ライフサイエンスコーパス: VRE

1 VRE and VSE isolates from each patient were closely rela

2 VRE BSI incidence was 6.5% of admissions (2.7 VRE BSI pe

3 VRE colonization (adjusted odds ratio [aOR] = 8.4; 95% c

4 VRE therapy is a particularly promising format to test t

5 VRE were initially isolated from 147 cultures, and the V

6 VRE-BMX provided the identification of 10 isolates of va

7 VRE-colonized patients bathed with chlorhexidine had a l

8 in the fidaxomicin group (5.9 vs 3.8 log(10) VRE/g stool; P = .01) but not the vancomycin group (5.3

9 not the vancomycin group (5.3 vs 4.2 log(10) VRE/g stool; P = .20).

10 RE BSI incidence was 6.5% of admissions (2.7 VRE BSI per 1000 BSI at-risk days).

11 ons, we probed the plasmids obtained from 75 VRE isolates for the presence of toxin-antitoxin (TA) ge

12 VRE) increases in hospitals, knowledge about VRE reservoirs and improved accuracy of epidemiologic me

13 70; P < .001) and 80% less likely to acquire VRE (IRR, 0.20; 95% CI, .08-.52; P < .001) after adjusti

14 ent of mice enabled exogenously administered VRE to efficiently and nearly completely displace the no

15 nits were significantly more likely to admit VRE carriers than were surgical units.

16 AdvanDx VRE EVIGENE, a commercial vanA/vanB DNA hybridization as

17 pediatric patients, mortality 30 days after VRE and VSE bacteremia was 20% (95% CI, 5.4%-59%) and 4.

18 eptide with potent in vitro activity against VRE (both VanA and VanB phenotypes).

19 has in vitro bacteriostatic activity against VRE, but its clinical use for serious enterococcal infec

20 se compounds possess potent activity against VRE, inhibiting growth of clinical isolates at concentra

21 vancin demonstrate in vitro activity against VRE.

22 n has in vitro bactericidal activity against VRE; however, clinical use of this compound for VRE has

23 esistance of antibiotic-treated mice against VRE.

24 eae restores colonization resistance against VRE and clears VRE from the intestines of mice.

25 The MIC values against VRE were more than 50-fold lower than those reported for

26 ovide even more potent antimicrobial agents [VRE minimum inhibitory concentration (MIC) = 0.01-0.005

27 All VRE subpopulations grew on V6 plates but were missed in

28 (Copan, Brescia, Italy) software to analyze VRE chromogenic agar and compared the results to technol

29 rence in CAPS between the VRE-DCS (n=13) and VRE-placebo (n=12) groups increased over time beginning

30 s previously associated with C difficile and VRE.

31 608) were similar discriminators of MRSA and VRE (c = 0.670 and c = 0.647, respectively).

32 The MICs for 9a, 9b, and 9c against MRSA and VRE (Van B phenotype) range from 0.12 to 0.25 mug/mL.

33 or rapid screening (PCR testing for MRSA and VRE and chromogenic screening for highly resistant Enter

34 MRSA and VRE are readily found on colonized patients and their en

35 c centers measured the incidence of MRSA and VRE colonization and BSI during a period of bathing with

36 ated the effect of surveillance for MRSA and VRE colonization and of the expanded use of barrier prec

37 o help ICU personnel better control MRSA and VRE in their units.

38 oped and standardized a registry of MRSA and VRE patients and created Web forms that infection preven

39 establishing metrics for monitoring MRSA and VRE rates in ICUs; promoting hand hygiene compliance; gu

40 ic dihydrazide), was active against MRSA and VRE with MIC's of 8.1 and 4.7 muM, respectively.

41 nd that the two Gram-positive ARBs (MRSA and VRE) were more resistant to UV disinfection than the two

42 t Gram-positive bacteria, including MRSA and VRE, rapid time-kill, avoidance of antibiotic resistance

43 ients may reduce the acquisition of MRSA and VRE.

