ObjectiveTo get a picture of the distribution of aminoglycoside-resistant genes in pseudomonas aeruginosa in China. MethodsWe electronically searched CBM, CNKI, VIP and WanFang Data for studies that reported aminoglycoside-resistant genes in pseudomonas aeruginosa in China from inception to December 2012. Two reviewers independently screened literature according to the inclusion and exclusion criteria, and extracted data. Then statistical analysis was performed using SPSS 17.0 software. ResultsA total of 1 144 strains of aminoglycoside-resistant pseudomonas aeruginosa from 10 provinces/cities were included. The positive rates of aac(3')-I, aac(3')-Ⅱ, aac(6')-I, aac(6')-Ⅱ, ant(2")-I, ant(3")-I and aph(3')-VI of aminoglycoside modifying enzyme genes were 13.3%, 40.1%, 21.6%, 40.3%, 38.1%, 23.7% and 2.9%, respectively to the north of Huai River, while the rates were 3.2%, 20.2%, 15.9%, 37.6%, 28.3%, 28.5% and 9.1%, respectively to the south of Huai River. The positive rates of rmtA, rmtB and armA of 16S rRNA methylases genes were 20.4%, 19.4% and 0.7%, respectively, while other 16S rRNA methylases genes were not found. ConclusionIn China, aminoglycoside modifying enzyme is the primary mechanism of pseudomonas aeruginosa aminoglycoside-resistant drugs, while 16S rRNA methylation enzyme mechanism is secondary.
There is a worldwide consensus that urgent action is needed to prevent and control multi-drug resistant organisms in health care settings, especially carbapenem-resistant Enterobacteriaceae (CRE), carbapenem-resistant Acinetobacter baumannii (CRAB) and carbapenem-resistant Pseudomonas aeruginosa (CRPsA). In 2017, to focus on this topic, World Health Organization organized experts worldwide to develop guidelines for the prevention and control of CRE, CRPsA and CRAB. In this paper, we introduced the background, development process, main measures, advantages and disadvantages of the guidelines to help infection prevention and control practitioners take actions properly based on the guidelines.
ObjectiveTo study the clinical features, short-term prognosis and risk factors of Pseudomonas Aeruginosa (P.aeruginosa) infection in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). MethodsThis study enrolled patients hospitalized for AECOPD in ten tertiary hospitals of China from September 2017 to July 2021. AECOPD patients with P.aeruginosa infection were included as case group, AECOPD patients without P.aeruginosa infection were randomly selected as control group from the same hospitals and same hospitalization period as the patients in case group, at a ratio of 2∶1. The differences in basic conditions, complications, clinical manifestations on admission and in-hospital prognosis between the two groups were compared, and the risk factors of P.aeruginosa infection were analyzed. ResultsA total of 14007 inpatients with AECOPD were included in this study, and 338 patients were confirmed to have P.aeruginosa infection during hospitalization, with an incidence rate of 2.41%. The in-hospital prognosis of AECOPD patients with P.aeruginosa infection was worse than that of the control group, which was manifested in higher hospital mortality (4.4% vs. 1.9%, P=0.02) and longer hospital stay [13.0 (9.0, 19.25)d vs. 11.0 (8.0, 15.0)d, P=0.002]. In terms of clinical features, the proportions of patients with cough, expectoration, purulent sputum, dyspnea in the case group were higher than those in the control group, and the inflammatory indicators (neutrophil ratio, erythrocyte sedimentation rate) and partial pressure of carbon dioxide in arterial blood gas were higher than those in the control group, while the serum albumin was significantly lower than that in the control group (all P<0.05). Multivariate logistic regression analysis showed that Parkinson's disease [odds ratio (OR)=5.14, 95% confidence interval (CI): 1.43 to 18.49, P=0.012], bronchiectasis (OR=4.97, 95%CI: 3.70 to 6.67, P<0.001), invasive mechanical ventilation (OR=2.03, 95%CI: 1.23 to 3.36, P=0.006), serum albumin<35 g/L (OR=1.40, 95%CI: 1.04 to 1.88, P=0.026), partial pressure of carbon dioxide ≥45 mm Hg (OR=1.38, 95%CI: 1.01 to 1.90, P=0.046) were independent risk factors for P.aeruginosa infection in AECOPD patients. ConclusionsP.aeruginosa infection has a relative high morbidity and poor outcome among AECOPD inpatients. Parkinson’s disease, bronchiectasis, invasive mechanical ventilation, serum albumin below 35 g/L, partial pressure of carbon dioxide ≥45 mm Hg are independent risk factors of P.aeruginosa infection in AECOPD inpatients.
