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Objective To analyze the drug resistance gene carrying situation of carbapenem-resistant Klebsiella pneumoniae (CRKP) and molecular epidemiological characteristics to provide a reference basis for studying the bacterial drug resistance.Methods A total of 37 clinically isolated strains of CRKP were collect ed from February 2016 to February 2017.The broth microdilution method was used to determine the strain drug susceptibility.The phenotypes of CRKP carbapenemases were detected by using the modified Hodge test and EDTA-imipenem synergistic method.The drug resistance genes of KPC-2,NDM-1 and OXA-48 were detected by PCR.The sequencing and internet comparison were performed for determining the genotype.The multilocus sequence typing (MLST) was adopted to conduct the genetic correlation study on the strains.The evolutionary trees were constructed by using the MEGA software and the genetic relationship was analyzed by using the eBURST software.Results The drug resistance to commonly used antibacterial drugs was over 90％.The KPC-2 gene was detected in all strains,3 strains simultaneously carried the NDM-1 gene,and other genes were negative.In MLST typing,25 strains were ST11,each 2 strains were ST524 and ST789,each 1 strain was ST35,ST29,ST1066 and ST244 respectively.Also a new ST type(2 strians) was confirmed by the PubMlst database and named as ST1792.The ST11 type group and non-ST11 type group had no statistical difference in the aspects of the age,sex,infection route and antibiotics use(P＜0.05).Conclusion Carrying KPC-2 gene is the main cause leading to bacterial resistance to carbapenem and ST11 type is the most popular clone type.
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Objective To study the drug resistance of multiple‐drug‐resistant Acinetobacter baumannii(MDR‐Ab) and its rela‐tive carbapenemases genes ,in order to provide references for rational use of antibacterial agents .Methods A total of 98 strains of Acinetobacter baumannii(Ab) were identified by using the MicroScan WalkAway96 automated microbial identification susceptibility testing system ,and the resistance genes ,including OXA‐23 ,OXA‐24 ,IMP ,VIM ,TEM and SHV ,were detected by using the poly‐merase chain reaction .DNA sequences of positive amplification products of the resistance gene were analysed .Results The drug re‐sistance rates of 98 strains of MDR‐Ab to penicillin class and cephalosporin class both were 100 .0% ,to imipenem and meropenem were 55 .1% and 54 .1% respectively ,to gentamicin ,amikacin and tobramycin were 100 .0% ,100 .0% and 87 .8% respectively ,to ciprofloxacin ,levofloxacin and gatifloxacin were 89 .8% ,91 .8% and 77 .6% respectively ,to sulfamethoxazole and rifampicin were 91 .8% and 100 .0% respectively ,to polymyxin B and polymyxin were 14 .3% and 11 .2% respectively ,to tetracycline ,minocycline and tigecycline were 100 .0% ,6 .1% and 4 .1% respectively .The results of resistance genes detection in 98 strains of MDR‐Ab showed that 70 strains carried TEM and OXA‐23 gene ,53 strains carried VIM gene ,41 strains carried IMP gene ,while OXA‐24 and SHV genes were not detected .DNA sequence analysis showed that the homology of OXA‐23 ,TEM ,IMP and VIM genes were 98% ,98% ,99% and 99% .Conclusion The condition of antibacterial resistance of MDR‐Ab in this area is very serious ,and TEM and OXA‐23 are the main drug resistance genes .Carrying multiple resistance genes is an important cause of MDR‐Ab resistance . The treatment of patients with Ab infection should be based on the results of drug sensitivity test for rational use of antibacterial a‐gents .
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Objective To investigate the distribution of vancomycin-resistant genes and virulence genes in vancomycin-resistant Enterococcus (VRE) isolates from intensive care unit (ICU).Methods A total of 180 anal swabs were collected from patients in ICU in Tianjin Medical University General Hospital during September 2012 and May 2013.VRE strains were screened by ChromID agar method.Vitek 2 Compact system was used in drug sensitivity test,and the sensitivities to vancomycin and teicoplanin were further determined using Kirby-Bauer disk diffusion method.Vancomycin resistant genes vanA,vanB,vanC1 and virulence genes esp,hyl were detected by polymerase chain reaction(PCR).Results Nineteen strains of vancomycin resistant Enterococcusfaecium were isolated from 180 anal swabs.All 19 VRE isolates were resistant to both vancomycin and teicoplanin,while they were susceptible to linezolid and tigecycline.All VRE isolates carried vanA and esp genes,and hyl gene was positive in 10 isolates.Conclusions VRE isolates from ICU are highly resistant to commonly used antibacterial agents,and most isolates carry vancomycin-resistant genes and virulence genes.Linezolid and tigecycline may be recommended for VRE infection in ICU.
