AIM:To investigate the resistance of Helicobacter pylori(H.pylori) to ciprofloxacin(CIP),levofloxacin(LVX) and moxifloxacin(MOX) in the Beijing area and to elucidate the resistance mechanisms.METHODS:Seventy-nine H.py...AIM:To investigate the resistance of Helicobacter pylori(H.pylori) to ciprofloxacin(CIP),levofloxacin(LVX) and moxifloxacin(MOX) in the Beijing area and to elucidate the resistance mechanisms.METHODS:Seventy-nine H.pylori clinical strains,isolated from patients who had undergone upper gastrointestinal endoscopy in Peking University First Hospital from 2007 to 2009,were tested for their susceptibility to CIP,LVX and MOX using the E-test method.H.pylori strain 26695 was included in the susceptibility testing as a control strain.According to the minimal inhibitory concentration(MIC) values,a strain was classified as resistant to CIP,LVX or MOX when the MIC was > 1 μg/mL.We amplified by polymerase chain reaction(PCR) and sequenced the quinolone resistance-determining regions of the gyrA and gyrB genes from 29 quinolone-resistant and 16 quinolone-susceptible H.pylori strains selected at random.RESULTS:In this study,the resistance rates of H.pylori to CIP,LVX or MOX were 55.7%(44/79),and the primary resistance rates were 26.6%(21/79).Patients with secondary resistance had received LVX in previous eradication treatments,but not MOX or CIP.Forty-five strains,including 29 CIP,LVX or MOX-resistant strains(MIC:1.5-32 μg/mL) and 16 susceptible strains,were selected randomly from the 79 strains and used in PCR analysis.Among these 45 strains,27 resistant strains had mutations in the gyrA gene,including 11 strains with mutations corresponding to Asp-91(MIC:2-32 μg/mL),one of which also had a mutation corresponding to Val-150,and 16 strains had mutations at Asn-87(MIC:4-32 μg/mL),three of which also had mutations corresponding to Arg-140 or Val-150.In addition,Arg-140,Val-150 or Ala-97 mutations were separately detected in three susceptible strains.Analysis of the gyrB gene showed that one strain of low resistance had a mutation corresponding to Ser-457 that coexisted with an Asp-91 mutation.There was a significant difference in the occurrence of mutations in the gyrA gene between CIP,LVX and MOX-resistant and-susceptible s展开更多
Mechanisms of bacterial resistance to fluoro-quinolones may be grouped intothree principal categories: gene mutations of DNA topoisomerase Ⅱ (GyrA or GyrB), DNA topoisomeraseⅣ ( ParC or ParE), decrease of outer memb...Mechanisms of bacterial resistance to fluoro-quinolones may be grouped intothree principal categories: gene mutations of DNA topoisomerase Ⅱ (GyrA or GyrB), DNA topoisomeraseⅣ ( ParC or ParE), decrease of outer membrane permeation and upregulation of multi-drug effluxpump (active efflux system). Efflux pumps are transport proteins removing toxic substrates(including virtually all classes of clinically relevant antibiotics) from cells to the externalenvironment. These proteins exist in both Gram positive bacteria and Gram negative bacteria as wellas in fungi and mammalian (tumour) cells. It has been reported that alkaloid reserpine and carbonylcyanide m-chlorophenylhydrazone (CCCP) can inhibit NorA multi-drug efflux. In order to explore theuniversality of drug efflux in microorganisms, 85 strains of Acinetobacter baumannii (A. baumannii)were tested using reserpine and CCCP. The quinolone-resistant-determining region (QRDR) of gyrA andparC genes in 35 isolates of A. baumannii were amplified by polymerase chain reaction (PCR) andsequenced by DNA sequencer. The correlation between resistant mutation regularity and bacterial drugefflux were analysed.展开更多
基金Supported by A Grant from the Beijing Medicine Researchand Development Fund,No 2005-1008
文摘AIM:To investigate the resistance of Helicobacter pylori(H.pylori) to ciprofloxacin(CIP),levofloxacin(LVX) and moxifloxacin(MOX) in the Beijing area and to elucidate the resistance mechanisms.METHODS:Seventy-nine H.pylori clinical strains,isolated from patients who had undergone upper gastrointestinal endoscopy in Peking University First Hospital from 2007 to 2009,were tested for their susceptibility to CIP,LVX and MOX using the E-test method.H.pylori strain 26695 was included in the susceptibility testing as a control strain.According to the minimal inhibitory concentration(MIC) values,a strain was classified as resistant to CIP,LVX or MOX when the MIC was > 1 μg/mL.We amplified by polymerase chain reaction(PCR) and sequenced the quinolone resistance-determining regions of the gyrA and gyrB genes from 29 quinolone-resistant and 16 quinolone-susceptible H.pylori strains selected at random.RESULTS:In this study,the resistance rates of H.pylori to CIP,LVX or MOX were 55.7%(44/79),and the primary resistance rates were 26.6%(21/79).Patients with secondary resistance had received LVX in previous eradication treatments,but not MOX or CIP.Forty-five strains,including 29 CIP,LVX or MOX-resistant strains(MIC:1.5-32 μg/mL) and 16 susceptible strains,were selected randomly from the 79 strains and used in PCR analysis.Among these 45 strains,27 resistant strains had mutations in the gyrA gene,including 11 strains with mutations corresponding to Asp-91(MIC:2-32 μg/mL),one of which also had a mutation corresponding to Val-150,and 16 strains had mutations at Asn-87(MIC:4-32 μg/mL),three of which also had mutations corresponding to Arg-140 or Val-150.In addition,Arg-140,Val-150 or Ala-97 mutations were separately detected in three susceptible strains.Analysis of the gyrB gene showed that one strain of low resistance had a mutation corresponding to Ser-457 that coexisted with an Asp-91 mutation.There was a significant difference in the occurrence of mutations in the gyrA gene between CIP,LVX and MOX-resistant and-susceptible s
文摘Mechanisms of bacterial resistance to fluoro-quinolones may be grouped intothree principal categories: gene mutations of DNA topoisomerase Ⅱ (GyrA or GyrB), DNA topoisomeraseⅣ ( ParC or ParE), decrease of outer membrane permeation and upregulation of multi-drug effluxpump (active efflux system). Efflux pumps are transport proteins removing toxic substrates(including virtually all classes of clinically relevant antibiotics) from cells to the externalenvironment. These proteins exist in both Gram positive bacteria and Gram negative bacteria as wellas in fungi and mammalian (tumour) cells. It has been reported that alkaloid reserpine and carbonylcyanide m-chlorophenylhydrazone (CCCP) can inhibit NorA multi-drug efflux. In order to explore theuniversality of drug efflux in microorganisms, 85 strains of Acinetobacter baumannii (A. baumannii)were tested using reserpine and CCCP. The quinolone-resistant-determining region (QRDR) of gyrA andparC genes in 35 isolates of A. baumannii were amplified by polymerase chain reaction (PCR) andsequenced by DNA sequencer. The correlation between resistant mutation regularity and bacterial drugefflux were analysed.
