripheral tissues. Integral parameters describing the area under the bacterial count-time curve (AUBC), the area between the normal growth curve, and the killing curve of bacteria exposed to antibiotic (ABBC), and the second parameter expressed as a percentage of its maximal hypothetical value (ABBC/ABBCmax) were calculated. All three parameters correlated well with EA (AUBC, r = 0.93; ABBC, r = -0.88; ABBC/ABBCmax, r = -0.91) and with MIC2 (r = 0.94, -0.94, and -0.95, respectively) but not with MIC1. Both EA and MIC2 can be considered reliable predictors of the antibacterial effect of ampicillin-sulbactam in an in vitro model. These correlations suggest that in vitro kinetic-dynamic models might be useful to reexamine established susceptibility breakpoints obtained with data based on the MIC1 (MICs obtained with constant levels of beta-lactamase inhibitors). These data also suggest that quantitative determinations of bacterial beta-lactamase production and MICs based on the component concentration ratio observed in vivo might be useful predictors of the effect of ampicillin-sulbactam and other beta-lactam-inhibitor combinations.


2008 ◽  
Vol 52 (8) ◽  
pp. 2929-2932 ◽  
Author(s):  
Vincent Cattoir ◽  
Patrice Nordmann ◽  
Jesus Silva-Sanchez ◽  
Paula Espinal ◽  
Laurent Poirel

ABSTRACT A novel QnrB-like plasmid-mediated resistance determinant, QnrB19, was identified from an Escherichia coli clinical isolate from Colombia. Its gene was associated with an ISEcp1-like insertion element that did not act as a promoter for its expression. Using an in vitro model of transposition, we showed that the ISEcp1-like element was able to mobilize the qnrB19 gene.


2005 ◽  
Vol 73 (2) ◽  
pp. 1034-1043 ◽  
Author(s):  
Laura Q. Leverton ◽  
James B. Kaper

ABSTRACT The hallmark of enteropathogenic Escherichia coli (EPEC) infection is the ability of EPEC to cause attaching and effacing (A/E) lesions on intestinal epithelium. This event is reproducible in in vitro tissue culture models of infection. We used real-time PCR to measure transcription from several locus of enterocyte effacement (LEE) operons (LEE1 to LEE5) and from bfp during a 5-h infection of HEp-2 cells with EPEC. We found that after the initial formation of A/E lesions, which occurs as early as 5 min postinfection, EPEC continues to increase transcription from LEE3 to LEE5 as well as from bfp. These levels are maximized by 3 h postinfection and remain constant throughout the course of infection. This increase in transcription from LEE3 to LEE5 occurs when LEE1 (ler) transcription is decreasing. EspA, EspB, intimin, Tir, and bundle-forming pilus expression is detectable during the entire 5-h infection. These results indicate that the EPEC genes involved in localized and intimate adherence are continually expressed after the initial stages of A/E lesion formation on host cells.


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