ライフサイエンスコーパス: enterococci

1 bacterales predominated (56% compared to 21% enterococci).

2 ve matrix molecules adhesin of collagen from enterococci).

3 sistance to vancomycin (vancomycin-resistant enterococci).

4 esistant S. aureus, and vancomycin-resistant enterococci.

5 are unit (ICU)-acquired bacteremia caused by enterococci.

6 idal antibiotic to treat multidrug-resistant enterococci.

7 eing due to staphylococci, streptococci, and enterococci.

8 susceptibility testing of staphylococci and enterococci.

9 ble on Vitek 2 for testing staphylococci and enterococci.

10 iding new insights into the evolution of the enterococci.

11 reatment of periodontal infections involving enterococci.

12 tified fines as the single best predictor of enterococci.

13 orphological and biochemical similarities to enterococci.

14 d Enterococcus faecalis accounted for 32% of enterococci.

15 -resistant Staphylococcus aureus as well as enterococci.

16 s murinus and Lactobacillus reuteri, but not enterococci.

17 nhanced potency against vancomycin-resistant enterococci.

18 ncomycin-susceptible and multidrug-resistant enterococci.

19 All samples were analyzed for E. coli and enterococci.

20 ng staphylococci, listeriae, clostridia, and enterococci.

21 surfaces compared with previous results for enterococci.

22 patients infected with vancomycin-resistant enterococci.

23 during the treatment of vancomycin-resistant enterococci.

24 nomes, found that the ebp locus is unique to enterococci.

25 bottles containing Staphylococcus aureus or enterococci.

26 o prevent infections by antibiotic-resistant enterococci.

27 rmediate S. aureus, and vancomycin-resistant Enterococci.

28 ) enzyme promotes intestinal colonization by enterococci.

29 S. aureus strains as well as in Listeria and Enterococci.

30 occurs at the expense of resident intestinal enterococci.

31 tablished new breakpoints for daptomycin and enterococci.

32 liably detected 48 environmental isolates of enterococci.

33 ntimicrobial design against these pathogenic enterococci.

34 fect on GIT colonization is universal across enterococci.

35 zation of the gut can lead to eradication of enterococci.

36 gonistic correlation with enterobacteria and enterococci.

37 antibacterial agents against drug-resistant enterococci.

38 s sunlight inactivation rates of E. coli and enterococci.

39 28.7%), followed by streptococci (20.4%) and enterococci (13.1%).

40 The microflora comprised staphylococci, enterococci (2.2 log(10)CFU/g) and lactic acid bacteria

41 followed by Staphylococcus aureus (21%) and enterococci (21%).

42 Multidrug-resistant E. coli (31%) and enterococci (22%) were found at nearly all sites, wherea

43 er discharge) with Escherichia coli uidA and enterococci 23S rRNA concentrations in sediment cores fr

44 thogens (including Staphylococcus aureus and enterococci), a mode of action distinct from that of oth

45 etween environmental factors and dry-weather enterococci abundance.

46 Enterococci account for nearly 10% of all nosocomial inf

47 ion for testing of Staphylococcus aureus and enterococci against vancomycin, daptomycin, and linezoli

48 at any colony count (Spearman's r=0.322 for enterococci and 0.272 for group B streptococci).

49 Culturable enterococci and a suite of environmental variables were

50 laboratory variability in the measurement of enterococci and Bacteroidales concentrations from standa

51 Enterococci and C. perfringens, but not E. coli, showed

52 patients with more comorbidity and a rise in enterococci and coagulase-negative staphylococcal infect

53 atality was similar for infections caused by enterococci and coagulase-negative staphylococci (CoNS;

54 s was placed on detecting species of Vibrio, enterococci and coliforms.

55 The virulence of enterococci and CoNS in a setting of CRBSI seems compara

56 s defined as antibiotic therapy to which the enterococci and copathogen, where applicable, were susce

57 epressed photoinactivation of sewage-sourced enterococci and E. coli after correcting for UVB light s

58 First order decay rate constants of both enterococci and E. coli were between 1 and 2 d(-1) under

59 Enterococci and Enterobacteriaceae counts were very low

60 ght serve as alternatives to the traditional enterococci and Escherichia coli faecal indicators.

