ライフサイエンスコーパス: C. difficile

1 ortant factor in the host immune response to C. difficile.

2 rategies to counter antibiotic resistance of C. difficile.

3 dy the pathogenesis of the obligate anaerobe C. difficile.

4 n Rag1(-/-) mice increased susceptibility to C. difficile.

5 cture observed in HIOs colonized with viable C. difficile.

6 tional potentially virulent organisms beyond C. difficile.

7 coded and phase-variable antiphage system in C. difficile.

8 a critical role for ILC1s in defense against C. difficile.

9 rotein CwpV provides antiphage protection in C. difficile.

10 t increase the adherence and colonization of C. difficile.

11 changes and lead to varied susceptibility to C. difficile.

12 ed by asymptomatic colonization by toxigenic C. difficile.

13 -)) mice (which additionally lack ILCs) with C. difficile.

14 veloped a CRISPR-Cas9 mutagenesis system for C. difficile.

15 oviding evidence for an endogenous source of C. difficile.

16 zed patients with diarrhea were cultured for C. difficile.

17 Epidemic C. difficile 027/ST1 caused the majority of infections d

18 infected hospital patients from the epidemic C. difficile 027/ST1 lineage, and to distinguish between

19 mperature sensitivity, grew more slowly than C. difficile 630 Deltaerm and was less thermotolerant.

20 an insertional mutation in the dnaK gene of C. difficile 630 Deltaerm.

21 Cefoperazone-treated mice were infected with C. difficile 630 spores and treated with vancomycin afte

22 or putative c-di-GMP metabolism proteins in C. difficile 630.

23 of the prior room occupant increase risk for C. difficile acquisition while antibiotic exposure, gast

24 e interval [CI], 1.15-1.18) and incidence of C. difficile (adjusted odds ratio, 1.42; 95% CI, 1.09-1.

25 sirable properties for repositioning as anti-C. difficile agents.

26 Although the C. difficile Alr2 racemase is the sixth most highly expr

27 typic and genotypic resistance mechanisms in C. difficile and addresses susceptibility test methods a

28 provided fecal samples to assess killing of C. difficile and changes to components of the microbiome

29 of FMT immediately after vancomycin cleared C. difficile and decreased cytotoxicity within 1 week.

30 for the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism by which this b

31 , many of these factors are not conserved in C. difficile and few novel factors have been identified.

32 lprotectin has antimicrobial effects against C. difficile and is an essential component of the innate

33 iverse organisms--the eubacteria E. coli and C. difficile and the archeon H. volcanii--could be align

34 ts have shown antimicrobial activity against C. difficile and toxin A/B neutralization capacity in vi

35 itive, 866 of 1447 (60%) contained toxigenic C. difficile, and fecal toxin was detected in 511 of 866

36 d persistently colonized with high levels of C. difficile, and the gut microbiota in these mice persi

37 atural design of human microbiome evasion of C. difficile, and this method may provide a prototypic p

38 Several important mechanisms for C. difficile antibiotic resistance have been described,

39 onse to the increasing medical burden, a new C. difficile antibiotic, fidaxomicin, was approved in 20

40 The two main virulence factors of C. difficile are the large toxins, TcdA and TcdB, which

41 Extraintestinal manifestations of C. difficile are uncommon and rarely reported.

42 otics reduce colonization resistance against C. difficile are unknown yet important for development o

43 tools for research, diagnosis and therapy of C. difficile associated disease.

44 patial and temporal inflammatory patterns of C. difficile-associated colitis.

45 rity of intestinal inflammation in mice with C. difficile-associated colitis.

46 n, was approved in 2011 for the treatment of C. difficile-associated diarrhea.

47 cile, excess dietary Zn severely exacerbated C. difficile-associated disease by increasing toxin acti

48 With limited treatment options, the rise of C. difficile-associated disease has spurred on the searc

49 require antibiotics and tested negative for C. difficile at 8 weeks; thus, 96.7% (29 of 30) achieved

50 ex case with CDI were screened for toxigenic C. difficile by culturing rectal swabs.

