The treatment of endogenous infections caused by commensal Escherichia coli are often complicated by antibiotic resistance. Strains of resistant E. coli in the gastrointestinal tract serve as a reservoir of resistance determinants, and dissemination of resistance genes is often facilitated by conjugative plasmids. It is important to understand these plasmids in order to track the movement of resistance determinants between populations.
Three faecal E. coli isolates from a healthy adult were examined. Two of these (838-98B and -3B) were resistant to ampicillin (Ap), streptomycin (Sm) and sulphamethoxazole (Su). The other (838-50A) was susceptible. 838-50A and -3B were indistinguishable by biochemical and molecular analysis (API20E, phylogenetic group PCR, RAPD). 838-98B was a distinct strain. B/O plasmid replicons were detected in both resistant isolates using PCR-based plasmid replicon typing. A B/O replicon was not detected in the susceptible strain. This suggested that a plasmid bearing a B/O replicon might be responsible for ApSmSu resistance. Conjugation experiments with a laboratory adapted E. coli strain (UB5201) confirmed that the movement of a B/O plasmid from both 838-98B and -3B conferred ApSmSu resistance. Plasmid sequencing revealed that an identical B/O plasmid, p838B-R (94.8kb), was present in 838-98B and -3B, and carried ApSmSu resistance determinants. p838B-R was also observed to mobilise small plasmids, allowing the direction of in situ transfer to be determined.
The observed transfer of antibiotic resistance plasmid p838B-R between two unrelated strains in the gastrointestinal tract highlights the important role commensal bacteria play in the spread of resistance determinants. While not well documented, the association of B/O-type plasmids with antibiotic resistance is evident not only through p838B-R but also other available plasmid sequences. Further studies will allow us to determine the extent to which these plasmids influence antibiotic resistance in commensal E. coli.