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.
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.
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.
Objective To evaluate the efficacy and safety of colistin in the treatment of severe infections. Methods PubMed, ISI Web of Knowledge and Wanfang databases were searched. The initial literatures and references listed in the literature were manually searched. Controlled studies were analyzed using RevMan 5. 0 software.Results Eleven studies were enrolled, including five prospective studies and six retrospective studies. Pooled analysis showed that, compared with other therapies, treatment with colistin in severe infections did not improve 28 or 30-day mortality, clinical symptoms, or bacteria clearance,however, increased the risk of kidney damage. Subgroup analysis showed that colistin did not improve symptoms, mortality ( which was even higher in the patients with drug resistant bacteria infection) , or kidney damage in drug resistant bacteria infections and ventilator associated pneumonia ( VAP) compared with the other antibiotic group. Conclusions Colistin is not superior to the other antibiotics in severe infections.However, there are some shortcomings in our meta-analysis due to limited high-quality RCTs, thus welldesigned RCTs are still needed before final conclusion is made.
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.
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.
摘要:目的:探讨老年耐亚胺培南铜绿假单胞菌(IRPA)感染的危险因素以指导临床救治。 方法:采用病例对照研究,选取四川省人民医院干部科2006年1月~2008年12月IRPA院内感染老年患者32例,并随机选择同时期敏感铜绿假单胞菌院内感染48例作为对照,采用单因素(t检验,χ2检验)及多因素Logistic回归进行分析。结果:IRPA分离率为34.8%,IRPA对抗生素的耐药性远远高于敏感铜绿假单胞菌组,但对阿米卡星敏感率达81.3%。单因素分析发现,下列因素与IRPA感染有关:高龄、住院时间≥4周、高急性生理和慢性健康状况(APACHEⅡ)评分、慢性肺部疾病(慢性阻塞性肺疾病COPD/支气管扩张)、分离出IRPA前2周用过亚胺培南/美罗培南、早期联用抗生素、院内获得性肺炎(HAP)。多因素Logistic回归分析表明:长程住院［比值比(OR)= 14.887］,APACHEⅡ评分≥16分(OR=38.908)以及分离出IRPA前2周用过亚胺培南/美罗培南(OR =12.945)是IRPA感染的独立危险因素。结论:长程住院、APACHEⅡ评分≥16分以及亚胺培南/美罗培南的使用是IRPA感染的危险因素。IRPA对阿米卡星敏感率相对较高,但治疗难度大。Abstract: Objective: To study the infection status and risk factors of nosocomial infection caused by imipenemresistant Pseudomonas aeruginosa (IRPA) in elderly patients. Methods: By a casecontrol study, the data of 32 cases of IRPA nosocomial infections were analyzed from Jan. 2006. to Dec. 2008 in cadres Ward of Sichuan Provincial People’s Hospital; 48 cases of Imipenemsensitive pseudomonas aeruginosa infection were randomized as control. Univariate analysis (T test and chisquare test )and multivariate logistic regression analysis were used for statistics. Results: The resistance to antibiotics of IRPA is much higher than the sensitive group.81.3％ of IRPA were sensitive to amikacin. According to univariate analysis,the factors associated with the infection caused by IRPA were age, length of stay in hospital more than 4 weeks, high score of APACHEⅡ, chronic pulmonary disease (COPD/bronchiectasis),imipenem/meropenem used 2 weeks before isolation of IRPA, early combination therapy of antibiotics and hospital acquired pneumonia (HAP). Multivariate logistic regression analysis identified three independent factors: Length of stay in hospital more than 4 weeks, APACHEⅡ score≥16 and imipenem/meropenem used 2 weeks before isolation of IRPA. Conclusion: Long length of stay in hospital, APACHEⅡ score ≥16 and previous imipenem/meropenem use were independent risk factors for IRPA infection. Although the sensitivity of IRPA to amikacin was relatively high, it was difficult to treat in clinical practice.
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.