61 linical significance of daptomycin-resistant enterococci and evolving microbiologic, pharmacokinetic-

62 ull, and canine fecal sources, monitoring of enterococci and fecal coliform, and measurement of chemi

63 an and by Etest in Staphylococcus aureus and enterococci and found that the Microscan panel GP 29 had

64 inant FIB sources to the surf zone: sand for enterococci and groundwater for E. coli.

65 l activity that acts on the cell membrane of enterococci and is often used off-label to treat patient

66 Vancomycin-resistant enterococci and Klebsiella pneumoniae carbapenemase-prod

67 e LiaFSR membrane stress response pathway in enterococci and many other Gram-positive organisms.

68 tor' of the cell envelope stress response in enterococci and many other Gram-positive organisms.

69 tive bacteria including vancomycin-resistant enterococci and methicillin-resistant Staphylococcus aur

70 serious infections caused by staphylococci, enterococci and other Gram-positive bacteria.

71 raM is a promising vaccine candidate against enterococci and other gram-positive pathogens.

72 faecalis harbouring pPD1 replaces indigenous enterococci and outcompetes E. faecalis lacking pPD1.

73 dasjon were analyzed for E. coli, intestinal enterococci and somatic coliphages through cultivation a

74 stant superbugs such as vancomycin-resistant Enterococci and Staphylococci has become a major global

75 pectrum efficacy against multidrug resistant enterococci and Staphylococcus aureus.

76 che competition among enterococci or between enterococci and the intestinal microbiota.

77 ains are active against vancomycin-resistant enterococci and vancomycin-resistant Staphylococcus aure

78 ip to human fecal markers (HFMs; crAssphage, enterococci) and anthropogenic antibiotic resistance mar

79 ndicator bacteria (FIB, Escherichia coli and enterococci) and six human-associated markers (two bacte

80 ach other and with total coliforms, E. coli, enterococci, and biochemical oxygen demand (Kendall's ta

81 the development of DAP resistance (DAP-R) in enterococci, and blocking this stress response system ha

82 Gram-negative bacteria, vancomycin-resistant enterococci, and Clostridium difficile) were rarely dete

83 indicator bacteria (FIBs; Escherichia coli, enterococci, and Clostridium perfringens) exhibited biph

84 us spp. other than Streptococcus pneumoniae, enterococci, and Enterobacteriaceae.

85 culture-based results of E. coli, intestinal enterococci, and thermotolerant Campylobacter spp. in su

86 Enterococci are a major cause of bloodstream infections

87 Vancomycin-resistant enterococci are a major cause of nosocomial infections b

88 Enterococci are also leading opportunistic hospital path

89 Enterococci are among the earliest members of this commu

90 The enterococci are an ancient genus that evolved along with

91 Enterococci are an important cause of healthcare-associa

92 Vancomycin-resistant enterococci are an important cause of healthcare-associa

93 Enterococci are commensal organisms of the gastrointesti

94 Enterococci are common members of the gut microbiome and

95 ions of fecal indicator bacteria E. coli and enterococci are commonly used to evaluate the microbial

96 Enterococci are Gram-positive bacteria that normally col

97 The enterococci are low-GC Gram-positive bacteria that have

98 Enterococci are major contributors of hospital-acquired

99 Enterococci are opportunistic pathogens, hard to eradica

100 why, among the vast diversity of gut flora, enterococci are so well adapted to the modern hospital e

101 Enterococci are the leading cause of nosocomial infectio

102 fecal indicator bacteria (FIB), E. coli and enterococci, are measured throughout the summer, resulti

103 ost fossil records, place the origins of the enterococci around the time of animal terrestrialization

104 coli; EC), culturable enterococci (ENT), and enterococci as analyzed by qPCR (QENT).

105 Despite the importance of enterococci as hospital pathogens, the vast majority liv

106 nt amplification (HDA), for the detection of enterococci as markers for fecal pollution in water.

107 aphylococcus aureus and vancomycin-resistant Enterococci as well as hemolytic activity.

