ライフサイエンスコーパス: streptococci

1 =0.322 for enterococci and 0.272 for group B streptococci).

2 and (3) binding to bacteria (e.g., viridans streptococci).

3 here as PgfS (protein glycosyltransferase of streptococci).

4 ng facultative anaerobic Firmicutes, such as streptococci.

5 rgeted genetic manipulation in this group of streptococci.

6 ococcus pneumoniae from other viridans group streptococci.

7 mechanism in S. mutans and possibly in other streptococci.

8 nscriptional activation of cytokine genes by streptococci.

9 first virus documented to be active against streptococci.

10 development and bacterial coaggregation with streptococci.

11 discrete cluster within those of other oral streptococci.

12 red to be the most cariogenic among all oral streptococci.

13 g the only known alternative sigma factor in streptococci.

14 phylcoccus aureus strains as well as group B streptococci.

15 lagen bound in vitro by certain serotypes of streptococci.

16 ional relationship between PerR and PolA1 in streptococci.

17 sk approximation test for the beta-hemolytic streptococci.

18 functional orthologue was reported in other streptococci.

19 d adhesins expressed by most indigenous oral streptococci.

20 enes, Streptococcus agalactiae, and viridans streptococci.

21 in a parallel way in all pyogenic and bovis streptococci.

22 or inducible CC resistance in beta-hemolytic streptococci.

23 e agents that target S. gordonii and related streptococci.

24 S. aureus but strong compared to binding of streptococci.

25 cal pyrogenic exotoxin A and possibly viable streptococci.

26 es and a polymerase in the rps loci of these streptococci.

27 to contribute to P. gingivalis adherence to streptococci.

28 tem in S. aureus may also differ compared to streptococci.

29 is the first of its kind to be identified in streptococci.

30 val plaque, such as the oralis group of oral streptococci.

31 increased the adherence of P. gingivalis to streptococci.

32 Veillonellae also coaggregate with streptococci.

33 erably higher than the G+C contents of other streptococci.

34 binding adhesin AbpA and a sortase B in oral streptococci.

35 n the single MPhi response to beta-hemolytic streptococci.

36 methicillin-susceptible S. aureus, and 5.0% streptococci.

37 host defense mechanism against Gram-positive Streptococci.

38 oduction of hydrogen peroxide (H2O2) by oral streptococci.

39 anginosus group, S aureus, and group A beta-streptococci.

40 Twelve percent had positive results for streptococci.

41 the exploitation of the diabetic eye by the streptococci.

42 /-) mice display higher levels of indigenous streptococci.

43 e enhanced by the presence of oral commensal streptococci.

44 ating Streptococcus pneumoniae from viridans streptococci.

45 oropharyngeal secretions containing biofilm streptococci.

46 ococci and capsular polysaccharides (CPS) in streptococci.

47 ptor substrate binding from GtfC homologs in streptococci.

48 broad spectrum of bacteria, including other streptococci.

49 r organism group level (e.g., viridans group streptococci), 11% positivity with discordant microbiolo

50 e (2 of 7), Pseudomonas aeruginosa (2 of 4), streptococci (2 of 5), or coagulase-negative staphylococ

51 mon (57%), followed by the viridans group of streptococci (20%).

52 isms were staphylococci (28.7%), followed by streptococci (20.4%) and enterococci (13.1%).

53 6, 46.8%), Gram-negative rods (34/126, 27%), streptococci (32/126, 25.4%), and a Gram-positive rod (1

54 (AST) with 13 agents was performed on 2,013 streptococci (938 Streptococcus pneumoniae isolates; 396

55 Group B streptococci, a major cause of sepsis, induce inflammato

56 rich in Candida are also rich in mitis group Streptococci,a community pattern associated with pathoge

57 unique sortase/adhesion substrate system in streptococci adapted to the oral environment rich in sal

58 Oral streptococci adhere to tooth-immobilized glycoprotein 34

59 co-aggregated strongly with receptor-bearing streptococci, agglutinated with sialidase-treated red bl

60 The anaerobic isolation of anginosus group streptococci (AGS) from respiratory specimens containing

61 n the presence or absence of anginosus group streptococci (AGS) were compared.

