Vancomycin-intermediate resistance in Staphylococcus aureus

Keiichi Hiramatsu; Yuki Kayayama; Miki Matsuo; Yoshifumi Aiba; Michie Saito; Tomomi Hishinuma; Akira Iwamoto

doi:10.1016/j.jgar.2014.04.006

Vancomycin-intermediate resistance in Staphylococcus aureus

J Glob Antimicrob Resist. 2014 Dec;2(4):213-224. doi: 10.1016/j.jgar.2014.04.006. Epub 2014 Jun 7.

Authors

Keiichi Hiramatsu¹, Yuki Kayayama², Miki Matsuo², Yoshifumi Aiba², Michie Saito², Tomomi Hishinuma², Akira Iwamoto²

Affiliations

¹ Juntendo University Research Center for Infection Control Science, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan. Electronic address: khiram06@juntendo.ac.jp.
² Juntendo University Research Center for Infection Control Science, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.

PMID: 27873679
DOI: 10.1016/j.jgar.2014.04.006

Abstract

Vancomycin-intermediate Staphylococcus aureus (VISA) and its precursor hetero-VISA (hVISA) were discovered almost 20 years ago and have continued to be a stumbling block in the chemotherapy of methicillin-resistant S. aureus (MRSA). Unlike vancomycin resistance mediated by the van gene in enterococci and staphylococci, VISA is generated by accumulation of mutations. It displays diverse and intriguing genetic mechanisms underlying its resistance phenotype. Here we make a brief note on our recent understanding of the genetics of hVISA, VISA and the newly discovered phenotype 'slow VISA' (sVISA).

Keywords: Pre-hVISA; VISA; Vancomycin; hVISA; rpoB mutation; sVISA.

Publication types

Review