JAC Advance Access published online on April 21, 2004
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkh217
© 2004 by The British Society for Antimicrobial Chemotherapy
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1 Bristol Centre for Antimicrobial
Research, Department of Pathology and Microbiology, University of
Bristol, Medical Sciences Building, University Walk, Bristol BS8
1TD; Department of Medical
Microbiology, Barts and
The London School of Medicine and Dentistry, Queen Mary, University
of London, Turner Street, London E1 2AD;
* To whom correspondence should be addressed. E-mail: v.i.enne{at}bristol.ac.uk.
Objectives: Despite a 97% reduction
in clinical sulphonamide usage, the prevalence of sulphonamide resistance
among Escherichia coli has remained constant in
the UK. Genetic linkage of sulphonamide resistance to other resistances
is thought important for this maintenance, but the finding also
implies that sulphonamide resistance exerts little fitness cost.
To test this hypothesis, we examined the fitness impact of four
naturally occurring sul2-coding plasmids upon their
hosts. Methods: The fitness impact of the plasmids
upon E. coli was determined by pairwise growth
competition in a minimal medium. The DNA sequence of plasmid p9123
was obtained by primer walking and PCR. Results: Three of the four sul2-coding
plasmids studied imposed fitness costs on their hosts. The fourth plasmid,
a 6.2 kb resistance element carrying sul2, strA and strB designated p9123, conferred a 4% fitness advantage
upon its original clinical host and also on E. coli K12
JM109. The complete sequence of p9123 revealed eight open reading
frames, including five of unknown function. There was no obvious
gene to which the fitness advantage might be attributed. Conclusions: The novel finding that p9123 can
improve host fitness may explain why this plasmid and its close
relatives are so widespread among enteric bacteria. In addition
to other factors such as co-selection of sulphonamide resistance
by other agents, the fitness advantage conferred by plasmids such
as p9123 may have contributed to the maintenance of sulphonamide
resistance in the UK in the absence of clinical selection pressure.
These data indicate that once antibiotic resistance has been established
on mobile genetic elements, it may be difficult to eliminate.
Revised February 24, 2004
Accepted March 2, 2004
Original article
Enhancement of host fitness by the sul2-coding
plasmid p9123 in the absence of selective pressure
2 Bristol Centre for Antimicrobial
Research, Department of Pathology and Microbiology, University of
Bristol, Medical Sciences Building, University Walk, Bristol BS8
1TD;
3 Antibiotic Resistance Monitoring & Reference
Laboratory, Specialist and Reference Microbiology Division,
Health Protection Agency, 61 Colindale Avenue, London NW9 5HT, UK
4 Department of Medical
Microbiology, Barts and
The London School of Medicine and Dentistry, Queen Mary, University
of London, Turner Street, London E1 2AD;
Abstract 
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