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Objective@#To investigate the in vitro antibacterial activity of triclosan combined with different antibacterial agents against triclosan-resistant multidrug-resistant Acinetobacter baumannii (A.baumannii).@*Methods@#A total of 626 A. baumannii strains were collected from the First Affiliated Hospital of Wenzhou Medical University from 2016 to 2017. The sensitivity of these A. baumannii strains to common antibiotics was detected by VITEK 2-compact automatical microbiological analyzer and the minimum inhibitory concentrations (MIC) of triclosan were detected by agar dilution method. Checkerboard method was used to detect the changes in MIC values of triclosan against 16 triclosan-resistant multidrug-resistant A. baumannii strains after it was used in combination with four external ointments, including gentamicin, erythromycin, chloramphenicol and kanamycin, and three common antibiotics of imipenem, meropenem and ciprofloxacin, respectively. Fractional inhibitory concentration index (FICI) was used to evaluate the joint bacteriostatic effects.@*Results@#Among the 626 A. baumannii strains, 17 were resistant to triclosan with a drug resistance rate of 2.7% (17/626). These triclosan-resistant strains had high MIC values for ciprofloxacin, imipenem, ceftazidime and other commonly used clinical antibiotic and most of them were multidrug-resistant. After triclosan was used in combination with seven different antibacterial drugs, the MIC values of all drugs decreased to various degrees compared with those when they were used alone. Triclosan in combination with gentamicin, chloramphenicol and ciprofloxacin showed synergistic effects on 62.5%, 56.25% and 62.5% of the 16 strains and additive effects on 37.5%, 43.75% and 37.5%, respectively. When it was used in combination with erythromycin, kanamycin, imipenem and meropenem, synergistic effects on 37.5%, 25%, 12.5% and 12.5%, additive effects on 37.5%, 56.25%, 62.5% and 62.5%, and indifferent effects on 25%, 18.75%, 25% and 25% of the strains were detected, respectively. No antagonistic effect was found between triclosan and any of the above antibiotics.@*Conclusions@#Triclosan combined with gentamicin, chloramphenicol and ciprofloxacin had better in vitro antibacterial effects against the triclosan-resistant multidrug-resistant A. baumannii strains in this study with synergistic and additive effects. Some indifferent effects were found between triclosan and kanamycin, erythromycin, imipenem and meropenem, but no antagonistic effects were detected.
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Objective To investigate the in vitro antibacterial activity of triclosan combined with different antibacterial agents against triclosan-resistant multidrug-resistant Acinetobacter baumannii ( A. bau-mannii) . Methods A total of 626 A. baumannii strains were collected from the First Affiliated Hospital of Wenzhou Medical University from 2016 to 2017. The sensitivity of these A. baumannii strains to common an-tibiotics was detected by VITEK 2-compact automatical microbiological analyzer and the minimum inhibitory concentrations ( MIC) of triclosan were detected by agar dilution method. Checkerboard method was used to detect the changes in MIC values of triclosan against 16 triclosan-resistant multidrug-resistant A. baumannii strains after it was used in combination with four external ointments, including gentamicin, erythromycin, chloramphenicol and kanamycin, and three common antibiotics of imipenem, meropenem and ciprofloxacin, respectively. Fractional inhibitory concentration index ( FICI) was used to evaluate the joint bacteriostatic effects. Results Among the 626 A. baumannii strains, 17 were resistant to triclosan with a drug resistance rate of 2. 7％ (17/626). These triclosan-resistant strains had high MIC values for ciprofloxacin, imipenem,ceftazidime and other commonly used clinical antibiotic and most of them were multidrug-resistant. After tri-closan was used in combination with seven different antibacterial drugs, the MIC values of all drugs de-creased to various degrees compared with those when they were used alone. Triclosan in combination with gentamicin, chloramphenicol and ciprofloxacin showed synergistic effects on 62. 5％, 56. 25％ and 62. 5％of the 16 strains and additive effects on 37. 5％, 43. 75％ and 37. 5％, respectively. When it was used in combination with erythromycin, kanamycin, imipenem and meropenem, synergistic effects on 37. 5％, 25％, 12. 5％ and 12. 5％, additive effects on 37. 5％, 56. 25％, 62. 5％ and 62. 5％, and indifferent effects on 25％, 18. 75％, 25％ and 25％ of the strains were detected, respectively. No antagonistic effect was found between triclosan and any of the above antibiotics. Conclusions Triclosan combined with genta-micin, chloramphenicol and ciprofloxacin had better in vitro antibacterial effects against the triclosan-resist-ant multidrug-resistant A. baumannii strains in this study with synergistic and additive effects. Some indiffer-ent effects were found between triclosan and kanamycin, erythromycin, imipenem and meropenem, but no antagonistic effects were detected.
