高链霉素抗性铜绿假单胞菌菌株对链霉素（SM）的抗性机制。

Mechanisms of streptomycin(SM)-resistance of highly SM-resistant Pseudomonas aeruginosa strains.

作者信息

Kono M, O'Hara K

出版信息

J Antibiot (Tokyo). 1976 Feb;29(2):169-75. doi: 10.7164/antibiotics.29.169.

DOI:10.7164/antibiotics.29.169

PMID:819408

Abstract

Three clinical isolates, K-Ps 94, K-Ps 97 and K-Ps 102, of Pseudomonas aeruginosa having R factor and showing MIC of more than 51,200 mcg/ml to streptomycin (SM), were examined for mechanisms of SM-resistance. Among the strains, K-Ps 94 and K-Ps 102 had R factor conferring SM-resistance. In K-Ps 94, the mechanism of SM-resistance was mainly owing to SM-phosphorylating enzyme and also owing to decreased permeability by an R factor, kR94. In K-Ps 97, it was considered to be due to SM-adenylylating enzyme by the chromosomal gene but not R factor, kR97. In K-Ps 102, the reduced permeability of the cell membrane to SM by an R factor, kR102, and the reduced affinity of the ribosome to the drug by the chromosomal gene contributed to the mechanisms of SM-resistance.

摘要

对三株具有R因子且对链霉素（SM）的最低抑菌浓度（MIC）超过51200微克/毫升的铜绿假单胞菌临床分离株K-Ps 94、K-Ps 97和K-Ps 102进行了链霉素耐药机制研究。在这些菌株中，K-Ps 94和K-Ps 102具有赋予链霉素耐药性的R因子。在K-Ps 94中，链霉素耐药机制主要归因于链霉素磷酸化酶，同时也归因于R因子kR94导致的通透性降低。在K-Ps 97中，认为是由染色体基因而非R因子kR97产生的链霉素腺苷酸化酶所致。在K-Ps 102中，R因子kR102导致细胞膜对链霉素的通透性降低，以及染色体基因导致核糖体对药物的亲和力降低，共同构成了链霉素耐药机制。