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

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

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

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

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

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

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

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

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

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

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

13 Enterococcal bacteremia has been associated with high ca

14 Enterococcal bacteremia is a frequent infectious complic

15 ICU-acquired enterococcal bacteremia is associated with increased cas

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

17 Enterococcal bacteremia was independently associated wit

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

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

20 her antibiotic therapy alters the outcome of enterococcal bacteremia.

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

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

23 bacteremia, 4 were directly associated with enterococcal bacteremia.

24 modeling to estimate ICU mortality caused by enterococcal bacteremia.

25 ical and economic outcomes for patients with enterococcal bacteremia.

26 Seventy enterococcal bacteremias in 52 patients were identified.

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

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

29 MEB represented approximately 5% of all enterococcal bacteremias.

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

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

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

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

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

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

36 >100 additional genes with unknown roles in enterococcal biology.

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

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

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

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

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

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

43 , respectively, compared to patients without enterococcal BSI.

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

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

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

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

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

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

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

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

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

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

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

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

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

57 ve plasmid pPD1 expressing bacteriocin 21 in enterococcal colonization.

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

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

60 The enterococcal, conjugative, cytolysin plasmid pAD1 confer

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

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

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

64 The enterococcal cytolysin is a virulence factor consisting

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

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

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

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

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

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

71 Enterococcal domination was increased 3-fold by metronid

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

73 nique target for therapeutic intervention in enterococcal endocarditis.

74 opment of immunological approaches to combat enterococcal endocarditis.

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

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

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

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

79 A previously undescribed enterococcal enteropathy was associated with preretinal

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

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

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

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

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

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

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

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

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

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

90 Enterococcal IE may be more frequent than generally thou

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

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

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

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

95 f traits contributing to the pathogenesis of enterococcal infection.

96 detected more episodes of streptococcal and enterococcal infection.

97 d inflammation contributes to the control of enterococcal infection.

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

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

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

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

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

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

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

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

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

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

108 options for the treatment and prevention of enterococcal infections.

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

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

111 l antimicrobial targets for the treatment of enterococcal infections.

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

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

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

115 n5385 consist of directly repeated copies of enterococcal IS1216.

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

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

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

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

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

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

122 Thirty-five enterococcal isolates were recovered from dogs diagnosed

123 Twenty enterococcal isolates were tested, including Enterococcu

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

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

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

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

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

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

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

131 56, IS257, and IS1216) of staphylococcal and enterococcal origin.

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

133 nfection and have important implications for enterococcal pathogenesis.

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

135 tive structural genes coding for the various enterococcal pheromones.

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

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

138 gions previously found in staphylococcal and enterococcal plasmids.

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

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

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

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

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

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

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

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

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

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

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

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

151 Enterococcal species are among the predominant causative

152 Although many enterococcal species can colonize humans, only Enterococ

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

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

155 Enterococcal species of bacteria are now acknowledged as

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

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

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

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

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

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

162 differences were identified between several enterococcal species.

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

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

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

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

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

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

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

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

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

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

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

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

175 To characterize enterococcal surface antigens that are targets of opsoni

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

177 Enterococcal surface protein, Esp, has been reported to

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

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

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

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

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

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

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

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

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

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

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

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