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 BSI is associated with lowest OS and highest NRM com

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

5 VRE therapy is a particularly promising format to test t

6 nfidence interval [CI]: 1.2, 2.4; P = .004), VRE (OR = 2.1; CI: 1.2, 3.8; P = .01), ESBL (OR = 1.6; C

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

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

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

10 70; P < .001) and 80% less likely to acquire VRE (IRR, 0.20; 95% CI, .08-.52; P < .001) after adjusti

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

12 Against VRE, 40 mM DAU for 120 min showed a > 94% kill rate, p <

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

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

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

16 vancin demonstrate in vitro activity against VRE.

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

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

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

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

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

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

23 s previously associated with C difficile and VRE.

24 level trends, while changes in AmpC ESBL and VRE appeared to be independent.

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

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

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

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

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

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

31 elevant bacterial strains including MRSA and VRE.

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

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

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

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

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

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

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

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

40 Together, this study presents potential anti-VRE therapeutic options to provide alternatives for prob

41 re implemented, and no further IR-associated VRE transmissions have been observed.

42 Both VRE colonization (odds ratio [OR], 0.64; 95% CI, 0.51 to

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

44 astrointestinal tract reduce colonization by VRE and represent potential probiotic agents to re-estab

45 e observed that the intestinal domination by VRE of patients hospitalized to receive allogeneic bone

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

47 ed from sequential stool samples provided by VRE-dominated patients revealed an unanticipated level o

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

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

50 in-treated mice colonized with a single CFU, VRE rapidly diversified and expanded into distinct linea

51 cidal therapeutic target that may help clear VRE from the intestines of dominated patients, as occurs

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

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

54 possessing improved potency against clinical VRE strains from MIC = 2 mug/mL (acetazolamide) to MIC =

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

56 the rapid diversification of host-colonizing VRE populations, with implications for epidemiologic tra

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

58 To combat VRE, we have repurposed the FDA-approved carbonic anhydr

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

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

61 abolic cue is a potential target to decrease VRE colonization and subsequent transmission of antibiot

62 em use, which may have resulted in decreased VRE colonization and infection and perhaps, in turn, dec

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

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

65 al vancomycin were no more likely to develop VRE within 3 months than metronidazole-treated patients

66 al vancomycin were no more likely to develop VRE within 3 months than metronidazole-treated patients

67 sly unappreciated subspecies dynamics during VRE domination that appeared to be stable from 16S rRNA

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

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

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

71 Vancomycin-resistant enterococci (VRE) are a major cause of hospital-acquired infections.

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

73 Vancomycin-resistant enterococci (VRE) are the second leading cause of hospital-acquired i

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

75 cidence of vancomycin-resistant Enterococci (VRE) colonization after receiving OVP, adverse effects a

76 cidence of vancomycin-resistant Enterococci (VRE) colonization after receiving OVP, adverse effects,

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

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

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

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

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

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

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

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

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

86 (CDI) and vancomycin-resistant enterococci (VRE) infections prevented in the intervention phase, bas

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

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

89 isting ICU vancomycin-resistant Enterococci (VRE) surveillance program.

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

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

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

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

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

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

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

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

98 essure for vancomycin-resistant Enterococci (VRE).

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

100 de against vancomycin-resistant enterococci (VRE).

101 ed against vancomycin-resistant Enterococci (VRE).

102 ation with vancomycin-resistant enterococci (VRE).

103 ainst many vancomycin-resistant enterococci (VRE).

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

105 ifficile, vancomycin-resistant Enterococcus (VRE) and ICU-acquired bloodstream infection (UABSIs) wer

106 Vancomycin-resistant Enterococcus (VRE) are highly antibiotic-resistant and readily transmi

107 impact of vancomycin-resistant Enterococcus (VRE) bloodstream infection (BSI) on outcomes of allogene

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

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

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

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

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

113 ifficile, vancomycin-resistant Enterococcus (VRE), and ICU-acquired bloodstream infections (UABSIs) f

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

115 s (MRSA), vancomycin-resistant enterococcus (VRE), extended-spectrum cephalosporin resistance in Ente

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

117 s (MRSA), vancomycin-resistant Enterococcus (VRE), Pseudomonas aeruginosa (PA), and Candida albicans

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

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

120 tions for vancomycin-resistant Enterococcus (VRE).

