title: Protection of Salmonella by ampicillin-resistant Escherichia coli in the presence of otherwise lethal drug concentrations.
abstract: Microbial systems have become the preferred testing grounds for experimental work on the evolution of traits that benefit other group members. This work, based on conceptual and theoretical models of frequency-dependent selection within populations, has proven fruitful in terms of understanding the dynamics of group beneficial or 'public goods' traits within species. Here, we expand the scope of microbial work on the evolution of group-beneficial traits to the case of multi-species communities, particularly those that affect human health. We examined whether beta-lactamase-producing Escherichia coli could protect ampicillin-sensitive cohorts of other species, particularly species that could cause human disease. Both beta-lactamase-secreting E. coli and, surprisingly, those engineered to retain it, allowed for survival of a large number of ampicillin-sensitive cohorts of Salmonella enterica serovar Typhimurium, including both laboratory and clinical isolates. The Salmonella survivors, however, remained sensitive to ampicillin when re-plated onto solid medium and there was no evidence of gene transfer. Salmonella survival did not even require direct physical contact with the resistant E. coli. The observed phenomenon appears to involve increased release of beta-lactamase from the E. coli when present with S. enterica. Significantly, these findings imply that resistant E. coli, that are not themselves pathogenic, may be exploited, even when they are normally selfish with respect to other E. coli. Thus, Salmonella can gain protection against antibiotics from E. coli without gene transfer, a phenomenon not previously known. As a consequence, antibiotic-resistant E. coli can play a decisive role in the survival of a species that causes disease and may thereby interfere with successful treatment.
authors: Department of Biology, Program on Disease Evolution, University of Louisville, Louisville, KY, USA. mhper101@gwise.louisville.edu
authors: Michael H
authors: MH
authors: Perlin
authors: Denise R
authors: DR
authors: Clark
authors: Courtney
authors: C
authors: McKenzie
authors: Himati
authors: H
authors: Patel
authors: Nikki
authors: N
authors: Jackson
authors: Cecile
authors: C
authors: Kormanik
authors: Cayse
authors: C
authors: Powell
authors: Alexander
authors: A
authors: Bajorek
authors: David A
authors: DA
authors: Myers
authors: Lee A
authors: LA
authors: Dugatkin
authors: Ronald M
authors: RM
authors: Atlas
mesh_terms: D000667:Ampicillin / Q000494:pharmacology*; D000668:Ampicillin Resistance; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D004926:Escherichia coli / Q000187:drug effects* / Q000201:enzymology / Q000235:genetics; D005818:Genetic Engineering; D012475:Salmonella / Q000187:drug effects*; D001618:beta-Lactamases / Q000235:genetics / Q000378:metabolism
chemical_list: D000900:Anti-Bacterial Agents; D000667:Ampicillin; D001618:beta-Lactamases