Prevalence and Expression of the Plasmid-Mediated Quinolone Resistance Determinant qnrA1

ABSTRACT Since its discovery, qnrA has been found in most common Enterobacteriaceae. Ciprofloxacin MICs conferred by different qnrA-positive plasmids could range from 0.1 μg/ml to 2 μg/ml in Escherichia coli J53. The reasons for different ciprofloxacin MICs conferred by qnrA have not been fully clarified. Five hundred forty-one consecutive gram-negative clinical strains that were resistant or intermediate to ciprofloxacin and that were isolated in Shanghai in 2005 were screened for qnrA by PCR. For qnrA-positive isolates, the transferability of quinolone resistance was determined by conjugation and mutations within the quinolone resistance-determining region (QRDR) of gyrA and parC. aac(6′)-Ib-cr was detected and qnrA RNA expression was determined using real-time reverse transcription-PCR for transconjugants with different ciprofloxacin MICs. The qnrA gene was detected in 7 of the 541 clinical isolates. Quinolone resistance was transferred in four strains by conjugation. Mutations in the QRDR of gyrA and parC were detected in five qnrA-positive clinical strains with higher ciprofloxacin MICs. Of four qnrA-bearing plasmids in E. coli J53, pHS4 and pHS5 conferred ciprofloxacin MICs of 0.094 to 0.125 μg/ml; pHS3, which harbored the aac(6′)-Ib-cr gene as well, conferred a ciprofloxacin MIC of 0.25 μg/ml, and pHS6, which had both the aac(6′)-Ib-cr gene and a high expression level of qnrA, had a ciprofloxacin MIC of 1.0 μg/ml. The prevalence of qnrA appeared to be higher in Enterobacter cloacae than in other Enterobacteriaceae. The coexistence of qnrA and aac(6′)-Ib-cr in a single plasmid and increased qnrA expression can account for the different levels of ciprofloxacin resistance seen in transconjugants.

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Genetic interplay between type II topoisomerase enzymes and chromosomal ccdAB toxin-antitoxin in E. coli

10.1101/2021.09.24.461737 ◽

2021 ◽

Author(s):

Jay Wook Joong Kim ◽

Vincent Blay ◽

Portia Mira ◽

Miriam Barlow ◽

Manel Camps

Keyword(s):

Public Health ◽

Genetic Markers ◽

Indirect Effect ◽

Quinolone Resistance ◽

Type Ii ◽

Topoisomerase Iv ◽

E Coli ◽

Resistance Evolution ◽

Selective Pressures ◽

Ciprofloxacin Resistance

Fluoroquinolones are one of the most widely used class of antibiotics. They target two type II topoisomerase enzymes: gyrase and topoisomerase IV. Resistance to these drugs, which is largely caused by mutations in their target enzymes, is on the rise and becoming a serious public health risk. In this work, we analyze the sequences of 352 extraintestinal E. coli clinical isolates to gain insights into the selective pressures shaping the type II topoisomerase mutation landscape in E. coli. We identify both Quinolone Resistance-Determining Region (QRDR) and non-QRDR mutations, outline their mutation trajectories, and show that they are likely driven by different selective pressures. We confirm that ciprofloxacin resistance is specifically and strongly associated with QRDR mutations. By contrast, non-QRDR mutations are associated with the presence of the chromosomal version of ccdAB, a toxin-antitoxin operon, where the toxin CcdB is known to target gyrase. We also find that ccdAB and the evolution of QRDR mutation trajectories are partially incompatible. Finally, we identify partial deletions in CcdB and additional mutations that likely facilitate the compatibility between the presence of the ccdAB operon and QRDR mutations. These "permissive" mutations are all found in ParC (a topoisomerase IV subunit). This, and the fact that CcdB-selected mutations frequently map to topoisomerase IV, strongly suggests that this enzyme (in addition to gyrase) is likely a target for the toxin CcdB in E. coli, although an indirect effect on global supercoiling cannot be excluded. This work opens the door for the use of the presence of ccdB and of the proposed permissive mutations in the genome as genetic markers to assess the risk of quinolone resistance evolution and implies that certain strains may be genetically more refractory to evolving quinolone resistance through mutations in target enzymes.