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

122 We developed a Virtual Research Environment (VRE) which facilitates rapid integration of new tools an

123 s were seen for all main organisms excluding VRE with greatest reductions for MRSA (97%), Pseudomonas

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

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

126 vancomycin-resistant Enterococcus faecalis (VRE), and another undergoes spontaneous cyclizations to

127 vancomycin-resistant Enterococcus faecalis (VRE).

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

129 Vancomycin-resistant Enterococcus faecium (VRE) is a leading cause of hospital-acquired infections.

130 Vancomycin-resistant Enterococcus faecium (VRE) is a major cause of nosocomial infections.

131 i-vancomycin-resistant Enterococcus faecium (VRE) therapy.

132 y vancomycin-resistant Enterococcus faecium (VRE), a leading cause of hospital-acquired infections(1,

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

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

135 f vancomycin-resistant Enterococcus faecium (VRE), Klebsiella pneumoniae, and Escherichia coli in the

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

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

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

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

140 /=10 mg/kg total body weight) daptomycin for VRE-BSI.

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

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

143 Patients were followed for VRE isolated from a clinical culture within 3 months.

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

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

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

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

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

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

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

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

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

153 g method for removing medium components from VRE cells.

154 C. difficile isolates from VRE swabs, and from C. difficile-positive stool samples,

155 2008 through 2012 were analyzed as 3 groups-VRE BSI, non-VRE BSI, without BSI-according to BSI statu

156 ce and humans, impairs separation of growing VRE diplococci, causing the formation of long chains and

157 Of 7128 patients, 258 (3.2%) had VRE BSI, 2398 (33.6%) had non-VRE BSI, and 4472 (63%) ha

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

159 ntact precautions are important for hospital VRE control programs.

160 ns for epidemiologic tracking of in-hospital VRE transmission and susceptibility to antibiotic treatm

161 to 93.68 cases per 10,000 hospitalizations), VRE infection (from 24.15 to 15.76 per 10,000), carbapen

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

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

164 ed survival and microbiological clearance in VRE-BSI.

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

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

167 to the quantitation of these metabolites in VRE.

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

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

170 ew agents targeting vancomycin resistance in VRE.

171 09 and 2018, there was an associated rise in VRE bloodstream infections in hospitals where contact pr

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

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

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

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

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

177 Integrating VRE colonization status with risk factors for developing

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

179 nfold reduction in the density of intestinal VRE colonization.

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

181 omponent response regulator liaR that locked VRE in diplococcal mode, impaired biofilm formation, and

182 We describe a cluster of 4 LR-VRE infections among a group of liver and multivisceral

183 ancomycin-resistant Enterococcus faecium (LR-VRE) in solid organ transplant recipients remain uncommo

184 This cluster of LR-VRE in transplant recipients highlights the possible sho

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

186 In multivariable models, VRE BSI was associated with lower OS (relative risk [RR]

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

188 Most VRE isolates recovered after fidaxomicin treatment had e

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

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

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

192 These mutant VRE strains were deficient in host colonization because

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 No patients developed new VRE colonization with only 1 patient reporting mild gast

196 No patients developed new VRE colonization, with only 1 patient reporting mild gas

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

198 The median time to VRE BSI and non-VRE BSI were D11 and D15, respectively.

199 2012 were analyzed as 3 groups-VRE BSI, non-VRE BSI, without BSI-according to BSI status at 100 days

200 258 (3.2%) had VRE BSI, 2398 (33.6%) had non-VRE BSI, and 4472 (63%) had no BSI.

