ライフサイエンスコーパス: difficile

1 patients with diarrhea were cultured for C. difficile.

2 egies to counter antibiotic resistance of C. difficile.

3 eptibility to pathogens, such as Clostridium difficile.

4 athogens, Bacillus anthracis and Clostridium difficile.

5 ant factor in the host immune response to C. difficile.

6 LFAs for influenza, malaria, and Clostridium difficile.

7 la, and the potential pathobiont Clostridium difficile.

8 additive effect on the risk of contracting C difficile.

9 oped a CRISPR-Cas9 mutagenesis system for C. difficile.

10 ding evidence for an endogenous source of C. difficile.

11 Quality control ranges for Clostridium difficile (0.12 to 1 mug/ml) and Eggerthella lenta (brot

12 ected hospital patients from the epidemic C. difficile 027/ST1 lineage, and to distinguish between th

13 rature sensitivity, grew more slowly than C. difficile 630 Deltaerm and was less thermotolerant.

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

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

16 the prior room occupant increase risk for C. difficile acquisition while antibiotic exposure, gastric

17 nterval [CI], 1.15-1.18) and incidence of C. difficile (adjusted odds ratio, 1.42; 95% CI, 1.09-1.85)

18 able properties for repositioning as anti-C. difficile agents.

19 Although the C. difficile Alr2 racemase is the sixth most highly express

20 ic and genotypic resistance mechanisms in C. difficile and addresses susceptibility test methods and

21 ts, investigating infection with Clostridium difficile and an immune-modulatory probiotic.

22 oduced by the bacterial pathogen Clostridium difficile and are responsible for the pathology associat

23 the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism by which this bina

24 hospitalized patients tested for Clostridium difficile and determine the correlation between pretest

25 the CD27L endolysin that targets Clostridium difficile and the CS74L endolysin that targets Clostridi

26 f proton pump inhibitor use with Clostridium difficile and ventilator-associated pneumonia have raise

27 ve, 866 of 1447 (60%) contained toxigenic C. difficile, and fecal toxin was detected in 511 of 866 (5

28 aureus, vancomycin-resistant enterococci, C difficile, and multidrug-resistant Acinetobacter.

29 ral design of human microbiome evasion of C. difficile, and this method may provide a prototypic prec

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

31 e, excess dietary Zn severely exacerbated C. difficile-associated disease by increasing toxin activit

32 th limited treatment options, the rise of C. difficile-associated disease has spurred on the search f

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

34 683 subjects were positive for toxigenic C. difficile by direct toxigenic culture, and 141 of 682 su

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

36 Stool was tested for C. difficile by toxin enzyme immunoassay (EIA) and toxigeni

37 In the intestinal pathogen Clostridium difficile, c-di-GMP inhibits flagellar motility and toxi

38 Asymptomatic carriers of C difficile can spread their infection to other patients.

39 ifficile infection (CDI) and asymptomatic C. difficile carriage, the diagnostic predictive value of N

40 Importation of C. difficile cases (acute care: patients with recent long-t

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

42 is an effective tool for verification of C. difficile clinical testing criteria and safe reduction o

43 reasons, including the high prevalence of C. difficile colonization and the inability of hospitals to

44 uteri with glycerol was effective against C. difficile colonization in complex human fecal microbial

45 The diarrheal pathogen Clostridium difficile consists of at least six distinct evolutionary

46 Regionally, C difficile decline was driven by elimination of fluoroqui

47 the HIV-1-derived Gag Ag or the Clostridium difficile-derived toxin B resulted in significant inhibi

48 There is no stand-alone Clostridium difficile diagnostic that can sensitively and rapidly de

49 herapy for prevention and amelioration of C. difficile disease.

