The introduction of the antibiotics into clinical practice has significantly reduced the mortality of infectious diseases. Although chromosomally mediated β-1actamase is natural in many genera of bacteria, the intens...The introduction of the antibiotics into clinical practice has significantly reduced the mortality of infectious diseases. Although chromosomally mediated β-1actamase is natural in many genera of bacteria, the intensive use of antibiotics is the main cause for the increasing emergence of new β-1actamases. So far, more than 340 β-lactamases have been identified,1 among which, more than 200 are extended-spectrum β-lactamases （ESBLs）.2 The most prevalent β-lactamases are class A enzymes, including SHV and TEM. Genes encoding these enzymes generally located in large transferable plasmids. The dissemination of these plasmids attributes to the increasing incidence and spread of v-lactam resistance. It is important to investigate the prevalence and allelic distribution of genes encoding β-lactamase in the bacterial population in order to prevent the emergence of ESBLs in those bacteria and the spread of ESBLs in the clinical setting.展开更多
文摘The introduction of the antibiotics into clinical practice has significantly reduced the mortality of infectious diseases. Although chromosomally mediated β-1actamase is natural in many genera of bacteria, the intensive use of antibiotics is the main cause for the increasing emergence of new β-1actamases. So far, more than 340 β-lactamases have been identified,1 among which, more than 200 are extended-spectrum β-lactamases （ESBLs）.2 The most prevalent β-lactamases are class A enzymes, including SHV and TEM. Genes encoding these enzymes generally located in large transferable plasmids. The dissemination of these plasmids attributes to the increasing incidence and spread of v-lactam resistance. It is important to investigate the prevalence and allelic distribution of genes encoding β-lactamase in the bacterial population in order to prevent the emergence of ESBLs in those bacteria and the spread of ESBLs in the clinical setting.
