scholarly journals High incidence of MDR and XDR Pseudomonas aeruginosa isolates obtained from patients with ventilator-associated pneumonia in Greece, Italy and Spain as part of the MagicBullet clinical trial

2019 ◽  
Vol 74 (5) ◽  
pp. 1244-1252 ◽  
Author(s):  
Astrid Pérez ◽  
Eva Gato ◽  
José Pérez-Llarena ◽  
Felipe Fernández-Cuenca ◽  
María José Gude ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Pseudomonas Aeruginosa ◽  
Molecular Epidemiology ◽  
Carbapenem Resistance ◽  
Clonal Diversity ◽  
Resistance Mechanisms ◽  
Ventilator Associated Pneumonia ◽  
Restriction Patterns ◽  
High Incidence ◽  
Tof Ms

Abstract Objectives To characterize the antimicrobial susceptibility, molecular epidemiology and carbapenem resistance mechanisms in Pseudomonas aeruginosa isolates recovered from respiratory tract samples from patients with ventilator-associated pneumonia enrolled in the MagicBullet clinical trial. Methods Isolates were collected from 53 patients from 12 hospitals in Spain, Italy and Greece. Susceptibility was determined using broth microdilution and Etest. MALDI-TOF MS was used to detect carbapenemase activity and carbapenemases were identified by PCR and sequencing. Molecular epidemiology was investigated using PFGE and MLST. Results Of the 53 isolates, 2 (3.8%) were considered pandrug resistant (PDR), 19 (35.8%) were XDR and 16 (30.2%) were MDR. Most (88.9%) of the isolates from Greece were MDR, XDR or PDR, whereas fewer of the isolates from Spain (33.3%) and Italy (43.5%) showed antibiotic resistance. Three Greek isolates were resistant to colistin. Overall, the rates of resistance of P. aeruginosa isolates to imipenem, ciprofloxacin, ceftolozane/tazobactam and ceftazidime/avibactam were 64.1%, 54.7%, 22.6% and 24.5%, respectively. All isolates resistant to ceftolozane/tazobactam and ceftazidime/avibactam (Greece, n = 10; and Italy, n = 2) carried blaVIM-2. Spanish isolates were susceptible to the new drug combinations. Forty-eight restriction patterns and 27 STs were documented. Sixty percent of isolates belonged to six STs, including the high-risk clones ST-111, ST-175 and ST-235. Conclusions MDR/XDR isolates were highly prevalent, particularly in Greece. The most effective antibiotic against P. aeruginosa was colistin, followed by ceftolozane/tazobactam and ceftazidime/avibactam. blaVIM-2 is associated with resistance to ceftolozane/tazobactam and ceftazidime/avibactam, and related to highly resistant phenotypes. ST-111 was the most frequent and disseminated clone and the clonal diversity was lower in XDR and PDR strains.

scholarly journals Molecular Epidemiology and Mechanisms of Carbapenem Resistance in Pseudomonas aeruginosa

2009 ◽  
Vol 53 (11) ◽  
pp. 4783-4788 ◽  
Author(s):  
José-Manuel Rodríguez-Martínez ◽  
Laurent Poirel ◽  
Patrice Nordmann
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Membrane Protein ◽  
Molecular Epidemiology ◽  
Outer Membrane ◽  
Outer Membrane Protein ◽  
Carbapenem Resistance ◽  
Resistance Mechanisms ◽  
Mechanisms Of Resistance ◽  
Genes Encoding ◽  
Imipenem Resistance

