Vancomycin-Resistant Enterococcus faecium Strains with Highly Similar Pulsed-Field Gel Electrophoresis Patterns Containing Similar Tn1546-Like Elements Isolated from a Hospitalized Patient and Pigs in Denmark

Vancomycin-resistant enterococci (VRE) have emerged as a worldwide problem (14). The consumption of vancomycin has been steadily increasing from 2,000 kg in 1984 to 10,312 kg in 1995 in the United States and from 200 to 1,222 kg in France (12). The oral use of avoparcin for growth promotion in pigs increased from 13,644 kg in 1989 to 24,117 kg in 1994 in Denmark (20). The frequency of isolation of VRE has increased (5) since isolation of the first VRE in England in 1986 (18). The mechanism of vancomycin resistance has been well characterized especially for the vanA gene cluster (14). Other resistance mechanisms named vanB, vanC, and vanD have been defined (14). Two theories on the selection for the presence of VRE prevail, and probably a combination of these theories has caused the development of VRE. One theory is that the use of the glycopeptide avoparcin as a growth promoter for animals in Europe has selected for vanA-positive VRE in the animal gut (1, 7, 16). Several studies have confirmed that avoparcin selects for VRE (2, 4). VRE have also been found in the environment (13, 17) and in nonhospitalized humans in Europe (8). The other theory is that the use of vancomycin in hospitals has selected for VRE. Studies of nonhospitalized humans and the environment in the United States, where avoparcin has not been approved for use, have failed to isolate VRE (6, 16). The genetic diversity of the vanA gene cluster encoded by Tn1546 has been investigated, and identical Tn1546-like elements in strains of human and animal origins were found (9, 11, 21). This indicates that these two reservoirs are not distinct and that exchange of Tn1546-like elements occurs. A study on a base pair variation in the vanX gene of Tn1546 suggests that the spread of VRE has occurred from animals to humans. While VRE isolated from humans contained either one or the other variant, pigs and poultry each had a unique base pair variant (10). Indistinguishable pulsed-field gel electrophoresis (PFGE) patterns of VRE strains isolated from a Dutch farmer and one of his turkeys have been obtained, indicating that humans and animals in close contact could harbor identical VRE (19). In Denmark, VRE is still present at a frequency of 20% among Enterococcus faecium isolates from pigs 3 years after the ban of use of avoparcin (3). From humans in Denmark VRE have been isolated in only six cases. One urine and four fecal isolates have been isolated from hospitalized patients, and one fecal isolate has been isolated from a healthy human. None of the patients had been treated with vancomycin. Among the isolates two of fecal origin were from the same patient carrier, isolated 6 months apart, and had identical SmaI PFGE patterns (Fig. 1). A third isolate of fecal origin from a hospitalized patient had a SmaI PFGE pattern (Fig. 1) highly similar to that of a VRE clone that is commonly found in Danish pigs (unpublished data). The Tn1546-like elements of the human and porcine isolates were identical (11). This person was interviewed by her doctor and had no association with any farms in Denmark and eats pork, beef, and poultry products. Since the highly similar PFGE pattern links this human isolate to a common porcine VRE clone, this provides further evidence for food-borne transmission of VRE from animals to humans.

FIG. 1.

PFGE SmaI patterns of VRE isolates of porcine and human origins in Denmark. Lanes 1 and 9, Lambda Ladder PFG Marker (New England Biolabs); lane 2, isolate 17243 (human); lane 3, isolate 17494 (human); lane 4, isolate 109 1A (human); lane 5, isolate 5979 (human); lane 6, isolate 86651 (human); lane 7, isolate 17575 (human); lane 8, isolate E 8 SV 3 (porcine). Isolates 17243 and 17494 (lane 2 and 3) were obtained from the same patient 6 months apart.