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β-Lactamase Production in Experimental Endocarditis Due to Aminoglycoside-Resistant Streptococcus faecalis
Journal article   Peer reviewed

β-Lactamase Production in Experimental Endocarditis Due to Aminoglycoside-Resistant Streptococcus faecalis

Mark Ingerman, Peter G. Pitsakis, Alan Rosenberg, M. Trexler Hessen, Elias Abrutyn, Barbara E. Murray and Matthew E. Levison
The Journal of infectious diseases, v 155(6), pp 1226-1232
Jun 1987
PMID: 3106510

Abstract

We used a β-lactamase-producing (βL+) strain of Streptococcus faecalis that also had high levels of resistance to all aminoglycosides to induce experimental endocarditis in rats. The rats were treated for five or 10 days with procaine penicillin, vancomycin, gentamicin, rifampin, or ciprofloxacin (alone or in various combinations), or with penicillin plus clavulanic acid. The levels of penicillin in serum and vegetations declined rapidly in the βL+-infected rats treated with procaine penicillin alone, unlike the sustained levels of penicillin in either βL−-infected rats treated with procaine penicillin or βL+-infected rats treated with penicillin plus clavulanic acid. For the βL+-infected rats, the enterococcal counts in vegetations were significantly reduced (>3 log10 cfu/g) only by vancomycin and by pencillin plus clavulanic acid. The efficacy of the latter regimen probably resulted from the inhibition of penicillin inactivation by clavulanic acid in vegetations infected with the βL+ strain. Our in vivo findings document the biologic significance of β-lactamase production.

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Collaboration types
Domestic collaboration
Web of Science research areas
Immunology
Infectious Diseases
Microbiology
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