108 , including staphylococci, streptococci, and enterococci, as well as for the presence of 3 resistance

109 ersity of these and other mobile elements in enterococci, as well as the extent of recombination and

110 microbial source tracking (MST) tools using enterococci bacteriophages and evaluated their performan

111 a were assayed for fecal indicator bacteria (enterococci, Bacteroidales, and Escherichia coli) and a

112 mation of activity against staphylococci and enterococci because of oritavancin's sticking to vials a

113 nstrate that, in the absence of eep or sigV, enterococci bind significantly more lysozyme, providing

114 f enterococci showed rapid killing effect on enterococci by killing 99.9% of bacterial cells in 60 mi

115 reement for the testing of staphylococci and enterococci by the Vitek 2.

116 Staphylococcus aureus, vancomycin-resistant enterococci, C difficile, and multidrug-resistant Acinet

117 Field data indicate E. coli and enterococci can be transported 1 and 2 m, respectively,

118 n of mobile elements in hospital isolates of enterococci can include those that are inherently incomp

119 ring early stages of infection, internalized enterococci can prevent host cell (RAW264.7 cells, prima

120 care unit are enteric Gram-negative bacilli, enterococci, Candida species, and Pseudomonas aeruginosa

121 .06-.17]) after adjusting for infection with enterococci, Charlson score, discharge location, and cou

122 aphylococcus aureus and vancomycin-resistant Enterococci clinical isolates and inhibit mutant DNA gyr

123 Enterococci commonly cause hospital-acquired infections,

124 Enterococci concentrations in CR increased toward presen

125 Mean enterococci concentrations were of 100 most probable num

126 whereas coagulase-negative staphylococci and enterococci consistently increased over the years.

127 While enterococci densities in the catch basins and wetland we

128 providing a more complete picture of natural enterococci diversity, 11 isolates of Enterococcus faeca

129 er counts of maternal total aerobes (TA) and enterococci (E) were associated with increased risk of i

130 short surf-zone residence times observed for enterococci (e-folding time 4 h) resulted from both rapi

131 challenging the prevailing commensal view of enterococci ecology.

132 ors that influence Escherichia coli (EC) and enterococci (ENT) concentrations, pathogen occurrence, a

133 This study explores the transport of enterococci (ENT) from naturally contaminated beach sand

134 e Escherichia coli (E. coli; EC), culturable enterococci (ENT), and enterococci as analyzed by qPCR (

135 The enterococci evolved over eons as highly adapted members

136 ploying a unique set of vancomycin-resistant Enterococci faecalis and Enterococci faecium clinical is

137 aphylococcus aureus and vancomycin-resistant Enterococci faecalis as well as their binding affinity f

138 Newly isolated Enterococci faecalis bacterial strains AIM06 (DSM100702)

139 comycin aglycon against vancomycin-resistant Enterococci faecalis previously reported.

140 ancomycin-resistant Enterococci faecalis and Enterococci faecium clinical isolates revealed that the

141 , enterococci surface protein (esp) found in Enterococci faecium, Bacteroides HF183, adenoviruses (AV

142 Unlike enterococci, fewer environmentally adapted E. coli strai

143 killed by GI tract flora, whereas commensal enterococci flourished.

144 n linezolid-nonsusceptible staphylococci and enterococci following a laboratory change in antimicrobi

145 ffected groundwater mixing zones, mobilizing enterococci from sand to water.

146 l sites, whereas 34.5% of E. coli and 28% of enterococci harboring multiple virulence factors were re

147 Enterococci have also recently emerged as opportunistic

148 uch as fecal coliforms, Escherichia coli, or enterococci have been used but these indicators generall

149 Enterococci have emerged as important nosocomial pathoge

150 onstrates the multiregional applicability of enterococci hosts in MST application and highlights the

151 Administration to treat vancomycin-resistant enterococci; however, resistance to this antibiotic appe

152 ects of the evolution of multidrug-resistant enterococci: (i) the accretion of mobile elements in E.

153 bitory activity against vancomycin-resistant Enterococci (IC50 40 nM), >270-fold more potent than the

154 the daptomycin susceptibility breakpoint for enterococci (ie, minimum inhibitory concentration [MIC]

155 There were steady state concentrations of enterococci in AB during c.1760-c.1860 and c.1910-c.2003

156 that dPCR is a viable option for enumerating enterococci in ambient water.

157 Notably, during dry weather the abundance of enterococci in dry sands at the mean high-tide line was

158 ancomycin resistance, that has emerged among enterococci in recent years.