51 of 683 subjects were positive for toxigenic C. difficile by direct toxigenic culture, and 141 of 682

52 ool samples (n = 312) positive for toxigenic C. difficile by the GeneXpert C. difficile/Epi tcdB PCR

53 n CD0386 is anchored to the peptidoglycan of C. difficile by the sortase SrtB and that an SPKTG pepti

54 Stool was tested for C. difficile by toxin enzyme immunoassay (EIA) and toxig

55 m difficile infection (CDI) and asymptomatic C. difficile carriage, the diagnostic predictive value o

56 Importation of C. difficile cases (acute care: patients with recent lon

57 Importation of acute care C. difficile cases was a greater concern for long-term c

58 d prevention efforts to reduce the spread of C. difficile, CDI remains a significant challenge to hea

59 The interactions between C. difficile cells and other bacteria and with host muco

60 ing is an effective tool for verification of C. difficile clinical testing criteria and safe reductio

61 Vancomycin treatment suppressed both C. difficile colonization and cytotoxin titers.

62 iming and location of the events surrounding C. difficile colonization and identifies potential targe

63 al reasons, including the high prevalence of C. difficile colonization and the inability of hospitals

64 reuteri with glycerol was effective against C. difficile colonization in complex human fecal microbi

65 After inducing susceptibility to C. difficile colonization via antibiotic administration,

66 In use, contact plates failed to detect C. difficile contamination (0/96 contact plates; 4 case

67 ling with a contact plate may fail to detect C. difficile contamination and result in false-negative

68 ination, and contact plates failed to detect C. difficile contamination below a detection limit of 10

69 ed the rapid and quantitative measurement of C. difficile contamination on surfaces with a sensitivit

70 a novel rapid method to detect and quantify C. difficile contamination on surfaces.

71 ative bacterial cultures showed a mean log10 C. difficile count (colony-forming units [CFU]) of 6.7 +

72 ereas metronidazole was associated with mean C. difficile counts 1.5-2 log10 higher at 10 days of tre

73 However, C. difficile counts increased within 7 days of completin

74 y; vancomycin treatment consistently reduced C. difficile counts to the limit of detection (2.0 log10

75 w therapy for prevention and amelioration of C. difficile disease.

76 tailed study shows that the SrtB enzyme from C. difficile does not play an essential role in pathogen

77 cy analysis was performed by using the Xpert C. difficile Epi test.

78 The Xpert C. difficile/Epi assay allows rapid, presumptive identif

79 for toxigenic C. difficile by the GeneXpert C. difficile/Epi tcdB PCR assay were tested with the rap

80 r retested samples from a second NAAT (Xpert C. difficile/Epi test; Cepheid, Sunnyvale, CA) found no

81 We compared Xpert C. difficile/Epi to multilocus sequence typing for ident

82 How C. difficile establishes initial colonisation of the hos

83 In mice colonized with C. difficile, excess dietary Zn severely exacerbated C.

84 Reservoirs of C. difficile extended to beyond the areas near the patie

85 inding and autoadenylylation activity of the C. difficile Fic domain protein are independent of the i

86 has been increased research into the role of C. difficile flagella in colonisation and adherence.

87 es on new insights into the specific role of C. difficile flagella in colonisation and toxin gene exp

88 hese results highlight the important role of C. difficile flagella in eliciting mucosal lesions as lo

89 The C. difficile flagella, which confer motility and chemota

90 ly correlated with the relative abundance of C. difficile from 16S rRNA gene sequencing (r(2) = -0.60

91 4 case wards), while sponge swabs recovered C. difficile from 29% (87/301) of the surfaces tested in

92 ficacy of each technique for the recovery of C. difficile from sites in the clinical environment that

93 ptimized method for the simple extraction of C. difficile gDNA using the QIAamp DNA minikit, which yi

94 introduces site-specific mutations into the C. difficile genome (20-50% mutation frequency).

95 e rapid and efficient modifications into the C. difficile genome.

96 C. difficile genotypes were determined by multilocus seq

97 The Vidas C. difficile glutamate dehydrogenase assay had performan

98 producers, with L. reuteri 17938 inhibiting C. difficile growth at a level on par with the level of

99 silico and validated some of them by testing C. difficile growth in the presence of various sulfur so

100 The anthelmintics broadly inhibited C. difficile growth in vitro via a membrane depolarizati

101 l, that B. intestinihominis can in fact slow C. difficile growth.

