scholarly journals Multicopy blaOXA-58 Gene as a Source of High-Level Resistance to Carbapenems in Acinetobacter baumannii

2007 ◽  
Vol 51 (7) ◽  
pp. 2324-2328 ◽  
Author(s):  
Alessia Bertini ◽  
Laurent Poirel ◽  
Sandrine Bernabeu ◽  
Daniela Fortini ◽  
Laura Villa ◽  
...  
Keyword(s):  
Genetic Variability ◽  
Acinetobacter Baumannii ◽  
Copy Number ◽  
Carbapenem Resistance ◽  
Recombination Process ◽  
University Hospital ◽  
Extra Copy ◽  
Multiple Copies ◽  
High Level ◽  
Level Resistance

ABSTRACT The mechanisms at the origin of heterogeneous carbapenem resistance levels observed among Acinetobacter baumannii isolates collected in 2005 in a large University Hospital of Rome, Italy, were investigated. These isolates were related and possessed similar plasmids carrying the carbapenem-hydrolyzing oxacillinase gene bla OXA-58 but showed variable levels of resistance to carbapenems. Analysis of sequences surrounding the bla OXA-58 gene showed genetic variability, with the presence in several isolates of multiple copies of the bla OXA-58 gene; this extra copy number was likely related to an IS26-mediated transposition or recombination process.

scholarly journals Emergence and Distribution of Plasmids Bearing the blaOXA-51-Like Gene with an Upstream ISAba1 in Carbapenem-Resistant Acinetobacter baumannii Isolates in Taiwan

2010 ◽  
Vol 54 (11) ◽  
pp. 4575-4581 ◽  
Author(s):  
Te-Li Chen ◽  
Yi-Tzu Lee ◽  
Shu-Chen Kuo ◽  
Po-Ren Hsueh ◽  
Feng-Yee Chang ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Copy Number ◽  
Recombinant Plasmid ◽  
Gene Dosage ◽  
Carbapenem Resistance ◽  
Carbapenem Resistant ◽  
Genomic Species ◽  
High Level

ABSTRACT The bla OXA-51-like gene with an upstream ISAba1 (ISAba1-bla OXA-51-like gene) was originally found on the chromosomes of carbapenem-resistant or -susceptible Acinetobacter baumannii isolates. However, a plasmid-borne ISAba1-bla OXA-51-like gene has recently been identified in Acinetobacter genomic species 13TU and several A. baumannii isolates in Taiwan, and all of the isolates are carbapenem resistant. This study aimed to characterize the plasmids bearing the ISAba1-bla OXA-51-like gene and their significance in A. baumannii. Among the 117 ISAba1-bla OXA-51-like-harboring isolates collected from 10 hospitals in Taiwan, 58 isolates (49.6%) from 24 clones had the genes located on plasmids that likely originated from a common progenitor. Among the 58 isolates, four had additional copy of the ISAba1-bla OXA-51-like gene on their chromosomes. Based on the analysis of these four isolates, the plasmid-located ISAba1-bla OXA-51-like gene appeared to be acquired via one-ended transposition (Tn6080). The isolates with a plasmid bearing the ISAba1-bla OXA-51-like gene had higher rates of resistance to imipenem (98% versus 46.6%; P < 0.001) and meropenem (98% versus 69%; P = 0.019) than those with the genes chromosomally encoded, which is most likely due to increased gene dosage provided by the higher copy number of associated plasmids. Transformation with a recombinant plasmid harboring only the ISAba1-bla OXA-51-like gene was enough to confer a high level of carbapenem resistance to A. baumannii, eliminating the possible contribution of other factors on the original plasmids. This study demonstrated that the carbapenem resistance-associated plasmids carrying the ISAba1-bla OXA-51-like gene are widespread in A. baumannii strains in Taiwan.

scholarly journals Multicity Outbreak of Carbapenem-Resistant Acinetobacter baumannii Isolates Producing the Carbapenemase OXA-40

