Assessment of the fitness impacts on Escherichia coli of acquisition of antibiotic resistance genes encoded by different types of genetic element.
OBJECTIVE
Little is known of the fitness cost that antibiotic resistance exerts on wild-type bacteria, especially in their natural environments. We therefore examined the fitness costs that several antibiotic resistance elements imposed on a wild-type Escherichia coli isolate, both in the laboratory and in a pig gut colonization model.


METHODS
Plasmid R46, Tn1 and Tn7 and a K42R RpsL substitution were separately introduced into E. coli 345-2 RifC, a rifampicin-resistant derivative of a recent porcine isolate. The insertion site of Tn1 was determined by DNA sequencing. The fitness cost of each resistance element was assessed in vitro by pairwise growth competition and in vivo by regularly monitoring the recovery of strains from faeces for 21 days following oral inoculation of organic piglets. Each derivative of 345-2 RifC carrying a resistance element was grown in antibiotic-free broth for 200 generations and the experiments to assess fitness were repeated.


RESULTS
RpsL K42R was found to impose a small fitness cost on E. coli 345-2 RifC in vitro but did not compromise survival in vivo. R46 imposed a cost both before and after laboratory passage in vitro, but only the pre-passage strain was at a disadvantage in vivo. The post-passage isolate had an advantage in pigs. Acquisition of Tn7 had no impact on the fitness of E. coli 345-2 RifC. Two derivatives containing Tn1 were isolated and, in both cases, the transposon inserted into the same cryptic chromosomal sequence. Acquisition of Tn1 improved fitness of E. coli 345-2 RifC in vitro and in vivo in the case of the first derivative, but in the case of a second, independent derivative, Tn1 had a neutral effect on fitness.


CONCLUSIONS
The fitness impact imposed on E. coli 345-2 RifC by carriage of antibiotic resistance elements was generally low or non-existent, suggesting that once established, resistance may be difficult to eliminate through reduction in prescribing alone.
Enne
V I
VI
Bristol Centre for Antimicrobial Research, Department of Pathology and Microbiology, University of Bristol, Medical Sciences Building, Bristol BS8 1TD, UK. v.i.enne@bristol.ac.uk
Delsol
A A
AA
Davis
G R
GR
Hayward
S L
SL
Roe
J M
JM
Bennett
P M
PM
D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D005075:Biological Evolution; D004251:DNA Transposable Elements; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics*; D004926:Escherichia coli / Q000187:drug effects* / Q000235:genetics* / Q000472:pathogenicity; D029968:Escherichia coli Proteins; D005243:Feces / Q000382:microbiology; D041981:Gastrointestinal Tract / Q000382:microbiology; D010957:Plasmids / Q000235:genetics; D000091243:Ribosomal Protein S9; D012269:Ribosomal Proteins / Q000187:drug effects / Q000235:genetics; D013307:Streptomycin / Q000494:pharmacology; D013552:Swine; D013553:Swine Diseases / Q000382:microbiology
D000900:Anti-Bacterial Agents; D004251:DNA Transposable Elements; D029968:Escherichia coli Proteins; D000091243:Ribosomal Protein S9; D012269:Ribosomal Proteins; C000717190:RpsI protein, E coli; C506766:RpsL protein, E coli; D013307:Streptomycin