ライフサイエンスコーパス: enterococcal

1 In stented patients, an antibiotic with anti-enterococcal activity should be chosen for PD prophylaxi

2 k for future studies to define signatures of enterococcal adaptation during bacteremia.

3 mphasizing the importance of this protein to enterococcal adaptation to the GIT.

4 suggests that PrgA can interact with another enterococcal adhesin, PrgB, and that these two proteins

5 is from 70% (modified Duke criteria) to 96% (enterococcal adjusted Duke criteria).

6 We investigated the importance of enterococcal aggregation substance (AS) and enterococcal

7 with the C-terminal enzymatic domain of the enterococcal alkaline phosphatase (PhoZ) revealed that t

8 uis and S. uberis, as well as representative enterococcal and staphylococcal species (including MRSA

9 ributed among E. faecalis isolates and other enterococcal and staphylococcal species.

10 s-reactive against other clinically relevant enterococcal and staphylococcal strains.

11 ophosphate oxidases (GlpOs) from a number of enterococcal and streptococcal sources contain a conserv

12 ovalbumin antigen or in formulation with an enterococcal antigen.

13 However, the enterococcal autolytic factors GelE and Atn (also known

14 Mixed-population (heterogeneous) enterococcal bacteremia (MEB) is rarely reported.

15 cs of and identify specific risk factors for enterococcal bacteremia following liver transplantation,

16 iexperimental study compared inpatients with enterococcal bacteremia from 1 February 2012 to 9 Septem

17 Enterococcal bacteremia has been associated with high ca

18 Enterococcal bacteremia is a frequent infectious complic

19 ICU-acquired enterococcal bacteremia is associated with increased cas

20 entamicin for the treatment of uncomplicated enterococcal bacteremia may pose harm to children with l

21 tients in the 2016-2022 Vancomycin-Resistant Enterococcal Bacteremia Outcomes Study (VENOUS) cohort e

22 Enterococcal bacteremia was independently associated wit

23 the 15 deaths (29%) among the patients with enterococcal bacteremia, 4 were directly associated with

24 For enterococcal bacteremia, a daptomycin fAUC/MIC >27.43 wa

25 Among patients with monomicrobial enterococcal bacteremia, receipt of effective antimicrob

26 her antibiotic therapy alters the outcome of enterococcal bacteremia.

27 3) were associated with vancomycin-resistant enterococcal bacteremia.

28 ce is an independent predictor of death from enterococcal bacteremia.

29 that assessed outcomes in daptomycin-treated enterococcal bacteremia.

30 bacteremia, 4 were directly associated with enterococcal bacteremia.

31 modeling to estimate ICU mortality caused by enterococcal bacteremia.

32 ical and economic outcomes for patients with enterococcal bacteremia.

33 Seventy enterococcal bacteremias in 52 patients were identified.

34 terococcus faecium isolates (18), and 49% of enterococcal bacteremias were polymicrobial.

35 ry tree complications were present in 34% of enterococcal bacteremias.

36 MEB represented approximately 5% of all enterococcal bacteremias.

37 enterococcal aggregation substance (AS) and enterococcal binding substance (EBS) in rabbit models of

38 ion substance (AS) and its cognate receptor, enterococcal binding substance (EBS), were compared for

39 contribute to the overall composition of the enterococcal biofilm and that the regulatory role of sig

40 The molecular mechanisms involved in enterococcal biofilm formation are only now beginning to

41 d-type gene, we have designated EF1809 ebrA (enterococcal biofilm regulator).

42 Therefore, AhrC and Eep can be classified as enterococcal biofilm-associated virulence factors.

43 lls mimics aspects of fratricide observed in enterococcal biofilms, where both are mediated by the At

44 >100 additional genes with unknown roles in enterococcal biology.

45 h infection-derived and outbreak strains, in enterococcal blood isolates from 2002 was determined.