ABSTRACT The contributions of different mechanisms of resistance to carbapenems among a collection of imipenem- and meropenem-nonsusceptible Pseudomonas aeruginosa isolates were investigated. This screening included the recently reported extended-spectrum cephalosporinases (ESACs) weakly hydrolyzing carbapenems. Eighty-seven percent of the studied isolates were resistant to imipenem. Genes encoding metallo-β-lactamases or carbapenem-hydrolyzing oxacillinases were not identified. The main mechanism associated with imipenem resistance was the loss of outer membrane protein OprD. Identification of overexpressed ESACs and loss of OprD were observed for 65% of the isolates, all being fully resistant to imipenem. Resistance to meropenem was observed in 78% of the isolates, with all but one also being resistant to imipenem. Overexpression of the MexAB-OprM, MexXY-OprM, or MexCD-OprJ efflux systems was observed in 60% of the isolates, suggesting the contribution of efflux mechanisms in resistance to meropenem. The loss of porin OprD and the overproduction of ESACs were observed in 100% and 92% of the meropenem-resistant isolates, respectively. P. aeruginosa can very often accumulate different resistance mechanisms, including ESAC production, leading to carbapenem resistance.

Molecular epidemiology and mechanisms of carbapenem resistance in Pseudomonas aeruginosa isolates from Chinese hospitals

2010 ◽  
Vol 35 (5) ◽  
pp. 486-491 ◽  
Author(s):  
Jie Wang ◽  
Jian-ying Zhou ◽  
Ting-ting Qu ◽  
Ping Shen ◽  
Ze-qing Wei ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Molecular Epidemiology ◽  
Carbapenem Resistance

scholarly journals Pseudomonas aeruginosa carbapenem resistance mechanisms in Spain: impact on the activity of imipenem, meropenem and doripenem

2011 ◽  
Vol 66 (9) ◽  
pp. 2022-2027 ◽  
Author(s):  
E. Riera ◽  
G. Cabot ◽  
X. Mulet ◽  
M. Garcia-Castillo ◽  
R. del Campo ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Carbapenem Resistance ◽  
Resistance Mechanisms

Molecular epidemiology and carbapenem resistance of Pseudomonas aeruginosa isolated from patients with burns

2021 ◽  
Vol 30 (2) ◽  
pp. 135-141 ◽  
Author(s):  
Younes Khalili ◽  
Mohammad Yousef Memar ◽  
Safar Farajnia ◽  
Khosro Adibkia ◽  
Hossein Samadi Kafil ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Molecular Epidemiology ◽  
Real Time ◽  
Real Time Pcr ◽  
Random Amplified Polymorphic Dna ◽  
Carbapenem Resistance ◽  
Efflux Pumps ◽  
Common Mechanism ◽  
Care Hospital ◽  
Burn Care

Objective: The aim of this study was to investigate the molecular epidemiology and carbapenem resistance mechanisms of Pseudomonas aeruginosa isolated from patients with burns in Azerbaijan, Iran. Method: Pseudomonas aeruginosa was isolated from 38 patients with burns. Disk diffusion and agar dilution methods were used to determine antibiotic susceptibility patterns. The overproduction of AmpC β-lactamase and efflux pumps were detected by phenotypic methods. The presence of carbapenemase-encoding genes was detected by multiplex polymerase chain reaction (PCR). Expression of the OprD gene and MexAB efflux pumps were also evaluated with real-time PCR. Random amplified polymorphic DNA typing (RAPD-PCR) was used for genotyping of carbapenem-resistant Pseudomonas aeruginosa (CRPA). Results: Minimum inhibitory concentration (MIC) assays demonstrated high levels of resistance to all classes of antibiotics except colistin and polymyxin B. The initial screening by carbapenem disks indicated 24 isolates (63.15%) as CRPA. Different mechanisms of carbapenem resistance were observed, including carbapenemase production (8.4%), overexpression of AmpC (25%) and decreased expression of OprD (75%). The overexpression of MexAB efflux pumps was detected in 19 (79.1%) isolates by phenotypic assay or real-time PCR. The resistance to carbapenem was multifactorial in most cases (58.3%). The RAPD genotyping revealed different patterns with nine clusters. Conclusion: According to our results, the prevalence of CRPA is at an alarming level. Our results did not demonstrate an epidemic clone. The most common mechanism of carbapenem resistance was decreased expression of OprD. Therefore, we suggest a reconsideration in the management of CRPA infections of patients in our burn care hospital in Azerbaijan, Iran.

