Transposons Vancomycin

Acquired resistance to the glycopeptides is transposon-mediated and has so far been largely confined to the enterococci. This has been a problem clinically because many of these strains have been resistant to all other antibiotics and were thus effectively untreatable. Fortunately, the enterococci are not particularly pathogenic and infections have been confined largely to seriously ill, long-term hospital patients. Two types of acquired glycopeptide resistance have been described (Woodford et al. 1995). The VanA phenotype is resistant to vancomycin and teicoplanin, whereas VanB is resistant... 

Inducible resistance to high levels of vancomycin in enterococci is mediated by transposon Tn 1546 or related transposons [262, 263]. The transposition of Tn 1546 into plasmids with a broad host range or into con-jugative transposons would enable resistance to spread to 5. aureus which can exchange genetic information with enterococci [260]. Plasmid-mediated resistance to vancomycin has been successfully conjugated, in laboratory experiments, from enterococci to S. aureus, provided that erythromycin (6) and not vancomycin was used as the selective agent [265], It was only a question of time before such an event was shown to occur clinically [266, 267] and vancomycin resistance has now been found in an MRSA strain [268]. The seriousness of this cannot be over-emphasized. 

High-level vancomycin-resistance in S. aureus (MIC >32 pg/mL) has resulted from a con-jugative plasmid into which the Van A transposon was integrated by an interspecies horizontal gene tranter from E. faecaUs to a methicillin-resistant strain ofS. aureus. 

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