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Objective The pathogenesis of intractable epilepsy was explored by examining the expression of the P-gp , GST-Pi as well as MDR1 in peripheral blood of the patients with intractable epilepsy. The potential of the above mentioned three genes as the biomarkers for treatment of intractable epilepsy was investigated. Methods Thirty-one sub?jects with refractory epilepsy, 33 subjects under good circumstances by antiepileptic drugs, and 37 healthy subjects were included in the present study. fluorescence quantitative polymerase chain reaction and flow cytometry were used to detect mRNA levels of MDR1 and GST-Pi and P-gp of MDR1 in the peripheral blood of the patients, respectively. Results The expression levels of MDR1 and GST-Pi were significantly higher in the AEDs intractable group(1.36±0.14,0.585±0.257) than in the treatment group(0.82±0.15,0.309±0.217, P<0.05)The expression levels of MDR1 and GST-Pi were signifi?cantly higher in the AEDs treatment group than in the normal group(0.27±0.07,0.134±0.223,P<0.05). The expression levels of P-gp were significantly higher in the AEDs of the intractable group(0.104±0.084)than in the treatment group (0.063 ± 0.030, P<0.05). The GST-Pi gene expression levels were significantly higher in three(0.535 ± 0.256)or two (0.425±0.254)kinds of antiepileptic drugs combination therapy than in single drug treatment(0.267±0.265, P<0.05). Leucocyte P-gp levels were significantly higher in combination therapy of three kinds of antiepileptic drugs(0.141 ± 0.096)than in combination therapy of two kinds of antiepileptic drugs(0.071±0.020)or in monotherapy(0.050±0.020, P<0.05). Conclusion MDR1 and GST-Pi gene expression levels of peripheral blood can be used as the reference in?dex for treatment of intractable epilepsy and the resistant index of combination treatment for intractable epilepsy.
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OBJECTIVE To understand the drug resistance genes in Klebsiella pneumoniae (KPN) isolate resistance to 18 kinds of antibacterials which included imipenem and meropenem. METHODS We detected 36 kinds of drug resistance genes for the strain of KPN by PCR method,included the beta-lactamases genes,blaTEM,blaSHV,blaLEN,blaOKP,(blaCTX-M-1,2 and 9) groups,(blaOXA-1,2 and 10) groups,CARB,PER,VEB and GES; the genes of metallo-beta-lactamases genes,IMP,VIM and KPC; the AmpC genes,DHA,ACT,MOX and LAT; the aminoglycosides resistant genes,aac(3)-Ⅰ,aac(3)-Ⅱ,aac(6')-Ⅰb,aac(6')-Ⅱ,ant(2″)-Ⅰ and ant(3″)-Ⅰ; the quinolones resistant gene qnr; the TMP resistant genes,dfrA1 and dfrA17; the disinfectant-sulfanilamide resistantgene,qacE△1-sul1;the integron genes,intⅠ-1,intⅠ-2 and intⅠ-3; and the transposon genes,tnpA and merA.RESULTS We found 9 kinds of drug resistance genes in this KPN isolate. They were the beta-lactamases genes,blaTEM and blaSHV; the metallo-beta-lactamasesgene blaKPC-2; the aminoglycosides resistant genes,aac(3)-Ⅱ and ant(3″)-Ⅰ; the quinolones resistant gene qnr; the TMP resistant gene dfrA17; the disinfectant-sulfanilamide resistant gene qacE△1-sul1 and the integron genes intⅠ-1. CONCLUSIONS We discovere multiple drug resistant genes (some in the chromosome,some are plasmid-mediated) in this isolate. We also find the infrequent plasmid-mediated drug resistant gene blaKPC-2. We think it's concerned with the pan-resistant and the multi-drug resistant genes in this KPN,and we must pay highly attention to this isolate in clinic.
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Objective To investigate the genetic features of pan-drag resistant pseudomonas aeruginosa. Methods The susceptibilities to 14 antibacterial agents were detected in pseudomonas aerations by K-B paper diffusing method. A strain of pan-drug resistant pseudomonas aeruginosa was selected randomly, and was used to amplify genes for β-Lactam antibiotic resistance (TEM, SHV, CTX-M-1 group,CTX-M-2 group, CTX-M-9 group, OXA-1 group, OXA-2 group, OXA-10 group, PER, GES, VEB,CARB, LCR, BEL, DHA, IMP, VIM, SPM, GIM, SIM and oprD2), aminoglycosidase drug resistance genes (including aminoglycosides modification enzymes gent,16S rRNA methylase gene) and genetic markers of plasmid (traA and traF), integrons (tnpA, tnpU and merA), transposons Ⅰ (int Ⅰ 1 ) by PCR,and the sequences of above genes were analyzed. Results The pseudomonas aeruginosa was resistant to all 14 antibacterial agents, and the following genes were positive in PCR: TEM-1 and CARB-3 types of genes for β-Lactam antibiotic resistance (deletion of oprD2), aac (6')-Ⅱ and ant (2")-Ⅰ of aminoglycosidase resistance genes, transposons Ⅰ (int Ⅰ 1 ), and the merit of integrons. Conclusions Pseudomonas aeruginosa shows high resistance to most antibacterial agents, which should draw attention in clinic.
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OBJECTIVE:To screen and analyze the ?-lactamases-resistant genes in imipenem-resistant pseudomonas aeruginosa (IMPRPa). METHODS: ?-lactamases-resistant genes including IMP,VIM and OprD2 in 60 clinically isolated IMPRPa strains were detected by polymerase chain reaction (PCR),and sequence analysis was performed on the PCR amplified products of some of IMP and VIM genes. RESULTS: Of the 60 IMPRPa strains,?-lactamases-resistant positive genes were as follows: IMP gene was positive in 7 strains,VIM gene was positive in 18 strains,and both IMP and VIM genes were positive in 3 strains. Sequencing of the PCR products of IMP and VIM genes were IMP-1 and VIM-2 types,and OprD2 gene deletion was noted in 29 strains. CONCLUSION: OprD2 protein channel deletion and metal-producing ?-lactamases are the chief mechanisms for the resistance of IMPRPa to imipenem.