44 elevant bacterial strains including MRSA and VRE.

45 tal use and increased C difficile, MRSA, and VRE prevalence.

46 ibacterial activities against MRSA, MRSE and VRE (MIC = 0.003-0.78 microM).

47 C = 0.59-9.38 microM) against MRSA, MRSE and VRE biofilms while showing minimal red blood cell lysis

48 n activities to date against MRSA, MRSE, and VRE biofilms (MBEC = 0.2-12.5 muM), as well as the effec

49 (MBEC < 10 muM), MRSE (MBEC = 2.35 muM), and VRE (MBEC = 0.20 muM) biofilms while 11 and 12 demonstra

50 of vancomycin-resistant pathogens (VRSA and VRE), the studies pave the way for the examination of sy

51 good activity against MRSA, VISA, VRSA, and VRE and moderate activity against E. coli.

52 Determining when to use empiric anti-VRE antibiotic therapy in this population remains a clin

53 thod of guiding rational use of empiric anti-VRE antimicrobial therapy in patients with hematological

54 Performance was assessed using S. aureus, VRE, and vancomycin-intermediate and -susceptible isolat

55 ity 30 days after infection was 38% for both VRE (95% CI, 25%-54%) and VSE cases (95% CI, 21%-62%).

56 ting, we found that intestinal domination by VRE preceded bloodstream infection in patients undergoin

57 le, of whom 226 (7.5%) were detected only by VRE surveillance cultures.

58 little propensity for acquired resistance by VRE and that their durability against such challenges as

59 In two cases, VRE presence was missed by Vitek2.

60 populations isolated from mice that cleared VRE following microbiota reconstitution revealed that re

61 lonization resistance against VRE and clears VRE from the intestines of mice.

62 tly detected 101 well-characterized clinical VRE isolates with no cross-reactivity in 27 non-VRE and

63 re chromogenic media, which included Colorex VRE (BioMed Diagnostics, White City, OR) or Oxoid VRE (O

64 No difference in 60-day VRE-BSI recurrence was observed between treatment groups

65 y; (2) microbiologic failure; and (3) 60-day VRE-BSI recurrence.

66 f a diverse intestinal microbiota to densely VRE-colonized mice eliminates VRE from the intestinal tr

67 There is a simple method to detect VRE subpopulations that may be missed by Vitek2.

68 chlorhexidine had a lower risk of developing VRE bacteremia (relative risk 3.35; 95% confidence inter

69 ota to densely VRE-colonized mice eliminates VRE from the intestinal tract.

70 he microbiota are ineffective at eliminating VRE, administration of obligate anaerobic commensal bact

71 ltures for vancomycin-resistant enterococci (VRE) and methicillin-resistant Staphylococcus aureus (MR

72 outcome of vancomycin-resistant enterococci (VRE) and vancomycin-sensitive enterococci (VSE) infectio

73 ed by both vancomycin-resistant enterococci (VRE) and vancomycin-susceptible enterococci (VSE).

74 Vancomycin-resistant enterococci (VRE) are an important cause of health care-acquired infe

75 Vancomycin-resistant enterococci (VRE) are common hospital pathogens that are resistant to

76 ptions for vancomycin-resistant enterococci (VRE) bloodstream infection (BSI) are limited.

77 ishment of vancomycin-resistant enterococci (VRE) colonization by depleting nutrients within cecal co

78 (MRSA) and vancomycin-resistant enterococci (VRE) due to the scope of the medical threat posed by the

79 Vancomycin-resistant enterococci (VRE) escape the bactericidal action of vancomycin by che

80 (MRSA) and vancomycin-resistant enterococci (VRE) for extended periods of time and temperatures using

81 illance of vancomycin-resistant enterococci (VRE) from rectal swabs in patients at high risk for VRE

82 olation of vancomycin-resistant enterococci (VRE) from stool specimens.