46 Ninety-three patients had enterococcal bloodstream infection (BSI) during the firs

47 tance on clinical outcome for 83 episodes of enterococcal bloodstream infection (BSI; 22 with vancomy

48 Frequency of enterococcal bloodstream infection (E-BSI) is increasing

49 ci (VRE), appropriate antibiotic therapy for enterococcal bloodstream infections (EBSI) can be delaye

50 l therapy (EET) on outcomes of patients with enterococcal bloodstream infections (EBSI) is unclear.

51 Patients with recalcitrant enterococcal bloodstream infections are at greater risk

52 MRSA bloodstream infection, (3) characterize enterococcal bloodstream infections, (4) demonstrate the

53 high-level aminoglycoside resistance in 815 enterococcal bloodstream isolates.

54 was 68.2% overall, ranging between 58.0% for enterococcal BSI without sepsis and 96.4% for pneumococc

55 , respectively, compared to patients without enterococcal BSI.

56 peptide had activity similar to that of the enterococcal cAM373 AIFILAS.

57 Drosophila could be cured of enterococcal carriage by antibiotic treatment and could

58 the cell surface and drastically reduced the enterococcal cell binding to immobilized fibronectin.

59 ggest that LiaR is a master regulator of the enterococcal cell membrane response to diverse antimicro

60 anchorless EfbA protein was localized to the enterococcal cell outer surface and bound to immobilized

61 cognition of its binding ligand (EBS) on the enterococcal cell surface, as indicated by increased tra

62 The enterococcal cell surface-associated protein, Esp, enhan

63 against actively dividing exponential phase enterococcal cells and bactericidal activity against non

64 ve suggested that AS-mediated aggregation of enterococcal cells could involve the binding of this pro

65 s also effectively inhibited the adhesion of enterococcal cells to a collagen substrate, suggesting t

66 ctivity against nondividing stationary phase enterococcal cells.

67 al meningitis in rabbits, staphylococcal and enterococcal central venous catheter infections in rats,

68 ference method for 134 staphylococcal and 84 enterococcal clinical isolates.

69 ial resistance, such as vancomycin-resistant enterococcal colonization of the gastrointestinal tract.

70 n of commensal bacteria in a murine model of enterococcal colonization of the gut can lead to eradica

71 ve plasmid pPD1 expressing bacteriocin 21 in enterococcal colonization.

72 detailed characterization of this important enterococcal conjugation protein and virulence factor.

73 ional readthrough in the pheromone-inducible enterococcal conjugative plasmid pCF10.

74 The enterococcal, conjugative, cytolysin plasmid pAD1 confer

75 on of important functions encoded within the enterococcal core genome may also be controlled by multi

76 Thus, we have defined conserved genes in the enterococcal core genome that influence GIT colonization

77 ied CTns, the Bacteroides CTn CTnDOT and the enterococcal CTn Tn916.

78 The enterococcal cytolysin is a toxic, two-component ribosom

79 The enterococcal cytolysin is a virulence factor consisting

80 y a well-characterized strain expressing the enterococcal cytolysin was found to be detrimental to Dr

81 Increased damage is mediated by enterococcal cytolysin, and involves both physical inter

82 ce a two-component lantibiotic homologous to enterococcal cytolysin.

83 ique opportunities to study the evolution of enterococcal disease by direct observation, as well as t

84 ly little is known about the pathogenesis of enterococcal disease.

85 ole for the cytolysin in the pathogenesis of enterococcal disease.

86 man health, and where substantial additional enterococcal diversity is likely to be found.

87 As a predictor of outcomes, enterococcal domination increased the risk of Vancomycin

88 Enterococcal domination was increased 3-fold by metronid

89 tidis and conjugal transfer of Tn916 from an enterococcal donor to M. arthritidis.

90 mpact of early administration of active anti-enterococcal empirical therapy (EET) on outcomes of pati

91 Enterococcal endocarditis (EE) is a growing entity in We

92 at gls24 is important in the pathogenesis of enterococcal endocarditis.

93 nique target for therapeutic intervention in enterococcal endocarditis.