2006 ◽  
Vol 50 (9) ◽  
pp. 2941-2945 ◽  
Author(s):  
Karen Lolans ◽  
Thomas W. Rice ◽  
L. Silvia Munoz-Price ◽  
John P. Quinn
Keyword(s):  
Acinetobacter Baumannii ◽  
Carbapenem Resistance ◽  
The United States ◽  
Nucleotide Sequencing ◽  
Sequencing Analysis ◽  
Carbapenem Resistant ◽  
Extended Care ◽  
Care Facilities ◽  
High Level ◽  
First Time

ABSTRACT During 2005 we detected a multicity outbreak of infections or colonization due to high-level imipenem-resistant Acinetobacter baumannii (MIC, 64 μg/ml). One hundred isolates from diverse sources were obtained from seven acute-care hospitals and two extended-care facilities; 97% of the isolates belonged to one clone. Susceptibility testing of the first 42 isolates (January to April 2005) revealed broad resistance profiles. Half of the isolates were susceptible to ceftazidime, with many isolates susceptible only to colistin. The level of AmpC β-lactamase expression was stronger in isolates resistant to ceftazidime. PCR and subsequent nucleotide sequencing analysis identified bla OXA-40. The presence of an OXA-40 β-lactamase in these isolates correlated with the carbapenem resistance. By Southern blot analysis, a bla OXA-40-specific probe revealed that the gene was both plasmid and chromosomally located. This is the first time in the United States that such carbapenem resistance in A. baumannii has been attributable to a carbapenemase.

scholarly journals Carbapenemase Production of Clinical Isolates Acinetobacter baumannii and Pseudomonas aeruginosa from a Bulgarian University Hospital

Folia Medica ◽  
2017 ◽  
Vol 59 (4) ◽  
pp. 413-422 ◽  
Author(s):  
Atanaska P. Petrova ◽  
Irina D. Stanimirova ◽  
Ivan N. Ivanov ◽  
Michael M. Petrov ◽  
Tsonka M. Miteva-Katrandzhieva ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Acinetobacter Baumannii ◽  
Insertion Sequence ◽  
Susceptibility Testing ◽  
Transmembrane Protein ◽  
Carbapenem Resistance ◽  
University Hospital ◽  
Gram Negative ◽  
Main Factors ◽  
Hospital Wards

AbstractBackground: Production of Bla OXA-23, OXA-24, OXA-58 and hyperexpression of OXA-51 due to ISAba1 insertion sequence are the leading causes of carbapenem resistance in Acinetobacter baumannii. The loss of OprD transmembrane protein and the overexpression of some effl ux pumps are considered to be the main factors for carbapenem resistance in Pseudomonas aeruginosa whereas metallo-enzymes’ production has a secondary role. Aim: Тo examine the carbapenem resistance due to carbapenemase production among clinically signifi cant Gram-negative non-fermenters from St George University hospital, Plovdiv: A. baumannii and P. aeruginosa. Materials and methods: Forty three A. baumannii and 43 P. aeruginosa isolates, resistant or with intermediate resistance to imipenem and/or meropenem were included in the study. They were collected from patients admitted in 14 various hospital wards between 2010 and 2014. Both phenotypic and genetic methods were used for identifi cation and antimicrobial susceptibility testing. Results: All A. baumannii demonstrated carbapenemase production determined by a modifi ed Hodge test whereas P. aeruginosa isolates did not show this phenomenon. OXA-23 genes were determined in 97.7% (42 out of 43) of A. baumannii isolates indistinguishable from the sequence of the classical ARI-1 gene. OXA-24, OXA-58 and overexpression of OXA-51 were not registered in any of the isolates. All P. aeruginosa were negative for blaVIM and blaIMP genes. Conclusion: The leading cause of carbapenem resistance in A. baumannii isolates from our hospital is the carbapenemase production due to the expression of OXA- 23 gene, whereas in P. aeruginosa - the loss of transmembrane OprD protein and the effl ux pumps’ hyperexpression are suspected to be the main mechanisms.

scholarly journals Extended-Spectrum Cephalosporinase in Acinetobacter baumannii

2010 ◽  
Vol 54 (8) ◽  
pp. 3484-3488 ◽  
Author(s):  
José-Manuel Rodríguez-Martínez ◽  
Patrice Nordmann ◽  
Esthel Ronco ◽  
Laurent Poirel
Keyword(s):  
Acinetobacter Baumannii ◽  
Clinical Isolate ◽  
Site Directed Mutagenesis ◽  
Directed Mutagenesis ◽  
Extended Spectrum ◽  
Class C ◽  
High Level ◽  
Level Resistance

