铜绿假单胞菌中新型的β内酰胺酶介导的羧苄青霉素抗性

发布时间：2018-06-26 21:58

  本文选题：铜绿假单胞菌 + 羧苄青霉素　； 参考：《西北大学学报(自然科学版)》2016年06期

【摘要】：为了探究铜绿假单胞菌抗羧苄青霉素的机制,通过基因敲除以及克拉维酸钾和羧苄青霉素协同实验对羧苄青霉素抗性菌株进行研究。在对羧苄青霉素具有抗性的转座突变体基础上敲除amp C后,其对羧苄青霉素抗性没有变化;8株羧苄青霉素抗性转座突变体菌株克拉维酸钾协同实验呈阳性。基因组中预测为β内酰胺酶的PA5514基因的敲除突变菌株及过表达菌株对氨苄青霉素以及羧苄青霉素的敏感性也没有变化。结果说明amp C及PA5514表达升高并不是羧苄青霉素抗性转座突变体抗性产生的原因,基因组中存在新的受克拉维酸钾抑制的β内酰胺酶可能是铜绿假单胞菌抗羧苄青霉素的一种新机制。同时,克拉维酸钾与羧苄青霉素联合使用能够提高羧苄青霉素对铜绿假单胞菌抗性菌株的治疗效果。
[Abstract]:In order to investigate the mechanism of resistance of Pseudomonas aeruginosa to Carbenicillin, the resistant strains were studied by gene knockout and synergistic experiments of potassium clavulanate and carbenicillin. After knockout amp C on the basis of transposable mutants resistant to carbenicillin, there was no change in resistance to carbenicillin in 8 strains of carbenicillin resistant mutants, potassium clavulanate synergistic test was positive. The sensitivity of the knockout mutant and overexpression strain of PA5514 gene predicted to 尾 lactamase to ampicillin and carbenicillin did not change. The results showed that the increased expression of amp C and PA5514 was not the cause of resistance to Carbenicillin resistance translocation mutants. The existence of new 尾 lactamases inhibited by potassium clavulanate in the genome may be a new mechanism of resistance of Pseudomonas aeruginosa to carbenicillin. At the same time, the combination of potassium clavulanate and carbenicillin could improve the therapeutic effect of carbenicillin against Pseudomonas aeruginosa.
【作者单位】： 西北大学生命科学学院/西部资源及现代生物技术教育部重点实验室;
【分类号】：R364.5
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本文编号：2071544