scholarly journals Evaluation of different phenotypic tests for detection of metallo-β-lactamases in imipenem-resistant Pseudomonas aeruginosa

2017 ◽  
Vol 9 (04) ◽  
pp. 249-253 ◽  
Author(s):  
Rohit Sachdeva ◽  
Babita Sharma ◽  
Rajni Sharma
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Large Scale ◽  
Wide Spectrum ◽  
Carbapenem Resistance ◽  
Resistance Mechanisms ◽  
Clinical Samples ◽  
Resistant Strains ◽  
Synergy Test ◽  
Phenotypic Tests ◽  
Simple Screening

Abstract PURPOSE: Pseudomonas aeruginosa causes a wide spectrum of infections including bacteremia, pneumonia, urinary tract infection, etc., Metallo-beta-lactamase (MBL) producing P. aeruginosa is an emerging threat and cause of concern as they have emerged as one of the most feared resistance mechanisms. This study was designed to know the prevalence of MBL production in P. aeruginosa and to evaluate the four phenotypic tests for detection of MBL production in imipenem-resistant clinical isolates of P. aeruginosa. METHODS: Totally, 800 isolates of P. aeruginosa isolated from various clinical samples were evaluated for carbapenem resistance and MBL production. All imipenem-resistant strains were tested for carabapenemase production by modified Hodge test. Screening for MBL production was done by double-disc synergy test and combined disc test (CDT). Confirmation of MBL production was done by the E-test (Ab BioDisk, Solna, Sweden). RESULTS: Out of the 800 isolates of P. aeruginosa, 250 isolates were found resistant to imipenem. Based on the results of E-test, 147 (18.37%) isolates of P. aeruginosa were positive for MBL production. The CDT has the highest sensitivity and specificity for the detection of MBL production as compared to other tests. CONCLUSION: The results of this study are indicative that MBL production is an important mechanism of carbapenem resistance among P. aeruginosa. Use of simple screening test like CDT will be crucial step toward large-scale monitoring of these emerging resistant determinants. Phenotypic test for MBL production has to be standardized, and all the isolates should be routinely screened for MBL production.

scholarly journals 485. Clinical and Molecular Epidemiology of Carbapenem Non-susceptible Citrobacter sp.

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S237-S238
Author(s):  
Ahmed Babiker ◽  
Daniel R Evans ◽  
Marrisa P Griffifth ◽  
Roberta T Mettus ◽  
Christi L McElheny ◽  
...  
Keyword(s):  
Molecular Epidemiology ◽  
Medical Center ◽  
Carbapenem Resistance ◽  
Healthcare Setting ◽  
Antibiotic Consumption ◽  
Resistance Mechanisms ◽  
University Of Pittsburgh ◽  
Trends Over Time ◽  
Epidemiological Trends ◽  
Healthcare Associated