ABSTRACT An AmpC-type β-lactamase conferring high-level resistance to expanded-spectrum cephalosporins and monobactams was characterized from an Acinetobacter baumannii clinical isolate. This class C β-lactamase (named ADC-33) possessed a Pro210Arg substitution together with a duplication of an Ala residue at position 215 (inside the Ω-loop) compared to a reference AmpC cephalosporinase from A. baumannii. ADC-33 hydrolyzed ceftazidime, cefepime, and aztreonam at high levels, which allows the classification of this enzyme as an extended-spectrum AmpC (ESAC). Site-directed mutagenesis confirmed the role of both substitutions in its ESAC property.

scholarly journals Prevalence and association of PCR ribotypes of Clostridium difficile isolated from symptomatic patients from Warsaw with macrolide-lincosamide-streptogramin B (MLSB) type resistance

2006 ◽  
Vol 55 (2) ◽  
pp. 207-213 ◽  
Author(s):  
Hanna Pituch ◽  
Jon S. Brazier ◽  
Piotr Obuch-Woszczatyński ◽  
Dorota Wultańska ◽  
Felicja Meisel-Mikołajczyk ◽  
...  
Keyword(s):  
Clostridium Difficile ◽  
University Hospital ◽  
Erythromycin Resistance ◽  
Toxin B ◽  
Pcr Ribotyping ◽  
Methylase Gene ◽  
High Level ◽  
The University ◽  
Antibiotic Associated Diarrhoea ◽  
Level Resistance

Isolates (79 in total) of Clostridium difficile obtained over a 2 year period from 785 patients suspected of having C. difficile-associated diarrhoea (CDAD) and being hospitalized in the University Hospital in Warsaw were characterized by toxigenicity profile and PCR ribotyping. Furthermore, their susceptibility to clindamycin and erythromycin was determined. Among the 79 C. difficile isolates, 35 were classified as A+B+, 1 as A+B+CDT+, 36 as A−B+ and 7 as A−B−. A total of 21 different PCR ribotypes was detected. Two main A+B+ strains circulated in our hospital: ribotype 014 and ribotype 046. Unexpectedly, the predominant PCR ribotype was type 017, a known A−B+ strain, and this accounted for about 45·5 % of all isolates cultured from patients with CDAD. Isolates belonging to PCR ribotype 017 were found in cases from epidemics of antibiotic-associated diarrhoea in the internal and surgery units. High-level resistance (MIC⩾256 mg l−1) to clindamycin and erythromycin was found in 39 (49 %) of the C. difficile isolates. Interestingly, 34 (94 %) of macrolide-lincosamide-streptogramin B (MLSB) type resistance strains did not produce toxin A, but produced toxin B and were A−B+ ribotype 017. Thirty-seven of the high-level resistance strains harboured the erythromycin-resistance methylase gene (ermB). C. difficile isolates (2/29) that had high-level clindamycin and erythromycin resistance, and belonged to PCR ribotype 046, were ermB negative. These investigations revealed that the predominant C. difficile strain isolated from symptomatic patients hospitalized in University Hospital in Warsaw was MLSB-positive clindamycin/erythromycin-resistant PCR ribotype 017.

scholarly journals β-lactamase genes in carbapenem resistance Acinetobacter baumannii isolates from a Turkish university hospital

2019 ◽  
Vol 13 (01) ◽  
pp. 50-55
Author(s):  
Umut Safiye Say Coskun ◽  
Emel Caliskan ◽  
Asegul Copur Cicek ◽  
Halbay Turumtay ◽  
Cemal Sandalli
Keyword(s):  
Acinetobacter Baumannii ◽  
Resistance Genes ◽  
Antimicrobial Agents ◽  
Low Frequency ◽  
Carbapenem Resistance ◽  
University Hospital ◽  
High Rate ◽  
Automated System ◽  
Diffusion Method ◽  
Disk Diffusion Method