159 qPCR and dPCR quantification of enterococci in the 24 environmental samples were signifi

160 The anatomical distribution of enterococci in the Drosophila GI tract was determined by

161 er microflora and examined the occurrence of enterococci in the gastrointestinal consortium of Drosop

162 Tidal forcing modulated the abundance of enterococci in the water, as both turbidity and enteroco

163 lonization of the gut by replacing commensal enterococci in their niche.

164 a bacteriocin ("gallocin") is shown to kill enterococci in vitro.

165 more than half of the observed variation in enterococci in water and dry sands.

166 In contrast, in midstream urine, enterococci (in 10% of cultures) and group B streptococc

167 (7.1%) patients, of which 76 were caused by enterococci (incidence rate, 3.0 per 1000 patient-days a

168 mong these organisms were several species of enterococci, including Enterococcus faecalis, Enterococc

169 revealed the antibacterial activity against enterococci-infected Wistar albino rats.

170 ot increase the risk of vancomycin-resistant Enterococci infection at 3 or 6 months compared to metro

171 increasing in frequency, representing 25% of enterococci infections in intensive care units.

172 ifficile infection, and vancomycin-resistant enterococci infections prevented in the intervention pha

173 Daptomycin resistance in enterococci is often mediated by the LiaFSR system, whic

174 f linezolid-nonsusceptible staphylococci and enterococci is providing a challenge for many susceptibi

175 ance to glycopeptide antibiotics in clinical enterococci is regulated by the VanSARA two-component si

176 or almost half of the erythromycin resistant enterococci isolated from the wetland.

177 In antimicrobial susceptibilty testing, all Enterococci isolates were cefazolin-resistant.

178 Translocating enterococci lead to hepatic inflammation and hepatocyte

179 Enterococci may have been primed to emerge among the van

180 horter for enteric Gram-negative bacilli and enterococci (means, 3.6 h and 2.3 h shorter, respectivel

181 We considered five fecal indicators: enterococci measured by culture and quantitative polymer

182 The test for enterococci measured by culture was the poorest predicto

183 The test for enterococci measured by qPCR was the best predictor of t

184 inactivation rates of wastewater E. coli and enterococci measured in clear marine water by researcher

185 t routine monitoring programs using discrete enterococci measurements may be biased by tides and othe

186 lates are inhibited [MIC(90)], 0.06 mug/mL), enterococci (MIC(90), </= 0.008 to 0.5 mug/mL), and stre

187 g linezolid-nonsusceptible staphylococci and enterococci, MicroScan results showed the highest catego

188 gens such Staphylococcus aureus (n = 45) and enterococci (n = 19) were 98% and 95%, respectively.

189 subgroups, staphylococci, streptococci, and enterococci (n = 217) and "related genera" (n = 81).

190 A challenge panel of enterococci (n = 50) and staphylococci (n = 50), includi

191 Systemic infections with multidrug-resistant enterococci occur subsequent to gastrointestinal coloniz

192 vailable on the antimicrobial sensitivity of enterococci of subgingival origin, this study evaluates

193 rtant in the killing mechanism of pathogenic enterococci on copper surfaces.

194 s and could modulate niche competition among enterococci or between enterococci and the intestinal mi

195 howed evidence of bladder E. coli but not of enterococci or group B streptococci, which are often iso

196 asmic membrane depolarization, not seen with enterococci or methicillin resistant Staphylococcus aure

197 arent MDROs (P = .009), vancomycin-resistant enterococci (P = .008), multidrug-resistant gram-negativ

198 ewetting mechanism that sustained culturable enterococci populations in high-tide sands.

199 yl lipidation modulated vancomycin-resistent Enterococci potency.

200 Pathogenic streptococci and enterococci primarily rely on the conserved secretory (S

201 te for infection, colonization of the GIT by enterococci remains poorly understood.

202 e about 0.1 and 0.2 for log(E. coli) and log(enterococci), respectively, and in most cases was statis

203 nsidered to be the most important species of enterococci responsible for blood stream infections in c

204 odification in the daptomycin breakpoint for enterococci should be considered.