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Structural Modification of Lipopolysaccharide Conferred by mcr-1 in Gram-Negative ESKAPE Pathogens

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00580-17 ◽

2017 ◽

Vol 61 (6) ◽

Cited By ~ 49

Author(s):

Yi-Yun Liu ◽

Courtney E. Chandler ◽

Lisa M. Leung ◽

Christi L. McElheny ◽

Roberta T. Mettus ◽

...

Keyword(s):

Structural Changes ◽

Lipid A ◽

Colistin Resistance ◽

Gram Negative ◽

Content Type ◽

Clinical Strains ◽

E Coli ◽

The Family ◽

Phosphoethanolamine Transferases ◽

Eskape Pathogens

ABSTRACT mcr-1 was initially reported as the first plasmid-mediated colistin resistance gene in clinical isolates of Escherichia coli and Klebsiella pneumoniae in China and has subsequently been identified worldwide in various species of the family Enterobacteriaceae. mcr-1 encodes a phosphoethanolamine transferase, and its expression has been shown to generate phosphoethanolamine-modified bis-phosphorylated hexa-acylated lipid A in E. coli. Here, we investigated the effects of mcr-1 on colistin susceptibility and on lipopolysaccharide structures in laboratory and clinical strains of the Gram-negative ESKAPE (Enterococcus faecium, Staphylococcus aureus, K. pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) pathogens, which are often treated clinically by colistin. The effects of mcr-1 on colistin resistance were determined using MIC assays of laboratory and clinical strains of E. coli, K. pneumoniae, A. baumannii, and P. aeruginosa. Lipid A structural changes resulting from MCR-1 were analyzed by mass spectrometry. The introduction of mcr-1 led to colistin resistance in E. coli, K. pneumoniae, and A. baumannii but only moderately reduced susceptibility in P. aeruginosa. Phosphoethanolamine modification of lipid A was observed consistently for all four species. These findings highlight the risk of colistin resistance as a consequence of mcr-1 expression among ESKAPE pathogens, especially in K. pneumoniae and A. baumannii. Furthermore, the observation that lipid A structures were modified despite only modest increases in colistin MICs in some instances suggests more sophisticated surveillance methods may need to be developed to track the dissemination of mcr-1 or plasmid-mediated phosphoethanolamine transferases in general.

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Ciprofloxacin Resistance in Hospital and Community-acquired Urinary Tract Infections by Escherichia coli: A Systematic Review and Meta-analysis

10.1101/2020.04.09.034041 ◽

2020 ◽

Author(s):

Guanyu Zhou ◽

Xiaoju Lv

Keyword(s):

Systematic Review ◽

Urinary Tract ◽

Urinary Tract Infections ◽

Main Concern ◽

Gram Negative Bacteria ◽

Gram Negative ◽

E Coli ◽

Ciprofloxacin Resistance ◽

Tract Infections ◽

Hospital Acquired

AbstractIn recent years, antimicrobial resistance has been increasingly reported. One main concern is the resistance of gram-negative bacteria like E. coli to ciprofloxacin (fluoroquinolones). Gram-negative bacteria are the main cause of community and hospital-acquired urinary tract infections (UTI). We aimed to review and analyze the data on ciprofloxacin resistance in hospital and community-acquired UTI. A literature search of three electronic databases (PubMed, Medline, and Cochrane) was performed. We considered the papers that were published from January 2004 to May 2019. The search yielded a total of 16097 studies besides 31 studies from a manual search. Filtering yielded 1297 relevant full-text papers. Eighty-three papers, equivalent of 99 cohorts, were finally included in this systematic review and in the analysis. The analysis results suggest that pooled ciprofloxacin resistance for community and hospital-acquired E. coli UTI is 0.27 (95% CI 0.246–0.303) and 0.30 (95% CI 0.22–0.38), respectively. Pooled resistance rates according to regions are 0.43 (95% CI 0.31–0.54) for Asia ensued by Africa 0.31 (95% CI 0.22–0.35), the Middle East 0.21(95% CI 0.13-0.30), Europe 0.18 (95% CI 0.13-0.22), and Australia 0.06 (95% CI 0.04-0.08). The pooled estimates revealed that ciprofloxacin resistance was higher in developing countries compared to that in developed countries, 0.35 (95% CI 0.30-0.40) and 0.13 (95% CI 0.10-0.16), respectively. Finally, plotting resistance over time deemed statistically significant (n= 79, r= 0.29, p= 0.038). Our findings suggest that ciprofloxacin resistance among UTI patients is a highly prevalent and serious issue. The suggested risks are low-income, acquiring hospital infection, and falling in highly-vulnerable regions like Asia and Africa. We also shed light on some approaches to correct the perception of patients and general practitioners (GPs) for antibiotic usage. We also suggest ideas to impede the progress of the post-antibiotic era in countries known for high antibiotic resistance.