62 caused by pathogens other than S. aureus or streptococci (all P < 0.05).

63 Findings of 1 military study using hemolytic streptococci also suggested that there was significant p

64 riptional regulator of capsule production in streptococci, although the regulatory mechanism is unkno

65 nguinis is a member of the viridans group of streptococci and a leading cause of the life-threatening

66 ary Interbacterial interactions between oral streptococci and actinomyces and their adherence to toot

67 directly facilitate coaggregation with oral streptococci and Actinomyces biofilm development require

68 distinct bacteria, for example, between oral streptococci and actinomyces, are central to dental plaq

69 control samples, combined with milleri group streptococci and actinomycetes in 33% and 26% of cases,

70 ofilm strategies to fight infections by oral streptococci and beyond.

71 er increase in the concentrations of group B streptococci and Candida albicans, Escherichia coli, and

72 ns involved in haem uptake found in pyogenic streptococci and Clostridium novyi.

73 more effectively than other species of oral streptococci and depended upon the salivary film on HA.

74 Pathogenic streptococci and enterococci primarily rely on the conse

75 ide receptors present on the surface of oral streptococci and epithelial cells.

76 distinguishable from those caused by group B streptococci and has been associated with considerable m

77 actoferrin in their saliva that kills mutans streptococci and have reduced proximal decay.

78 n B (SpeB) is a protease secreted by group A streptococci and known to degrade a wide range of host a

79 two groups were observed in levels of mutans streptococci and lactobacilli at all time-points.

80 Salivary levels of mutans streptococci and lactobacilli were enumerated at baselin

81 upstream of fap1 is also highly conserved in streptococci and lactobacilli.

82 thought to be essential in others, including streptococci and lactococci.

83 rolide resistance in commensal oropharyngeal streptococci and lung function.

84 oirs of resistance genes for more pathogenic streptococci and may be implicated in some non-oral infe

85 on as a receptor for HA-encapsulated Group A streptococci and mediate lymphatic dissemination in mice

86 e harboured in some, but not all, pathogenic streptococci and related Gram-positive organisms, openin

87 The accessory Sec (SecA2/Y2) systems of streptococci and staphylococci are dedicated to the tran

88 ne-rich repeat glycoproteins identified from streptococci and staphylococci are important for bacteri

89 ch repeat glycoproteins (SRRPs) conserved in streptococci and staphylococci are important for bacteri

90 The SecA2 proteins of streptococci and staphylococci are paralogues of SecA an

91 The accessory Sec systems of streptococci and staphylococci mediate the transport of

92 of bacterial adhesins found in a variety of streptococci and staphylococci that have been implicated

93 lycoproteins (SRRPs) are highly conserved in streptococci and staphylococci.

94 re important bacterial adhesins conserved in streptococci and staphylococci.

95 ant bacterial adhesins that are conserved in streptococci and staphylococci.

96 SecA2, Gap1, and Gap3 are conserved in many streptococci and staphylococci.

97 ed abundant atypical bacteria in addition to streptococci and staphylococci.

98 g family of bacterial adhesins found in many streptococci and staphylococci; they play important role

99 The streptococci and strain PK1910 formed interdigitated thr

100 M5 streptococci and the DeltaNH(2) mutant were resistant to

101 Although immune responses against group A streptococci and the heart have been correlated with ant

102 competition between pioneer colonizing oral streptococci and the survival mechanisms of S. mutans in

103 could deter the adherence of pathogenic oral streptococci and thereby prevent the onset of infections

104 Streptococci and veillonellae occur in mixed-species col

105 and thawing, on indigenous coliforms, fecal streptococci, and antibiotic-resistant (AR) bacteria, an

106 isolates into two subgroups, staphylococci, streptococci, and enterococci (n = 217) and "related gen

107 ifferent organisms, including staphylococci, streptococci, and enterococci, as well as for the presen

108 urden of disease being due to staphylococci, streptococci, and enterococci.

109 orming units of total micro-organisms, total streptococci, and mutans streptococci by an order of mag

110 vity against Enterococci, Staphylococci, and Streptococci, and other Gram-positive bacteria.