ObjectiveTo explore the relationship between imipenem-resistant Pseudomonas aeruginosa (IRPA) and outer membrane porin protein OprD2 gene mutation.MethodsIRPA strains (n=30) and imipenem-sensitive Pseudomonas aeruginosa strains (n=30) isolated from the clinical specimens in the First Affiliated Hospital of Chengdu Medical College from December 2018 to December 2019 were collected. Bacteria identification and drug sensitivity experiments were performed by VITEK-2 Compact combined with Kirby-Bauer method. Quantitative real-time polymerase chain reaction was used to detect the expression levels of OprD2 gene in the imipenem-resistant group and the imipenem-sensitive group, and then the strains with decreased expression were sequenced.ResultsThe expression level of OprD2 gene in the imipenem-resistant group was significantly lower than that in the imipenem-sensitive group (P=0.048). Compared with the X63152 sequence, all the 11 Pseudomonas aeruginosa strains with significantly decreased OprD2 expression carried genetic variation, which occurred in coding regions. The variation sites presented diversity. The missense mutation of c.308C→G, c.344A→C, c.379G→C, c.471G→C, c.508T→C, c.553G→C, c.556-558CCG→GGC and c.565-566TG→AC caused amino acid change in the loop L2 and L3 of OprD2 porin, which affected the binding to imipenem. In addition, the mutations at 127, 169-171, 175, 177, 604, 628-630, 688, 719, 785, 826, 828, 842-843, 886, 901, 928-930, 934, 936, 944-945, 1039, 1041 and 1274 all resulted in the changes of amino acid. We also detected a deletion (c.1114-1115delAT) and other nonsense mutations. Large fragment deletion of OprD2 gene occurred in Strain 12. ConclusionsThe mutation and deletion of OprD2 gene can reduce the expression lever of OprD2 gene, leading to the resistance to imipenem of Pseudomonas aeruginosa. The variation of OprD2 gene of IRPA from clinical strains is diverse.
Objective To systematically review the resistance of pseudomonas aeruginosa to quinolone in China. Methods Such databases as CNKI, WanFang Data, CBM, VIP, PubMed, EMbase and The Cochrane Library were electronically searched from inception to December 2012, for relevant studies on the resistance mechanism of pseudomonas aeruginosa to quinolone. Two reviewers independently screened literature according to inclusion and exclusion criteria. Then, meta-analysis was performed using RevMan 5.0 software. Results Totally 19 studies were included, involving 723 strains of quinolone-resistant pseudomonas aeruginosa. The statistical results showed that, in the areas to the north of Huai River, the detection rates of gyrA, gyrB, parC and parE were 88.0%, 13.3%, 31.4% and 16.7%, respectively; and in the areas to the south of Huai River, they were 64.6%, 50.0%, 35.4% and 16.7%, respectively. The detection rates of plasmid mediated resistant genes aac (6’)-Ib-cr was 0 (0/66) in the areas to the north of Huai River, and 39% (25/64) in the areas to the south of Huai River. The outer membrane protein expression rate of active efflux system was 68.1%. Conclusion In China, gyrA gene mutation and the active efflux system mainly account for pseudomonas aeruginosa’s resistance to quinolone. DNA topoisomerase IV abnormalities and plasmid mediated resistance is the secondary mechanism.
Objective To investigate the mutations of quinolone resistance determinational region ( QRDR) in fluoroquinolon-resistant Pseudomonas aeruginosa strains isolated from patients with nosocomial pneumonia. Methods Eight-four Pseudomonas aeruginosa strains isolated from patients with nosocomial pneumonia in Xinhua Hospital during January 2006 to December 2007, from whom fluoroquinolon-resistant resisitant ( case) and fluoroquinolon-susceptible ( control ) Pseudomona aeruginosa were identified. The mutation of QRDR was tested by restriction fragment length polymorphism ( RFLP) and gene sequencing.The relationship between QRDR mutations and clinical prescription was analyzed. Results Mutation in QRDR was found in 42 isolates among the 50 fluoroquinlon-resisitant isolates( 84. 0% ) , while no mutation was found in fluoroquinlon-susceptible isolates. The mutation in GyrB Ser464 was found in 34 isolates ( 68. 0% ) . There was statistical difference in the usage of β-lactams between the GyrB-Ser464-mutated group and the non-GyrB-Ser464-mutated group( OR = 11. 3, P = 0. 003 and OR = 3. 5, P = 0. 023) , also in the time of fluoroquinolon usage before isolated ( P = 0. 038) . Conclusions The mutation of QRDR is contributing to fluoroquindor-resisitance of Pseudomona aeruginosa, most of which lies in GyrB Ser464.Abuse of β-lactams and fluoroquinolon may be the risk factors of mutation in GyrB Ser464.