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Prevalence of Ciprofloxacin Resistance Among Gram-Negative Bacilli at a Specialist Hospital in Saudi Arabia

Bangladesh Journal of Medical Science ◽

10.3329/bjms.v11i4.12604 ◽

2012 ◽

Vol 11 (4) ◽

pp. 317-321

Author(s):

Shamweel Ahmad

Keyword(s):

Bacterial Species ◽

Treatment Options ◽

Medical Science ◽

Surrogate Marker ◽

Quinolone Resistance ◽

Cross Resistance ◽

Multi Drug Resistance ◽

Gram Negative ◽

Ciprofloxacin Resistance ◽

Tract Infections

Background: Resistance to antimicrobials of different structural classes including fluoroquinolones has arisen in a multitude of bacterial species both in the community and the hospitals. This may complicate the therapeutic management of infections. Decreased susceptibility to fluoroquinolones arises mainly by singlestep mutations in the gyrA and parC genes, which encode the fluoroquinolones targets, the topoisomerase enzymes, conferring cross resistance to all fluoroquinolones. Accumulation of multiple mutations in several genes confers increasing level of resistance associated with clinical failure. However, even low level resistance can generate therapeutic failure. In 1998, some mobile elements with a potential for the horizontal transfer of the quinolone resistance genes were described. The loci which are responsible for this plasmid-mediated quinolone resistance, which have been designated as qnrA, qnrB and qnrS, have been identified in the Enterobacteriaceae species. Aim: To evaluate the susceptibility pattern of the isolates to various antibiotics and to know the prevalence rate of ciprofloxacin resistance in our hospital. Materials & Methods: A total of 916 gram-negative bacilli (GNB) were isolated from different clinical specimens over a period of nine months, were subjected to antibiotic susceptibility testing. Isolates with resistance or with a decreased susceptibility to ciprofloxacin (£20 mm) were then screened for their minimum inhibitory concentration(MIC) by using the E-test. Results: Out of 916 GNB, 321 (35%) isolates were resistant to ciprofloxacin. The MIC of these isolates ranged from 4 to >32?g/ml.Conclusion: The resistance rate to ciprofloxacin was 35% in our study. Most of the ciprofloxacin resistant isolates were from urinary tract infections (UTI). The ciprofloxacin resistance was also closely associated with multi-drug resistance, thus limiting the treatment options. Ciprofloxacin resistance can be used as a general surrogate marker of multidrug resistance, thus limiting the already restricted treatment options. The considerably high MIC values for ciprofloxacin in this study reflected the extent of the treatment problems for these resistant isolates and a need for the continuous evaluation of the commonly used antibiotics. DOI: http://dx.doi.org/10.3329/bjms.v11i4.12604 Bangladesh Journal of Medical Science Vol. 11 No. 04 Oct12

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Improvement of Gram-negative Susceptibility to Fluoroquinolones After Implementation of a Pre-Authorization Policy for Fluoroquinolone Use: A Decade-Long Experience

Open Forum Infectious Diseases ◽

10.1093/ofid/ofx162.048 ◽

2017 ◽

Vol 4 (suppl_1) ◽

pp. S19-S19

Author(s):

Rachael A Lee ◽

Morgan Scully ◽

Danielle F Kunz ◽

T Aaron Jones ◽

Bernard Camins ◽

...

