http://jac.oxfordjournals.org/cgi/conte ... t/56/3/544
JAC Advance Access originally published online on July 22, 2005
Journal of Antimicrobial Chemotherapy 2005 56(3):544-551; doi:10.1093/jac/dki255
Assessment of the fitness impacts on Escherichia coli of acquisition of antibiotic resistance genes encoded by different types of genetic element
V. I. Enne1,*, A. A. Delsol2, G. R. Davis1, S. L. Hayward1, J. M. Roe2 and P. M. Bennett1
1 Bristol Centre for Antimicrobial Research, Department of Pathology and Microbiology, University of Bristol, Medical Sciences Building, University Walk, Bristol BS8 1TD, UK; 2 Division of Animal Health and Husbandry, Department of Clinical Veterinary Science, University of Bristol, Langford BS40 5DU, UK
Received 4 March 2005; returned 27 April 2005; revised 3 June 2005; accepted 23 June 2005
* Corresponding author. Tel: +44-117-9287522; Fax: +44-117-9287896; E-mail: email@example.com
Objectives: 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.
(I added the bold type for emphasis. Resistant strains may be at a disadvantage in the lab, but not in the host animal or human. Also note that the paper says it may be difficult to get rid of the resistant strains once they are established, so contrary to what you might believe, they aren't reverting quickly to non-resistant strains even when the antibiotic use stops.)