50 s may cause diarrhoea, including Clostridium difficile, drugs (e.g. laxatives, antibiotics) and enter

51 ot reported at this institution (Clostridium difficile, enteroaggregative Escherichia coli, enteropat

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

53 r toxigenic C. difficile by the GeneXpert C. difficile/Epi tcdB PCR assay were tested with the rapid

54 etested samples from a second NAAT (Xpert C. difficile/Epi test; Cepheid, Sunnyvale, CA) found no fal

55 We compared Xpert C. difficile/Epi to multilocus sequence typing for identifi

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

57 ing and autoadenylylation activity of the C. difficile Fic domain protein are independent of the inhi

58 e results highlight the important role of C. difficile flagella in eliciting mucosal lesions as long

59 The C. difficile flagella, which confer motility and chemotaxis

60 ecting ultraviolet [UV-C] light except for C difficile, for which bleach and UV-C were used); bleach;

61 uaternary ammonium disinfectant except for C difficile, for which bleach was used); UV (quaternary am

62 ultidrug-resistant organisms and Clostridium difficile from inadequately disinfected environmental su

63 s for the detection of toxigenic Clostridium difficile from unformed (liquid or soft) stool samples.

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

65 apid and efficient modifications into the C. difficile genome.

66 C. difficile genotypes were determined by multilocus sequen

67 oducers, with L. reuteri 17938 inhibiting C. difficile growth at a level on par with the level of gro

68 The anthelmintics broadly inhibited C. difficile growth in vitro via a membrane depolarization

69 Clostridium difficile has become one of the most common bacterial pa

70 Unlike in B. subtilis, SpoIIQ of Clostridium difficile has intact LytM zinc-binding motifs.

71 mic shotgun sequencing (MSS) for Clostridium difficile identification in diarrhea stool samples.

72 The incidence of C difficile in England declined by roughly 80% after 2006,

73 nd that asymptomatic carriers of toxigenic C difficile in hospitals increase risk of infection in oth

74 ewardship may help reduce the incidence of C difficile in long-term care settings.

75 tory data, and the detection of toxigenic C. difficile in stool does not necessarily confirm the diag

76 dition to sensitively detecting toxigenic C. difficile in stool, on-demand PCR may also be used to ac

77 enesis; however, the survival strategy of C. difficile in the challenging gut environment still remai

78 mark, screening all patients for toxigenic C difficile in the intestine upon admittance, from October

79 t of recurrent infections (i.e., Clostridium difficile) in the human gut and as a general research to

80 Long-term care C difficile incidence (minimum, 0.6 case per 10 000 reside

81 unted for 75% of the regional variation in C difficile incidence (R2 = 0.75).

82 Drivers of differences in Clostridium difficile incidence across acute and long-term care faci

83 ught to obtain a comprehensive picture of C. difficile incidence and risk factors in acute and long-t

84 dence, with a 1% increase in a facility's C. difficile incidence being associated with a 0.53% increa

85 Only 25% of the variation in regional C difficile incidence in long-term care remained unexplain

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

87 6 in all criteria: 2 measures of Clostridium difficile incidence, incidence of drug-resistant pathoge

88 association between network structure and C. difficile incidence, with a 1% increase in a facility's

89 Network-matched C difficile-infected controls without arthritis were rando

90 rrelation between pretest probability for C. difficile infection (CDI) and assay results.

91 tests (NAATs) do not distinguish Clostridium difficile infection (CDI) and asymptomatic C. difficile

92 ction and inflammation which characterize C. difficile infection (CDI) are primarily due to the Rho-g

93 hat most cases of hospital-onset Clostridium difficile infection (CDI) are unrelated to other cases o

94 Little is known about pediatric Clostridium difficile infection (CDI) epidemiology.

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

96 factors for and transmission of Clostridium difficile infection (CDI) in China have been reported.