Keyword(s):

Hospital Setting ◽

Enterobacter Cloacae ◽

Antibiotic Use ◽

Resistant Bacteria ◽

Antibiotic Prescribing ◽

Gram Negative ◽

E Coli ◽

Authorization Policy ◽

Acinetobacter Spp ◽

Hospital Acquired

Abstract Background Antibiotic use is a well-known risk factor for acquisition of drug-resistant bacteria and community antibiotic prescribing can drive high rates of resistance within the hospital setting. Owing to concerns over increasing fluoroquinolone (FQ) resistance among Gram-negative organisms at UAB Hospital, our stewardship program implemented a pre-authorization policy. The goal of this study was to assess the relationship between hospital fluoroquinolone use and antibiotic resistance. Methods In 2006, the inpatient formulary was consolidated to only ciprofloxacin and moxifloxacin with implementation of guidelines for use to limit inpatient prescribing. Any use outside of these guidelines required approval from an infectious diseases physician. Organism-specific data were obtained from the clinical microbiology database and FQ use was obtained from the hospital database. Correlations were calculated using Pearson’s coefficient. Results From 1998 to 2004, FQ use peaked at 173 days of therapy (DOT)/1,000 patient-days, but has remained below 60 DOT/1,000 patient-days since restriction implementation (Figure 1). FQ susceptibility was documented for five common Gram-negative isolates, P. aeruginosa, Acinetobacter spp., Enterobacter cloacae, E. coli, and K. pneumoniae, over an 18-year period (1998–2016). Common hospital acquired pathogens, including Pseudomonas aeruginosa, Acinetobacter spp. and Enterobacter cloacae improved in their susceptibilities to fluoroquinolones. Acinetobacter went from 35% to over 50% susceptible in the preceding 10 years after the policy. Pseudomonas improved from 50% susceptible to over 70% and Enterobacter improved from less than 50% to over 90% susceptible. Interestingly this improvement was not seen for E. coli which continued to show a decline in susceptibility from over 90% to near 60% in 2016. Conclusion In a large academic hospital setting, FQ susceptibility for common hospital-acquired GNRS improved significantly with the introduction of a restricted use program. A continued decline in E. coli FQ susceptibility suggests resistance rates may be driven by outpatient and community antibiotic use and thus, outpatient stewardship programs are necessary to prevent further spread of FQ resistance. Disclosures All authors: No reported disclosures.

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Characterization of plasmid-mediated quinolone resistance by the qnrS gene in Escherichia coli isolated from healthy chickens and pigs

Veterinární Medicína ◽

10.17221/108/2009-vetmed ◽

2009 ◽

Vol 54 (No. 10) ◽

pp. 473-482 ◽

Cited By ~ 10

Author(s):

H.-C. Kuo ◽

C.-C. Chou ◽

C. Tu ◽

S.-R. Gong ◽

C.-L. Han ◽

...

Keyword(s):

Escherichia Coli ◽

Blot Hybridization ◽

Southern Blot Hybridization ◽

Quinolone Resistance ◽

E Coli ◽

Sequence Variations ◽

Southern Blot Hybridization Analysis ◽

Ciprofloxacin Resistance ◽

Polymerase Chain

The prevalence of qnr and qepA genes in 660 Escherichia coli isolates was investigated in healthy animals from 30 pig farms and 30 chicken farms in Taiwan from January 2005 to February 2006 by the polymerase chain reaction. The qnrS gene, but not qnrA, qnrB, and qepA were detected in 12/360 pig isolates (3.33%) and in 6/300 chicken isolates (2%). Southern blot hybridization analysis indicated that qnrS was located on plasmids ranging in size from 50–165 kb. Eleven of the 18 qnrS positive isolates which showed a high ciprofloxacin resistance phenotype (minimum inhibitory concentration ≥ 8 mg/l) also had amino acid sequence variations in chromosomal quinolone resistance-determining regions of gyrA and parC. Only two qnrS-positive isolates carried the aac(6’)-Ib-crvariant that mediates FQ acetylation. For the high percentage resistance of cephalosporins, the blaCTX-M gene was also examined in qnrS-positive isolates. The blaCTX-M gene was detected in fifteen isolates (15/18, 83.3%) of which 12 isolates were blaCTX-M-1 and three isolates were blCTX-M-15. This study demonstrated a close linkage between the qnrS gene and blaCTX-M-1, suggesting CTX-M and Qnr-based mechanisms might be co-emerging in E. coli strains isolated from healthy chickens and pigs under selective pressure of quinolone and cephalosporine administration.

