Vancomycin-Resistant Enterococci, Point Barrow, Alaska, USA

To the Editor: An increasing number of bacterial infections are now diffi cult or impossible to treat (1) because of the misuse of antimicro-bial drugs and the epidemic spread of bacterial resistance to these drugs (2). The most alarming reports are of me-thicillin-resistant Staphylococcus au-reus, extended-spectrum β-lactamase producers, and vancomycin-resistant enterococci (VRE). Although knowledge about dissemination mechanisms is poor, the spread of resistance clearly is not restricted to hospitals but occurs also in the community and in the natural environment (3,4). Since the 1990s, the epidemiology in the United States has shifted so that most VRE are Enterococcus faecium. Recent studies indicate clonal spread of the E. faecium CC17 lineage in clinical isolates, exhibiting high-level ampi-cillin and fl uoroquinolone resistance and harboring an enterococcal surface protein–coding esp gene (5,6). During a polar research expedition to the Beringia region in 2005, we collected fecal samples from birds at sites with no or low human population. The aim was to investigate the current status of resistance dissemination into remote areas of the world. The study site in Alaska was located on the tundra halfway between the city of Barrow and Point Barrow, the northernmost point of the United States (71°23′20″N, 156°28′45″W). Fecal samples from glaucous gulls (Larus hyperboreus) were enriched (18 h at 37°C) in brain–heart infusion broth (Becton Dickinson, Franklin Lakes, NJ, USA) supplemented with aztreonam and vancomycin (10 mg/L and 4 mg/L, respectively; ICN Bio-lowed by spreading on chromID VRE plates (bioMérieux, Marcy l'Etoile, France) and incubated for 48 h at 37°C. Typical colonies were isolated and species identifi ed by biochemical testing, including the Phoenix Automated Microbiology System (Becton Dickinson). MIC was determined for vancomycin, teicoplanin, ampicillin, and ciprofl oxacin by using Etest strips (AB Biodisk, Solna, Sweden), and the presence of vanA, vanB, and esp genes was established by PCR with previously described primers (7,8) (esp primers esp11 and esp12). Cultures showed 2 isolates of E. faecium; MICs for vancomycin and teicoplanin were >256 and 96 μg/mL, respectively, for both isolates. Geno-typing determined that they harbored vanA. Isolates exhibited high-level am-picillin and ciprofl oxacin resistance; MICs were >256 and >32 μg mL, respectively for both isolates. They also harbored the esp gene. Isolates came from 2 of 33 sampled glaucous gulls, a species confi ned to the Arctic regions, that have limited southbound migration during the nonbreeding season. Clinical isolates of VRE were fi rst found in the …