83 caused by vancomycin-resistant enterococci (VRE) has become an important clinical challenge and comp

84 (MRSA) and vancomycin-resistant Enterococci (VRE) have now arisen and are of major concern.

85 to detect vancomycin-resistant enterococci (VRE) in 750 stool specimens.

86 control of vancomycin-resistant enterococci (VRE) in hospitals also requires consideration of vancomy

87 eening for vancomycin-resistant enterococci (VRE) in rectal and stool specimens has been recommended

88 ction with vancomycin-resistant enterococci (VRE) increases in hospitals, knowledge about VRE reservo

89 nized with vancomycin-resistant enterococci (VRE) is central to the containment of this agent within

90 istance in vancomycin-resistant enterococci (VRE) is due to an alternative cell wall biosynthesis pat

91 SA) and/or vancomycin-resistant enterococci (VRE) on at least 1 occasion by any of 5 healthcare syste

92 m clinical vancomycin-resistant enterococci (VRE) strains.

93 (MRSA) and vancomycin-resistant enterococci (VRE) that are known to exert a high level of resistance

94 erred upon vancomycin-resistant enterococci (VRE) through the replacement of peptidoglycan (PG) stem

95 tion, more vancomycin-resistant enterococci (VRE) were recovered with CVRE than BEAV.

96 as well as vancomycin-resistant enterococci (VRE) with minimum inhibitory concentrations (MICs) rangi

97 us (MRSA), vancomycin-resistant enterococci (VRE), and ceftazidime-resistant (CAZ(r)) and ciprofloxac

98 ve against vancomycin-resistant enterococci (VRE), and fluoroquinolones with improved potency against

99 detecting vancomycin-resistant enterococci (VRE), and the results were available 24 to 48 h sooner.

100 valence of vancomycin-resistant enterococci (VRE), appropriate antibiotic therapy for enterococcal bl

101 (MRSA) and vancomycin-resistant enterococci (VRE), has reached a critical state.

102 s, such as vancomycin-resistant enterococci (VRE), necessitates the development of new antimicrobials

103 o identify vancomycin-resistant enterococci (VRE), was evaluated for the detection of vanA in Staphyl

104 ed against vancomycin-resistant Enterococci (VRE).

105 ation with vancomycin-resistant enterococci (VRE).

106 d) against vancomycin-resistant Enterococci (VRE).

107 ainst many vancomycin-resistant enterococci (VRE).

108 (MRSA) and vancomycin-resistant Enterococci (VRE).

109 ynamics of vancomycin-resistant enterococci (VRE).

110 (MRSA) or vancomycin-resistant enterococci (VRE).

111 ative" for vancomycin-resistant enterococci (VRE).

112 de against vancomycin-resistant enterococci (VRE).

113 I; 22 with vancomycin-resistant enterococci [VRE] and 61 with vancomycin-susceptible enterococci [VSE

114 [MRSA] and vancomycin-resistant enterococci [VRE]) or rapid screening (PCR testing for MRSA and VRE a

115 MRSA) and vancomycin-resistant Enterococcus (VRE) among ICU patients.

116 bacterium vancomycin-resistant Enterococcus (VRE) can exceed 10(9) organisms per gram of feces, even

117 creen for vancomycin-resistant enterococcus (VRE) colonization.

118 MRSA) and vancomycin-resistant enterococcus (VRE) have achieved significant rates of colonization and

119 RSA), and vancomycin-resistant Enterococcus (VRE) in patients with and without penicillin "allergy" a

120 atment of vancomycin-resistant Enterococcus (VRE) infections is limited by the paucity of effective a

121 I) to due vancomycin-resistant Enterococcus (VRE) is an important complication of hematologic maligna

122 MRSA) and vancomycin-resistant Enterococcus (VRE) is driving the development of new technologies to i

123 utable to vancomycin-resistant Enterococcus (VRE) strains have become increasingly prevalent over the

