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青紫霉素对铜绿假单胞菌的活性:耐药菌株诱导的磷酸化使其失活

Activity of lividomycin against Pseudomonas aeruginosa: its inactivation by phosphorylation induced by resistant strains.

作者信息

Kobayashi F, Yamaguchi M, Mitsuhashi S

出版信息

Antimicrob Agents Chemother. 1972 Jan;1(1):17-21. doi: 10.1128/AAC.1.1.17.

Abstract

The antibacterial activity and enzymatic inactivation of lividomycin, a new aminoglycosidic antibiotic, were studied with 13 strains of Pseudomonas aeruginosa. The minimal inhibitory concentration of lividomycin was 12.5 to 25 mug/ml, and three strains were resistant to high concentrations of lividomycin (more than 200 mug/ml). It was found that P. aeruginosa TI-13 and K-11, highly lividomycin-resistant strains of clinical origin, strongly inactivated the drug. The third resistant strain, Km-41/R, was developed in vitro. Unlike the other resistant strains, Km-41/R, was developed in vitro. Unlike the other resistant strains, Km-41/R did not inactivate the drug, indicating that different mechanisms were involved in lividomycin resistance. By use of a cell-free extract from P. aeruginosa TI-13, the inactivation of lividomycin was found to be caused by the formation of a monophosphorylated product of the drug.

摘要

用13株铜绿假单胞菌研究了新氨基糖苷类抗生素青紫霉素的抗菌活性及酶失活作用。青紫霉素的最小抑菌浓度为12.5至25微克/毫升,有3株菌对高浓度的青紫霉素(超过200微克/毫升)耐药。发现临床来源的高度耐青紫霉素的铜绿假单胞菌TI-13和K-11能使该药物强烈失活。第三株耐药菌株Km-41/R是在体外产生的。与其他耐药菌株不同,Km-41/R不会使药物失活,这表明青紫霉素耐药涉及不同机制。通过使用铜绿假单胞菌TI-13的无细胞提取物,发现青紫霉素的失活是由该药物单磷酸化产物的形成引起的。

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