102 oratory data, and the detection of toxigenic C. difficile in stool does not necessarily confirm the d

103 addition to sensitively detecting toxigenic C. difficile in stool, on-demand PCR may also be used to

104 hogenesis; however, the survival strategy of C. difficile in the challenging gut environment still re

105 n addition to the infection due to toxigenic C. difficile in the gastrointestinal tract of susceptibl

106 ammatory response, which are associated with C. difficile in these models, including in mice challeng

107 sought to obtain a comprehensive picture of C. difficile incidence and risk factors in acute and lon

108 ncidence, with a 1% increase in a facility's C. difficile incidence being associated with a 0.53% inc

109 ce being associated with a 0.53% increase in C. difficile incidence of neighboring facilities.

110 he association between network structure and C. difficile incidence, with a 1% increase in a facility

111 level of intestinal mucosa is a hallmark of C. difficile-induced infections, we propose that the pan

112 correlation between pretest probability for C. difficile infection (CDI) and assay results.

113 35 isolates from hospitalized patients with C. difficile infection (CDI) and two environmental ward

114 ptible hosts, other predisposing factors for C. difficile infection (CDI) are identified, including a

115 truction and inflammation which characterize C. difficile infection (CDI) are primarily due to the Rh

116 ncidence, severity and costs associated with C. difficile infection (CDI) have increased dramatically

117 in infants is unclear, and the existence of C. difficile infection (CDI) in this population is contr

118 ain BI/NAP1/027 is associated with increased C. difficile infection (CDI) rates and severity, and the

119 The pathogenesis of C. difficile infection (CDI) results from the interactio

120 The continued increase in C. difficile infection (CDI) suggests that it has surpas

121 spores greatly contributes to the spread of C. difficile infection (CDI), and the resistance of spor

122 izing antitoxin antibodies are protective in C. difficile infection (CDI), as demonstrated, in part,

123 ence of facility-onset laboratory-identified C. difficile infection (CDI), defined as a person with a

124 iagnosis and, potentially, for management of C. difficile infection (CDI).

125 Ms was associated with a marked reduction of C. difficile infection (CDI).

126 specimens from patients suspected of having C. difficile infection (CDI).

127 esponsible for the pathology associated with C. difficile infection (CDI).

128 as in the United States to identify cases of C. difficile infection (stool specimens positive for C.

129 prolonged loss of colonization resistance to C. difficile infection and dense colonization by vancomy

130 mics of clindamycin antibiotic treatment and C. difficile infection and predicts therapeutic probioti

131 ch intestinal bacteria provide resistance to C. difficile infection and their in vivo inhibitory mech

132 bacterium, is associated with resistance to C. difficile infection and, upon administration, enhance

133 vancomycin exposure and reduced the odds of C. difficile infection by >95%.

134 sociated with in vitro and in vivo models of C. difficile infection for drug screening and lead optim

135 We monitored patients with C. difficile infection in a UK hospital over a 2-year pe

136 function have been shown to protect against C. difficile infection in animal models and reduce recur

137 nd administration of these agents to prevent C. difficile infection in high-risk patients, although n

138 nteric pathogens; however, their role during C. difficile infection is undefined.

139 However, bringing a new treatment for C. difficile infection to market involves particular cha

140 The estimated number of first recurrences of C. difficile infection was 83,000 (95% CI, 57,000 to 108

141 The incidence of C. difficile infection was significantly lower in patien

142 A total of 15,461 cases of C. difficile infection were identified in the 10 geograp

143 As an alternative approach to controlling C. difficile infection, a series of bile acid derivative

144 Metronidazole or oral vancomycin can cure C. difficile infection, and administration of these agen

145 In a sample of cases of C. difficile infection, specimens were cultured and isol

146 In an animal model for C. difficile infection, the SrtB mutant caused disease a

147 y immune pathways that mediate recovery from C. difficile infection, we challenged C57BL/6, Rag1(-/-)

148 factor that causes diseases associated with C. difficile infection.

149 e prevention of TcdB-induced cytotoxicity in C. difficile infection.

150 applications for treatment and prevention of C. difficile infection.

151 and therapeutics for individuals at risk of C. difficile infection.