124 ected for vancomycin-resistant Enterococcus (VRE) surveillance as well as from clinical C. difficile

125 s (MRSA), vancomycin-resistant Enterococcus (VRE), and MDR Enterobacteriaceae Fecal metagenomes were

126 , such as vancomycin-resistant Enterococcus (VRE), is a dangerous and costly complication of broad-sp

127 , such as vancomycin-resistant Enterococcus (VRE), is a growing clinical problem that increasingly de

128 tion with vancomycin-resistant Enterococcus (VRE), leading to bloodstream infection in hospitalized p

129 MRSA) and vancomycin-resistant Enterococcus (VRE), while also exhibiting a minimal potential to induc

130 MRSA) and vancomycin-resistant enterococcus (VRE).

131 niae, and vancomycin-resistant Enterococcus (VRE).

132 MRSA) and vancomycin-resistant enterococcus (VRE).

133 uated for vancomycin-resistant enterococcus (VRE).

134 e to vancomycin-resistant (VR) enterococcus (VRE) and methicillin-resistant Staphylococcus aureus (MR

135 nergistically with virtual reality exposure (VRE) therapy for the treatment of PTSD.

136 vancomycin-resistant Enterococcus faecalis (VRE) and 2 patients with infectious crystalline keratiti

137 vancomycin-resistant Enterococcus faecalis (VRE).

138 erococcus faecium and Enterococcus faecalis (VRE).

139 vancomycin-resistant Enterococcus faecalis (VRE).

140 , vancomycin-resistant Enterococcus faecium (VRE FCM) (16), vancomycin-susceptible Enterococcus faeca

141 , vancomycin-resistant Enterococcus faecium (VRE), and beta-lactam-resistant Klebsiella pneumoniae.

142 , vancomycin-resistant Enterococcus faecium (VRE), Escherichia coli SMS-3-5, and Pseudomonas aerugino

143 ; however, clinical use of this compound for VRE has not been well studied, and the reports of resist

144 r daptomycin doses need to be considered for VRE-BSI treatment.

145 Stool was cultured for VRE and Candida species before and after therapy.

146 ded 112 patients treated with daptomycin for VRE-BSI and with evaluable clinical outcomes.

147 /=10 mg/kg total body weight) daptomycin for VRE-BSI.

148 re or after transplant was a risk factor for VRE bacteremia (odds ratio [OR], 3.3 [95% CI, 1.3-8.3] a

149 ed a prediction score using risk factors for VRE BSI and evaluated the model's predictive performance

150 Treatment with linezolid for VRE-BSI resulted in significantly higher treatment failu

151 ing a plausible pathophysiological model for VRE BSI in patients with hematological malignancy.

152 omycin are the primary treatment options for VRE-BSI, but optimal treatment is unclear.

153 ctive surveillance of high-risk patients for VRE colonization can aid in reducing HAIs; however, thes

154 om rectal swabs in patients at high risk for VRE carriage.

155 eOhm VanR assay is a good screening test for VRE in our population of predominantly vanA-colonized pa

156 (P = 0.0001 versus CIP(r) GNB), and that for VRE was 186.0 days (P = 0.0004 versus CIP(r) GNB).

157 Thus, current reliable therapies for VRE appear to be limited, and clinical data that use the

158 sozyme resistance and enhanced virulence for VRE grown in the presence of vancomycin.

159 All four VRE isolates and 2/4 VSE isolates were vanA positive.

160 g method for removing medium components from VRE cells.

161 Further, VRE-BMX was capable of identifying patients colonized wi

162 he same cornea at the end of therapy for her VRE keratitis.

163 the available laboratory methods to identify VRE in clinical specimens.

164 eacetylation, and increased O-acetylation in VRE when grown in the presence of vancomycin.

165 ed survival and microbiological clearance in VRE-BSI.

