scholarly journals High-level resistance to gentamicin in clinical isolates of Streptococcus (Enterococcus) faecium.

1988 ◽  
Vol 32 (10) ◽  
pp. 1528-1532 ◽  
Author(s):  
G M Eliopoulos ◽  
C Wennersten ◽  
S Zighelboim-Daum ◽  
E Reiszner ◽  
D Goldmann ◽  
...  
Keyword(s):  
Enterococcus Faecium ◽  
Clinical Isolates ◽  
High Level ◽  
Level Resistance

scholarly journals Molecular aspects of high-level resistance to sulbactam-cefoperazone in Klebsiella oxytoca clinical isolates.

1996 ◽  
Vol 40 (9) ◽  
pp. 1988-1994 ◽  
Author(s):  
K Kimura ◽  
Y Arakawa ◽  
S Ohsuka ◽  
H Ito ◽  
K Suzuki ◽  
...  
Keyword(s):  
Klebsiella Oxytoca ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Point Of View ◽  
Clinical Isolates ◽  
Beta Lactamase ◽  
Beta Lactamases ◽  
Molecular Aspects ◽  
High Level ◽  
Level Resistance

Nine Klebsiella oxytoca strains which demonstrated resistance to the combination of sulbactam and cefoperazone were isolated from geographically separate hospitals in Japan in 1995. Among them, K. oxytoca SB23 showed high-level resistance to sulbactam-cefoperazone (MIC > 128 micrograms/ml) and aztreonam (MIC, 128 micrograms/ml). The sulbactam-cefoperazone resistance was not transferred from strain SB23 to Escherichia coli CSH2 by conjugation, beta-Lactamase RbiA, produced by strain SB23, was purified, and the molecular mass was estimated to be 29 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Kinetic parameters for RbiA revealed that cefoperazone and aztreonam were hydrolyzed efficiently by this enzyme. Moreover, ceftazidime and imipenem were also hydrolyzed weakly by RbiA, although strain SB23 did not show any resistance to these agents. Clavulanate, sulbactam, and tazobactam failed to block the hydrolysis of cefoperazone by RbiA. The structural gene of RbiA (blaRBI) was cloned and sequenced, and the deduced amino acid sequence of RbiA demonstrated high-level similarities to those of the beta-lactamases found in K. oxytoca D488, E23004, and plasmid-mediated MEN-1, which have been classified into Bush functional group 2be. Although RbiA demonstrates high-level molecular similarity to the enzymes in group 2be, from an enzymological point of view, this enzyme might be differentiated from the enzymes in that group. Hybridization analysis revealed that beta-lactamase genes highly similar to blaRBI were generally encoded on the chromosome of the sulbactam-cefoperazone-resistant clinical isolates of K. oxytoca tested in the study, despite their different derivations. This observation suggests that sulbactam-cefoperazone-resistant A. oxytoca strains which produce RbiA-type beta-lactamases have been proliferating in many hospitals in Japan.

Rapid Emergence of High-Level Resistance to Quinolones in Campylobacter jejuni Associated with Mutational Changes in gyrA and parC

1998 ◽  
Vol 42 (12) ◽  
pp. 3276-3278 ◽  
Author(s):  
Amera Gibreel ◽  
Eva Sjögren ◽  
Bertil Kaijser ◽  
Bengt Wretlind ◽  
Ola Sköld
Keyword(s):  
Campylobacter Jejuni ◽  
Quinolone Resistance ◽  
Clinical Isolates ◽  
High Level ◽  
Chromosomal Mutations ◽  
Rapid Emergence ◽  
Level Resistance

ABSTRACT Quinolone resistance in clinical isolates of Campylobacter jejuni in Sweden increased more than 20-fold at the beginning of the 1990s. Resistance to 125 μg of ciprofloxacin per ml in clinical isolates was associated with chromosomal mutations in C. jejuni leading to a Thr-86-Ile substitution in thegyrA product and a Arg-139-Gln substitution in theparC product.

Multiple-Antibiotic Resistance of Enterococcus faecalis and Enterococcus faecium from Cecal Contents in Broiler Chicken and Turkey Flocks Slaughtered in Canada and Plasmid Colocalization of tetO and ermB Genes

2011 ◽  
Vol 74 (10) ◽  
pp. 1639-1648 ◽  
Author(s):  
CINDY-LOVE TREMBLAY ◽  
ANN LETELLIER ◽  
SYLVAIN QUESSY ◽  
MARTINE BOULIANNE ◽  
DANIELLE DAIGNAULT ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Enterococcus Faecalis ◽  
Resistance Genes ◽  
Enterococcus Faecium ◽  
Broiler Chicken ◽  
Multidrug Resistant ◽  
Poultry Meat ◽  
Antimicrobial Resistance Genes ◽  
High Level ◽  
Level Resistance

