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The use of antimicrobial growth promoters has caused the development of resistance in a number of important pathogenic bacterial species. Furthermore, most cases in which antimicrobials belonging to one single class of antibiotics have been used as therapeutic drugs for both humans and animals have resulted in the development of cross resistance to these drugs. Some of the bacteria developing resistance are pathogenic to animals or man, and the development of resistance to growth promoters and related therapeutic drugs has limited the therapeutic options for these bacteria. In the case of E. faecium, resistance has developed towards very important "last resort" antimicrobials. Although the full public health consequences of the development of resistance through the use of antimicrobial growth promoters have not yet been determined, there is nevertheless a need to take precautionary actions in order to prevent further development of resistance towards a number of antimicrobials used as growth promoters.

The satA gene encoding streptogramin A resistance was detected in virginiamycin-resistant Enterococcus faecium isolates from pigs and broilers. The satA gene was present in 22 of 89 (25%) virginiamycin-resistant E. faecium isolates. It was shown that the satA gene and other gene(s) encoding streptogramin resistance could be transferred between isogenic E. faecium strains at frequencies ranging from 2.3 x 10(-4) to 2.2 x 10(-3) transconjugants per donor.

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In this study, internal size variations in the VanA gene cluster Tn1546, encoding resistance to glycopeptides, is described. Studies of previously uncharacterized size variations of an internal region, encoding the vanX and vanY genes of Tn1546, revealed that these variations were due to the presence of the IS sequence, IS1216V. This IS sequence has previously been found integrated in Tn1546. Integration of the IS1216V element created both deletions and a duplication in a non-essential region of Tn1546. In several isolates, the entire vanY gene was deleted, proving that this gene is non-essential for vancomycin resistance.

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