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Objective@#To evaluate the in vitro antibiotic effects of colistin combined with meropenem, levofloxacin or fosfomycin against colistin-heteroresistant Acinetobacter baumannii (A.baumannii).@*Methods@#A total of 576 A. baumannii clinical isolates were collected from the First Affiliated Hospital of Wenzhou Medical University from 2014 to 2015. Minimal inhibitory concentrations (MICs) of colistin against A. baumannii were detected by broth dilution method. Colistin-heteroresistant A. baumannii isolates were screened using population analysis profiles (PAPs). MICs of colistin combined with meropenem, levofloxacin or fosfomycin, and the four drugs used alone against colistin-heteroresistant A. baumannii were detected by checkerboard method and broth dilution method. Fractional inhibitory concentration index (FICI) was calculated to evaluate antibiotic effects.@*Results@#None of the 576 A. baumannii isolates was resistant to colistin as indicated by the broth dilution method. Nine colistin-heteroresistant A. baumannii isolates were identified using PAPs. Compared with the MICs of colistin used alone, the MICs of colistin used in combination with meropenem, levofloxacin or fosfomycin against colistin-heteroresistant isolates were all decreased. Colistin-meropenem combination showed synergistic (55.6%), additive (33.3%) and indifferent effects (11.1%), but no antagonistic effect. Colistin-levofloxacin combination showed synergistic (55.6%), additive (22.2%) and indifferent effects (22.2%), but no antagonistic effect. Colistin-fosfomycin combination showed synergistic (77.8%) and additive (22.2%) effects, but no indifferent or antagonistic effect.@*Conclusion@#In vitro use of colistin in combination with meropenem, levofloxacin or fosfomycin has synergistic and additive antibacterial effects against colistin-heteroresistant A. baumannii. Combinations of colistin-meropenem and colistin-levofloxacin have fewer indifferent effects and no antagonistic effect.
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Objective To investigate the drug resistant genes against carbapenems,aminoglycosides and quinolones and the molecular epidemiology of clinical isolates of Acinetobacter baumannii.Methods Forty non-duplicate strains of Acinetobacter baumannii were collected from clinical specimens in First Affiliated Hospital of Wenzhou Medical University.The identification of strains was conducted by Vitek 2 Compact system.The susceptibilities to antimicrobials commonly used were determined by agar plate dilution method and broth microdilution method.The presence of class B metalloenzyme-encoding genes (blaIMP,blaVIM,blaNDM,blaSIM,blaGIM),class D cabapenemase-encoding genes (blaOXA-23,blaOXA-48,blaOXA-58),16S rRNA methylase genes (armA,rmtB) and quinolone resistance-determining regions (QRDR) in gyrA and parC were detected by polymerase chain reaction (PCR) and sequenced.Chromosomal or plasmid location of blaOXA-23 and armA genes were assessed by Southern blot.Multiple loci sequence classification (MLST) was performed to analyze the molecular epidemiology of these strains.Results All of the 40 isolates were multi-drug resistant Acinetobacterbaumannii (MDR-AB) and showed high level resistance to all of the tested antimicrobial agents excluding colistin and tigecycline.The positive rates of blaOXA-23 and armA were 90％ and 95％,respectively.All of the 40 isolates carried QRDR mutations in gyrA and parC genes,leading to the Ser83→ Leu and the Ser80→ Leu amino-acid substitutions,respectively.Southern blot showed the chromosomal location of blaOXA-23 and armA genes.Six different ST (ST191,ST381,ST373,ST426,ST208 and ST207) were assigned for these isolates by MLST and the most dominant clones were ST191 (23/40) and ST381 (10/40).Conclusions The predominant cabapenemase-encoding gene and 16S rRNA methylase gene of Acinetobacter baumannii isolates in First Affiliated Hospital of Wenzhou Medical University are blaOXA-23 and armA,respectively,which may be located on the chromosome and vertically transmit the drug resistance.ST191 MDR-AB with blaOXa-23 and armA gene clonally spread in this hospital.
