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Acquired inducible antimicrobial resistance in Gram-positive bacteria

机译:在革兰氏阳性细菌中获得的诱导型抗菌素耐药性

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摘要

A major contributor to the emergence of antibiotic resistance in Gram-positive bacterial pathogens is the expansion of acquired, inducible genetic elements. Although acquired, inducible antibiotic resistance is not new, the interest in its molecular basis has been accelerated by the widening distribution and often ‘silent’ spread of the elements responsible, the diagnostic challenges of such resistance and the mounting limitations of available agents to treat Gram-positive infections. Acquired, inducible antibiotic resistance elements belong to the accessory genome of a species and are horizontally acquired by transformation/recombination or through the transfer of mobile DNA elements. The two key, but mechanistically very different, induction mechanisms are: ribosome-sensed induction, characteristic of the macrolide–lincosamide–streptogramin B antibiotics and tetracycline resistance, leading to ribosomal modifications or efflux pump activation; and resistance by cell surface-associated sensing of β-lactams (e.g., oxacillin), glycopeptides (e.g., vancomycin) and the polypeptide bacitracin, leading to drug inactivation or resistance due to cell wall alterations.
机译:革兰氏阳性细菌病原体中抗生素耐药性出现的主要原因是获得性,可诱导性遗传元件的扩展。尽管获得性诱导型抗生素耐药性并不是新生事物,但是由于负责任成分的分布扩大和通常“无声”扩散,这种耐药性的诊断挑战以及治疗革兰氏可用药物的局限性,已加速了其分子基础的兴趣。阳性感染。获得的可诱导的抗生素抗性元件属于物种的辅助基因组,并且通过转化/重组或通过移动DNA元件的转移水平获得。两种关键但机制上非常不同的诱导机制是:核糖体诱导的诱导,大环内酯-林可酰胺-链霉菌素B抗生素的特性和四环素抗性,导致核糖体修饰或外排泵激活。 β-内酰胺(例如,奥沙西林),糖肽(例如,万古霉素)和多肽杆菌肽的细胞表面相关感测引起的抗性和耐药性,由于细胞壁改变而导致药物失活或抗性。

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