Antimicrobial resistanee and resistant genes of Pseudomonas aeruginosa
10.3760/cma.j.issn.1674-2397.2009.03.007
- VernacularTitle:铜绿假单胞菌耐药性分析及耐药基因检测
- Author:
Tianmei ZHOU
;
Daojun YU
;
Xiaoqin DONG
;
Qiang SHEN
;
Tao WANG
;
Wenjuan TONG
;
Xiang FANG
- Publication Type:Journal Article
- Keywords:
Pseudomonas aeruginosa;
Antimicrobials;
Drug resistance;
Resistance gene
- From:
Chinese Journal of Clinical Infectious Diseases
2009;2(3):154-158
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the trend of antimicrobial resistance and the prevalence of resistant genes in Pseudomonas aeruginosa strains isolated from Hangzhou First People's Hospital.Methods Antimicrobial susceptibilities of 1489 Pseudomonas aeruginosa strains isolated from 2003 to 2007 were statistically analyzed using WHONET.MICs of 11 antimicrobisis to 36 multi-drug-resistant Pseudomonas aerugionosa strains were determined by agar dilution method.Genes of β-lactamases(BLA)and aminoglycoside-modifying enzymes(AMEs)were detected by PCR and the PCR products were sequenced.Results The resistant rates to aztreonam,imipenem,ceftazidime,cefepime,piperacillin,piperacillin/tazobactam.cefoperazone/sulbactam,ciprofloxacin,levofloxacin,gentamicin and amikacin were increased from 13.4%,10.6%,8.7%,7.9%,12.7%,12.7%,6.7%, 15.8%,20.5%,24.7% and 10.9%in 2003 to 35.3%,40.9%,18.4%, 32.4%,32.9%,32.0%,21.9%,37.8%,38.6%, 39.4% and 34.8% in 2007.respectively.Hish MICs of 11 antimicrobiMs for multi-drug resistant Pseudomonas aerouginosa were determined with MIC90≥128 μg/mL.In 36 multi-drug resistant Pseudomonas aeruginosa strains,21(58.3%)strains carried β-lactamase genes and 32 strains(88.9%)carried aminoglycosidemodifying enzyme genes,while the deletion rate of oprD2 was 80.6%(29/36).Conclusions The resistant rates to common antibiotics of Pseudomonas aeruginosa have increased.resulting in multi-drug resistance.Genes of β-lactamases and aminoglycoside-medifying enzymes are prevalent in multi-drug resistant Pseudomonas aeruginosa strains,with the common deletion of oprD2.
