Characterization of a novel extended-spectrum beta-lactamase from Pseudomonas aeruginosa

Nordmann, Patrice; Ronco, E; Naas, Thierry; Duport, Catherine; Michel-Briand, Y; Labia, Roger

doi:10.1128/aac.37.5.962

Cited by 192 publications

(156 citation statements)

References 37 publications

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“…Ceftazidime is an important and effective antimicrobial agent for the therapy of serious infections due to multidrug resistance in P. aeruginosa. A surge in ceftazidime resistance in human clinical isolates of P. aeruginosa results from the production of acquired β-lactamase, the constitutive overproduction of AmpC, or an activation of the MexAB-OprM or MexXY-OprM efflux systems (Lindberg et al, 1987;Li et al, 1994;Stapleton et al, 1995;Nordmann and Guibert, 1998;Aires et al, 1999;Kuga et al, 2000;Masuda et al, 2000;Livermore, 2002). The molecular mechanism of canine ceftazidime resistance in P. aeruginosa isolates still requires further clarification.…”

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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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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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“…GES-1 is reported to not be closely related to any other plasmid-mediated β-lactamase; nevertheless, it demonstrates 36% homology to a carbenicillinase produced by Proteus mirabilis 11 . The PER-1 β-lactamase was first discovered in strains of P. aeruginosa isolated from patients in Turkey 15 . There are limited reports describing the prevalence of the OXA, VEB, PER, and GES types of ESBLs in clinical isolates of P. aeruginosa in Iran.…”

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confidence: 99%

Distribution of the bla OXA , bla VEB-1 , and bla GES-1 genes and resistance patterns of ESBL-producing Pseudomonas aeruginosa isolated from hospitals in Tehran and Qazvin, Iran

Amirkamali

Naserpour-Farivar

Azarhoosh

et al. 2017

Rev. Soc. Bras. Med. Trop.

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Introduction:Pseudomonas aeruginosa is one of the most common nosocomial pathogens. The emergence of extended spectrum β-lactamases (ESBLs) has been increasingly reported as a major clinical concern worldwide. The main aim of the present study was to determine the distribution of bla OXA , bla PER-1, bla VEB-1, and bla GES-1 genes among ESBL-producing P. aeruginosa isolated from two distinct provinces in Iran. Methods: In this study, a total of 75 (27.5%) ESBL-producing isolates were identified from 273 P. aeruginosa isolates collected from patients in Qazvin and Tehran. Phenotypic detection of ESBLs and antimicrobial susceptibility testing were performed according to the Clinical and Laboratory Standards Institute guidelines. PCR and sequencing were employed to detect bla OXA-1 , bla OXA , bla GES-1, bla PER-1 , and bla VEB-1 genes. Isolate genetic relationships were evaluated by repetitive extragenic palindromic sequence-based PCR (REP-PCR). Results: In total, 59 (78.7%) of the ESBLproducing isolates showed multidrug resistance. The highest rates of susceptibility were observed against colistin (75 isolates, 100%) and polymyxin B (75, 100%) followed by amikacin (44, 58.7%), and piperacillin-tazobactam (40, 53.3%). The bla OXA-1 (37.3%) gene was the most common of the genes investigated, followed by bla OXA-4 (32%), bla GES-1 (16%), and bla VEB-1 (13.3%). REP-PCR identified three different genotypes: types A (89.3%), B (6.7%), and C (4%). Conclusions: We found a significant presence of bla OXA-1 , bla OXA-4 , bla GES-1, and bla VEB-1 genes among P. aeruginosa isolates, highlighting the need for suitable infection control strategies to effectively treat patients and prevent the further distribution of these resistant organisms.

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“…In 1991, PER-1 producing strains of P. aeruginosa were found in Turkey [4] and have been reported in European countries and USA [8ϳ12]. However, there had been no reports on the emergence of PER-1 producing strains of P. aeruginosa in Asian countries, although some strains of Acinetobacter spp.…”

Section: Discussionmentioning

confidence: 99%

“…Although the production of ESBL has been reported primarily in Enterobacteriaceae, there are few reports on the isolation of ESBL-producing P. aeruginosa [3]. PER-1-type blactamase was first detected as an ESBL in P. aeruginosa and was reported to hydrolyze various b-lactams except for imipenem, oxacillin and cephamycins [4,5]. Although there had been no reports on clinical isolates in Japan, PER-1 producing highly resistant strains have been found to be prevalent in P. aeruginosa and Acinetobacter spp.…”

Section: Introductionmentioning

confidence: 99%

Occurrence of PER-1 Producing Clinical Isolates of Pseudomonas aeruginosa in Japan and their Susceptibility to Doripenem

et al. 2006

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The acquisition of resistance by extendedspectrum b-lactamases (ESBL) has been reported primarily for Enterobacteriaceae, but there are few reports on the isolation of ESBL-producing Pseudomonas aeruginosa. PER-1-type ESBL producing P. aeruginosa has been found in various regions around the world but there are no reports of clinical isolates in Japan. During our susceptibility surveillance studies over a 10 year period, we found four clinical isolates resistant to ceftazidime due to production of PER-1. They were resistant to ceftazidime but susceptible in the presence of clavulanic acid, a class A b -lactamase inhibitor. The strains had the ability to hydrolyze ceftazidime. They also had the gene for PER-1-type ESBL. This is the first report of the isolation of PER-1 producing strains in Japan. These four strains were resistant to ceftazidime, cefepime and aztreonam with MICs of 64 mg/ml or more, but were more susceptible to carbapenem antibiotics. In particular, doripenem, which is a novel carbapenem antibiotic, showed good antibacterial activity with a MIC of 2 or 4 mg/ml, which was more potent than meropenem and imipenem. Doripenem also showed good therapeutic efficacy against a systemic infection of mice with a PER-1 producing strain, and was also more potent in vivo than imipenem or meropenem.

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Characterization of a novel extended-spectrum beta-lactamase from Pseudomonas aeruginosa

Cited by 192 publications

References 37 publications

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

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

Distribution of the bla OXA , bla VEB-1 , and bla GES-1 genes and resistance patterns of ESBL-producing Pseudomonas aeruginosa isolated from hospitals in Tehran and Qazvin, Iran

Occurrence of PER-1 Producing Clinical Isolates of Pseudomonas aeruginosa in Japan and their Susceptibility to Doripenem

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