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pubmed:abstractText |
It was shown that a strain of Serratia liquefaciens harbors a conjugative R-plasmid responsible for reistance to the following 14 antibiotics: ampicillin, carbenicillin, cephalothin, butirosin, neomycin, paramomycin, kanamycin, lividomycin, gentamicin, tobramycin, streptomycin, tetracycline, sulfonamide, and chloramphenicol, which belong to five families, the beta-lactamines, the aminoglycosides, the tetracyclines, the sulfonamides, and the phenicols. Resistance to th 14 antibiotics was cotransferred by in vitro conjugation between S. liquefaciens and strains of Escherichia coli. Mating between S. liquefaciens and E. coli also occurred in vivo, in the digestive tract of axenic mice and gnotobiotic mice associated with the whole human fecal flora. It was also shown that mating between these two strains occurred even when the donor S. liquefaciens strain was only transient in the digestive tract of the gnotobiotic host animals. A dense population of Bacteroides (10(10) viable cells per g of fresh feces) did not hinder this mating. All the matings occurred in the absence of an antibiotic selection pressure, and the resulting transferred strain of E. coli did not have the same colonizing capacity as the recipient parental strain. However, during antibiotic administration to mice, and even after the end of the drug intake, the transconjugant became established in the dominant population and replaced the parental recipient strain.
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