ライフサイエンスコーパス: enterococci

1 ve matrix molecules adhesin of collagen from enterococci).

2 eing due to staphylococci, streptococci, and enterococci.

3 susceptibility testing of staphylococci and enterococci.

4 ble on Vitek 2 for testing staphylococci and enterococci.

5 iding new insights into the evolution of the enterococci.

6 reatment of periodontal infections involving enterococci.

7 tified fines as the single best predictor of enterococci.

8 orphological and biochemical similarities to enterococci.

9 d Enterococcus faecalis accounted for 32% of enterococci.

10 -resistant Staphylococcus aureus as well as enterococci.

11 s murinus and Lactobacillus reuteri, but not enterococci.

12 nhanced potency against vancomycin-resistant enterococci.

13 ncomycin-susceptible and multidrug-resistant enterococci.

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

15 surfaces compared with previous results for enterococci.

16 patients infected with vancomycin-resistant enterococci.

17 liably detected 48 environmental isolates of enterococci.

18 during the treatment of vancomycin-resistant enterococci.

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

20 ntimicrobial design against these pathogenic enterococci.

21 bottles containing Staphylococcus aureus or enterococci.

22 fect on GIT colonization is universal across enterococci.

23 o prevent infections by antibiotic-resistant enterococci.

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

25 ylococcus aureus, and glycopeptide-resistant enterococci.

26 for 69% of the staphylococci and 25% of the enterococci.

27 lasmid-encoded mazEF is indeed functional in enterococci.

28 hods for the ID and AST of staphylococci and enterococci.

29 taphylococci and 14.3% VM errors (2/14) with enterococci.

30 ermediate S. aureus and vancomycin-resistant enterococci.

31 , including drug-resistant staphylococci and enterococci.

32 ential target for species differentiation of enterococci.

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

34 gonistic correlation with enterobacteria and enterococci.

35 antibacterial agents against drug-resistant enterococci.

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

37 occurs at the expense of resident intestinal enterococci.

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

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

40 idal antibiotic to treat multidrug-resistant enterococci.

41 terobacteriaceae, 18%; Pseudomonas spp., 5%, enterococci, 12%).

42 28.7%), followed by streptococci (20.4%) and enterococci (13.1%).

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

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

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

46 In total, 424 isolates were tested: 90 enterococci; 232 Staphylococcus aureus isolates, includi

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

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

49 etween environmental factors and dry-weather enterococci abundance.

50 Enterococci account for nearly 10% of all nosocomial inf

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

52 in 28.5% very major (VM) errors (4/14) with enterococci (all E. faecium) but none (0/22) with staphy

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

54 Culturable enterococci and a suite of environmental variables were

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

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

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

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

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

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

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

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

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

64 Enterococci and Enterobacteriaceae counts were very low

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

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

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

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

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

70 Vancomycin-resistant enterococci and Klebsiella pneumoniae carbapenemase-prod

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

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

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

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

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

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

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

78 pectrum efficacy against multidrug resistant enterococci and Staphylococcus aureus.

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

80 Both the percentage of E. faecium among the enterococci and the proportion of vancomycin-resistant E

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

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

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

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

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

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

87 for example, Staphylococcus, Streptococcus, Enterococci, and Pseudomonas there is a renewed interest

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

89 Enterococci are a major cause of bloodstream infections

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

91 Enterococci are also leading opportunistic hospital path

92 The enterococci are an ancient genus that evolved along with

93 Enterococci are an important cause of healthcare-associa

94 Enterococci are commensal organisms of the gastrointesti

95 Enterococci are common members of the gut microbiome and

96 iology laboratories report that 80 to 90% of enterococci are Enterococcus faecalis, whereas E. faeciu

97 Enterococci are Gram-positive bacteria that normally col

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

99 Antibiotic-resistant enterococci are major causes of hospital-acquired infect

100 Enterococci are major contributors of hospital-acquired

101 Enterococci are opportunistic pathogens and among the le

102 Enterococci are opportunistic pathogens, hard to eradica

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

104 Enterococci are the leading cause of nosocomial infectio

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

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

107 systems, significantly more streptococci and enterococci as a group were detected by VTI.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 Enterococci commonly cause hospital-acquired infections,

127 Enterococci concentrations in CR increased toward presen

128 Mean enterococci concentrations were of 100 most probable num

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

130 While enterococci densities in the catch basins and wetland we

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

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

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

134 challenging the prevailing commensal view of enterococci ecology.

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

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

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

138 The enterococci evolved over eons as highly adapted members

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

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

141 Newly isolated Enterococci faecalis bacterial strains AIM06 (DSM100702)

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

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

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

145 Unlike enterococci, fewer environmentally adapted E. coli strai

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

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

148 Recent studies have shown that enterococci form biofilms independently of Esp expressio

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

150 ns: vancomycin-susceptible staphylococci and enterococci, glycopeptide-intermediate-resistant Staphyl

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

152 More recently, enterococci have been associated with biofilms, which ar

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

154 Enterococci have emerged as one of the leading causes of

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

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

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

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

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

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

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

162 The advent of vancomycin-resistant enterococci in the 1990s and the threat posed by vancomy

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

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

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

166 Little is known about the ecological role of enterococci in the GI tract consortia.

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

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

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

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

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

172 (7.1%) patients, of which 76 were caused by enterococci (incidence rate, 3.0 per 1000 patient-days a

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

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

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

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

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

178 trains of E. faecalis, E. faecium, and other enterococci isolated from blood cultures of patients at

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

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

181 Translocating enterococci lead to hepatic inflammation and hepatocyte

182 Enterococci may have been primed to emerge among the van

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

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

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

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

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

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

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

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

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

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

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

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

195 s the horizontal transfer of the PAI between enterococci of porcine and human origin.

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

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

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

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

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

201 If the total number of vancomycin-resistant enterococci patients in the ICU were reduced by 50%, the

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

203 yl lipidation modulated vancomycin-resistent Enterococci potency.

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

205 of challenge and clinical staphylococci and enterococci recovered from patients in a tertiary-care m

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

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

208 Enterococci species and Staphylococcus aureus were the m

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

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

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

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

217 Over this 10-year period, the percentage of enterococci that were identified as E. faecium increased

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

219 For the enterococci, there was 100% CA and 99.3% EA.

220 For enterococci, there was 97.3% CA.

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

222 The ability of enterococci to adapt and respond to different environmen

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 artum infections due to vancomycin-resistant enterococci (VRE) and the possible spread of vancomycin

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

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

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

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

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

241 it the establishment of vancomycin-resistant enterococci (VRE) colonization by depleting nutrients wi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 ransmission dynamics of vancomycin-resistant enterococci (VRE).

275 coccus aureus (MRSA) or vancomycin-resistant enterococci (VRE).

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

277 infection (BSI; 22 with vancomycin-resistant enterococci [VRE] and 61 with vancomycin-susceptible ent

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

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

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

281 cci [VRE] and 61 with vancomycin-susceptible enterococci [VSE]) in 77 patients with neutropenia.

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 All S. aureus isolates and enterococci were correctly identified by the Phoenix pan

285 All 36 vancomycin-resistant enterococci were detected by the Phoenix system.

286 Enterococci were detected only in PEG tube biofilms and

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

288 The enterococci were further identified as Enterococcus hira

289 Enterococci were identified to the species level using s

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

291 Enterococci were not observed, nor were DNA sequences am

292 However, enterococci were recently shown to persist in environmen

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

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

295 Staphylococci and enterococci were the most common agents.

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

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

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

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

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