97 Clostridium difficile infection (CDI) is a frequent complication in

98 Clostridium difficile infection (CDI) is an important hospital-acqui

99 Clostridium difficile infection (CDI) is common after liver transpla

100 Clostridium difficile infection (CDI) is facilitated by alteration o

101 Managing recurrent Clostridium difficile infection (CDI) presents a significant challen

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

103 Variation in Clostridium difficile infection (CDI) rates between healthcare insti

104 Clostridium difficile infection (CDI) represents an important exampl

105 cacy of probiotics in preventing Clostridium difficile infection (CDI), but guidelines do not recomme

106 romising treatment for recurrent Clostridium difficile infection (CDI), but its true effectiveness re

107 e of facility-onset laboratory-identified C. difficile infection (CDI), defined as a person with a po

108 Clostridium difficile infection (CDI), the most common health care-a

109 ng acute kidney injury (AKI) and Clostridium difficile infection (CDI), were also considered.

110 t on the laboratory diagnosis of Clostridium difficile infection (CDI).

111 ecimens from patients suspected of having C. difficile infection (CDI).

112 ts of dietary supplementation on Clostridium difficile infection (CDI).

113 onsible for the pathology associated with C. difficile infection (CDI).

114 United States for patients with Clostridium difficile infection (CDI).

115 important for protection against Clostridium difficile infection (CDI).

116 nosis and, potentially, for management of C. difficile infection (CDI).

117 effective therapy for recurrent Clostridium difficile infection (CDI).

118 health care facility-associated Clostridium difficile infection (HO-CDI) is overdiagnosed for severa

119 AZO) shortage and hospital-onset Clostridium difficile infection (HO-CDI) risk in 88 US medical cente

120 Recurrent Clostridium difficile infection (RCDI) is associated with repeated a

121 Clostridium difficile infection after LT was associated with higher

122 we identified 4885 cases of hospital-onset C difficile infection among 1 289 929 admissions to study

123 nd a further 1625 cases of community-onset C difficile infection among 455 508 adults registered in p

124 mong exposed patients and the incidence of C difficile infection among exposed patients in the intent

125 Similarly, the incidence of C difficile infection among exposed patients was not chang

126 Participants with signs and symptoms of C difficile infection and a positive diagnostic test resul

127 The odds of C difficile infection and epinephrine administration were

128 Although all cases had community-onset C difficile infection and fewer comorbidities, they were m

129 at shows potential in treatment of initial C difficile infection and in providing sustained benefit t

130 lts aged 60 years and older with confirmed C difficile infection at 86 European hospitals.

131 erved in subjects with recurrent Clostridium difficile infection but is observed in the same set of s

132 ncomycin exposure and reduced the odds of C. difficile infection by >95%.

133 Clostridium difficile infection causes severe complications and freq

134 population comprising all individuals with C difficile infection confirmed by the presence of free to

135 ewardship should be a central component of C difficile infection control programmes.

136 First, if C difficile infection declines in England were driven by r

137 Second, if C difficile infection declines were driven by improvements

138 The incidence of Clostridium difficile infection has increased among children.

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

140 nction have been shown to protect against C. difficile infection in animal models and reduce recurren

141 The primary outcomes were rate of C difficile infection in exposed and unexposed patients an

142 Clostridium difficile infection in LT recipients was associated with

143 The detection and diagnosis of Clostridium difficile infection in pediatric populations have some u

144 Clostridium difficile infection is a growing problem in healthcare s

145 Clostridium difficile infection is the leading cause of hospital-acq

146 Clostridium difficile infection is the leading cause of hospital-acq

147 Clostridium difficile infection is the most common health-care-assoc

148 Clostridium difficile infection occurred in 27 (14%) of 192 patients

149 ears vs <75 years), and number of previous C difficile infection occurrences.