Introduction: The spread of Acinetobacter baumannii, resistant to most of the available antimicrobial agents, is a serious health problem. The high rate of carbapenem resistance among Acinetobacter baumannii isolates is considered as a threat to public health. In this study, we aimed to determine the antibiotic resistance and related genes in carbapenem-resistant Acinetobacter baumannii isolates. Methodology: Ninety six isolates of A. baumannii were included. Antimicrobial susceptibility was performed by Phoenix Automated System and disk diffusion method. Carbapenem resistane was characterized by scrneeing of resistance genes such as blaTEM, blaSHV, blaCTX-M1-2, blaPER, blaVEB, blaKPC, blaGES, blaNDM, blaVIM, blaIMP and blaOXA23-24-51-58 using multiplex polymerase chain reaction. Results: Resistance for the levofloxacin, gentamicin, amikacin, and tigecycline were determined as 96.9%, 93.7%, 72.9% and 45.8% respectively. Colistin was the only susceptible antibiotic against all clinical isolates. All isolates were defined as multidrug resistance and of these, 31.2% were extensively drug-resistant (sensitive only to colistin). BlaOXA-51­  and blaOXA-23 genes were detected in 100% strains while blaTEM was found in only 2% strains. There was no amplification for the blaSHV, blaCTX-M1-2, blaPER, blaVEB, blaKPC, blaGES blaNDM, blaVIM, blaIMP and blaOXA24-58 genes. Conclusions: The high frequency of blaOXA-23 and low frequency of blaTEM gene was observed that indicate prevalence of a variety of A. baumannii strains. The rates of resistance genes vary from region to region. Studies are required for the prevention and control of A. baumannii infection and to formulate the strategies of antibiotic usage.

scholarly journals A Plasmid-Borne blaOXA-58 Gene Confers Imipenem Resistance to Acinetobacter baumannii Isolates from a Lebanese Hospital

2008 ◽  
Vol 52 (11) ◽  
pp. 4115-4120 ◽  
Author(s):  
Raffaele Zarrilli ◽  
Domenico Vitale ◽  
Anna Di Popolo ◽  
Maria Bagattini ◽  
Ziad Daoud ◽  
...  
Keyword(s):  
Acinetobacter Baumannii ◽  
Insertion Sequence ◽  
Carbapenem Resistance ◽  
Multidrug Resistant ◽  
Open Reading Frames ◽  
Mosaic Structure ◽  
University Hospital ◽  
Origins Of Replication ◽  
Imipenem Resistance ◽  
Reading Frames

ABSTRACT We investigated the basis of the carbapenem resistance of 17 multidrug-resistant Acinetobacter baumannii clinical isolates collected from 2004 to 2005 at the Saint George University Hospital in Beirut, Lebanon. A. baumannii isolates were clonally related and were susceptible to colistin and trimethoprim-sulfamethoxazole, susceptible or intermediate to ampicillin-sulbactam and meropenem, and resistant to all other antimicrobials. Conjugation experiments demonstrated that resistance to imipenem could be transferred along with a plasmid containing the carbapenem-hydrolyzing oxacillinase bla OXA-58 gene. The plasmid that we called pABIR was 29,823 bp in size and showed a novel mosaic structure composed of two origins of replication, four insertion sequence (IS) elements, and 28 open reading frames. The bla OXA-58 gene was flanked by IS18 and ISAba3 elements at the 5′ and 3′ ends, respectively. The production of the carbapenem-hydrolyzing oxacillinase OXA-58 was apparently the only mechanism for carbapenem resistance in A. baumannii isolates causing the outbreak at the Lebanese Hospital.

