In vitro susceptibilities of clinical isolates of vancomycin-resistant enterococci

Abstract

Recent studies have reported RP59500 (Synercid) (quinupristin-dalfopristin), a semisynthetic streptogramin, to have good in vitro activity against certain enterococcal strains, including vancomycin-resistant strains of Enterococcus faecium (3-5). The purpose of the present study was to determine the in vitro activity of this new compound against a larger sample of resistant strains of enterococci and to compare its activity with those of several currently available antimicrobials. We analyzed 1,044 strains of vancomycin-resistant enterococci (990 E. faecium and 54 E. faecalis) which had been isolated from clinical specimens at 52 New Jersey hospitals between March 1993 and February 1996. Following identification of isolates to species level, MICs were determined by broth microdilution (6). The results are summarized in Table 1. All isolates demonstrated resistance to vancomycin (MIC Ն 32 g/ml); 803 (76.9%) were also resistant to teicoplanin (MIC Ն 32 g/ml). RP59500 had excellent activity against most isolates of E. faecium, with 968 (97.8%) inhibited at a concentration of 1 g/ml or less, making it the most active agent of those we tested. This supports data obtained in prior studies involving vancomycinresistant E. faecium which have reported a range of MICs from 0.06 to 32 g,/ml, with MICs at which 90% of isolates are inhibited (MIC 90) between 0.5 and 16 g/ml (2-5, 7). RP59500 was considerably less active against E. faecalis, with only one-third of strains inhibited at 4 g/ml, an observation consistent with earlier findings (3-5). In addition, the MIC 50 s and MIC 90 s of RP59500 for the two species were not affected by differences in the vancomycin resistance phenotype (1). Like that to RP59500, resistance to ampicillin was found to be species specific, with E. faecium (MIC 90 Ն 128 g/ml) significantly more likely to be resistant to ampicillin (MIC Ն 16 g/ml) than E. faecalis (MIC 90 ϭ 2 g/ml). High-level resistance to gentamicin, defined by a MIC of Ͼ500 g/ml, was

Lack of Efficacy of Oral Bacitracin Plus Doxycycline for the Eradication of Stool Colonization with Vancomycin‐Resistant Enterococcus faecium

“…Bacitracin has limited oral absorption, has excellent in vitro activity against VRE [27], and has been shown to suppress bowel flora when Ͼ100,000 U daily is administered [28]. Doxycycline has in vitro activity [29,30], achieves adequate fecal levels [31] to have activity against VRE, and has shown clinical efficacy against VRE [17,30]. Nord and Heimdahl showed that administration of oral doxycycline for 7 days decreased the number of enterococci in the feces by 2-3 logs [31] but also led to a significant increase in doxycyclineresistant strains.…”

Chloramphenicol Resistance in Vancomycin-Resistant Enterococcal Bacteremia: Impact of Prior Fluoroquinolone Use?

“…31 A report of in vitro susceptibilities of 1,044 strains of VRE (990 Enterococcus faecium and 54 Enterococcus faecalis) from New Jersey hospitals between 1993 and 1996 found that 92.1% of Enterococcus faecium strains, but only 68.5% of Enterococcus faecalis strains, were susceptible to chloramphenicol. 32 Transferable plasmids mediating resistance to multiple antibiotics, including chloramphenicol, are well known in Enterococcus faecalis. 11 We noted clustering of many cases of chloramphenicol-resistant VRE in two areas of the hospital (data not shown).…”

Transmission of VanA-Type Vancomycin-Resistant Enterococci andvanAResistance Elements between Chicken and Humans at Avoparcin-Exposed Farms

“…Environmental reservoirs of vana-type vancomycin-resistant enterococci (VRE) were first reported from Europe in 1993.16 These reservoirs are related to widespread use of the glycopeptide avoparcin as a growth-promoting feed additive in European animal husbandry.1 [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] carrying VRE in their gastrointestinal tract have been suggested as a likely source of VanA VRE infection in humans, 4 and several studies have focused on possible transmission lines between humans and animals. The occurrence of VRE in chicken carcasses and commercial meat products4 '17,19 im-plies the risk of VRE transmission through the food chain and could explain the detection of VRE in fecal samples from healthy volunteers,25 out-patients,17'25 and newly admitted hospital patients.5 A case of possible VRE transmission from colonized animal to human by direct wound inoculation was recently reported in a community-acquired infection in a food industry worker.7 This observation suggests a mode of VRE transmission through direct contact between humans and colonized animals.…”