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 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 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.
ObjectiveTo observe the effectiveness and safety of pseudomonas aeruginosa preparation in treating refractory seroma after breast cancer surgery.MethodsA total of 76 patients with refractory seroma after breast cancer surgery who underwent surgery from October 2018 to August 2019 in our hospital were selected. The subjects were randomly divided into two groups. The patients in the control group (n=36) adopted negative pressure drainage connected with indwelling needle in the lower position of the seroma chamber; on the basis, patients in the experimental group (n=400) were injected with pseudomonas aeruginosa preparation into the seroma chamber. The drainage time, total drainage volume, recurrence rate, and incidence of complications of the two groups were compared.ResultsThere were 4 cases in the experimental group and 3 cases in the control group were lost followed-up, so only 69 cases enrolled in data analysis. The drainage time, total drainage volume, and the recurrence rate of the experimental group were all shorter or less than those of the control group (P<0.05). But there was no significant difference in the incidence of complications between the experimental group and the control group (P>0.05), such as fever, inflamed skin, and infection of incision.ConclusionPseudomonas aeruginosa preparation is an effective treatment for refractory seroma after breast cancer surgery, which can shorten the drainage time and promote wound healing.
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.
In this research a strain of isolated Pseudomonas alcaligenes which causes degradation of dexamethasone was acclimated further and its proteins of every position in the bacterium were separated by the osmotic shock method. The separated intracellular proteins which had the highest enzyme activity were extracted by the salting out with ammonium sulfate and were purified with the cation exchange chromatography and gel chromatography. The purified proteins which was active to cause degradation of dexamethasone had been detected were cut with enzyme and were analyzed with mass spectrometry. The results showed that the degradation rate to dexamethasone by acclimated Pseudomonas alcaligenes were increased from 23.63% to 52.84%. The degrading enzymes were located mainly in the intracellular of the bacteria and its molecular weight was about 41 kD. The specific activity of the purified degrading enzymes were achieved to 1.02 U·mg-1. Its 5-peptide amino acid sequences were consistent with some sequences of the isovaleryl-CoA dehydrogenase. The protein enzyme may be a new kind degrading enzyme of steroidal compounds. Our experimental results provided new strategies for cleanup of dexamethasone in water environment with microbial bioremediation technique.
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 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.