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粪肠球菌对青霉素 - 庆大霉素协同作用耐药的一种新机制。

A novel mechanism of resistance to penicillin-gentamicin synergism in Streptococcus faecalis.

作者信息

Moellering R C, Murray B E, Schoenbaum S C, Adler J, Wennersten C B

出版信息

J Infect Dis. 1980 Jan;141(1):81-6. doi: 10.1093/infdis/141.1.81.

Abstract

A patient with enterococcal endocarditis, who relapsed after repeated courses of apparently adequate treatment with ampicillin plus gentamicin, was subsequently cured with ampicillin-tobramycin therapy. The organisms isolated from this patient were strains of Streptococcus faecalis that were resistant to penicillin (or ampicillin)-gentamicin synergism but not to penicillin (or ampicillin)-tobramycin synergism. The mechanism of resistance in these strains appears to be related to a specific defect in the intracellular uptake of gentamicin (but not tobramycin) in the presence of penicillin.

摘要

一名患有肠球菌性心内膜炎的患者,在接受了多次看似足够疗程的氨苄西林加庆大霉素治疗后复发,随后采用氨苄西林-妥布霉素治疗得以治愈。从该患者分离出的菌株为粪肠球菌,对青霉素(或氨苄西林)-庆大霉素协同作用耐药,但对青霉素(或氨苄西林)-妥布霉素协同作用不耐药。这些菌株的耐药机制似乎与在青霉素存在的情况下庆大霉素(而非妥布霉素)细胞内摄取的特定缺陷有关。

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