111 n of 305 clinical isolates of staphylococci, streptococci, and related genera by comparing direct col

112 am-positive bacteria, including enterococci, streptococci, and staphylococci, and antibodies against

113 has conventionally been associated with the streptococci, and when it is caused by other organisms,

114 The expression level of arcA in streptococci appears to be controlled by both cis and tr

115 g evidence that suggests that oral commensal streptococci are cocolonized with Pseudomonas aeruginosa

116 Streptococci are common human colonizers with a species-

117 Staphylococci and streptococci are considered predominant causes of wound

118 for genetic transformation, yet no pyogenic streptococci are known to develop competence.

119 Streptococci are not an infrequent cause of periprosthet

120 Streptococci are predominant bacterial species in the or

121 is without purulent drainage, beta-hemolytic streptococci are presumed to be the predominant pathogen

122 Mutans streptococci are strongly implicated in caries induction

123 e clinical relevance since staphylococci and streptococci are the most common causes of nosocomial NI

124 ogens (e.g., enterococci, staphylococci, and streptococci) are Gram-positive (G+), their conjugation

125 Lactobacillus species, in addition to mutans streptococci, are risk markers for early childhood carie

126 Hence, the role of mutans streptococci as a primary caries pathogen appears less p

127 ences of F. necrophorum and groups A and C/G streptococci as agents of bacterial pharyngitis in child

128 tact and invasive procedures, have overtaken streptococci as the most common cause of the disease.

129 ar interactions between Actinomyces and oral streptococci as well as host cells during the developmen

130 r peptide designed for this SNP kills mutans streptococci associated with caries by >1 log.

131 ny phage are induced and transferred to host streptococci at a site where host organisms are more pre

132 ral competitors, including health-associated Streptococci, became dominant.

133 tious disease frequently caused by commensal streptococci, but the contribution of host factors in bi

134 ro-organisms, total streptococci, and mutans streptococci by an order of magnitude.

135 ide of SOF inhibited binding of fibulin-1 to streptococci by approximately 45%.

136 The above results suggest that the streptococci can use phage HLs to degrade glycosaminogly

137 Beta-hemolytic group C and G streptococci cause a considerable invasive disease burde

138 onii by an RPS-dependent mechanism, and both streptococci coaggregated with PK1910, which was used as

139 fections and that the presence of these oral streptococci contributes to improved lung function.

140 al arginine biosynthesis was inefficient and streptococci could not grow aerobically at low arginine

141 minal sequence of the M protein from group A streptococci defines the serotype of the organism and co

142 Patients with IE caused by oral streptococci differ from patients with IE caused by nono

143 In summary, C. albicans and commensal oral streptococci display a synergistic interaction with impl

144 ide that was shown to aggregate several oral streptococci displayed limited aggregation and also nons

145 ce of periapical abscesses and oral viridans streptococci DNA-positive thrombi was found (odds ratio,

146 Streptococci do so during a transient period of competen

147 mycin resistance can occur in beta-hemolytic streptococci due to the presence of an erm gene.

148 ent a unique anti-infection strategy by oral streptococci during polymicrobial infections.

149 ies (pneumococci, staphylococci, and group B streptococci) during the exponential growth phase (desig

150 The prophages of S. equi and other streptococci encode intracellular HLs which are reported

151 For streptococci, export of the SraP homologs requires a spe

152 otein, we constructed a mutant of M5 group A streptococci expressing an M protein with a deletion of

153 Endocarditis-inducing streptococci form multilayered biofilms in complex with

154 It was observed that C. albicans and streptococci formed a synergistic partnership where C. a

155 as identified from 11 (22%) and 15 (31%) and streptococci from 15 (31%) and 20 (41%) of the specimens

156 ty data for staphylococci and beta-hemolytic streptococci from 52 U.S. medical centers that locally t

157 edictive values for the detection of group B streptococci from Lim enrichment broth with sheep blood

158 ion between C. albicans and three species of streptococci from the viridans group, which are ubiquito

159 d immunity against the two conserved group A streptococci (GAS) Ags, streptococcal C5a peptidase and

160 Group A streptococci (GAS) are a common cause of bacterial phary

161 Group A streptococci (GAS) are highly prevalent human pathogens

162 nce responder/sensor (CovR/S) mutant group A streptococci (GAS) are serious human pathogens of multip

163 ole-genome sequencing of serotype M3 group A streptococci (GAS) from oropharyngeal and invasive infec

164 ur epidemiologic studies on invasive Group A Streptococci (GAS) infections identified specific HLA cl

165 syndrome in childhood to antecedent group A streptococci (GAS) is unclear.