152 ILC1- or ILC3-associated proteins following C. difficile infection.

153 rapeutic probiotic interventions to suppress C. difficile infection.

154 reatment antibiotics and drastically reduced C. difficile infection.

155 rotective against enteric infections besides C. difficile infection.

156 deaths within 30 days after the diagnosis of C. difficile infection.

157 n their network position, detects 80% of the C. difficile infections using only 2% of hospitals as se

158 The burden of C. difficile infections was exacerbated with the outbrea

159 No Clostridium difficile colonization or C. difficile infections were reported.

160 ol samples from a patient with two recurrent C. difficile infections.

161 The regulatory pathways by which C. difficile initiates spore formation are poorly unders

162 The results revealed that C. difficile is present as a minority member of communit

163 Although C. difficile is strictly anaerobic, it survives in aerob

164 ) culture filtrates from a panel of clinical C. difficile isolates and (ii) 149 adult stool specimens

165 Although cultured C. difficile isolates can be reliably subtyped by variou

166 whole-genome sequencing (WGS) of consecutive C. difficile isolates from 6 English hospitals over 1 ye

167 en used to characterize tens of thousands of C. difficile isolates from cases of disease.

168 C. difficile isolates from these patients then were anal

169 e MIC values of the anthelmintics against 16 C. difficile isolates of defined PCR-ribotype.

170 Genotypic and phenotypic screening of C. difficile isolates revealed multiple PCR ribotypes pr

171 Here, we hypothesized that Alr2 could affect C. difficile l-alanine-induced spore germination in a de

172 ne of five clonal lineages of human virulent C. difficile, lacks TcdA expression but causes widesprea

173 B flagellin in the 023 and 027 hypervirulent C. difficile lineages by mutagenesis of five putative gl

174 at major impurities and variants of the anti-C. difficile mAb are degradation species of the heavy ch

175 Vegetative C. difficile, microinjected into the lumen of HIOs, pers

176 ved efficacious in murine sepsis and hamster C. difficile models of disease.

177 ilocus sequence typing for identification of C. difficile NAP1 and found "very good" agreement at 97.

178 allows rapid, presumptive identification of C. difficile NAP1.

179 samples identified by PCR and qPCR and five C. difficile-negative diarrhea controls were studied.

180 gies identified, consisting predominantly of C. difficile, norovirus, cytomegalovirus, and bacterial

181 cile infection (stool specimens positive for C. difficile on either toxin or molecular assay in resid

182 e in hospital length of stay, development of C. difficile, or total hospital cost.

183 During a C. difficile outbreak, a strain from this clade was foun

184 robial community that preferentially targets C. difficile outgrowth and toxicity, a finding consisten

185 tilization of specific probiotics to prevent C. difficile overgrowth (8/8); (4) staff education regar

186 Despite the importance of sporulation to C. difficile pathogenesis, the molecular mechanisms cont

187 We investigated the performance of the C. difficile PCR cycle threshold (CT ) for predicting fr

188 ll decrease of 19%, and reduced noncompliant C. difficile PCR orders (orders <7 days after a previous

189 ed in the transpeptidation reaction with the C. difficile peptidoglycan.

190 uccessfully treated case of catheter-related C. difficile peritonitis in a patient undergoing periton

191 In patients receiving tolevamer, C. difficile persisted in high counts during treatment;

192 Three patients with early, self-limiting C. difficile-positive diarrhea did not require antibioti

193 he primary efficacy end point was absence of C. difficile-positive diarrhea during an 8-week follow-u

194 Twenty-two C. difficile-positive diarrhea samples identified by PCR

195 C. difficile was detected in 90.9% of C. difficile-positive samples using 16S rRNA gene sequen

196 g, and C. difficile was detected in 86.3% of C. difficile-positive samples using MSS.

197 ymptomatic carriers or progression of latent C. difficile present on admission to active infection.

198 C. difficile produces two large toxins, TcdA and TcdB, w

199 On colonisation, C. difficile produces two toxins that lead to disease, w

200 Here we show C. difficile proteins CD2537 and CD3392 are functional s

201 We compared the Qiagen artus C. difficile QS-RGQ kit, a new nucleic acid amplificatio

202 gative predictive value for the Qiagen artus C. difficile QS-RGQ test were 100%, 89.5%, 60.9%, and 10

203 id or the chromosome of locked 'ON' cells of C. difficile R20291, CwpV conferred antiphage protection

204 -days) and explained 72% of the variation in C. difficile rates.

