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Antimicrob Agents Chemother. 2018 Oct 24;62(11). pii: e01158-18. doi: 10.1128/AAC.01158-18. Print 2018 Nov.

Adjunctive Clavulanic Acid Abolishes the Cefazolin Inoculum Effect in an Experimental Rat Model of Methicillin-Sensitive Staphylococcus aureus Endocarditis.

Miller WR1,2, Singh KV3,2, Arias CA3,2,4,5,6, Murray BE3,2,4.

Author information

1
Center for Antimicrobial Resistance and Microbial Genomics, UTHealth, McGovern Medical School, Houston, Texas, USA William.R.Miller@uth.tmc.edu.
2
Department of Internal Medicine, Division of Infectious Diseases, UTHealth, McGovern Medical School, Houston, Texas, USA.
3
Center for Antimicrobial Resistance and Microbial Genomics, UTHealth, McGovern Medical School, Houston, Texas, USA.
4
Department of Microbiology and Molecular Genetics, UTHealth, McGovern Medical School, Houston, Texas, USA.
5
Center for Infectious Diseases, UTHealth, School of Public Health, Houston, Texas, USA.
6
Molecular Genetics and Antimicrobial Resistance Unit, International Center for Microbial Genomics, Universidad El Bosque, Bogota, Colombia.

Abstract

We tested the ability of clavulanic acid to restore the efficacy of cefazolin against Staphylococcus aureus TX0117, which exhibits the cefazolin inoculum effect (CzIE). In the rat infective endocarditis model, the coadministration of cefazolin plus clavulanic acid resulted in a significant reduction of bacterial counts (7.1 ± 0.5 log10 CFU/g) compared to that with cefazolin alone (2 ± 0.6 log10 CFU/g; P < 0.0001). The addition of a β-lactamase inhibitor may be a viable strategy for overcoming the CzIE.

KEYWORDS:

Staphylococcus aureus; animal models; cefazolin; clavulanic acid; infective endocarditis; inoculum effect

PMID:
30150459
PMCID:
PMC6201062
[Available on 2019-04-24]
DOI:
10.1128/AAC.01158-18

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