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Clinical strain of Staphylococcus aureus inactivates and causes efflux of macrolides
Author(s) -
L Wondrack,
Mark A. Massa,
Bingwei Yang,
Joyce A. Sutcliffe
Publication year - 1996
Publication title -
antimicrobial agents and chemotherapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.07
H-Index - 259
eISSN - 1070-6283
pISSN - 0066-4804
DOI - 10.1128/aac.40.4.992
Subject(s) - efflux , staphylococcus aureus , microbiology and biotechnology , erythromycin , strain (injury) , escherichia coli , esterase , biology , staphylococcus , bacteria , chemistry , enzyme , antibiotics , biochemistry , gene , genetics , anatomy
Searching through a collection of 124 Staphylococcus aureus clinical strains, we found one isolate, strain 01A1032, that inactivates 14- and 16-membered macrolides. The products of inactivation were purified from supernatant fluids of cultures exposed to erythromycin for 3 h and were found to be identical to products of inactivation from Escherichia coli strains that encode either an EreA or EreB esterase. Further, strain 01A1032 was shown to be resistant to azithromycin, a 15-membered macrolide, by an alternate mechanism, efflux. Thus, strain 01A1032 harbors determinants encoding an esterase activity that hydrolyzes 14- and 16-membered macrolides and a macrolide efflux system.

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