94 opment of immunological approaches to combat enterococcal endocarditis.

95 role for the protein in the pathogenesis of enterococcal endocarditis.

96 tis isolate and sera from four patients with enterococcal endocarditis.

97 gelE DeltasprE mutants) in a rabbit model of enterococcal endocarditis.

98 A previously undescribed enterococcal enteropathy was associated with preretinal

99 nce GIT colonization through their effect on enterococcal envelope integrity and antimicrobial resist

100 APH(3')-IIIa is an enterococcal enzyme that is responsible for the ATP-depe

101 (allo-HCT), we describe a high incidence of enterococcal expansion, which was associated with graft-

102 ccus HDA assay successfully discriminated 15 enterococcal from 15 non-enterococcal reference strains

103 the antibiotic treated hospital patient--the enterococcal genome is evolving in a pattern characteris

104 copies of the redundant 23s rRNA gene in the enterococcal genome.

105 a 10-15-fold increase in the activity of the enterococcal glycerol kinase.

106 d the C-terminal extension that is unique to enterococcal GpsB homologs.

107 usion, although Vitek broth can support good enterococcal growth, this medium does not sufficiently s

108 etected 1515 patients with E-BSI and 65 with enterococcal IE (4.29% of all episodes of E-BSI, 16.7% o

109 ients with E-BSI who are at very low risk of enterococcal IE (and therefore do not require TEE) and t

110 core <4 points suggested a very low risk for enterococcal IE and that TEE could be obviated.

111 Enterococcal IE may be more frequent than generally thou

112 Enterococcal IE was more frequent in the SEV group (36.5

113 a case-control study (patients with/without enterococcal IE) in our center.

114 We developed a bedside predictive score for enterococcal IE-Number of positive blood cultures, Origi

115 aused by S. aureus, with increasing rates of enterococcal IE.

116 ion was only minimally altered by subsequent enterococcal infection and was not suppressed by inhibit

117 However, the risk of vancomycin-resistant enterococcal infection or colonization is significantly

118 ling, this monoclonal identified the site of enterococcal infection, providing a rare example of mole

119 f traits contributing to the pathogenesis of enterococcal infection.

120 detected more episodes of streptococcal and enterococcal infection.

121 d inflammation contributes to the control of enterococcal infection.

122 ibiotic resistances, making the treatment of enterococcal infections an increasingly difficult proble

123 Enterococcal infections can be difficult to treat becaus

124 been an increase in the number of nosocomial enterococcal infections caused by strains resistant to v

125 ly assayed sera collected from patients with enterococcal infections for the presence of anti-Ace A a

126 sr-mediated virulence in the pathogenesis of enterococcal infections in humans.

127 idly, to the point where over one-quarter of enterococcal infections in intensive care units are now

128 tomycin resistance during therapy of serious enterococcal infections is a major clinical issue.

129 gainst VRE, but its clinical use for serious enterococcal infections is unclear due to low serum leve

130 of vancomycin resistance and association of enterococcal infections with significant mortality warra

131 ptomycin (DAP) is a key drug against serious enterococcal infections, but the emergence of resistance

132 nosocomial pathogen, yet the pathogenesis of enterococcal infections, particularly of urinary tract i

133 The prevalence and severity of enterococcal infections, the mortality rate from such in

134 It has also been used "off-label" for Enterococcal infections.

135 a serious threat to the treatment of serious enterococcal infections.

136 options for the treatment and prevention of enterococcal infections.

137 y be useful for prophylaxis and treatment of enterococcal infections.

138 tive for some strains of multidrug-resistant enterococcal infections.

139 riate treatment of patients with deep-seated enterococcal infections.

140 d be harnessed to combat multidrug-resistant enterococcal infections.

141 l antimicrobial targets for the treatment of enterococcal infections.

142 nuary 2007, reducing gentamicin treatment in enterococcal infective endocarditis from 4 to 6 weeks to

143 the epa variability as a key determinant for enterococcal intestinal colonization.

144 n5385 consist of directly repeated copies of enterococcal IS1216.