166 Group A streptococci (GAS) may engage different sets of virulenc

167 Myonecrosis due to group A streptococci (GAS) often develops at sites of nonpenetra

168 Group A streptococci (GAS) secrete streptokinase, a specific act

169 For invasive serotype M3 group A streptococci (GAS) strains, the gene encoding regulator

170 reconstructions of NAD metabolism in group A streptococci (GAS), combined with focused experimental t

171 ing protein (PAM) from Gram-positive group-A streptococci (GAS), represents an epitope within PAM tha

172 Group B streptococci (GBS) are beta-hemolytic Gram-positive bact

173 Group B streptococci (GBS) are one of the leading causes of life

174 pB assay (GOSB) for the detection of group B streptococci (GBS) from an 18- to 24-h LIM broth.

175 describe the population structure of group B streptococci (GBS) isolated from infected and colonized

176 Group B streptococci (GBS), a leading cause of neonatal sepsis a

177 5.1-9.8; p<0.0001) driven mainly by group B streptococci (GBS), and in adults aged 65 years or older

178 ty of pathogens, including fungi and group B streptococci (GBS), are thought to be major virulence fa

179 Group B streptococci (GBS; Streptococcus agalactiae) are a major

180 Group B streptococci (GBS; Streptococcus agalactiae) are beta-he

181 reptococcus pneumoniae isolates; 396 group B streptococci [GBS]; 369 viridans group streptococci [VGS

182 Group G streptococci (GGS) are important bacterial pathogens in

183 assay correctly detected all beta-hemolytic streptococci (group A, n = 19; group C/G, n = 5).

184 Beta-hemolytic streptococci had a 20.2% erythromycin resistance rate an

185 beta-Hemolytic streptococci had MIC(90) values ranging between <or=0.01

186 differences in activity among staphylococci, streptococci, Haemophilus spp., and Moraxella catarrhali

187 investigating the infectivity of desiccated streptococci has used broth-grown, planktonic population

188 Oral streptococci have been associated with systemic diseases

189 New, often noncultured, oral streptococci have been identified, and their phenotypic

190 Oral streptococci have evolved diverse strategies to survive

191 lis strains (unlike Enterococcus faecium and streptococci) have a single pilus locus.

192 respiratory disease, such as oral commensal streptococci, have not been investigated.

193 Compared to streptococci, however, SraP is predicted to differ in it

194 IM) analysis to determine the species of the streptococci identified by pyrosequencing.

195 Oral streptococci IE incidence did not increase either in the

196 CR-based system for the detection of group B streptococci in antepartum screening samples enriched in

197 Similar to planktonic cells, the streptococci in biofilms were also able to induce platel

198 the platelet is a host factor for commensal streptococci in the circulation to consolidate biofilm f

199 enterococci (in 10% of cultures) and group B streptococci (in 12% of cultures) were not predictive of

200 The most prevalent streptococci included species typically associated with

201 The arsenal of virulence factors deployed by streptococci includes streptococcal collagen-like (Scl)

202 eptococcus pneumoniae from other mitis group streptococci, including differentiation of S. pneumoniae

203 ' microbiota was characterized by a panel of streptococci, including S. mutans, S. sobrinus, and Stre

204 ll-conserved protein that is present in many streptococci, including S. mutans.

