ライフサイエンスコーパス: streptococci

1 here as PgfS (protein glycosyltransferase of streptococci).

2 =0.322 for enterococci and 0.272 for group B streptococci).

3 pes that promote opsonophagocytic killing of streptococci.

4 Twelve percent had positive results for streptococci.

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

6 e enhanced by the presence of oral commensal streptococci.

7 ating Streptococcus pneumoniae from viridans streptococci.

8 oropharyngeal secretions containing biofilm streptococci.

9 ococci and capsular polysaccharides (CPS) in streptococci.

10 ptor substrate binding from GtfC homologs in streptococci.

11 broad spectrum of bacteria, including other streptococci.

12 ng facultative anaerobic Firmicutes, such as streptococci.

13 rgeted genetic manipulation in this group of streptococci.

14 ococcus pneumoniae from other viridans group streptococci.

15 ) is widely distributed among oral commensal streptococci.

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

17 , including some cocci in chains, suggesting streptococci.

18 nscriptional activation of cytokine genes by streptococci.

19 first virus documented to be active against streptococci.

20 development and bacterial coaggregation with streptococci.

21 discrete cluster within those of other oral streptococci.

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

23 phylcoccus aureus strains as well as group B streptococci.

24 lagen bound in vitro by certain serotypes of streptococci.

25 ional relationship between PerR and PolA1 in streptococci.

26 sk approximation test for the beta-hemolytic streptococci.

27 functional orthologue was reported in other streptococci.

28 d adhesins expressed by most indigenous oral streptococci.

29 enes, Streptococcus agalactiae, and viridans streptococci.

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

31 or inducible CC resistance in beta-hemolytic streptococci.

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

33 cal pyrogenic exotoxin A and possibly viable streptococci.

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

35 to contribute to P. gingivalis adherence to streptococci.

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

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

38 occus spp., including mitis and mutans group streptococci.

39 ely high antimicrobial efficacy against oral streptococci.

40 the exploitation of the diabetic eye by the streptococci.

41 g the only known alternative sigma factor in streptococci.

42 ribed, in all likelihood it is not unique to streptococci.

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

44 lishment of oral health-associated commensal streptococci.

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

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

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

48 host defense mechanism against Gram-positive Streptococci.

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

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

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

52 nt causal microorganisms were viridans group streptococci (18.6%), Staphylococcus aureus (15.6%), and

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

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

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

56 by Staphylococcus aureus (43%), followed by streptococci (26%) and Gram negative rods (18%).

57 6, 46.8%), Gram-negative rods (34/126, 27%), streptococci (32/126, 25.4%), and a Gram-positive rod (1

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

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

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

61 Oral streptococci adhere to tooth-immobilized glycoprotein 34

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

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

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

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

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

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

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

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

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

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

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

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

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 regulatory circuit also exists in pathogenic streptococci and is likely conserved among Gram-positive

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

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

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

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

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

84 rolide resistance in commensal oropharyngeal streptococci and lung function.

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

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

87 f hydrogen peroxide-producing oral commensal streptococci and nitrite has been shown to mediate the g

88 summary, our data demonstrate that commensal streptococci and nitrite provide protection against S. m

89 i (Sg) potently inhibited adherence of Pg to streptococci and reduced Pg virulence in a mouse model o

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

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

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

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

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

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

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

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

98 re important bacterial adhesins conserved in streptococci and staphylococci.

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

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

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

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

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

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

105 Streptococci and veillonellae occur in mixed-species col

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

107 acterial pathogens, including staphylococci, streptococci, and borrelia, likewise produce virulence f

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

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

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

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

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

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

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

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

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

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

118 Streptococci are common human colonizers with a species-

119 Staphylococci and streptococci are considered predominant causes of wound

120 beta-Hemolytic streptococci are frequently implicated in necrotizing so

121 beta-Hemolytic streptococci are highly prevalent in NSTIs, and in our p

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

123 Streptococci are not an infrequent cause of periprosthet

124 Streptococci are predominant bacterial species in the or

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

126 Mutans streptococci are strongly implicated in caries induction

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

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

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

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

131 Our results highlight mammalian streptococci as a rich source of unusual enzymatic chemi

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

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

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

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

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

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

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

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

140 Interestingly, however, some species of oral streptococci can antagonize the phenotypes induced by P.

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

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

143 In most streptococci, competence is regulated by ComRS signaling

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

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

146 tion of impetigo lesions containing pyogenic streptococci declined following MDA.

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

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

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

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

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

152 Streptococci do so during a transient period of competen

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

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

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

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

157 arms) but the proportion containing pyogenic streptococci fell significantly (63% vs 23%, P < .01).

158 Endocarditis-inducing streptococci form multilayered biofilms in complex with

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

160 Streptococci frequently cause infective endocarditis (IE

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

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

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

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

165 ing fasciitis and myositis caused by group A streptococci (GAS) are among the most fulminating infect

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

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

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

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

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

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

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

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

174 tion to invasive infection caused by group A streptococci (GAS).

175 Group B Streptococci (GBS) are bacteria associated with preterm

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

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

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

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

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

181 5.1-9.8; p<0.0001) driven mainly by group B streptococci (GBS), and in adults aged 65 years or older

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

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

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

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

186 beta-Hemolytic streptococci grew in 31%, and clindamycin resistance was

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

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

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

190 Oral streptococci have been associated with systemic diseases

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

192 Oral streptococci have evolved diverse strategies to survive

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

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

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

196 Oral streptococci IE incidence did not increase either in the

197 llite prophages are widely distributed among streptococci in a structured manner, and constitute two

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

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

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

201 tive Enterobacteriaceae in nine patients and streptococci in three patients.

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

203 The most prevalent streptococci included species typically associated with

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

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

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

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

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

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

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

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

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

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

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

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

216 clindamycin resistance among beta-hemolytic streptococci infections (1.86; 1.10-3.16).

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

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

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

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

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

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

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

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 Subsequent to the interaction with streptococci, MPhi changed their immunophenotype and gai

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

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

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

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

234 Oral streptococci often harbor capsular polysaccharide (PS) s

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 outcomes and the presence of beta-hemolytic streptococci or clindamycin-resistant beta-hemolytic str

238 endovascular infection are not present, most streptococci or Enterobacterales bacteremias do not requ

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

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

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

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

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

244 limb loss among patients with beta-hemolytic streptococci-particularly clindamycin-resistant strains-

245 Streptococci plus MPO produced potent synergistic microb

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

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

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

249 Porphyromonas gingivalis (Pg) with commensal streptococci promotes Pg colonization of the oral cavity

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

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

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

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

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

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

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

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

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

259 example, Bifidobacteria, staphylococci, and streptococci significantly decreased on cessation of bre

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

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

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

263 s, Rothia, Haemophilus, Corynebacterium, and Streptococci spp.

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

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

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

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

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

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

270 nsing-regulated BGCs in mammalian microbiome streptococci that code for ribosomally synthesized and p

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

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

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

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

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

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

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

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

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

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

281 us, Streptococcus pneumoniae, beta-hemolytic streptococci, vancomycin-resistant Enterococcus, and Ent

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

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

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

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

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

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

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

289 The presence of beta-hemolytic streptococci was associated with greater risk of amputat

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

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

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

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

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

295 occi or clindamycin-resistant beta-hemolytic streptococci were calculated using log-binomial regressi

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

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

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

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

300 hatic dissemination and show that metastatic streptococci within infected lymph nodes resist and subv