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Objective To investigate the mechanisms of tigecycline nonsusceptibility in carbapen-ems-resistant Acinetobacter baumannii ( CRAB) strains in order to provide a theoretical basis for a reasonable use of antibiotics and the control of nosocomial infection .Methods Susceptibility testing of 120 non-dupli-cate CRAB strains to tigecycline was performed by using the broth microdilution method .Minimal inhibitory concentrations ( MIC) of tigecycline against the A.baumannii strains were determined by using the broth mi-crodilution method before and after exposing the strains to Carbonylcyanide-m-chlorophenylhydrazone (CCCP), which was the efflux pump inhibitor .Polymerase chain reaction (PCR) was used to amply the ef-flux pumps genes including adeB, adeJ, adeG, abeM, adeE, adeRS, tetX and tetX1.The real-time PCR was performed to measure the expression of efflux pumps genes including adeB, adeJ, adeG, abeM and adeE.Results A total of 120 CRAB strains were collected including 13 (10.8%) tigecycline non-suscep-tible A.baumannii (TNAB) strains and 107 (89.2%) tigecycline susceptible A.baumannii (TSAB) strains.The MIC values of tigecline to the 120 CRAB strains were in a range of 0.25 μg/ml to 8 μg/ml. The adeR and adeJ genes were detected in 90.0%and 92.5%of the 120 CRAB strains, respectively.The positive rates of adeB, adeS, adeG and abeM genes among the 120 CRAB strains were all 94.2%.None of the three genes including adeE, tetX and tetX1 were detected .The mean expression levels of adeB and adeJ in TNAB strains were respectively increased by 18.69 folds and 5.46 folds as compared with those in sensi-tive strains.No significant increase in the expression of adeG and abeM genes was observed in TNAB strains . A 4-fold decrease in the MIC was observed in 8 out of 13 TNAB isolates treated with 10 μg/ml of CCCP .The CCCP could partially reverse the resistance pattern of tigecycline .Conclusion The efflux pump sys-tems of adeABC and adeIJK rather than the abeFGH and abeM systems might play an important role in reduc-ing the tigecycline susceptibility in carbapenems-resistant A.baumannii strains.
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OBJECTIVE To analyze the risk factors and the drug-resistance of nosocomial acquired lung infection by Chryseobacterium meningosepticum.METHODS A retrospective investigation of the clinical correlative data and the drug sensitivity results of 60 cases with nosocomial acquired lung infection by C.meningosepticum from Jan 2004 to Jan 2006 was conducted in local hospital.RESULTS The patients were mainly distributed at ICU,respiration and neurosurgery wards.They had severe underlying diseases(100.0%),tracheal intubation(56.7%),central venous catheter(25.0%) and urine catheter(16.7%) treatments and applications of more than three antibiotics(68.3%).The drug-resistance of C.meningosepticum was serious.The antibiotic drugs which had higher susceptibility ratio were cefoperazone/sulbactam,fluoroquinolones,et al.CONCLUSIONS The main risk factors of nosocomial acquired lung infection by C.meningosepticum are severe underlying diseases,various invasive treatments,long-term hospitalization and inappropriate use of broad spectrum antibiotics.Clinical isolates are multi-drug resistant to many kinds of antibiotics.