205 his study, we discovered that oral commensal streptococci, including Streptococcus parasanguinis, Str

206 l) proteins are widely present in pathogenic streptococci, including Streptococcus pyogenes, S. agala

207 is shared by the pyogenic, mutans, and bovis streptococci, including the clinically relevant pathogen

208 as been shown to impact virulence in several streptococci, including the human pathogen Streptococcus

209 Conversely, the presence of streptococci increased the ability of C. albicans to inv

210 the distribution of homologs of SMU.1297 in streptococci indicates that this protein is essential fo

211 w that NO plays an important role in Group B streptococci-induced transcriptional activation of cytok

212 Cases with streptococci infection were 10 times more likely to have

213 , with multidrug-resistant staphylococci and streptococci infections posing major threats to human he

214 eract metabolically; lactic acid produced by streptococci is a carbon source for veillonellae.

215 ggest that the adherence of P. gingivalis to streptococci is driven by a protein-protein interaction

216 tance to hydrogen peroxide and iron in other streptococci is that encoding nonheme iron-containing fe

217 model, a community consisting of RPS-bearing streptococci juxtaposed with veillonellae was targeted b

218 Salivary levels of Bifidobacteria, mutans streptococci, lactobacilli, and yeasts were correlated w

219 of total cultivable microbes, including oral streptococci, lactobacilli, Streptococcus mutans, and Ca

220 Escherichia coli, Enterococcus spp., group B streptococci, Lactobacillus crispatus, and Staphylococcu

221 uncovered novel regulatory pathways by which streptococci link environmental carbohydrate availabilit

222 Individual mediators, salivary log10 mutans streptococci, log10 lactobacilli, and fluoride level, di

223 Streptococcus pneumoniae and viridans group streptococci may result in misidentification of these or

224 These findings raise the possibility that streptococci may survive in the environment and be trans

225 ction and oral bacteria, especially viridans streptococci, may be associated with the development of

226 portion of macrolide-resistant oropharyngeal streptococci (median change, 27.7% [IQR, 0.04% to 41.1%]

227 The mitis group streptococci (MGS) are widespread in the oral cavity and

228 occi (MIC(90), </= 0.008 to 0.5 mug/mL), and streptococci (MIC(90), </= 0.008 to 0.12 mug/mL), includ

229 t pro-inflammatory cytokines induced by oral streptococci might play a role in the pathogenesis of vi

230 Mutans streptococci (MS) are key organisms associated with the

231 pneumoniae (n = 13; 21%), and beta-hemolytic Streptococci (n = 5; 8%).

232 Intrageneric coaggregation of streptococci occurs when a lectin-like adhesin on one st

233 ed, which demonstrated high levels of viable streptococci of both species.

234 the vaginal (staphylococci) or oral mucosa (streptococci) of the body.

235 neumoniae from all but one other mitis group streptococci (one S. mitis isolate generated an OD-value

236 Unlike the CiaRH system in other streptococci, only the ciaH-null mutant displays defecti

237 Microorganisms were categorized as oral streptococci or nonoral pathogens using an expert-valida

238 ntrols had definite IE caused either by oral streptococci or nonoral pathogens, respectively.

239 g 41 episodes in which enterococcus, group B streptococci, or both were found in midstream urine, E.

240 /pyrosequencing as containing staphylococci, streptococci, or enteric Gram-negative rods had target-s

241 ne neuropsychiatric disorder associated with streptococci" (PANDAS) with small choreiform movements r

242 Streptococci plus MPO produced potent synergistic microb

243 increasing emergence of multi-drug resistant streptococci poses a serious threat to public health wor

244 esponse to a protein antigen from cariogenic streptococci, potentially through suppressive SOCS compo

245 Recent studies indicate that streptococci produce and respond to several secreted pep

246 Certain oral streptococci produce H(2)O(2) under aerobic growth condi

247 In many streptococci, quorum sensing utilizes secreted, linear p

248 Several oral streptococci, relative to A. naeslundii, produced protea

249 w function by DprA impacted its evolution in streptococci relying on ComE to regulate comX expression

250 phagosome acidification, we demonstrate that streptococci reside in a phagosome and that acidificatio

251 itive for F. necrophorum, GAS, and group C/G streptococci, respectively.

252 ylococcus aureus, Enterococcus faecalis, and streptococci, respectively.