Abstract Background Carbapenem non-susceptible Citrobacter sp. (CNSC) are becoming increasingly recognized as healthcare-associated (HA) pathogens, but data on clinical and molecular epidemiology, species diversity and mechanisms of carbapenem resistance are lacking. Methods We reviewed patients at University of Pittsburgh Medical Center with CNSC positive cultures from 2000 to 2018. The diversity of CNSC species among a subset of isolates from all UPMC sites was confirmed by 16S rRNA typing, and the presence of carbapenemase enzymes in the same isolates was determined by PCR amplificon. Minimum inhibitory concentrations (MICs) were determined by broth microdilution. Significance of epidemiological trends over time was determined by linear regression, and correlation with antibiotic consumption was determined by cross-correlation using STATA v15. Results Between 2000 and 2018, 3% (78/2817) of all Citrobacter sp. were CNS. CNSC rates increased from 4% in 2000 to 10% in 2018 (R2 = 0.206, P = 0.05), as did carbapenem consumption (6.5–34.5 DDDs/1000, R2 = 0.831, P < 0.001) (Figure 1). Twenty-one isolates from 19 patients were available for additional analysis. Patients had multiple comorbidities (84%), frequently acquired CNSC in the healthcare setting (84%), were colonized with other organisms (68%), and had high rates of in-hospital mortality/discharge to hospice (47%) (Table 1). C. freundii was the dominant species identified (16/21), followed by C. farmeri (2/21), C. koseri (2/21), and C. werkmanii (1/21). Carbapenemases were identified in 14 isolates, including KPC (n = 12), NDM (n = 2), and OXA-48 (n = 1) (Table 2). Isolates were frequently susceptible to ceftazidime–avibactam (MIC median [IQR]: 2[0.5,8]) 81%) and meropenem-vaborbactam (86%) (MIC median [IQR] 0.12[0.3,0.5]) (Table 2). Conclusion CNSC species are diverse, have emerged as an HA pathogen at our center, and cause high rates of mortality. Further studies, including ongoing genome sequencing and analysis, are required to better elucidate CNSC diversity and resistance mechanisms. Disclosures All authors: No reported disclosures.

Distribution of carbapenem resistance mechanisms in clinical isolates of XDR Pseudomonas aeruginosa

2019 ◽  
Vol 38 (8) ◽  
pp. 1547-1552 ◽  
Author(s):  
Annalisa De Rosa ◽  
Nico T. Mutters ◽  
Claudio M. Mastroianni ◽  
Stefan J. Kaiser ◽  
Frank Günther
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Carbapenem Resistance ◽  
Resistance Mechanisms ◽  
Clinical Isolates

scholarly journals Problematic clinical isolates of Pseudomonas aeruginosa from the university hospitals in Sofia, Bulgaria: current status of antimicrobial resistance and prevailing resistance mechanisms

2007 ◽  
Vol 56 (7) ◽  
pp. 956-963 ◽  
Author(s):  
Tanya Strateva ◽  
Vessela Ouzounova-Raykova ◽  
Boyka Markova ◽  
Albena Todorova ◽  
Yulia Marteva-Proevska ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antimicrobial Agents ◽  
Carbapenem Resistance ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Clinical Isolates ◽  
Current Status ◽  
University Hospitals ◽  
Active Efflux ◽  
Genes Encoding

A total of 203 clinical isolates of Pseudomonas aeruginosa was collected during 2001–2006 from five university hospitals in Sofia, Bulgaria, to assess the current levels of antimicrobial susceptibility and to evaluate resistance mechanisms to antipseudomonal antimicrobial agents. The antibiotic resistance rates against the following antimicrobials were: carbenicillin 93.1 %, azlocillin 91.6 %, piperacillin 86.2 %, piperacillin/tazobactam 56.8 %, ceftazidime 45.8 %, cefepime 48.9 %, cefpirome 58.2 %, aztreonam 49.8 %, imipenem 42.3 %, meropenem 45.5 %, amikacin 59.1 %, gentamicin 79.7 %, tobramycin 89.6 %, netilmicin 69.6 % and ciprofloxacin 80.3 %. A total of 101 of the studied P. aeruginosa isolates (49.8 %) were multidrug resistant. Structural genes encoding class A and class D β-lactamases showed the following frequencies: bla VEB-1 33.1 %, bla PSE-1 22.5 %, bla PER-1 0 %, bla OXA-groupI 41.3 % and bla OXA-groupII 8.8 %. IMP- and VIM-type carbapenemases were not detected. In conclusion, the studied clinical strains of P. aeruginosa were problematic nosocomial pathogens. VEB-1 extended-spectrum β-lactamases appear to have a significant presence among clinical P. aeruginosa isolates from Sofia. Carbapenem resistance was related to non-enzymic mechanisms such as a deficiency of OprD proteins and active efflux.

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