205 vancomycin-resistant and control strains of enterococci showed rapid killing effect on enterococci b

206 nt in wastewater such as fecal coliforms and enterococci showed that 1-log reduction could be achieve

207 Enterococci species and Staphylococcus aureus were the m

208 zation, several fecal bacteria, particularly Enterococci species, are present in human intestinal flo

209 5-4 mug/mL against the MDR Staphylococci and Enterococci species.

210 red upon adaptation to terrestrial life when Enterococci split from marine ancestors 400 million year

211 ugh many medically relevant pathogens (e.g., enterococci, staphylococci, and streptococci) are Gram-p

212 in and evernimicin, possess activity against Enterococci, Staphylococci, and Streptococci, and other

213 al exposure against two vancomycin-resistant enterococci strains where its activity proved more durab

214 important gram-positive bacteria, including enterococci, streptococci, and staphylococci, and antibo

215 G1RF_11271, and OG1RF_11272 are found in all enterococci, suggesting that their effect on GIT coloniz

216 ith other sewage-associated markers, namely, enterococci surface protein (esp) found in Enterococci f

217 icantly higher concentrations of E. coli and enterococci than soil collected from the latrine floor.

218 w treatment options for infections caused by enterococci that are resistant to ampicillin and vancomy

219 Enterococci that evade phage therapy by developing resis

220 of chip-based digital PCR (dPCR) to quantify enterococci, the fecal indicator recommended by the Unit

221 For enterococci, there was 97.3% CA.

222 PrgA was necessary for extensive binding of enterococci to abiotic surfaces and development of robus

223 ating transfer of vancomycin resistance from enterococci to methicillin-resistant strains of S. aureu

224 a were used to evaluate sands as a source of enterococci to nearshore waters, and to assess the relat

225 the precise traits that now allow pathogenic enterococci to survive desiccation, starvation, and disi

226 The susceptibility of the enterococci to vancomycin and teicoplanin was determined

227 multidrug resistant hospital pathogens, the enterococci, to their origin hundreds of millions of yea

228 Genetic markers for enterococci, total Bacteroides, and human-associated Bac

229 ce slope on the release of Escherichia coli, enterococci, total coliforms, and dissolved chloride fro

230 ed time-series study of vancomycin-resistant enterococci transmission in a hematology ward.

231 cteria (FIB), including Escherichia coli and enterococci, trigger coastal beach advisories and signal

232 its bioactivity against vancomycin-resistant enterococci (Van A and Van B phenotypes of VRE).

233 en acquired, and has disseminated throughout enterococci, via horizontal transfer of mobile genetic e

234 rveillance cultures for vancomycin-resistant enterococci (VRE) and methicillin-resistant Staphylococc

235 factors and outcome of vancomycin-resistant enterococci (VRE) and vancomycin-sensitive enterococci (

236 cteremia caused by both vancomycin-resistant enterococci (VRE) and vancomycin-susceptible enterococci

237 Vancomycin-resistant enterococci (VRE) are a major cause of hospital-acquired

238 Vancomycin-resistant enterococci (VRE) are an important cause of health care-

239 Vancomycin-resistant enterococci (VRE) are the second leading cause of hospit

240 Treatment options for vancomycin-resistant enterococci (VRE) bloodstream infection (BSI) are limite

241 HCFA-CDI), incidence of vancomycin-resistant Enterococci (VRE) colonization after receiving OVP, adve

242 HCFA-CDI), incidence of vancomycin-resistant Enterococci (VRE) colonization after receiving OVP, adve

243 occus aureus (MRSA) and vancomycin-resistant enterococci (VRE) due to the scope of the medical threat

244 Vancomycin-resistant enterococci (VRE) escape the bactericidal action of vanc

245 occus aureus (MRSA) and vancomycin-resistant enterococci (VRE) for extended periods of time and tempe

246 routine surveillance of vancomycin-resistant enterococci (VRE) from rectal swabs in patients at high

247 V) for the isolation of vancomycin-resistant enterococci (VRE) from stool specimens.

248 of infections caused by vancomycin-resistant enterococci (VRE) has become an important clinical chall

249 occus aureus (MRSA) and vancomycin-resistant Enterococci (VRE) have now arisen and are of major conce

250 their ability to detect vancomycin-resistant enterococci (VRE) in 750 stool specimens.