205 itors on ventilator-associated pneumonia and C. difficile remain unclear.

206 recovery of colonization resistance against C. difficile requires the restoration of a specific comm

207 he hypothesis that, in a mouse model of CDI, C. difficile resides in multicellular communities (biofi

208 that spoIIQ or spoIIIAH deletion mutants of C. difficile result in anomalous engulfment, and that di

209 with 869 episodes with diarrhea but negative C. difficile results.

210 indicated that the NAPCR1 variant belongs to C. difficile ribotype 012 and sequence type 54, as does

211 sampling to assess the in vitro recovery of C. difficile ribotype 027 contamination ( approximately

212 tative TcdA epitope sequences across several C. difficile ribotypes and homologous repeat sequences w

213 This study identified three sublineages of C. difficile RT017 that are circulating in London.

214 ct evenly split sublineages (SL1 and SL2) of C. difficile RT017 that contain multiple independent clo

215 dates in late-stage clinical development for C. difficile, S. aureus, and P. aeruginosa Basic, precli

216 f the sortase in the cell wall biogenesis, a C. difficile sortase knockout strain was constructed by

217 rt on the structural characterisation of the C. difficile sortase.

218 the sixth most highly expressed gene during C. difficile spore formation, a previous study reported

219 d 21b, was found to be a potent inhibitor of C. difficile spore germination and poorly permeable in a

220 C. difficile spore germination is triggered in response

221 eractions between gut microbial products and C. difficile spore germination, growth, and toxin produc

222 s, therapies that are more effective against C. difficile spores and less damaging to the resident ga

223 These results suggest that C. difficile spores can respond to a diverse set of amin

224 Persistence of C. difficile spores greatly contributes to the spread of

225 Alr2 has little to no role in germination of C. difficile spores in rich medium.

226 Current methods to detect C. difficile spores on surfaces are not quantitative, la

227 C. difficile spores were able to germinate within 6 h po

228 ated ( approximately 1.34 +/- 6.88 CFU/cm(2) C. difficile spores).

229 CDI initiates with ingestion of C. difficile spores, germination in the gastrointestinal

230 ol the adherence of the CotB coat protein to C. difficile spores, indicating that these proteins regu

231 t l- and d-serine are also co-germinants for C. difficile spores.

232 These results provide further evidence that C. difficile sporulation is regulated differently from t

233 requirement for SpoIIID and sigma(K) during C. difficile sporulation, we analyzed spoIIID and sigK m

234 tic exposure of the prior room occupant, and C. difficile status of the prior room occupant increase

235 to investigate the role of selenoproteins in C. difficile Stickland metabolism and found that a Targe

236 onstructed the sulfur metabolism pathways of C. difficile strain 630 in silico and validated some of

237 rs in protected animals when challenged with C. difficile strain 630.

238 ium difficile 027/NAP1/BI is the most common C. difficile strain in the United States.

239 Nontoxigenic C. difficile strain M3 colonized the gastrointestinal tr

240 study defines the dynamics of infection with C. difficile strain VPI 10463 throughout the gastrointes

241 Therefore, CTD from different C. difficile strains may be a good immunogen for stimula

242 r biological roles in emerging hypervirulent C. difficile strains.

243 differential virulence potential seen among C. difficile strains.

244 of neutralizing TcdB from a diverse array of C. difficile strains.

245 30 June 2016 on consecutive inpatients with C. difficile test orders at an academic hospital.

246 rvention, 7.1% (164) and 9.1% (211) of 2,321 C. difficile test orders were canceled due to absence of

247 C. difficile test utilization decreased upon implementat

248 Outcome measures included C. difficile test utilization, HO-CDI incidence, oral va

249 %, and 100%, and those for the Cepheid Xpert C. difficile test were 100%, 90%, 62.2%, and 100%, respe

250 n (CDI), defined as a person with a positive C. difficile test without a positive test in the prior 8

251 s in stool specimens, with the Cepheid Xpert C. difficile test.

