Abstract
Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.
Publication types
-
Comparative Study
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adaptation, Physiological
-
Animals
-
Anti-Bacterial Agents / pharmacology*
-
Antiporters*
-
Carrier Proteins / genetics
-
Culture Media
-
Drug Resistance, Microbial / genetics*
-
Escherichia coli Proteins
-
Evolution, Molecular
-
Female
-
Fusidic Acid / pharmacology
-
Membrane Proteins / genetics
-
Mice
-
Mice, Inbred BALB C
-
Mutation*
-
Peptide Elongation Factor G / genetics
-
Ribosomal Proteins / genetics
-
Salmonella typhimurium / drug effects*
-
Salmonella typhimurium / genetics*
-
Salmonella typhimurium / growth & development
-
Salmonella typhimurium / metabolism
-
Selection, Genetic
-
Serial Passage
-
Streptomycin / pharmacology
-
Suppression, Genetic
Substances
-
Anti-Bacterial Agents
-
Antiporters
-
Carrier Proteins
-
Culture Media
-
Escherichia coli Proteins
-
Membrane Proteins
-
Peptide Elongation Factor G
-
Ribosomal Proteins
-
ribosomal protein S12
-
EmrE protein, E coli
-
Fusidic Acid
-
Streptomycin