253 However, as with many streptococci, Sg also produces high levels of the antimi

254 s, it is likely that the PerR orthologs from streptococci share a common mechanism of metal binding,

255 al surface protein with orthologues in other streptococci, show that it binds to the extracellar matr

256 ng microorganisms, Staphylococcus aureus and streptococci slightly declined, whereas coagulase-negati

257 e Neuropsychiatric Disorders Associated with Streptococci (so-called 'PANDAS').

258 eat-killed, sensitively co-aggregates mutans streptococci specifically.

259 e serine-rich glycoproteins are conserved in streptococci, staphylococci, and lactobacilli, and are r

260 IL-1beta-rich supernatant fluids from oral streptococci-stimulated or lipopolysaccharide-stimulated

261 he most common bacteria (54.6%), followed by Streptococci (Strep) species (20.8%), Staphylococcus aur

262 Group A streptococci (Streptococcus pyogenes or GAS) freshly iso

263 ites with many microbes, including commensal streptococci such as Streptococcus gordonii (Sg).

264 CRISPR-Cas systems are widespread in streptococci, suggesting that the interplay between CRIS

265 transformation is even more common among the streptococci than has been recognized.

266 tinct groups of glycosyltransferases in oral streptococci that are important for bacterial colonizati

267 he sigX genes of mutans, pyogenic, and bovis streptococci that uses a novel small, double-tryptophan-

268 e, we show that during coculture growth with streptococci, the oral pathogen Aggregatibacter actinomy

269 the bovis, salivarius and pyogenic groups of streptococci, the pheromone XIP is sensed by the intra-c

270 from many Gram-positive bacteria, including streptococci; therefore, how CtsR activity is modulated

271 logs are highly conserved in SRRP-containing streptococci, they share minimal homology with functiona

272 proteins, which contribute to the ability of streptococci to colonize and cause diseases in humans an

273 proteins might contribute to the ability of streptococci to colonize and infect the host.

274 The increased ability of streptococci to form biofilms in the presence of C. albi

275 ip where C. albicans promoted the ability of streptococci to form biofilms on abiotic surfaces or on

276 ent a basilar cistern inoculation of group B Streptococci to induce meningitis.

277 Identification of group G streptococci to the species level could have epidemiolog

278 e X state by permitting lysis of incompetent streptococci, uptake of DNA fragments, and integration o

279 Viridans group streptococci (VGS) are a heterogeneous group of medicall

280 The viridans group streptococci (VGS) are a heterogeneous group of organism

281 difficulty in distinguishing viridans group streptococci (VGS) by phenotype, analysis of 16S rRNA se

282 The viridans group streptococci (VGS) have been suggested to serve as reser

283 The incidence of IE caused by viridans group streptococci (VGS) in the United States after publicatio

284 due to beta-lactam-resistant viridans group streptococci (VGS) is a major factor driving empiric use

285 Identification of viridans group streptococci (VGS) to the species level is difficult bec

286 oup B streptococci [GBS]; 369 viridans group streptococci [VGS]; 290 beta-hemolytic streptococcus gro

287 Bacterial RNA within streptococci was also a dominant stimulus for murine imm

288 host survival after infection with wild-type streptococci was enhanced among flies overexpressing the

289 r endodontic infection, mainly oral viridans streptococci, was measured in 78.2% of thrombi, and peri

290 Gtf3 homologs only exist in SRRP-containing streptococci, we conclude that the Gtf3 homologs represe

291 hrough our analyses of P. aeruginosa and six Streptococci, we show that ensembles increase the qualit

292 Moreover, Gtf3 homologs from other streptococci were able to rescue the gtf3 knock-out muta

293 As a group, streptococci were commonly detected in these individuals

294 The streptococci were identified as Streptococcus oralis (RP

295 Fecal streptococci were more resistant to long-term freezing t

296 PK1910 grew only when streptococci were present.

297 ned by a growth-stimulatory effect since the streptococci were unaffected in their growth in plankton

298 er E. coli but not of enterococci or group B streptococci, which are often isolated with E. coli but

299 II proteins expressed by the oralis group of streptococci, which interact with P. gingivalis.

300 reptococcus groups A, C, and G; and 20 other streptococci) with the Phoenix system and a broth microd