MLST typing of Escherichia coli isolates overproducing AmpC {beta}-lactamase.
MLST typing of Escherichia coli isolates overproducing AmpC {beta}-lactamase.
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大肠杆菌分离株的 MLST 分型过量产生 AmpC {β}-内酰胺酶。
DOI：
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发表时间：
2009
影响因子：
5.2
通讯作者：
S. Corvec
中科院分区：
文献类型：
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作者：
A. Guillouzouic;N. Caroff;S. Dauvergne;D. Lepelletier;A. Perrin Guyomard;I. Kempf;A. Reynaud;S. Corvec
大肠杆菌是人和动物消化道的主要肠道需氧菌，也是人类最常见的致病菌。因此，该物种携带的抗性机制特别令人关注。这些机制之一是染色体AmpC β-内酰胺酶的过度产生，导致大多数β-内酰胺类药物（包括第三代头孢菌素）的MIC增加。AmpC过量产生是由ampC启动子中的各种突变（-42、-32和-11）引起的，这些突变增加了与RNA聚合酶共有启动子的同源性，
Escherichia coli is the major commensal aerobic bacterium of the digestive tract of humans and animals, but is also the most frequent human bacterial pathogen. As a consequence, resistance mechanisms carried by this species are of particular concern. One of these mechanisms is the overproduction of the chromosomal AmpC β-lactamase, leading to increased MICs of most β-lactams including third-generation cephalosporins. AmpC overproduction is caused by various mutations in the ampC promoter (–42, –32 and –11) increasing homology with the consensus promoter for RNA polymerase,