[Bacterial enteric pathogens' resistance to fluoroquinolones and last generation cephalosporines].

Maria Damian, Codruţa-Romanita Usein, Andi Marian Palade, Mădălina Băltoiu, Maria Condei, Simona Ciontea, Dorina Tatu-Chiţoiu
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引用次数: 0

Abstract

The increase of incidence of resistance to the antibiotics became the most worrisome subject within the clinical and research communities in the medical fields. Intrinsic resistance genetic mutations, horizontal transfer of mobile structures carrying genes coding for resistance to the antibiotics within the pan-microbial genome are representing the bacterial resistome which is bearing the genetic information regarding the defensive mechanisms developed by micro-organisms to protect themselves against antibiotics. Rice in the resistance of enteric bacteria, pathogens involved in a large number of human infections, to the cephalosporin of last generation and to the fluoroquinolones is a very actual subject in the medical area. Production of beta-lactamases with extended spectrum is the most important enzymatic defence system, developed by micro-organisms, consisting in the inactivation of beta-lactam antibiotics by destroying the beta-lactam ring. Enterobacteria are able to produce beta-lactamases of type TEM, SHV and/or CTX-M. Punctual mutations in nucleotide structure of bla genes, coding for beta-lactamases synthesis, are leading on production of a large diversity of enzymes with enlarged spectrum of activity (ESBL). At the beginning of 90's the first beta-lactamases resistance to clavulanic acid were detected and in our days more then 170 TEM, 120 SVH and 90 CTX-MESBLs are known. Escherichia coli strains are producing, firstly, TEM ESBLs, Klebsiella pneumoniae SHV ESBLs. and both are producing CTX-M type ESBLs, are resistant to the fluoroquinolones due to punctual mutations in nucleotide structure of gyr gene coding for gyrases production, enzymes involved in nucleic acids replication. Resistance to the antibiotics with extended activity is a public health threat due to their capacity of large spreading within bacterial population, when the coding structures are located on mobile genetic structures. The menace increase when genes coding for fluoroquinolones resistance (qnr) are identified on such of structures.

[肠道细菌病原体对氟喹诺酮类药物和上一代头孢菌素的耐药性]。
抗生素耐药发生率的上升已成为医学界临床和研究界最为担忧的问题。固有耐药基因突变,泛微生物基因组中携带抗生素耐药基因的移动结构的水平转移,代表了细菌耐药组,它承载着微生物为保护自己免受抗生素侵害而形成的防御机制的遗传信息。水稻在肠道细菌中的耐药性,涉及大量人类感染的病原体,对上一代头孢菌素和氟喹诺酮类药物的耐药性是医学领域一个非常现实的课题。广谱β -内酰胺酶的产生是微生物发展的最重要的酶防御系统,包括通过破坏β -内酰胺环使β -内酰胺类抗生素失活。肠杆菌能够产生TEM、SHV和/或CTX-M型的β -内酰胺酶。编码β -内酰胺酶合成的bla基因核苷酸结构的准时突变导致了具有扩大活性谱(ESBL)的多种酶的产生。在90年代初,首次检测到对克拉维酸耐药的β -内酰胺酶,目前已知有170多个TEM, 120个SVH和90个CTX-MESBLs。大肠杆菌菌株首先产生TEM ESBLs,肺炎克雷伯菌SHV ESBLs。两者都产生CTX-M型ESBLs,对氟喹诺酮类药物具有耐药性,这是由于编码gyr基因的核苷酸结构的准时突变,gyr基因编码的gyrase生产,参与核酸复制的酶。当编码结构位于可移动的遗传结构上时,对具有扩展活性的抗生素的耐药性由于其在细菌群体中大规模传播的能力而成为公共卫生威胁。当在这些结构上发现编码氟喹诺酮类药物耐药性(qnr)的基因时,威胁就会增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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