Persistence: a copacetic and parsimonious hypothesis for the existence of non-inherited resistance to antibiotics

• Type of Material: Article
• Authors: Bruce R. Levin, Emory University; Jenniffer Concepción-Acevedo, Emory University; Klas I. Udekwu, Karolinska Institutet
• Language: English
• Date: 2014-08-02
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2014 Elsevier Ltd. All rights reserved.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): https://doi.org/10.1016/j.mib.2014.06.016
• Title of Journal or Parent Work: Current Opinion in Microbiology
• Volume: 0
• Start Page: 18
• End Page: 21
• Grant/Funding Agency: Hesselman Fund; US National Institutes of General Medical Science; Swedish Research Council
• Grant/Funding Information: Support for this endeavor has been provided by the US National Institutes of General Medical Science, GM098175 (BRL) and the Hesselman Fund (travel) and a Swedish Research Council junior investigator grant, VR # 2012-3564, (KU).
• Keywords: phenotypic resistance; antibiotics
• Subject - Topics: Bacteria; Drug resistance in microorganisms

Abstract

We postulate that phenotypic resistance to antibiotics, persistence, is not an evolved (selected-for) character but rather like mutation, an inadvertent product of different kinds of errors and glitches. The rate of generation of these errors is augmented by exposure to these drugs. The genes that have been identified as contributing to the production of persisters are analogous to the so-called mutator genes; they modulate the rate at which these errors occur and/or are corrected. In theory, these phenotypically resistant bacteria can retard the rate of microbiological cure by antibiotic treatment.