166 condary outcomes, there was no difference in VRE acquisition with the intervention (difference, 0.89

167 -Ala, d-Ala-d-Ala, and d-Ala-d-Lac levels in VRE were then determined in the presence of variable van

168 Given this ubiquity of mazEF in VRE and the deleterious activity of the MazF toxin, disr

169 to the quantitation of these metabolites in VRE.

170 type on damage to ARGs was only observed in VRE and P. aeruginosa, the latter potentially because of

171 l biosynthesis and modification processes in VRE that contribute to lysozyme resistance and enhanced

172 lysis demonstrated significant reductions in VRE bacteremia (p = 0.02) following the introduction of

173 ew agents targeting vancomycin resistance in VRE.

174 that kills gram-positive bacteria, including VRE.

175 that kills Gram-positive bacteria, including VRE.

176 atment of gram-positive keratitis, including VRE, and is both significantly more comfortable and less

177 sis of clinical cultures alone and increased VRE precaution days by 2.4-fold (unit range, 2.0-2.6-fol

178 Secondary outcomes included individual VRE acquisition, MRSA acquisition, frequency of health c

179 sistant Enterococcus bloodstream infections (VRE-BSIs) are associated with significant mortality.

180 sistant Enterococcus bloodstream infections (VRE-BSIs) are becoming increasingly common.

181 n with B. producta, which directly inhibited VRE growth.

182 Integrating VRE colonization status with risk factors for developing

183 esiella genus enable clearance of intestinal VRE colonization and may provide novel approaches to pre

184 nfold reduction in the density of intestinal VRE colonization.

185 e, represents an important approach to limit VRE transmission.

186 While C. bolteae did not directly mediate VRE clearance, it enabled intestinal colonization with B

187 aluated a prototype chromogenic agar medium (VRE-BMX; bioMerieux, Marcy l'Etoile, France) used to rec

188 RSA, and 30.1% (95% CI, 12.5% to 50.4%) more VRE infections than expected compared with control subje

189 Most VRE isolates recovered after fidaxomicin treatment had e

190 against Gram-positive bacteria (e.g., MRSA, VRE, PRSP (penicillin-resistant Streptococcus pneumoniae

191 biological tests were used to identify MRSA, VRE, and CAZ(r) and CIP(r) GNB.

192 problematic fluoroquinolone-resistant MRSA, VRE, and S. pneumoniae, and the possibility to offer pat

193 Of 301 patients, 247 (82%) had negative VRE cultures and 252 (84%) had negative Candida species

194 the CDM was accurate at identifying negative VRE plates, which comprised 84% (87,973) of the specimen

195 isolates with no cross-reactivity in 27 non-VRE and related culture isolates.

196 , color distinction, and breakthrough of non-VRE organisms vary among the chromogenic media tested an

197 -treated patients had reduced acquisition of VRE (7% vs 31%, respectively; P < .001) and Candida spec

198 ly than vancomycin to promote acquisition of VRE and Candida species during CDI treatment.

199 barrier precautions to reduce acquisition of VRE and MRSA and the subsequent development of healthcar

200 cal contents and limiting the association of VRE with the mucus layer.

201 n vivo, significantly reducing the burden of VRE in infected worms.

202 weekly intervals would predict clearance of VRE or MRSA from colonized patients.

203 Clearance of VRE remains a challenging goal that, if achieved, would

204 eillance markedly increases the detection of VRE, despite variability across patient-care units.

205 lture was more specific for the detection of VRE.

206 Anaerobic growth of VRE was assessed in cecal contents and cecal mucus of mi

207 edictive values for prompt identification of VRE-colonized patients in hospitals with relatively high

208 agnostic testing for early identification of VRE.

209 e care units; and (5) defining the impact of VRE bacteremia and daptomycin susceptibility on patient

210 tive pretreatment cultures, the incidence of VRE and Candida species acquisition was compared.