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Lacticaseicin 30 and Colistin as a Promising Antibiotic Formulation against Gram-Negative β-Lactamase-Producing Strains and Colistin-Resistant Strains

Antibiotics ◽

10.3390/antibiotics11010020 ◽

2021 ◽

Vol 11 (1) ◽

pp. 20

Author(s):

Désiré Madi-Moussa ◽

Yanath Belguesmia ◽

Audrey Charlet ◽

Djamel Drider ◽

Françoise Coucheney

Keyword(s):

Pathogenic Bacteria ◽

Therapeutic Option ◽

Klebsiella Oxytoca ◽

Health Concern ◽

Cross Resistance ◽

Gram Positive ◽

Gram Negative ◽

Clinical Strains ◽

E Coli ◽

Gram Positive Bacteria

Antimicrobial resistance is a global health concern across the world and it is foreseen to swell if no actions are taken now. To help curbing this well announced crisis different strategies are announced, and these include the use of antimicrobial peptides (AMP), which are remarkable molecules known for their killing activities towards pathogenic bacteria. Bacteriocins are ribosomally synthesized AMP produced by almost all prokaryotic lineages. Bacteriocins, unlike antibiotics, offer a set of advantages in terms of cytotoxicity towards eukaryotic cells, their mode of action, cross-resistance and impact of microbiota content. Most known bacteriocins are produced by Gram-positive bacteria, and specifically by lactic acid bacteria (LAB). LAB-bacteriocins were steadily reported and characterized for their activity against genetically related Gram-positive bacteria, and seldom against Gram-negative bacteria. The aim of this study is to show that lacticaseicin 30, which is one of the bacteriocins produced by Lacticaseibacillus paracasei CNCM I-5369, is active against Gram-negative clinical strains (Salmonella enterica Enteritidis H10, S. enterica Typhimurium H97, Enterobacter cloacae H51, Escherichia coli H45, E. coli H51, E. coli H66, Klebsiella oxytoca H40, K. pneumoniae H71, K. variicola H77, K. pneumoniae H79, K. pneumoniae H79), whereas antibiotics failed. In addition, lacticaseicin 30 and colistin enabled synergistic interactions towards the aforementioned target Gram-negative clinical strains. Further, the combinations of lacticaseicin 30 and colistin prompted a drastic downregulation of mcr-1 and mcr-9 genes, which are associated with the colistin resistance phenotypes of these clinical strains. This report shows that lacticaseicin 30 is active against Gram-negative clinical strains carrying a rainbow of mcr genes, and the combination of these antimicrobials constitutes a promising therapeutic option that needs to be further exploited.

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Research of antimicrobial efficacy of modern antiseptic agents based on decamethoxine and povidone-iodine

Perioperaciina Medicina ◽

10.31636/prmd.v2i1.1 ◽

2019 ◽

Vol 2 (1) ◽

pp. 6-10 ◽

Cited By ~ 1

Author(s):

Oleksandr Nazarchuk

Keyword(s):

Antimicrobial Activity ◽

Povidone Iodine ◽

Antimicrobial Properties ◽

Infectious Complications ◽

Antimicrobial Efficacy ◽

Gram Positive ◽

Gram Negative ◽

Clinical Strains ◽

E Coli ◽

Enterococcus Spp

Under conditions of wide increased resistance of pathogens of infectious complications to antimicrobial agents, a considerable attention is paid to the use of antiseptic drugs. The research of their antimicrobial efficacy remains valid for substantiation of the rational use. The purpose was to carry out a comparative study of the antimicrobial efficacy of medicinal antiseptic agents based on decamethoxine and povidone-iodine. In the study there was examined antimicrobial activity of mentioned antiseptics against 682 clinical strains of microorganisms (A. baumannii, S. aureus, P. aeruginosa, Enterococcus spp., E. coli, Enterobacter spp., K. pneumoniae, Proteus spp.), isolated from patients with infectious complications. Minimum inhibitory and bactericidal concentrations of 1–2– 10 % iodine, 0.02 % decamethoxine (decasan) were determined. Antimicrobial efficacy of medicines, based on studied antiseptics was evaluated with the use of an index of antiseptic activity, calculated by means of commonly used methods. The study revealed high bactericidal properties of decasan against clinical strains of S. aureus, Enterococcus spp., E. coli, K. pneumoniae and Enterobacter spp. The advantages of antimicrobial activity of decamethoxine-based antseptis (decasan, p < 0.001) were proved. Iodine has expressed antimicrobial properties against Enterococcus spp., S. aureus, A. baumannii, bacteria of the Enterobacteriаcеae family and P. aeruginosa. It is proven that the dissolution of povidone-iodine leads to the reduction of the antimicrobial efficacy of 2 % antiseptic solution. There was found inefficacy of 1 % povidone-iodine against infectious agents (p < 0.001). Thus, the leading Gram-positive (S. aureus, Enterococci) and Gram-negative pathogens (Escherichia, Klebsiella, Enterobacteria, Acinetobacteria, Pseudomonas) have a sensitivity to iodine and to domestic preparation based on decamethoxin 0.02 % (decasan), with a definite advantage of the antimicrobial properties of the latter to Gram-positive and some Gram-negative microorganisms (p < 0.001).