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

202 RM compared with patients without BSI or non-VRE BSI.

203 tors for worse OS and increased NRM were non-VRE BSI, older age, advanced disease stage, UCB allograf

204 Compared with non-VRE BSI patients, VRE BSI patients were older, had advan

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

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

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

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

209 Multivariable models examined the effect of VRE BSI for overall survival (OS) and nonrelapse mortali

210 vember 2016 to November 2017 for evidence of VRE transmission.

211 Here we show that BP(SCSK) reduces growth of VRE by secreting a lantibiotic that is similar to the ni

212 Although the growth of VRE is inhibited by BP(SCSK) and L. lactis in vitro, onl

213 ole or oral vancomycin and had no history of VRE in the previous year.

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

215 agnostic testing for early identification of VRE.

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

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

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

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

220 analyses, we detected an overall increase of VRE infection following ASP (1.37 [1.10-1.69]).

221 patients revealed an unanticipated level of VRE population complexity that evolved over time.

222 A prolonged outbreak of VRE infections related to IR procedures with IV contrast

223 ventions that address the pathophysiology of VRE BSI have the potential of improving survival after H

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

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

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

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

228 be a significant driver of increased risk of VRE at the patient level.

229 be a significant driver of increased risk of VRE at the patient level.In this multicenter, retrospect

230 We evaluated the risk of VRE following oral vancomycin or metronidazole treatment

231 In patients at high risk of VRE infection, high abundance of the lantibiotic gene is

232 e equally likely to impact patients' risk of VRE.

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

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

235 The susceptibility of VRE isolates to fidaxomicin was assessed.

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

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

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

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

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

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

242 tively counteracting major types (VanABC) of VRE.

243 can affect both the fitness and virulence of VRE.

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

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

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

249 he primary outcome of acquisition of MRSA or VRE.

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

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

252 utcome of unit-attributable MRSA-positive or VRE-positive clinical cultures (figure 2), the HR for th

253 The fact that our VRE outbreak was discovered through WGS surveillance and

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

255 Compared with non-VRE BSI patients, VRE BSI patients were older, had advanced-stage acute le

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

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

258 ions to provide alternatives for problematic VRE infections.

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

260 nly BP(SCSK) colonizes the colon and reduces VRE density in vivo.

261 recognized cluster of 10 genetically related VRE (Enterococcus faecium) infections was discovered.

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

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

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

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

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

267 SA), vancomycin-resistant Enterococcus spp. (VRE), extended-spectrum beta-lactamase-producing organis

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

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

270 ost Microbe 2019;25:695-705.e5) reports that VRE undergo a morphotype switch in response to lithochol

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

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

273 95% CI, -200 to -120; P < .001) than did the VRE clinical prediction score (-30 DOT/1000 patient-days

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

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

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

277 microbiota caused by antibiotics can lead to VRE domination of the intestine, increasing a patient's

278 d with patient-derived faeces, resistance to VRE colonization correlates with abundance of the lantib

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

280 obiotic agents to re-establish resistance to VRE.

281 reverse antibiotic-induced susceptibility to VRE infection(3).

282 The median time to VRE BSI and non-VRE BSI were D11 and D15, respectively.

283 ions or low intestinal permeability to treat VRE infections in the gastrointestinal tract.

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

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

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

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

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

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

290 RSA (42%) and ESBL (34%); in LTACs they were VRE (55%) and ESBL (38%).

291 ifficile acquisitions, 11.1 to 3.5), whereas VRE acquisitions increased from 1.5 to 5.9.

292 6 to 4.2; acquisitions 11.1 to 3.5), whereas VRE admissions and acquisitions increased from 1.9 to 5.

293 procedure with contrast were associated with VRE infection (matched odds ratio [MOR], 16.72; 95% conf

294 -5.8; P = .007) correlated most closely with VRE BSI.

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

296 ta that contains Barnesiella correlates with VRE elimination.

297 al domination and bloodstream infection with VRE.

298 The patient with VRE keratitis developed a consecutive Candida keratitis

299 y were significantly higher in patients with VRE BSI.

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