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.
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
ObjectiveTo investigate the impact of postoperative application of Pseudomonas aeruginosa injection on recurrence free survival (RFS) and overall survival (OS) in patients with abnormal serum calcitonin levels following surgery for medullary thyroid carcinoma (MTC). MethodsA retrospective collection of data was conducted for 214 patients with abnormal serum calcitonin levels following MTC surgery at West China Hospital of Sichuan University from January 2015 to April 2024. Propensity score matching (1∶2) was utilized to match patients’ data to reduce confounding bias, comparing RFS and OS between patients who used (Pseudomonas group) and did not use (control group) Pseudomonas aeruginosa injection. ResultsAfter propensity score matching, 72 patients with abnormal postoperative calcitonin levels were included, with 24 in the Pseudomonas group and 48 in the control group. The median follow-up time for the 72 patients was 66 months (11–168 months). The 1-year RFS rates for the Pseudomonas group and the control group were 100% and 75.0%, respectively, and the 2-year RFS rates were 87.5% and 56.3%, respectively. The RFS in the Pseudomonas group was superior to that in the control group (χ2=4.791, P=0.029). The 5-year OS rates for the Pseudomonas group and the control group were 90.9% and 93.5%, respectively, with no significant difference between the two groups (χ2=0.469, P=0.491). The Cox proportional hazards regression model indicated that the median RFS was extended in the Pseudomonas group [25 months vs. 21 months, RR=0.350, 95%CI (0.135, 0.900), P=0.029], but there was no significant impact on OS [66 months vs. 69 months, RR=2.22, 95%CI (0.229, 21.444), P=0.503]. ConclusionPostoperative use of Pseudomonas aeruginosa injection in MTC patients with abnormal serum calcitonin level shows significant improvement in RFS, but no significant change in OS.
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 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 explore the role of CD4+CD25+ Treg cells in chronic pulmonary infection caused by Pseudomonas aeruginosa(PA).Methods Sixty SD rats were randomly divided into a PA group and a control group(n=30 in each group).Chronic lung infection model was established by implantation of silicone tube precoated with PA into the main bronchus.Twenty-eight days later Treg cells in peripheral blood were measured by fluorescence-activated cell sorting（FACS）.Levels of IL-10 and TGF-β in serum were assayed by ELISA.The expression of Foxp3 mRNA in spleen was measured by RT-PCR.Pathological changes of lung tissue were studed by HE staining.Results Treg/CD4+ T cells in the PA group were significantly more than those in the control group[（19.79±6.45）% vs （5.15±0.47）%，Plt;0.05].The levels of IL-10 and TGF-β were (231.52±54.48)pg/mL and （121.05±7.98）pg/mL in the PA group respectively，which were significantly higher than those in the control group[（35.43±23.56）pg/mL and （36.02±8.94）pg/mL].The expression of Foxp3 mRNA in the PA group was significantly higher compared with the control group(0.80±0.044 vs 0.25±0.054，Plt;0.05）.HE staining revealed that PA caused a intensive inflammatory reaction with lymphocytes infiltration.Conclusion CD4+CD25+ Treg cell is up-regulated and plays an important role in chronic lung infection caused by Pseudomonas aeruginosa.
Objectives
To retrospectively analyze the isolation rate and drug-resistance of pseudomonas aeruginosa in Fuwai Hospital of Chinese Academy of Medical Sciences from 2013 to 2016.
Methods
The specimens were collected and cultured. If the isolated bacteria were from the same part of the same patient, the first isolated strains were only counted. The isolated pathogens were identified and the drug-resistance were analyzed.
Results
A total of 1 404 pseudomonas aeruginosa were isolated. The majority of them were from postoperative recovery room of surgery department (62.1%) and ICU of internal medicine (22.3%). The specimen source were mainly from respiratory tract (75.7%), followed by blood (10.0%) and venous catheter (5.5%). The resistance rate of piperacillin and piperacillin/sulbactam to pseudomonas aeruginosa was 0.6% to 10.4%. The resistance rate of ceftazidime and cefepime was 0.3% to 11.7%. The resistance rate of imipenem and meropenem was 7.6% to 20.1%. The resistance rate of amikacin, gentamicin, and tobramycin was 0.3% to 3.2%. The resistance rate of ciprofloxacin and levofloxacin was 0.6% to 5.2%.
Conclusions
The isolates of pseudomonas aeruginosa are mainly from postoperative recovery room of surgery department and ICU of internal medicine . Imipenem and meropenem are not the best choices for pseudomonas aeruginosa infection. It has great value to combine piperacillin, piperacillin/sulbactam, ceftazidime and cefepime with aminoglycoside or quinolone antibiotics for the treatment of pseudomonas aeruginosa infection which will reduce drug resistance.
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 predictors for carbapenem-resistant Acinetobacter baumannii, Enterobacteriaceae and Pseudomonas aeruginosa (CR-AEP) as the pathogens of bloodstream infection (BSI) for intensive care unit (ICU) patients. Methods A retrospective case-control study based on ICU- healthcare-associated infection (HAI) research database was carried out. The patients who have been admitted to the central ICU between 2015 and 2019 in the ICU-HAI research database of West China Hospital of Sichuan University were selected. The included patients were divided into two groups, of which the patients with ICU-acquired BSI due to CR-AEP were the case group and the patients with BSI due to the pathogens other than CR-AEP were the control group. The clinical features of the two groups of patients were compared. Logistic regression model was used to identify the predictors of BSI due to CR-AEP.ResultsA total of 197 patients with BSI were included, including 83 cases in the case group and 114 cases in the control group. A total of 214 strains of pathogenic bacteria were isolated from the 197 BSI cases, including 86 CR-AEP strains. The results of multivariate logistic regression analysis showed that previous use of tigecycline [odds ratio (OR)=2.490, 95% confidence interval (CI) (1.141, 5.436), P=0.022] was associated with higher possibility for CR-AEP as the pathogens of BSI in ICU patients with BSI, while previous use of antipseudomonal penicillin [OR=0.497, 95%CI (0.256, 0.964), P=0.039] was associated with lower possibility for that. Conclusion Previous use of tigecycline or antipseudomonal penicillin is the predictor for CR-AEP as the pathogens of BSI in ICU patients with BSI.
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.
