The ingestion of resistant E. faecium of animal origin leads to detectable concentrations of the resistant strain in stools for up to 14 days after ingestion. The organisms survive gastric passage and multiply.

The MICs of vancomycin and avoparcin were determined for isolates of Enterococcus faecium and isolates of Enterococcus faecalis recovered from the feces of humans and animals in Denmark. Two hundred twenty-one of 376 (59%) isolates of E. faecium and 2 of 133 (1.5%) isolates of E. faecalis were resistant to vancomycin (MICs, 128 to > or = 256 micrograms/ml), and all vancomycin-resistant isolates were resistant to avoparcin (MICs, 64 to > or = 256 micrograms/ml). All vancomycin-resistant isolates examined carried the vanA, vanX, and vanR genes, suggesting that a gene cluster similar to that of the transposon Tn1546 was responsible for the resistance.

The consequences of using anti-microbial agents in a complex ecosystem like the animal intestine can be difficult to predict. We have looked at effects of modulations in growth of competing intestinal bacteria on transfer and establishment of new genetic elements in the intestinal microflora. For this purpose, we used tetracycline, which gradually reduces the growth rate of tetracycline-sensitive bacteria, as the concentration of this drug is increased. The effect of tetracycline on transfer and establishment of the plasmid RP4, which encodes resistance to this drug, in populations of Escherichia coli BJ4 colonizing the intestine was investigated. A tetracycline-sensitive E. coli BJ4 strain was allowed to establish in the gastrointestinal tract of mice, where after an isogenic E. coli BJ4 carrying RP4 was given to the mice per os. Tetracycline in the drinking water given to the animals was kept in concentrations that allowed the sensitive recipient strain to colonize the gut. A given 'window' between the highest and the lowest antibiotic doses tested was shown to be optimal for the establishment of transconjugants in the intestine. These observations are important for the evaluation of the effect of a given drug on the intestinal ecosystem. A reduced potential for growth of a given bacterial species, caused by the presence of sub-inhibitory concentrations of a bacteriostatic antibiotic, will facilitate establishment of competing (i.e. closely related) organisms, which have acquired resistance genes and therefore grow well in the presence of the drug.

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A new 3-h hybridization assay for detection of the staphylococcal mecA gene and the Staphylococcus aureus nuclease gene was evaluated by comparing the assay with existing genotypic and phenotypic methods. A total of 275 S. aureus strains were tested, including 257 epidemiologically unrelated strains (135 mecA-positive and 122 mecA-negative; collection I), and 18 strains with known borderline resistance to methicillin (collection II). Complete agreement was obtained for both collections when comparing the new assay with genotypic methods. We further evaluated a range of phenotypic susceptibility methods recommended in Europe and/or USA using the presence of the mecA gene as the defining standard. For collection I a high degree of agreement was found for both Etests (256 strains) and the oxacillin screen plate test (255 strains); the degree of agreement was lower for agar dilution methicillin (250 strains) and oxacillin 1 microg discs (239 strains). For the borderline strains a high degree of agreement was only obtained by the oxacillin screen plate test (17 of 18 strains). The other tests were less accurate, in the following order: agar dilution methicillin, Etest methicillin, Etest oxacillin and oxacillin discs with disagreement for four, five, nine and 13 strains, respectively. In conclusion, the new hybridization assay is a rapid and exact method for detecting the mecA gene and the S. aureus nuclease gene. This study confirms that phenotypic tests for methicillin resistance in S. aureus strains creates both false-susceptible and false-resistant results, especially for borderline resistant strains.