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The susceptibility to growth-promoting antibiotics of Enterococcus faecium isolates from pigs and chickens in Europe.

Research paper by Robin R Bywater, Malcolm M McConville, Ian I Phillips, Thomas T Shryock

Indexed on: 09 Aug '05Published on: 09 Aug '05Published in: The Journal of antimicrobial chemotherapy



Abstract

To establish the susceptibility of Enterococcus faecium isolates from pigs and chickens to antimicrobial growth promoters that either were or had been in use in the European Union.Samples were taken at abattoirs in two successive years (mid-1998-mid-1999, year 1; mid-1999-mid-2000, year 2) from chickens (France, The Netherlands, Sweden, UK) and pigs (Denmark, The Netherlands, Spain, Sweden). E. faecium was isolated from faecal samples at national laboratories and sent to a central laboratory where MICs of avilamycin, avoparcin, bacitracin, flavophospholipol, spiramycin, tylosin and virginiamycin were determined. Microbiological breakpoints were allocated on the basis of MIC distributions, and comparison was made between host species, country of origin and year of sample.In total, 2567 isolates were obtained from chickens and 1742 from pigs. In all countries, resistance to avoparcin (banned in 1997) was uncommon, but resistance to bacitracin and flavophospholipol was common (and was probably largely intrinsic). The prevalence of resistance was similar in chicken and pig isolates, with the exception of avilamycin, to which resistance was commoner among chicken isolates. The removal of four compounds as growth promoters (bacitracin, spiramycin, tylosin, virginiamycin) between years 1 and 2 appeared to result in a significant decrease in resistance to three of them-spiramycin, tylosin and virginiamycin, with no change in resistance to bacitracin, but an increase in resistance to avilamycin (not discontinued). Associated resistance was shown between some of the compounds.Resistance prevalence declined rapidly following removal of growth promoters in pigs and chickens, suggesting that in the absence of selective pressure, a susceptible population began to replace phenotypically resistant strains. Associated resistance between different compounds, where seen, could have resulted from either shared resistance mechanisms or from carriage of resistance genes on the same plasmid. Multiresistance to streptogramins, macrolides and glycopeptides was rare.