211 Cumulative incidence of VRE and VSE bacteremia was 6.6% (95% confidence interval

212 ay in engraftment increased the incidence of VRE bacteremia from 4.5% (95% CI, 2.9-6.6) if engrafted

213 The incidence of VRE is increasing rapidly, to the point where over one-q

214 Igamma markedly decreases in vivo killing of VRE in the intestine of antibiotic-treated mice.

215 Seventy-two percent of VRE-colonized patients and 94% of MRSA-colonized patient

216 We compared the performance of VRE-BMX with bile esculin azide agar supplemented with v

217 t enterococci (Van A and Van B phenotypes of VRE).

218 The positive predictive values (PPV) of VRE-BMX and BEAV at 24 h were 89.8% and 80.7%, respectiv

219 firmed by another method for the presence of VRE.

220 A decrease in the endemic prevalence of VRE also occurs with a decrease in the length of hospita

221 The admission prevalence of VRE was 2.2%-27.2%, with admission surveillance providin

222 shold of >/=5 points, per day probability of VRE BSI was increased nearly 4-fold.

223 s in hospitals with relatively high rates of VRE carriage.

224 id not significantly improve the recovery of VRE and resulted in decreased specificity.

225 d that VRE-BMX provided improved recovery of VRE from stool specimens, with the added advantage of be

226 This is the first report of VRE found in food animals in the United States.

227 s the factors that contribute to the rise of VRE as an important health care-associated pathogen, the

228 nterventions aimed at limiting the spread of VRE.

229 , selection of preexisting subpopulations of VRE with elevated fidaxomicin MICs was common during fid

230 C(90), 256 microg/mL), and subpopulations of VRE with elevated fidaxomicin MICs were common before th

231 The susceptibility of VRE isolates to fidaxomicin was assessed.

232 rol practices can reduce the transmission of VRE and aid in the prevention of hospital-acquired infec

233 Administration approval for the treatment of VRE (E. faecium) infections, namely, linezolid and quinu

234 ined, and novel targets for the treatment of VRE are lacking.

235 y novel protein targets for the treatment of VRE infections, we probed the plasmids obtained from 75

236 inezolid and daptomycin for the treatment of VRE-BSI among Veterans Affairs Medical Center patients a

237 ycin dose of >/=6 mg/kg for the treatment of VRE-BSI caused by daptomycin-susceptible VRE.

238 ion, is frequently used for the treatment of VRE-BSI.

239 r specimens plated on two different types of VRE chromogenic agar plates.

240 tively counteracting major types (VanABC) of VRE.

241 can affect both the fitness and virulence of VRE.

242 a first positive clinical culture of MRSA or VRE at least 48 hours postadmission (July 1, 1998-July 1

243 e primary outcome was acquisition of MRSA or VRE based on surveillance cultures collected on admissio

244 actice (control) on the incidence of MRSA or VRE colonization or infection in adult ICUs.

245 ereas control ICUs had a decrease in MRSA or VRE from 19.02 acquisitions per 1000 patient-days (95% C

246 a decrease in the primary outcome of MRSA or VRE from 21.35 acquisitions per 1000 patient-days (95% C

247 ts of colonization or infection with MRSA or VRE per 1000 patient-days at risk, adjusted for baseline

248 reviously infected or colonized with MRSA or VRE registered for admission to a study hospital from Ju

249 who were colonized or infected with MRSA or VRE were assigned to barrier precautions more frequently

250 who were colonized or infected with MRSA or VRE were assigned to care with contact precautions; all

251 tive in reducing the transmission of MRSA or VRE, although the use of barrier precautions by provider

252 ge of 37 h earlier for patients with MRSA or VRE.

253 he primary outcome of acquisition of MRSA or VRE.

254 ys without a decrease in recovery of MRSA or VRE.

