scholarly journals Pseudomonas aeruginosa Polynucleotide Phosphorylase Contributes to Ciprofloxacin Resistance by Regulating PrtR

2019 ◽  
Vol 10 ◽  
Author(s):  
Zheng Fan ◽  
Hao Chen ◽  
Mei Li ◽  
Xiaolei Pan ◽  
Weixin Fu ◽  
...  
2021 ◽  
Vol 9 (2) ◽  
pp. 388
Author(s):  
Marta Hernández-García ◽  
María García-Castillo ◽  
Sergio García-Fernández ◽  
Diego López-Mendoza ◽  
Jazmín Díaz-Regañón ◽  
...  

CrpP enzymes have been recently described as a novel ciprofloxacin-resistance mechanism. We investigated by whole genome sequencing the presence of crpP-genes and other mechanisms involved in quinolone resistance in MDR/XDR-Pseudomonas aeruginosa isolates (n = 55) with both ceftolozane-tazobactam susceptible or resistant profiles recovered from intensive care unit patients during the STEP (Portugal) and SUPERIOR (Spain) surveillance studies. Ciprofloxacin resistance was associated with mutations in the gyrA and parC genes. Additionally, plasmid-mediated genes (qnrS2 and aac(6′)-Ib-cr) were eventually detected. Ten chromosomal crpP-like genes contained in related pathogenicity genomic islands and 6 different CrpP (CrpP1-CrpP6) proteins were found in 65% (36/55) of the isolates. Dissemination of CrpP variants was observed among non-related clones of both countries, including the CC175 (Spain) high-risk clone and CC348 (Portugal) clone. Interestingly, 5 of 6 variants (CrpP1-CrpP5) carried missense mutations in an amino acid position (Gly7) previously defined as essential conferring ciprofloxacin resistance, and decreased ciprofloxacin susceptibility was only associated with the novel CrpP6 protein. In our collection, ciprofloxacin resistance was mainly due to chromosomal mutations in the gyrA and parC genes. However, crpP genes carrying mutations essential for protein function (G7, I26) and associated with a restored ciprofloxacin susceptibility were predominant. Despite the presence of crpP genes is not always associated with ciprofloxacin resistance, the risk of emergence of novel CrpP variants with a higher ability to affect quinolones is increasing. Furthermore, the spread of crpP genes in highly mobilizable genomic islands among related and non-related P. aeruginosa clones alert the dispersion of MDR pathogens in hospital settings.


Drugs ◽  
1995 ◽  
Vol 49 (Supplement 2) ◽  
pp. 175-176 ◽  
Author(s):  
G. Corti ◽  
F. Paradisi ◽  
E. Giganti ◽  
G. Buffini ◽  
E. Tortoli ◽  
...  

ANKEM Dergisi ◽  
2021 ◽  
Author(s):  
Nilüfer Uzunbayır Akel ◽  
Yamaç Tekintaş ◽  
Fethiye Ferda Yılmaz ◽  
İsmail Öztürk ◽  
Mustafa Ökeer ◽  
...  

Pseudomonas aeruginosa is one of the most important causes of hospital infections. Although different antibiotic groups are used for the treatment of P.aeruginosa infections, quinolone groups are distinguished by the advantages of oral administration. However, in recent years, resistance against members of this group has made treatment more difficult. The aim of this study was to investigate the epidemiological relationship and possible mechanisms of resistance in ciprofloxacin resistant P. aeruginosa isolates from Ege University Hospital. The identification of P.aeruginosa bacteria isolated from clinical samples in Ege University Medical Faculty Medical Microbiology Laboratory was determined by VITEK MS automated systems by VITEK compact, antimicrobial susceptibility. The epidemiological relationships of the ciprofloxacin resistant isolates were determined by Enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR). The presence of qnrA, qnrB, qnrS, qepA genes, the quinolone resistance genes and nfxB, mexR, the regulatory genes of the efflux pump, was determined by PCR. The phenylalanine-arginine β-naphthylamide (PAβN) assay was used to determine the activation of the efflux pump. Twenty-two isolates (26.5 %) were found resistant to ciprofloxacin. According to the ERIC-PCR results, 11 unrelated clones were detected. Ciprofloxacin minimum inhibitory concentration (MIC) values were decreased 2-64 times in 10 isolates in the presence of PAIN. No ciprofloxacin MIC change was detected in one isolate. The presence of pump regulatory genes was determined in 10 of the 11 representative isolates, while only qnrB of the genes associated with quinolone resistance was detected in seven representative isolates. qnrA, qnrS, qepA genes were not detected in any isolate. Ciprofloxacin resistant P.aeruginosa isolates are isolated from our hospital. It is noteworthy that the isolates belonging to different genetic groups are in circulation in clinics. Basic resistance mechanisms are thought to be efflux pumps and qnrB genes.