251 implies that control of vancomycin-resistant enterococci (VRE) in hospitals also requires considerati

252 Active screening for vancomycin-resistant enterococci (VRE) in rectal and stool specimens has been

253 As infection with vancomycin-resistant enterococci (VRE) increases in hospitals, knowledge abou

254 ile infection (CDI) and vancomycin-resistant enterococci (VRE) infections prevented in the interventi

255 patients colonized with vancomycin-resistant enterococci (VRE) is central to the containment of this

256 ancomycin resistance in vancomycin-resistant enterococci (VRE) is due to an alternative cell wall bio

257 us aureus (MRSA) and/or vancomycin-resistant enterococci (VRE) on at least 1 occasion by any of 5 hea

258 isolated from clinical vancomycin-resistant enterococci (VRE) strains.

259 bs from an existing ICU vancomycin-resistant Enterococci (VRE) surveillance program.

260 occus aureus (MRSA) and vancomycin-resistant enterococci (VRE) that are known to exert a high level o

261 tance is conferred upon vancomycin-resistant enterococci (VRE) through the replacement of peptidoglyc

262 atient population, more vancomycin-resistant enterococci (VRE) were recovered with CVRE than BEAV.

263 ureus (MRSA) as well as vancomycin-resistant enterococci (VRE) with minimum inhibitory concentrations

264 lococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), and ceftazidime-resistant (CAZ(r)) an

265 tides effective against vancomycin-resistant enterococci (VRE), and fluoroquinolones with improved po

266 r (84.8%) for detecting vancomycin-resistant enterococci (VRE), and the results were available 24 to

267 ncreasing prevalence of vancomycin-resistant enterococci (VRE), appropriate antibiotic therapy for en

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

269 terial species, such as vancomycin-resistant enterococci (VRE), necessitates the development of new a

270 ation assay to identify vancomycin-resistant enterococci (VRE), was evaluated for the detection of va

271 crobial peptide against vancomycin-resistant enterococci (VRE).

272 as demonstrated against vancomycin-resistant Enterococci (VRE).

273 ectal colonization with vancomycin-resistant enterococci (VRE).

274 s activity against many vancomycin-resistant enterococci (VRE).

275 selection pressure for vancomycin-resistant Enterococci (VRE).

276 ency (200-fold) against vancomycin-resistant Enterococci (VRE).

277 occus aureus (MRSA) and vancomycin-resistant Enterococci (VRE).

278 ve or "nonnegative" for vancomycin-resistant enterococci (VRE).

279 occus aureus [MRSA] and vancomycin-resistant enterococci [VRE]) or rapid screening (PCR testing for M

280 t enterococci (VRE) and vancomycin-sensitive enterococci (VSE) infections.

281 enterococci (VRE) and vancomycin-susceptible enterococci (VSE).

282 Enterococci was associated with population and river dis

283 decay of sewage-sourced Escherichia coli and enterococci was measured at multiple depths in a freshwa

284 breakpoint of <=4 mug/mL for daptomycin and enterococci was no longer appropriate.

285 erococci in the water, as both turbidity and enterococci were elevated during ebb and flood tides.

286 The enterococci were further identified as Enterococcus hira

287 Enterococci were identified to the species level using s

288 aphylococcus aureus, or vancomycin-resistant enterococci were included.

289 In bile cultures, enterobacterales and enterococci were isolated with equal frequencies of appr

290 Enterococci were not observed, nor were DNA sequences am

291 However, enterococci were recently shown to persist in environmen

292 ur cohort, higher maternal total aerobes and enterococci were related to increased risk of infant whe

293 nterococcus ; correlations between fines and enterococci were significant (p < 0.01), and generalized

294 Staphylococci and enterococci were the most common agents.

295 Listeria spp., S. lugdunensis, vanB-positive Enterococci) were included to fully evaluate the perform

296 Most isolates (27% of E. coli and 22% of enterococci) were recovered from the sediments that had

297 how that PPIs induce bacterial overgrowth of enterococci, which, in turn, exacerbate ethanol-induced

298 The very major error rate for enterococci with VITEK was 20.0%.

299 ed in combination with antibiotics to target enterococci within a dysbiotic microbiota.

300 esulted in clearance of vancomycin-resistant enterococci, without plasmid transfer.