This study was conducted to characterize the antimicrobial resistance determinants and investigate plasmid colocalization of tetracycline and macrolide genes in Enterococcus faecalis and Enterococcus faecium from broiler chicken and turkey flocks in Canada. A total of 387 E. faecalis and E. faecium isolates were recovered from poultry cecal contents from five processing plants. The percentages of resistant E. faecalis and E. faecium isolates, respectively, were 88.1 and 94% to bacitracin, 0 and 0.9% to chloramphenicol, 0.7 and 14.5% to ciprofloxacin, 72.6 and 80.3% to erythromycin, 3.7 and 41% to flavomycin, 9.6 and 4.3% (high-level resistance) to gentamicin, 25.2 and 17.1% (high-level resistance) to kanamycin, 100 and 94% to lincomycin, 0 and 0% to linezolid, 2.6 and 20.5% to nitrofurantoin, 3 and 27.4% to penicillin, 98.5 and 89.7% to quinupristin-dalfopristin, 7 and 12.8% to salinomycin, 46.7 and 38.5% (high-level resistance) to streptomycin, 95.6 and 89.7% to tetracycline, 73 and 75.2% to tylosin, and 0 and 0% to vancomycin. One predominant multidrug-resistant phenotypic pattern was identified in both E. faecalis and E. faecium (bacitracin, erythromycin, lincomycin, quinupristin-dalfopristin, tetracycline, and tylosin). These isolates were further examined by PCR and sequencing for the genes encoding their antimicrobial resistance. Various combinations of vatD, vatE, bcrR, bcrA, bcrB, bcrD, ermB, msrC, linB, tetM, and tetO genes were detected, and ermB, tetM, and bcrB were the most common antimicrobial resistance genes identified. For the first time, plasmid extraction and hybridization revealed colocalization of tetO and ermB genes on a ca. 11-kb plasmid in E. faecalis isolates, and filter mating experiments demonstrated its transferability. Results indicate that the intestinal enterococci of healthy poultry, which can contaminate poultry meat at slaughter, could be a reservoir for quinupristin-dalfopristin, bacitracin, tetracycline, and macrolide resistance genes.

scholarly journals Mechanisms of Resistance to Quinupristin-Dalfopristin among Isolates of Enterococcus faecium from Animals, Raw Meat, and Hospital Patients in Western Europe

2000 ◽  
Vol 44 (2) ◽  
pp. 433-436 ◽  
Author(s):  
Mehnam Soltani ◽  
David Beighton ◽  
John Philpott-Howard ◽  
Neil Woodford
Keyword(s):  
Enterococcus Faecium ◽  
Western Europe ◽  
European Countries ◽  
Mechanisms Of Resistance ◽  
Raw Meat ◽  
Hospital Patients ◽  
High Level ◽  
Level Resistance

ABSTRACT Twenty-eight quinupristin-dalfopristin-resistant isolates ofEnterococcus faecium from hospital patients and nonhuman sources in European countries were studied. High-level resistance (MICs, ≥32 μg/ml) was associated with the presence ofvat(E) (satG) (14 isolates [50%]) orvat(D) (satA) (6 isolates [21%]). These genes were not detected in eight (29%) isolates with lower levels of quinupristin-dalfopristin resistance (MICs, 4 to 16 μg/ml). This suggests the presence of further mechanisms of resistance to quinupristin-dalfopristin in E. faecium.

scholarly journals Susceptibility trends of zoliflodacin against multidrug-resistant Neisseria gonorrhoeae clinical isolates in Nanjing, China (2014-2018)

2020 ◽  
Author(s):  
Wenjing Le ◽  
Xiaohong Su ◽  
Xiangdi Lou ◽  
Xuechun Li ◽  
Xiangdong Gong ◽  
...  
Keyword(s):  
Neisseria Gonorrhoeae ◽  
Dna Sequencing ◽  
Multidrug Resistant ◽  
Quinolone Resistance ◽  
Clinical Isolates ◽  
Drug Resistant ◽  
Extended Spectrum ◽  
High Level ◽  
Level Resistance

