Diffusion of beta-lactam antibiotics through liposome membranes reconstituted from purified porins of the outer membrane of Pseudomonas aeruginosa.

The role of the outer membrane (OM) was investigated in relation to the high level of intrinsic antibiotic resistance of Pseudomonas aeruginosa ATCC 9027. OM penetration barriers were measured by comparing turbidimetric growth curves of EDTA-treated and normal cells exposed to carbenicillin, moxalactam (LY 127935), gentamicin, tobramycin, rifampin, novobiocin, and vancomycin. OM barriers were also measured for carbenicillin and moxalactam in P. aeruginosa strain K 799/61, a hypersusceptible mutant presumed to have lost its penetration barrier in the cell envelope. Most antibiotics penetrated the OM efficiently and there was little difference between the two strains. The evidence therefore suggests that intrinsic resistance of P. aeruginosa, especially to the beta-lactam antibiotics, is not mainly due to the OM. A penetration barrier situated deeper within the cell envelope is hypothesized, the size of which in relation to any antibiotic may be estimated by comparing the IC50 values of EDTA-treated cells of the two strains.

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Growing Menace of Antibacterial Resistance in Clinical Isolates ofPseudomonas aeruginosain Nepal: An Insight of Beta-Lactamase Production

BioMed Research International ◽

10.1155/2016/6437208 ◽

2016 ◽

Vol 2016 ◽

pp. 1-8 ◽

Cited By ~ 2

Author(s):

Shamshul Ansari ◽

Rabindra Dhital ◽

Sony Shrestha ◽

Sangita Thapa ◽

Ram Puri ◽

...

Keyword(s):

Pseudomonas Aeruginosa ◽

Antibiotic Resistance ◽

Opportunistic Pathogen ◽

Resistance Rate ◽

Diffusion Method ◽

Beta Lactamase ◽

Beta Lactam ◽

Beta Lactam Antibiotics ◽

Microbiological Methods ◽

Immunosuppressed Patients

Introduction. Pseudomonas aeruginosais the most frequently isolated organism as it acts as the opportunistic pathogen and can cause infections in immunosuppressed patients. The production of different types of beta-lactamases renders this organism resistant to many commonly used antimicrobials. Therefore, the aim of this study was to document the antibiotic resistance rate inPseudomonas aeruginosaisolated from different clinical specimens.Methods. Pseudomonas aeruginosarecovered was identified by standard microbiological methods. Antibiotic susceptibility testing was performed by modified Kirby-Bauer disc diffusion method following Clinical and Laboratory Standard Institute (CLSI) guidelines and all the suspected isolates were tested for the production of ESBLs, MBLs, and AmpC.Results.Out of total (178) isolates, 83.1% were recovered from the inpatient department (IPD). Majority of the isolates mediated resistance towards the beta-lactam antibiotics, while nearly half of the isolates were resistant to ciprofloxacin. Most of the aminoglycosides used showed resistance rate up to 75% but amikacin proved to be better option. No resistance to polymyxin was observed. ESBLs, MBLs, and AmpC mediated resistance was seen in 33.1%, 30.9%, and 15.7% isolates, respectively.Conclusions. Antibiotic resistance rate and beta-lactamase mediated resistance were high. Thus, regular surveillance of drug resistance is of utmost importance.

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Pseudomonas aeruginosa Resistance to beta-lactam antibiotics

Infectious Diseases Newsletter ◽

10.1016/0278-2316(91)90029-y ◽

1991 ◽

Vol 10 (12) ◽

pp. 97-101 ◽

Cited By ~ 1

Author(s):

B. Giwercman ◽

N. Høiby

Keyword(s):

Pseudomonas Aeruginosa ◽

Beta Lactam ◽

Beta Lactam Antibiotics

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A TEM-derived extended-spectrum beta-lactamase in Pseudomonas aeruginosa.

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.40.11.2488 ◽

1996 ◽

Vol 40 (11) ◽

pp. 2488-2493 ◽

Cited By ~ 47

Author(s):

P Mugnier ◽

P Dubrous ◽

I Casin ◽

G Arlet ◽

E Collatz

Keyword(s):

Pseudomonas Aeruginosa ◽

Clinical Strain ◽

Beta Lactamase ◽

Beta Lactam ◽

Aminoglycoside Resistance ◽

Double Mutation ◽

Extended Spectrum Beta Lactamase ◽

Beta Lactam Antibiotics ◽

Extended Spectrum ◽

High Level

A clinical strain of Pseudomonas aeruginosa, PAe1100, was found to be resistant to all antipseudomonal beta-lactam antibiotics and to aminoglycosides, including gentamicin, amikacin, and isepamicin. PAe1100 produced two beta-lactamases, TEM-2 (pI 5.6) and a novel, TEM-derived extended-spectrum beta-lactamase called TEM-42 (pI 5.8), susceptible to inhibition by clavulanate, sulbactam, and tazobactam. Both enzymes, as well as the aminoglycoside resistance which resulted from AAC(3)-IIa and AAC(6')-I production, were encoded by an 18-kb nonconjugative plasmid, pLRM1, that could be transferred to Escherichia coli by transformation. The gene coding for TEM-42 had four mutations that led to as many amino acid substitutions with respect to TEM-2: Val for Ala at position 42 (Ala42), Ser for Gly238, Lys for Glu240, and Met for Thr265 (Ambler numbering). The double mutation Ser for Gly238 and Lys for Glu240, which has so far only been described in SHV-type but not TEM-type enzymes, conferred concomitant high-level resistance to cefotaxime and ceftazidime. The novel, TEM-derived extended-spectrum beta-lactamase appears to be the first of its class to be described in P. aeruginosa.

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