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Extended-spectrum beta-lactamases and the permeability barrier.

机译:扩展光谱β-内酰胺酶和渗透性屏障。

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摘要

The outer membrane of Gram-negative bacteria represents a barrier for penetration of hydrophilic compounds. Loss of porins (water-filled protein channels) contributes to antimicrobial resistance, particularly when additional mechanisms of resistance are expressed. Many studies on the structure and regulation of porins in Escherichia coli K-12 are available, but there is little information concerning clinical isolates of this species. In Klebsiella pneumoniae, two major porins, OmpK35 and OmpK36, are produced, but many extended-spectrum beta-lactamase (ESBL)-producing K. pneumoniae isolates do not express OmpK35. Loss of both OmpK35 and OmpK36 in ESBL-producing K. pneumoniae causes resistance to cefoxitin, increased resistance to expanded-spectrum cephalosporins, and decreased susceptibility to carbapenems, particularly ertapenem. Porin loss also decreases the susceptibility to other non-beta-lactam compounds, such as fluoroquinolones, of ESBL-producing organisms.
机译:革兰氏阴性细菌的外膜代表了亲水化合物渗透的屏障。 悬浮虫(填充蛋白质通道)的丧失有助于抗微生物抗性,特别是当表达额外的抗性机制时。 许多关于大肠杆菌K-12中荚的结构和调节的研究,但几乎没有关于该物种的临床分离物的信息。 在Klebsiella肺炎群岛中,产生两个主要的孔蛋白,OMPK35和OMPK36,但许多扩展β-内酰胺酶(ESBL) - 肺炎肺炎分离物不表达OMPK35。 在ESBL的K.35和OMPK36中丧失肺炎肺炎肺炎导致对食半氧酸的抗性,对扩增光谱孢子的抗性增加,并降低对肉豆蔻蛋白的敏感性,特别是腹膜敏。 Porin损失还降低了对ESBL-生物体的其他非β-内酰胺化合物(例如氟喹诺酮类)的易感性。

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