145 g a rapid streptococcus test, and no further enterococcal isolate has been confirmed as E. durans.

146 ies have significantly shortened the time to enterococcal isolate identification compared with conven

147 For stool and clinical enterococcal isolates and 12 type strains, only Enteroco

148 ated the percentages of E. faecium among all enterococcal isolates and the percentages of E. faecium

149 Enterococcal isolates causing recalcitrant bacteremia we

150 istance phenotypes, with the majority of the enterococcal isolates exhibiting resistance to three or

151 method, 92 Enterobacteriaceae isolates and 9 enterococcal isolates were nonsusceptible to ERV accordi

152 Fifty-eight vancomycin-resistant enterococcal isolates were obtained from two patients ov

153 Thirty-five enterococcal isolates were recovered from dogs diagnosed

154 Twenty enterococcal isolates were tested, including Enterococcu

155 ey indicated that for clinically significant enterococcal isolates, laboratories in the San Francisco

156 ected resistance to ampicillin in 132 of 132 enterococcal isolates, while three isolates for which th

157 rs directed to vanA, vanB, vanC1, vanC2, and enterococcal ligase genes were used to detect and identi

158 hesin, aggregation substance, contributes to enterococcal localization or otherwise mediates adherenc

159 an ascending UTI model and is the first such enterococcal locus shown to be important in this site.

160 e observed, the medium used for detection of enterococcal motility must be selected carefully.

161 widely used in treatments of, in particular, enterococcal, mycobacterial, and severe Gram-negative ba

162 56, IS257, and IS1216) of staphylococcal and enterococcal origin.

163 characterized EfbA, which is encoded by the enterococcal orthologue of Streptococcus pneumoniae pavA

164 nfection and have important implications for enterococcal pathogenesis.

165 Moreover, the enterococcal pathogenicity island, in addition to coding

166 tioned with potent in vitro efficacy against enterococcal pathogens.

167 Enterococcal pheromone responsive conjugative plasmids l

168 tive structural genes coding for the various enterococcal pheromones.

169 mone cAM373, which induces a response by the enterococcal plasmid pAM373, has been of interest becaus

170 Two of these relaxase genes, pcfG from the enterococcal plasmid pCF10 and the ORF4 gene in the stre

171 gions previously found in staphylococcal and enterococcal plasmids.

172 es of a large family of pheromone-responsive enterococcal plasmids.

173 alis, we found that these phages require the enterococcal polysaccharide antigen (Epa) for productive

174 eviously, TX5179, a disruption mutant of the enterococcal polysaccharide antigen (epa) gene cluster o

175 nsferase located in a variable region of the enterococcal polysaccharide antigen (epa) locus.

176 h components of the major and variant region enterococcal polysaccharide antigen to engage in lytic i

177 utants involving the previously studied epa (enterococcal polysaccharide antigen) gene cluster, known

178 rinary tract infection and is the first such enterococcal polysaccharide locus shown to be important

179 njugates consisting of these proteins and an enterococcal polysaccharide to develop a vaccine with br

180 nd lung cancer patients, the presence of the enterococcal prophage in stools and expression of a TMP-

181 , these observations suggest that of the two enterococcal proteases, gelatinase is the principal medi

182 olonize the GIT, we identified two conserved enterococcal proteins (OG1RF_11271 and OG1RF_11272) that

183 Diheteroglycan was conjugated to these 2 enterococcal proteins.

184 Enterococcal PVE was associated with a higher risk of re

185 ly discriminated 15 enterococcal from 15 non-enterococcal reference strains and reliably detected 48

186 ring previous hospitalizations have elevated enterococcal relative abundances on NH admission and hig

187 ole to the RR-HK17 TCS as coordinator of the enterococcal response to specific nutritional conditions

188 In addition, compositional changes in the enterococcal rhamnopolysaccharide were noticed.

189 A suicide vector was generated with an enterococcal selectable marker in order to disrupt a gen

190 We have previously characterized two new enterococcal species (provisionally designated CDC PNS-E

191 Enterococcal species are among the predominant causative

192 Over 60 enterococcal species are now known.

193 Although many enterococcal species can colonize humans, only Enterococ

194 The 16S rRNA sequences of enterococcal species E. faecium, E. faecalis, E. gallina

195 hosts, including the rapid emergence of new enterococcal species following the End Permian Extinctio

196 The basis for host association of enterococcal species is unknown.

197 Enterococcal species of bacteria are now acknowledged as

198 ecium isolates or in 4 other less pathogenic enterococcal species tested.

