A combined phenotypic and genotypic method for the detection of Mex efflux pumps in Pseudomonas aeruginosa

Mesaros, Narcisa; Glupczynski, Youri; Avrain, Laëtitia; Caceres, Nancy E.; Tulkens, Paul M.; Bambeke, Françoise Van

doi:10.1093/jac/dkl504

Cited by 81 publications

(67 citation statements)

References 48 publications

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“…Finally out of the 30 drug resistant strains 9 became sensitive after adding curcumin (50μg/ml) with one or the other antimicrobial agents [Table /Fig-4]. Name of antimicrobials strains which became sensitive after adding PaβN(20µg/ml) n=30 strains which became sensitive after adding Curcumin (50µg/ml) A recent study showed that PAβN may be used for phenotypic screening for presence of efflux pump activity in clinical isolates of Pseudomonas aeruginosa along with genotypic methods [25]. Further, another study observed 4 to 8-fold reduction of meropenem MICs among Acinetobacter baumanii using PAβN as efflux pump inhibitor [26].…”

Section: Resultsmentioning

confidence: 99%

Possible Role of Curcumin as ection an Efflux Pump Inhibitor in Multi Drug Resistant Clinical Isolates of Pseudomonas aeruginosa

Negi

Prakash

Gupta

et al. 2014

JCDR

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Section: Resultsmentioning

confidence: 99%

Possible Role of Curcumin as ection an Efflux Pump Inhibitor in Multi Drug Resistant Clinical Isolates of Pseudomonas aeruginosa

Negi

Prakash

Gupta

et al. 2014

JCDR

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“…The ceftazidime MICs were determined by broth microdilution in the absence or presence of 50 mg/l PAβN (Sigma Aldrich, St Louis, MO, USA). The ceftazidime MICs decreased at least 4-fold in the presence of PAβN, likely due to overproduction of the efflux pumps as shown by the positive reaction in the efflux pump inhibition test (Mesaros et al, 2007).…”

Section: Efflux Pump Inhibition Testmentioning

confidence: 99%

Molecular mechanisms of ceftazidime resistance in Pseudomonas aeruginosa isolates from canine and human infections

Du¹,

Kuo²,

Cheng³

et al. 2010

Vet. Med. - Czech

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Sixty-six clinical P. aeruginosa isolates, 17 obtained from canine otitis specimens and 49 received from human patients with bloodstream infections, were collected between February 2007 and January 2008. The minimal inhibitory concentrations (MICs) of the antimicrobial agents of these isolates were determined. Multidrug resistance was common, with 23 (34.8%) isolates found to be ceftazidime resistant. To explore the mechanisms of ceftazidime resistance, PCR analyses were performed to detect drug-resistance genes. The prevalence rate of Ambler class A, B, and D β-lactamase genes were obtained, with bla TEM-1 100%, bla PSE-1 100%, bla OXA-2 96.2%, bla SHV-18 91.3%, bla OXA-17 78.3%, bla VIM-3 26.1%, bla OXA-10 21.7% and bla SHV-1 8.7%. An efflux inhibition assay with the PAβN compound was conducted. The ceftazidime resistance isolates were also tested by RT-qPCR to determine the mRNA expression levels of the oprM and ampC genes. Five (21.7%) of the ceftazidime resistance isolates appeared to overactivate the OprM efflux system. The ampD, ampE, and ampR genes and the ampC-ampR intergenic region were subsequently amplified and sequenced. Five (21.7%) of the ceftazidime resistance isolates from humans and canines had a point mutation in AmpR (Asp135-Asn, n = 3; Als194-Ser, n = 2), which induces AmpC overproduction from 10-to 80-fold. This study first reported ceftazidime resistance in P. aeruginosa from canine otitis specimens, which are closely related to ESBLs (50%), including the overproduction of AmpC (25%) and the OprM efflux system (25%). The ESBLs (100%) played an important role in all ceftazidime resistance isolates from humans, and either AmpC (21.1%) or OprM (21.1%) might be overexpressed within the same isolate. A human patient isolate (H307B) showed simultaneous expression of ESBLs, the OprM efflux system, and AmpC overproduction.

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“…Overexpression of efflux pump MexAB-OprM was established when the expression of mexB was 2-3 folds its expression level in the wild isolate PAO1 [19][20]. The expression level of oprD was also calibrated relative to PAO1 [21].…”

Section: Real-time Pcr Of Porin (Oprd) and Efflux Pumpmentioning

confidence: 99%

Molecular characterization of resistance mechanisms in Pseudomonas aeruginosa isolates resistant to carbapenems

Shaaban

Al‐Qahtani

Al‐Ahdal

et al. 2018

J Infect Dev Ctries

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Introduction: Emergence of carbapenem resistance in Pseudomonas aeruginosa increases the therapeutic dilemma. In this study, we investigated various mechanisms involved in the resistance of P. aeruginosa clinical isolates to carbapenems. Methodology: P. aeruginosa isolates were isolated from different clinical samples. The antimicrobial susceptibility was evaluated by disc diffusion method. Carbapenemases were detected among carbapenem resistant isolates. Expression level of mexB and oprD was determined by real-time PCR. Molecular relatedness among isolates was detected based on pulsed-field gel electrophoresis (PFGE). Results: Ninety P. aeruginosa isolates were purified from clinical specimens. High levels of resistance to imipenem and meropenem were detected in 16 isolates. PCR analysis of carbapenemases indicated the prevalence of Verona integron-encoded metallo-beta-lactamase (VIM); four isolates produced only VIM enzymes (VIM-1 or VIM-2), while the remaining twelve co-produced both VIM-1 or VIM-2 and NDM enzymes. Additionally, real-time PCR analysis elucidated high expression levels of mexB in seven of the carbapenem resistant isolates and low expression of oprD in seven isolates. The identified carbapenem-resistant isolates were clustered into eleven PFGE profiles where clusters E1 and E2 involved isolates exhibiting multiple carbapenemase genes (blaNDM-1, blaVIM-1 and blaVIM-2). Conclusion: Various mechanisms underlying carbapenem resistance have been detected in our P. aeruginosa cohort of isolates. Emergence of P. aeruginosa as a reservoir of multiple carbapenemases is increasing over time limiting the treatment options to this serious infection. This increases the urgency for infection control practices to reduce the incidence of this infection.

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A combined phenotypic and genotypic method for the detection of Mex efflux pumps in Pseudomonas aeruginosa

Abstract: The data plead for combining phenotypic and genotypic approaches in the diagnosis of efflux-mediated resistance in P. aeruginosa.

Cited by 81 publications

References 48 publications

Possible Role of Curcumin as ection an Efflux Pump Inhibitor in Multi Drug Resistant Clinical Isolates of Pseudomonas aeruginosa

Possible Role of Curcumin as ection an Efflux Pump Inhibitor in Multi Drug Resistant Clinical Isolates of Pseudomonas aeruginosa

Molecular mechanisms of ceftazidime resistance in Pseudomonas aeruginosa isolates from canine and human infections

Molecular characterization of resistance mechanisms in Pseudomonas aeruginosa isolates resistant to carbapenems

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