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Phenotypic and genotypic quinolone resistance in Escherichia coli underlining GyrA83/87 mutations as a target to detect ciprofloxacin resistance

Journal of Antimicrobial Chemotherapy ◽

10.1093/jac/dkaa189 ◽

2020 ◽

Vol 75 (9) ◽

pp. 2466-2470

Author(s):

Anaëlle Muggeo ◽

Emmanuelle Cambau ◽

Marlène Amara ◽

Maïté Micaëlo ◽

Béatrice Pangon ◽

...

Keyword(s):

Escherichia Coli ◽

Efflux Pump ◽

Bloodstream Infections ◽

Blood Cultures ◽

Quinolone Resistance ◽

E Coli ◽

Molecular Determinants ◽

Ciprofloxacin Resistance ◽

First Time

Abstract Background Quinolone resistance (QR) is one component of the MDR emerging in Escherichia coli and is of particular concern given the widespread use of fluoroquinolones. Objectives To characterize the QR phenotypes and genotypes in E. coli responsible for bloodstream infections and to propose molecular determinants that could be targeted to predict ciprofloxacin resistance. Methods E. coli isolates from blood cultures in three French hospitals were studied for quinolone MICs and characterization of genotypic QR determinants (QRg). Results Among 507 isolates tested for MICs, 148 (29.2%) were resistant to quinolones based on EUCAST breakpoints and 143 (28.2%) harboured at least one QRg. QRg were mainly mutations in the QRDR (138 isolates, 27.2%), with 55.8% of these isolates carrying at least three QRDR mutations. gyrA mutations predominated (92.8%) followed by parC (61.6%), parE (32.6%) and gyrB (1.4%) mutations. Only 4.7% of the isolates harboured a plasmid-mediated quinolone resistance (PMQR) gene: aac(6′)-Ib-cr (60.0%) or qnr (qnrS, qnrB) (32.0%). For the first time in France, we reported the qepA4 allele of the plasmid-encoded efflux pump QepA. Only five isolates carried PMQR without a QRDR mutation. The positive predictive value (PPV) for ciprofloxacin resistance was 100% for any QRg and 99.2% for gyrA mutations specifically. Conclusions QR observed in E. coli isolates involved in bloodstream infections is still mainly due to QRDR mutations, especially at codons GyrA83/87, which could be used as a molecular target to rapidly detect resistance.

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Mutant Prevention Concentrations of Four Carbapenems against Gram-Negative Rods

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.00033-10 ◽

2010 ◽

Vol 54 (6) ◽

pp. 2692-2695 ◽

Cited By ~ 18

Author(s):

Kim Credito ◽

Klaudia Kosowska-Shick ◽

Peter C. Appelbaum

Keyword(s):

Escherichia Coli ◽

Pseudomonas Aeruginosa ◽

Klebsiella Pneumoniae ◽

Acinetobacter Baumannii ◽

Gram Negative ◽

Clinical Strains ◽

E Coli

ABSTRACT We tested the propensities of four carbapenems to select for resistant Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and Acinetobacter baumannii mutants by determining the mutant prevention concentrations (MPCs) for 100 clinical strains with various ß-lactam phenotypes. Among the members of the Enterobacteriaceae family and A. baumannii strains, the MPC/MIC ratios were mostly 2 to 4. In contrast, for P. aeruginosa the MPC/MIC ratios were 4 to ≥16. The MPC/MIC ratios for β-lactamase-positive K. pneumoniae and E. coli isolates were much higher (range, 4 to >16 μg/ml) than those for ß-lactamase-negative strains.

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