199 After examining 6,028 genomes of 61 Enterococcal species using updated Phage_Finder software

200 iate E. faecium from certain newly described enterococcal species, a PCR-based assay was developed fo

201 , after controlling for severity of illness, enterococcal species, gram-negative copathogens, sex, ra

202 For Enterococcus faecalis and other enterococcal species, revised breakpoints of <=2 mug/mL-

203 Focusing our studies on the enterococcal species, we found that both E. faecalis and

204 inclusion of the strains in any of the known enterococcal species.

205 (strain SS-1729), and IV (strain SS-1728) of enterococcal species.

206 differences were identified between several enterococcal species.

207 as to whether E. flavescens is a legitimate enterococcal species.

208 onfidence interval, 0.29-0.93; P = 0.03) and enterococcal SSIs by 64% (relative risk, 0.36; 95% confi

209 he risk of resistant staphylococcal SSIs and enterococcal SSIs, but increase the risk of respiratory

210 and ceftriaxone inhibited colonization by an enterococcal strain devoid of low-affinity penicillin-bi

211 to test four VRE strains and one susceptible enterococcal strain from the Centers for Disease Control

212 smids encoding bacteriocins are common among enterococcal strains and could modulate niche competitio

213 omycin resistance, five vancomycin-resistant enterococcal strains and one vancomycin-susceptible beta

214 terial cells showed immune recognition of 22 enterococcal strains by the sera.

215 hat drive host association, we collected 886 enterococcal strains from widely diverse hosts, ecologie

216 -one percent (26 of 32) of streptococcal and enterococcal strains isolated from bacteremic patients e

217 vailability of draft genome sequences for 28 enterococcal strains of diverse origin, including the sp

218 The VEL assay identified all enterococcal strains with vanA and vanB genes.

219 roscopic method for accurate detection of 89 enterococcal strains, including 72 vanC enterococcal str

220 f 89 enterococcal strains, including 72 vanC enterococcal strains.

221 ions four times higher than the MIC for some enterococcal strains.

222 To characterize enterococcal surface antigens that are targets of opsoni

223 It was recently reported that enterococcal surface protein (esp) was more prevalent in

224 Enterococcal surface protein, Esp, has been reported to

225 nt Staphylococcus aureus (MRSA) carrying the enterococcal vanA gene complex and expressing high level

226 The enterococcal vanA gene was positively associated with 8

227 d not react with DNA probes specific for the enterococcal vanA or vanB gene, and showed characteristi

228 strains carrying the Tn1546 transposon-based enterococcal vancomycin resistant mechanism were identif

229 ial activity against both staphylococcal and enterococcal vancomycin-resistant pathogens.

230 S system, in contrast to results obtained in enterococcal VanRS systems.

231 ) appears to have no effect on the monomeric enterococcal VanS kinase involved in glycopeptide resist

232 ine may play an important role in modulating enterococcal virulence at sites of infection.

233 design of specific inhibitors targeting this enterococcal virulence factor and its orthologs in other

234 aecalis quorum-sensing locus (fsr) increases enterococcal virulence in multiple animal models.

235 Asc10 also increases enterococcal virulence in several models, and when donor

236 e the extent to which biological cues affect enterococcal virulence-associated gene expression, we us

237 sis, enabling us to dissect the mechanism of enterococcal virulence.

238 increased incidence of vancomycin-resistant enterococcal (VRE) isolates at area health care faciliti