252 r CDI should be considered prior to ordering C. difficile testing and must be taken into account when

253 clinical bioinformatics resources to prevent C. difficile testing of stools from patients without cli

254 II Fic domain protein in the human pathogen C. difficile that is not regulated by autoinhibition and

255 rulent strains of the human enteric pathogen C. difficile, the most serious cause of antibiotic-assoc

256 the vegetative cell surface or spore coat of C. difficile These include two dehydrogenases, AdhE1 and

257 ation also significantly reduces adhesion of C. difficile to Caco-2 intestinal epithelial cells but d

258 gut microbiota by antibiotic therapy allows C. difficile to colonise the colon.

259 s spores were able to reduce the adhesion of C. difficile to mucus-producing intestinal cells.

260 in these communities modulate the ability of C. difficile to successfully colonize and, thereby, caus

261 munoglobulin A, and immunoglobulin G against C. difficile toxin A were depressed in aged mice, and va

262 ng a carboxy-terminal segment (TcdA26-39) of C. difficile toxin A, no colonization occurs in protecte

263 xumab, a human monoclonal antibody, binds to C. difficile toxin B (TcdB), reducing recurrence presuma

264 Our study reveals a unique mechanism of C. difficile toxin neutralization by a monoclonal antibo

265 ntitative bacterial cultures, measurement of C. difficile toxin titers, quantitative polymerase chain

266 CDT, the third C. difficile toxin, is a binary actin-ADP-ribosylating t

267 d levels of select intestinal microbiota and C. difficile toxin.

268 The pathogen produces three protein toxins: C. difficile toxins A (TcdA) and B (TcdB), and C. diffic

269 ase 2 trial testing monoclonal antibodies to C. difficile toxins A and B for preventing CDI recurrenc

270 The C. difficile toxins contribute directly to CDI-associate

271 s, but expression of a third toxin, known as C. difficile transferase (CDT), is increasingly common.

272 difficile toxins A (TcdA) and B (TcdB), and C. difficile transferase toxin (CDT).

273 rveillance tool to identify varying rates of C. difficile transmission between institutions and there

274 symptomatic TS+/FT- and TS+/FT+ patients in C. difficile transmission in 2 UK regions.

275 ymptomatic TS+/FT- patients were a source of C. difficile transmission, although they accounted for l

276 center, subjects enrolled into phase 2 and 3 C. difficile treatment clinical trials (2003-2008) provi

277 The most popular C. difficile-typing technique is PCR ribotyping, and we

278 and/or oral vancomycin on susceptibility to C. difficile, vancomycin-resistant Enterococcus, carbape

279 This C. difficile variant elicited higher white blood cell co

280 at the pathogenic potential of this emerging C. difficile variant is due to the acquisition of hypoth

281 lucidated a more complex role of flagella in C. difficile virulence pertaining to the regulation of t

282 Upon colonization with C. difficile VPI 10463, the HIO epithelium is markedly d

283 Optimal efficacy in the hamster model of C. difficile was achieved with compounds that possessed

284 C. difficile was codetected with Clostridium perfringens

285 Toxigenic C. difficile was detected in 6.0% (27/451) after a media

286 samples using 16S rRNA gene sequencing, and C. difficile was detected in 86.3% of C. difficile-posit

287 C. difficile was detected in 90.9% of C. difficile-posit

288 mission was defined as possible if toxigenic C. difficile was detected in contacts, as probable if th

289 C. difficile was identified in 4.1% pantoprazole patient

290 C. difficile was isolated from stool samples from a pati

291 C. difficile was isolated from stool specimens in 432 (1

292 C. difficile was present on floors in approximately 90%

293 C. difficile was responsible for almost half a million i

294 of toxigenic, predominantly nonhypervirulent C. difficile, was low and no outbreaks were recorded ove

295 ns from a number of hypervirulent strains of C. difficile We used mass spectrometry (nano-LC-MS and M

296 ithin mucus-associated communities harboring C. difficile, we characterized bacterial populations in

297 Patients with testing ordered for C. difficile were enrolled and assigned a high, medium,

298 detes, Clostridium clusters XIVa and IV, and C. difficile were performed.

299 l samples with a positive initial screen for C. difficile were sequenced.

300 ing to monitor the persistence and spread of C. difficile within healthcare facilities could inform i