Outbreak of Infections in a Greek University Hospital Involving a Single Clone of High-Level Aminoglycoside-ResistantEnterococcus faecalis

2000 ◽  
Vol 21 (12) ◽  
pp. 786-789 ◽  
Author(s):  
Spyros Pournaras ◽  
Athanassios Tsakris ◽  
Mary E. Kaufmann ◽  
John Douboyas ◽  
Antonios Antoniadis
Keyword(s):  
Enterococcus Faecalis ◽  
Resistance Genes ◽  
University Hospital ◽  
Aminoglycoside Resistance ◽  
Single Clone ◽  
Aminoglycoside Resistance Genes ◽  
High Level ◽  
Level Resistance

Among 145Enterococcus faecalisisolates recovered during a 15-month period (April 1997-June 1998) in AHEPA University Hospital, Thessaloniki, Greece, 94 (65%) exhibited high-level resistance to gentamicin or streptomycin and 61 (42%) to both aminoglycosides; 73% of the high-level aminoglycoside-resistantE faecalisisolates belonged to a single clone carrying the geneaac(6')-Ie-aph(2”)-Ia. These findings differ from those of other regions, where high-level aminoglycoside-resistance genes are dispersed into genetically unrelated strains.

scholarly journals Outbreak of Infections Caused by Pseudomonas aeruginosa Producing VIM-1 Carbapenemase in Greece

2000 ◽  
Vol 38 (3) ◽  
pp. 1290-1292 ◽  
Author(s):  
Athanassios Tsakris ◽  
Spyros Pournaras ◽  
Neil Woodford ◽  
Marie-France I. Palepou ◽  
Gioia S. Babini ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Gel Electrophoresis ◽  
Pulsed Field Gel Electrophoresis ◽  
University Hospital ◽  
Pulsed Field ◽  
Serotype O ◽  
Class B ◽  
High Level ◽  
Level Resistance

Resistance to imipenem and meropenem was observed in 211 (16.5%) isolates of Pseudomonas aeruginosa recovered in a Greek university hospital during 1996 to 1998. In six isolates selected from throughout this period, high-level resistance to both carbapenems (MICs ≥ 128 μg/ml) was associated with production of the class B β-lactamase VIM-1. bla VIM-bearing isolates belonged to serotype O:12 and were indistinguishable by pulsed-field gel electrophoresis.

scholarly journals Genetic Factors Associated with Elevated Carbapenem Resistance in KPC-Producing Klebsiella pneumoniae

2010 ◽  
Vol 54 (10) ◽  
pp. 4201-4207 ◽  
Author(s):  
Brandon Kitchel ◽  
J. Kamile Rasheed ◽  
Andrea Endimiani ◽  
Andrea M. Hujer ◽  
Karen F. Anderson ◽  
...  
Keyword(s):  
United States ◽  
Klebsiella Pneumoniae ◽  
Copy Number ◽  
Gene Copy Number ◽  
Carbapenem Resistance ◽  
The United States ◽  
Gene Copy ◽  
Sequencing Analysis ◽  
Low Level ◽  
High Level

ABSTRACT In the United States, the most prevalent mechanism of carbapenem resistance among Enterobacteriaceae is the production of a Klebsiella pneumoniae carbapenemase (KPC). KPC-producing isolates often exhibit a range of carbapenem MICs. To better understand the factors that contribute to overall carbapenem resistance, we analyzed 27 KPC-producing K. pneumoniae isolates with different levels of carbapenem resistance, 11 with low-level (i.e., meropenem or imipenem MIC ≤ 4 μg/ml), 2 with intermediate-level (i.e., meropenem and imipenem MIC = 8 μg/ml), and 14 with high-level (i.e., imipenem or meropenem MIC ≥ 16 μg/ml) carbapenem resistance, that were received from throughout the United States. Among 14 isolates that exhibited high-level carbapenem resistance, Western blot analysis indicated that 10 produced an elevated amount of KPC. These isolates either contained an increased bla KPC gene copy number (n = 3) or had deletions directly upstream of the bla KPC gene (n = 7). Four additional isolates lacked elevated KPC production but had high-level carbapenem resistance. Porin sequencing analysis identified 22 isolates potentially lacking a functional OmpK35 and three isolates potentially lacking a functional OmpK36. The highest carbapenem MICs were found in two isolates that lacked both functioning porins and produced elevated amounts of KPC. The 11 isolates with low-level carbapenem resistance contained neither an upstream deletion nor increased bla KPC copy number. These results suggest that both bla KPC copy number and deletions in the upstream genetic environment affect the level of KPC production and may contribute to high-level carbapenem resistance in KPC-producing K. pneumoniae, particularly when coupled with OmpK36 porin loss.

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