河水:特拉细菌的耐药率低主要是与内在机制。
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Tacao M,科雷亚,戴安娜
河水:特拉细菌的耐药率低主要是与内在机制。
活细胞药物抵抗。2015年10月,21 (5):497 - 506。doi: 10.1089 / mdr.2015.0072。Epub 2015 6月2。
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26430939 (在PubMed]
- 文摘
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碳青霉烯类抗生素的方法来处理严重的抗多种抗菌素的细菌引起的感染。这些抗生素耐药性的发生率已经增加和新耐药机制已经出现。耐碳青霉烯的传播环境中一直被忽视。本研究的主要目的是评估的患病率和多样性特细菌河的生态系统。的存在经常报道carbapenemase-encoding基因检查。细菌的比例imipenem-resistant平均2.24 CFU /毫升。Imipenem-resistant菌株(n = 110)被确定为假单胞菌spp, Stenotrophomonas maltophilia,气单胞菌属spp,色素细菌haemolyticum, Shewanella xiamenensis,和肠杆菌科的成员。特拉细菌是高度耐喹诺酮类等其他beta-lactams,氨基甙类抗生素、氯霉素、四环素、磺胺甲恶唑/甲氧苄氨嘧啶。碳青霉烯耐药主要是与内在抗药性细菌有关。作为固有耐药机制,我们已经确定了在气单胞菌属的77.3% spp blaCphA基因,在所有美国maltophilia blaL1,在所有美国xiamenensis blaOXA-48-like。 As acquired resistance mechanisms, we have detected the blaVIM-2 gene in six Pseudomonas spp. (5.45%). Integrons with gene cassettes encoding resistance to aminoglycosides (aacA and aacC genes), trimethoprim (dfrB1b), and carbapenems (blaVIM-2) were found in Pseudomonas spp. Results suggest that carbapenem resistance dissemination in riverine ecosystems is still at an early stage. Nevertheless, monitoring these aquatic compartments for the presence of resistance genes and its host organisms is essential to outline strategies to minimize resistance dissemination.