ABSTRACTPreviously, we reported potent activity of a novel spiropyrimidinetrione, zoliflodacin, against N. gonorrhoeae isolates from symptomatic men in Nanjing, China, collected in 2013. Here, we investigated trends of susceptibilities of zoliflodacin in 986 gonococcal isolates collected from men between 2014 and 2018. N. gonorrhoeae isolates were tested for susceptibility to zoliflodacin and seven other antibiotics. Mutations in gyrA, gyrB, parC and parE genes were determined by PCR and DNA sequencing. The MIC of zoliflodacin for N. gonorrhoeae ranged from ≤0.002 to 0.25 mg/L; the overall MIC50s and MIC90s were 0.06 mg/L and 0.125mg/L in 2018, increasing two-fold from 2014. However, the percent of isolates with lower zoliflodacin MICs declined in each year sequentially while the percent with higher MICs increased yearly (P≤0.00001). All isolates were susceptible to spectinomycin but resistant to ciprofloxacin (MIC ≥1 μg/ml); 21.2% (209/986) were resistant to azithromycin (≥1 μg/ml), 43.4% (428/986) were penicillinase-producing (PPNG), 26.9% (265/986) tetracycline-resistant (TRNG) and 19.4% (191/986) were multi-drug resistant (MDR) isolates. Among 143 isolates with higher zoliflodacin MICs (0.125-0.25 mg/L), all had quinolone resistance associated double or triple mutations in gyrA; 139/143 (97.2%) also had mutations in parC. There were no D429N/A and/or K450T mutations in GyrB identified in the 143 isolates with higher zoliflodacin MICs; a S467N mutation in GyrB was identified in one isolate. We report that zoliflodacin has excellent in vitro activity against clinical gonococcal isolates, including those with high-level resistance to ciprofloxacin, azithromycin and extended spectrum cephalosporins.

scholarly journals Failure of VITEK2 to reliably detect vanB- mediated vancomycin resistance in Enterococcus faecium

2020 ◽  
Author(s):  
Sarah V. Walker ◽  
Martina Wolke ◽  
Georg Plum ◽  
Robert E. Weber ◽  
Guido Werner ◽  
...  
Keyword(s):  
Enterococcus Faecium ◽  
Vancomycin Resistance ◽  
Bacterial Suspension ◽  
Initial Growth ◽  
Low Level ◽  
Test Kit ◽  
Before And After ◽  
Vancomycin Resistant ◽  
High Level ◽  
Level Resistance

AbstractObjectivesThe increasing prevalence of vancomycin resistant enterococci (VRE) necessitates a reliable detection of VRE especially for low level resistance mediated by vanB in Enterococcus faecium. In this prospective study we analyzed if vanB mediated vancomycin resistance can be reliably detected by Vitek2.Methods1344 enterococcal isolates from routine clinical specimens were tested by Vitek2 (bioMérieux, Nürtingen, Germany). Additionally, a bacterial suspension (0.5 McFarland) was inoculated on a chromID VRE screening agar (bioMérieux) and incubated for 48 hours. If vancomycin was tested susceptible by Vitek2 but growth was detected on the screening agar a PCR for vanA/vanB was performed (GeneXpert vanA/B test kit, Cepheid, Frankfurt, Germany). MICs of vancomycin susceptible by Vitek but vanA/B positive isolates were determined before and after cultivation in a broth with increasing concentration of vancomycin.Results156/492 of E. faecium were VRE, predominantly vanB (87.0%) of which 14 were not identified as VRE by Vitek2 (sensitivity 91.0%). The majority (9/14) demonstrated high-level MICs by broth dilution. Even after exposure to increasing vancomycin concentrations MICs remained nearly identical. Three of the undetected isolates demonstrated initial growth on chromID VRE, after the vancomycin exposure additional 7 isolates demonstrated growth on chromID VRE.ConclusionsVitek2 fails to detect vanB mediated vancomycin resistance consistently, especially but not limited to low-level resistance. As this may lead to treatment failure and further dissemination of vanB VRE, additional methods (e.g. culture on VRE screening agar or PCR) are necessary to reliably identify vanB-positive enterococci in clinical routine.

scholarly journals Distribution of aminoglycoside resistance genes in recent clinical isolates of Enterococcus faecalis, Enterococcus faecium and Enterococcus avium

2001 ◽  
Vol 126 (2) ◽  
pp. 197-204 ◽  
Author(s):  
N. KOBAYASHI ◽  
MD. MAHBUB ALAM ◽  
Y. NISHIMOTO ◽  
S. URASAWA ◽  
N. UEHARA ◽  
...  
Keyword(s):  
Enterococcus Faecalis ◽  
Enterococcus Faecium ◽  
Clinical Isolates ◽  
University Hospital ◽  
Aminoglycoside Resistance ◽  
Genes Encoding ◽  
Enterococcal Species ◽  
Aminoglycoside Resistance Genes ◽  
Major Factors ◽  
High Level