Author(s):  
Zheng Fan ◽  
Xiaolei Pan ◽  
Dan Wang ◽  
Ronghao Chen ◽  
Tongtong Fu ◽  
...  

Pseudomonas aeruginosa is an opportunistic pathogen that shows high intrinsic resistance to a variety of antibiotics. The MexX-MexY-OprM efflux pump plays an important role in the bacterial resistance to aminoglycoside antibiotics. Polynucleotide phosphorylase (PNPase) is a highly conserved exonuclease that plays important roles in RNA processing and bacterial response to environmental stresses. Previously, we demonstrated that PNPase controls the tolerance to fluoroquinolone antibiotics by influencing the production of pyocin in P. aeruginosa. In this study, we found that mutation of the PNPase coding gene (pnp) in P. aeruginosa increases the bacterial tolerance to aminoglycoside antibiotics. We further demonstrate that upregulation of the mexXY genes is responsible for the increased tolerance in the pnp mutant. Furthermore, our experimental results revealed that PNPase controls translation of the armZ mRNA through its 5′ untranslated region (5′-UTR). ArmZ had previously been shown to positively regulate the expression of mexXY. Therefore, our results revealed a novel role of PNPase in the regulation of armZ and subsequently the MexXY efflux pump.


2008 ◽  
Vol 29 (8) ◽  
pp. 716-722 ◽  
Author(s):  
Paul P. Cook ◽  
Titu D. Das ◽  
Michael Gooch ◽  
Paul G. Catrou

Objective.We evaluated the effect of an antimicrobial management effort to decrease ciprofloxacin use on the antibiotic susceptibility of nosocomial Pseudomonas aeruginosa isolates.Design.Retrospective, observational study.Setting.Tertiary care teaching hospital with 731 beds.Methods.The study was conducted between January 1, 2001, and December 31, 2007. Linear regression analyses and Student t tests were used to determine significant changes in drug use among patients and antimicrobial susceptibility patterns among nosocomial P. aeruginosa isolates during the 84-month period.Results.Following implementation of a program to reduce oral and intravenous use of ciprofloxacin in 2005, there was a 56.6% reduction in ciprofloxacin use (P < .001). Significant reductions in the mean percentage of nosocomial P. aeruginosa isolates that were resistant to ciprofloxacin (from 45.0% to 35.2%; P < .002) and the mean incidence of ciprofloxacin resistance (from 0.77 to 0.67 isolates recovered per 1,000 patient-days; P = .03) were noted after implementation of this program. The total quantity of antipseudomonal antibiotics consumed decreased, but the use of certain antipseudomonal antibiotics (ie, cefepime and imipenem/meropenem) increased. Among nosocomial P. aeruginosa isolates, the prevalence of imipenem/meropenem resistance increased, whereas the prevalence of cefepime resistance did not. During the 84 months of the study, there was a significant association between ciprofloxacin use and the percentage of nosocomial P. aeruginosa isolates that were resistant to ciprofloxacin (p = 0.47; P = .011), but there was no correlation between ciprofloxacin use and the incidence of ciprofloxacin resistance (p = 0.21; P = .26).Conclusions.Major reductions in ciprofloxacin use were associated with small but significant improvements in the rate of ciprofloxacin susceptibility among nosocomial P. aeruginosa isolates. The impact of the program on other antipseudomonal agents was variable.


1995 ◽  
Vol 39 (10) ◽  
pp. 2248-2252 ◽  
Author(s):  
E. Cambau ◽  
E. Perani ◽  
C. Dib ◽  
C. Petinon ◽  
J. Trias ◽  
...  

1962 ◽  
Vol 55 (1-2) ◽  
pp. 231-232 ◽  
Author(s):  
G.A. Strasdine ◽  
Loretta A. Hogg ◽  
J.J.R. Campbell

Sign in / Sign up

Export Citation Format

Share Document