title: Persistence: a copacetic and parsimonious hypothesis for the existence of non-inherited resistance to antibiotics.
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.
authors.affiliation: Department of Biology, Emory University, Atlanta, GA 30322, USA. Electronic address: blevin@emory.edu.
authors.forename: Bruce R
authors.initials: BR
authors.lastname: Levin
authors.affiliation: Department of Biology, Emory University, Atlanta, GA 30322, USA.
authors.forename: Jeniffer
authors.initials: J
authors.lastname: Concepción-Acevedo
authors.affiliation: Swedish Medical Nanoscience Center, Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
authors.forename: Klas I
authors.initials: KI
authors.lastname: Udekwu
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001419:Bacteria / Q000187:drug effects / Q000235:genetics*; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D019143:Evolution, Molecular; D008826:Microbial Sensitivity Tests; D009154:Mutation / Q000187:drug effects*
chemical_list: D000900:Anti-Bacterial Agents
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