Aminoglycoside modifying enzymes (AMEs) are major factors which confer aminoglycoside resistance on bacteria. Distribution of genes encoding seven AMEs was investigated by multiplex PCR for 279 recent clinical isolates of enterococci derived from a university hospital in Japan. The aac(6′)-aph(2″), which is related to high level gentamicin resistance, was detected at higher frequency in Enterococcus faecalis (42·5 %) than in Enterococcus faecium (4·3 %). Almost half of E. faecalis and E. faecium isolates possessed ant(6)-Ia and aph(3′)-IIIa. The profile of AME gene(s) detected most frequently in individual strains of E. faecalis was aac(6′)-aph(2″)+ant(6)-Ia+aph(3′)-IIIa, and isolates with this profile showed high level resistance to both gentamicin and streptomycin. In contrast, AME gene profiles of aac(6′)-Ii+ant(6)-Ia+aph(3′)-IIIa, followed by aac(6′)-Ii alone, were predominant in E. faecium. Only one AME gene profile of ant(6)-Ia+aph(3′)-IIIa was found in Enterococcus avium. The ant(4′)-Ia and ant(9)-Ia, which have been known to be distributed mostly among Staphylococcus aureus strains, were detected in a few enterococcal strains. An AME gene aph(2″)-Ic was not detected in any isolates of the three enterococcal species. These findings indicated a variety of distribution profiles of AME genes among enterococci in our study site.

Canadian national survey of prevalence of antimicrobial resistance among clinical isolates of Streptococcus pneumoniae. Canadian Bacterial Surveillance Network.

1996 ◽  
Vol 40 (9) ◽  
pp. 2190-2193 ◽  
Author(s):  
A E Simor ◽  
M Louie ◽  
D E Low
Keyword(s):  
Streptococcus Pneumoniae ◽  
Antimicrobial Agents ◽  
Clinical Isolates ◽  
Beta Lactam ◽  
Surveillance Network ◽  
Antibiotic Resistant ◽  
Intermediate Resistance ◽  
Resistant Strains ◽  
High Level ◽  
Level Resistance

The antimicrobial susceptibilities of 1,089 clinical isolates of Streptococcus pneumoniae obtained from 39 laboratories across Canada between October 1994 and August 1995 were determined. A total of 91 isolates (8.4%) demonstrated intermediate resistance (MIC, 0.1 to 1.0 microgram/ml) and 36 (3.3%) had high-level resistance (MIC, > or = 2.0 micrograms/ml) to penicillin. Penicillin-resistant strains were more likely to have been recovered from normally sterile sites (P = 0.005) and to be cross-resistant to several beta-lactam and non-beta-lactam antimicrobial agents (P < 0.05). These results indicate that there has been a recent significant increase in the prevalence of antibiotic-resistant S. pneumoniae in Canada.

scholarly journals Sparfloxacin Resistance in Clinical Isolates ofStreptococcus pneumoniae: Involvement of Multiple Mutations in gyrA and parC Genes

1998 ◽  
Vol 42 (9) ◽  
pp. 2193-2196 ◽  
Author(s):  
Hideki Taba ◽  
Nobuchika Kusano
Keyword(s):  
Streptococcus Pneumoniae ◽  
Amino Acid ◽  
Antimicrobial Susceptibility ◽  
Susceptibility Testing ◽  
Clinical Isolates ◽  
Amino Acid Substitutions ◽  
Sequencing Analysis ◽  
High Level ◽  
Additional Nucleotide ◽  
Level Resistance

ABSTRACT Antimicrobial susceptibility testing revealed among 150 clinical isolates of Streptococcus pneumoniae 4 pneumococcal isolates with resistance to fluoroquinolones (MIC of ciprofloxacin, ≥32 μg/ml; MIC of sparfloxacin, ≥16 μg/ml). Gene amplification and sequencing analysis of gyrA andparC revealed nucleotide changes leading to amino acid substitutions in both GyrA and ParC of all four fluoroquinolone-resistant isolates. In the case of strains 182 and 674 for which sparfloxacin MICs were 16 and 64 μg/ml, respectively, nucleotide changes were detected at codon 81 in gyrA and codon 79 in parC; these changes led to an Ser→Phe substitution in GyrA and an Ser→Phe substitution in ParC. Strains 354 and 252, for which sparfloxacin MICs were 128 μg/ml, revealed multiple mutations in both gyrA and parC. These strains exhibited nucleotide changes at codon 85 leading to a Glu→Lys substitution in GyrA, in addition to Ser-79→Tyr and Lys-137→Asn substitutions in ParC. Moreover, strain 252 showed additional nucleotide changes at codon 93, which led to a Trp→Arg substitution in GyrA. These results suggest that sparfloxacin resistance could be due to the multiple mutations in GyrA and ParC. However, it is possible that other yet unidentified mutations may also be involved in the high-level resistance to fluoroquinolones in S. pneumoniae.

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