255 rt review of 31 patients with MRSA, MSSA, or VRE demonstrated that the Nanosphere BC-GP assay might h

256 BioMed Diagnostics, White City, OR) or Oxoid VRE (Oxoid, Basingstoke, United Kingdom).

257 For those with preexisting VRE, the change in concentration during treatment was co

258 For patients with preexisting VRE, the mean concentration decreased significantly in t

259 ation of broad-spectrum antibiotics promotes VRE colonization by down-regulating homeostatic innate i

260 ted the hypothesis that fidaxomicin promotes VRE and Candida species colonization less than vancomyci

261 eux, Marcy l'Etoile, France) used to recover VRE from clinical specimens.

262 antibiotic-treated mice dramatically reduces VRE colonization.

263 ollows: BEAV, 75.7% and 74.6%, respectively; VRE-BMX, 95.5% and 91.3%, respectively.

264 ollows: BEAV, 90.9% and 89.9%, respectively; VRE-BMX, 96.4% and 96.6%, respectively.

265 nt limitations for the treatment of a severe VRE infection (ie, endocarditis), combination of oritava

266 owever, the use of these compounds in severe VRE infections is hampered by the lack of in vivo bacter

267 d vancomycin-resistant Enterococcus species (VRE) using a laboratory-developed real-time PCR test and

268 Spectra VRE (Remel, Lenexa, KS) is a chromogenic medium designed

269 Spectra VRE and CAMPY are significantly more sensitive at 24 h t

270 , respectively, were 98% and 95% for Spectra VRE chromogenic agar (Remel, Lenexa, KS), 86% and 92% fo

271 (Campy; BD Diagnostics, Sparks, MD), Spectra VRE (Remel, Lenexa, KS), and bile-esculin-azide-vancomyc

272 The utility of the Spectra VRE media appeared to be significantly impacted by the a

273 Using Spectra VRE medium (Remel Diagnostics, Lenexa, KS), we identifie

274 of VRE-BSI caused by daptomycin-susceptible VRE.

275 oal that, if achieved, would reduce systemic VRE infections and patient-to-patient transmission.

276 In this initial evaluation, we found that VRE-BMX provided improved recovery of VRE from stool spe

277 MRSA study included 2,164 patients, and the VRE study included 1,948.

278 The difference in CAPS between the VRE-DCS (n=13) and VRE-placebo (n=12) groups increased o

279 To detect the VRE subpopulation, tryptic soy broth was inoculated from

280 ion rates were significantly greater for the VRE-DCS group (46% vs 8% at post-treatment; 69% vs 17% a

281 Patients in the VRE-DCS group showed earlier and greater improvement in

282 provement in PTSD symptoms compared with the VRE-placebo group.

283 n associated with colonization resistance to VRE, the specific bacterial species involved remain unde

284 veillance cultures in detecting unrecognized VRE in 14 patient-care units.

285 VanA resistant bacteria ( E. faecalis , VanA VRE) at a level accurately reflecting these binding char

286 icrobial activity (VSSA, MRSA, VanA and VanB VRE) and impressive potencies (MIC = 0.06-0.005 mug/mL)

287 bial activity (VSSA, MRSA, and VanA and VanB VRE) and impressive potencies against both vancomycin-se

288 vancomycin aglycon derivatives exhibit VanB VRE antimicrobial activity at levels that approach (typi

289 exhibits concentration-dependent activity vs VRE in vitro, yet the clinical impact of higher-dose str

290 o was administered 90 min before each weekly VRE session, to ensure peak plasma concentrations during

291 The exact mechanism by which VRE maintains its plasmid-encoded resistance genes is il

292 -5.8; P = .007) correlated most closely with VRE BSI.

293 Colonization with VRE before or after transplant was a risk factor for VRE

294 une defenses and restricts colonization with VRE.

295 ta that contains Barnesiella correlates with VRE elimination.

296 al domination and bloodstream infection with VRE.

297 The patient with VRE keratitis developed a consecutive Candida keratitis

298 and 2.7 (95% CI, 1.4-5.1) for patients with VRE and VSE BSIs, respectively, compared to patients wit

299 y were significantly higher in patients with VRE BSI.

300 ciated with lower mortality in patients with VRE-BSI.