Objective To examine the effects of Pseudomonas aeruginosa(PA)quorum-sensing systems on airway mucus hypersecretion．Methods Sixty Sprague-Dawley rats were intubated with a silicone tube pre-coated with PAO1(wild-type PA strain)，PAO1-JP2(quorum-sensing-mutant strain)or saline in the bronchus．After 28 days，the mRNA and protein expression of MUC5AC in the rats’bronchial epithelia were detected by RT-PCR，alcian blue／periodic acid—Schif(AB／PAS)staining and enzyme linked immunosorbent assay(ELISA)．Results In the PAO1 group，bronchiolar epithelium goblet cells by AB／PAS staining was significantly more than those in the PAO1-JP2 and control groups(both Plt;0．05)．The expression level of MUC5AC mRNA in the PAO1 group was significantly higher than those in the PAO1-JP2 and control groups(both P lt;0．05)．The ELISA showed that the concentration of MUC5AC protein in bronchoalveolar lavage fluid(BALF)in the PAO1 group was much higher than that in the PAO1-JP2 group(P lt;0．05)．Conclusion PA quorum-sensing system plays an important role in airway mucus hypersecretion
Objective To describe and compare the distributions of aminoglycosides modifying enzymes ( AMEs) in imipenem-resistant Pseudomonas aeruginosa ( IRPA) collected from5 cities in China. Methods A total of 146 strains of IRPA were collected from 5 cities of China ( Chengdu, Hangzhou, Beijing, Shanghai, and Guangzhou) . The polymerase chain reaction ( PCR) were used to amplify the genes of AMEs in IRPA. Results Six positive genotypes were amplified out of 16 genotypes of AMEs by PCR. The total positive rate of AMEs is 65. 06% . The positive rates of genes of aac( 3) -Ⅱ, aac( 6′) -Ⅰ, aac( 6′) -Ⅱ, ant( 2″) -Ⅰ, ant ( 3″) -Ⅰ and aph( 3′) -Ⅵ were 33. 6% , 15. 8% , 19. 9% , 28. 8% , 14. 4%, and 4. 8% , respectively. The genotypes of AMEs were discrepant in different areas as 6 genotypes in Huangzhou and Shanghai, 4 genotypes in Chengdu and Beijing, and 3 genotypes in Guangzhou. Conclusion The results show that the positive rate of AMEs genes is high in IRPA, and the distribution is discrepant among different areas.
Objective To explore the overall outcome and its factors of patients with carbapenem-resistant Pseudomonas aeruginosa bloodstream infection (CRPA-BSI). Methods A single-center, retrospective cohort study was carried out. The demographic and clinical data of all emergency patients and inpatients in West China Hospital of Sichuan University from 2017 to 2021 were collected. Firstly, the prognosis of patients with CRPA-BSI was compared with those with carbapenem-sensitive Pseudomonas aeruginosa bloodstream infection (CSPA-BSI). Then Cox regression was used to analyze the factors affecting the prognosis of CRPA-BSI patients. Results A total of 53 patients with CRPA-BSI and 175 patients with CSPA-BSI were enrolled, and they were 1∶1 matched according to the age-adjusted Charlson Comorbidity Index (aCCI) to control for confounding factors. When aCCI was similar, the incidence of poor prognosis in CRPA-BSI patients was significantly higher than that in CSPA-BSI patients [41.5% vs. 18.9%; relative risk=2.20, 95% confidence interval (CI) (1.16, 4.19), P=0.011]. The median length of hospital stay in the CRPA-BSI group was 3 d longer than that in the CSPA-BSI group but the difference was not statistically significant (29 vs. 26 d, P=0.388). With regard to prognostic factors, univariate Cox regression analyses showed that the highest temperature ≤39℃ (P=0.014), hepatobiliary and pancreatic diseases (P=0.011), days of central venous catheterization (P=0.025), days of indwelling urinary catheters (P=0.037), adjustment of medication duration according to drug sensitivity results (P=0.015) and Pitt bacteremia score (P=0.007) were related to the poor prognosis of CRPA-BSI patients. Multiple Cox regression analysis showed that hepatobiliary and pancreatic disease [hazard ratio (HR)=3.434, 95%CI (1.271, 9.276), P=0.015] and Pitt bacteremia score [HR=1.264, 95%CI (1.057, 1.510), P=0.010] were independently associated with poor outcome in CRPA-BSI patients. Conclusions The prognosis of CRPA-BSI patients is worsen than that of CSPA-BSI patients. Hepatobiliary and pancreatic diseases significantly increase the risk of poor outcome in CRPA-BSI patients. Pitt bacteremia score is a predictor of prognosis in patients with CRPA-BSI.
Objective To establish a rat model of chronic pulmonary infection by inoculating Pseudomonas aeruginosa to Sprague-Dawley(SD) rats.Metods Sixty SD rats were divided into 2 groups,ie.the P.aeruginosa group and the control group. Silicone tube precoated with P.aeruginosa was placed into the main bronchus. For the control group, sterile silicon tube was intubated. Results P ． aeruginosa was detected from lung tissue of rats in infected groups.Bacterial number was higher than 103cfu ／ g 28 days after inoculation.The pathological study showed fibrinous proliferation and granulomas formation in the lungs of infected rats 28 days after inoculation.Microscopy examination showed a inflammation predominantly with lymphocyte infiltration.In control group, no bacterial and pathological changes could be detected. Conclusions The animal model with P.aeruginosa chronic pulmonary infection can be established successfully by silicone tubes precoated with P.aeruginosa intubated into the main bronchus.