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 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
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.
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.
铜绿假单胞菌( Pseudomonas aeruginosa) 属于非发酵类假单胞菌, 广泛存在于自然界中, 也可广泛定植于人体消化道、呼吸道、皮肤及泌尿道等部位。20 世纪70 年代, 铜绿假单胞菌仅被认为是导致粒细胞缺乏患者发生致死性菌血症的病原体, 而到上世纪末及本世纪初, 铜绿假单胞菌已是医院获得性感染的主要病原体[ 1] 。在皮肤黏膜发生破坏( 如气管插管、烧伤、机械通气) , 免疫功能低下( 如中性粒细胞缺乏、细胞免疫功能缺陷) , 以及菌群失调的患者, 铜绿假单胞菌感染的发生率相当高。汪复等[ 2] 对国内主要地区的12所教学医院临床分离细菌资料的统计发现在所分离的革兰阴性菌中铜绿假单胞菌占16. 4% , 仅次于大肠埃希菌。在铜绿假单胞菌临床感染率不断增加的同时, 铜绿假单胞菌耐药率逐渐增加, 特别是耐多药( MDR) 或者泛耐药( PDR) 铜绿假单胞菌的出现, 给临床治疗铜绿假单胞菌感染带来了更大的挑战。本文主要对目前临床上铜绿假单胞菌肺部感染治疗中的难点及临床处理的过度与不足进行阐述。
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.
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.