150 nd addressed the use of FMTs for Clostridium difficile infection or inflammatory bowel disease, and m

151 rimary outcomes were prevalence density of C difficile infection per 1000 occupied bed-days in hospit

152 Hospital-onset C difficile infection prevalence densities were associated

153 red with predictions without intervention, C difficile infection prevalence density fell by 68% (mean

154 Community-onset C difficile infection prevalence density was predicted by

155 e density was predicted by recent hospital C difficile infection rates, introduction of mandatory sur

156 aily on days 1-10), stratified by baseline C difficile infection severity, cancer presence, age (>/=7

157 any antibiotics increase risk of Clostridium difficile infection through dysbiosis, epidemic C diffic

158 C difficile infection was detected in 2.6% of patients not

159 The incidence of C. difficile infection was significantly lower in patients

160 9 subjects treated for recurrent Clostridium difficile infection with fecal microbiota transplantatio

161 e arthritis affected 1.4% of children with C difficile infection yearly (95% CI 0.8%-2.3%).

162 As an alternative approach to controlling C. difficile infection, a series of bile acid derivatives h

163 s (antibiotic-days, incidence of Clostridium difficile infection, and in-hospital mortality).

164 dard-dose vancomycin for sustained cure of C difficile infection, and, to our knowledge, extended-pul

165 Amount of exposure correlated with risk of C difficile infection, from 2.2% in the lowest quartile to

166 infection, acute kidney injury, Clostridium difficile infection, or drug-related adverse reactions r

167 uency of complications including Clostridium difficile infection, readmission, and all-cause mortalit

168 nexpensive therapy for recurrent Clostridium difficile infection, yet its safety is thought to depend

169 The epidemiology of pediatric C difficile infection-associated reactive arthritis is poo

170 Incidence of C difficile infection-associated reactive arthritis was ca

171 Only 35% of cases of C difficile infection-associated reactive arthritis were c

172 icin are therapies of choice for Clostridium difficile infection.

173 clinical trial of antibiotic treatment for C difficile infection.

174 ilazole versus vancomycin for treatment of C difficile infection.

175 moting antibiotic resistance and Clostridium difficile infection.

176 ic source population and (2) children with C difficile infection.

177 tment antibiotics and drastically reduced C. difficile infection.

178 valuable patients with recurrent Clostridium difficile infection.

179 BACKGROUND & AIMS: Studies of Clostridium difficile infections (CDIs) among individuals with infla

180 ribing correlated highly with incidence of C difficile infections (cross-correlations >0.88), by cont

181 UK) and national data for the incidence of C difficile infections and antimicrobial prescribing data

182 ical determinants of clinical burdens from C difficile infections and ribotype distributions in a hea

183 a transplantation to face severe Clostridium difficile infections and to perform decolonization of pa

184 The incidence of C difficile infections caused by fluoroquinolone-resistant

185 C difficile infections caused by fluoroquinolone-resistant

186 particular antibiotics, then incidence of C difficile infections caused by resistant isolates should

187 strategies for the treatment of Clostridium difficile infections disrupt indigenous microbiota and c

188 ociated with substantial declines in total C difficile infections in northeast Scotland.

189 ociated with substantial declines in total C difficile infections in northeast Scotland.

190 the clinical and molecular epidemiology of C difficile infections in northeast Scotland.

191 The control of Clostridium difficile infections is an international clinical challe

192 heir network position, detects 80% of the C. difficile infections using only 2% of hospitals as senso

193 The burden of C. difficile infections was exacerbated with the outbreak o

194 ars to explain the decline in incidence of C difficile infections, above other measures, in Oxfordshi

195 ocomial infections, 1000 to 5000 Clostridium difficile infections, and 2 to 6 cases of anaphylaxis an

196 omly selected at the time of cohort member C difficile infections.

197 cts of asymptomatic carriers on nosocomial C difficile infections.

198 Clostridium difficile is a clinically significant pathogen that caus

199 Clostridium difficile is a gastrointestinal pathogen but how the bac

200 Clostridium difficile is a major nosocomial pathogen that produces t

201 antibiotic-associated diarrhea, Clostridium difficile is a serious problem in health care facilities

202 Clostridium difficile is a significant concern as a nosocomial patho

203 egative (FT-) in transmission of Clostridium difficile is currently unknown.

204 The pathogenicity of Clostridium difficile is linked to its ability to produce two toxins

205 Although C. difficile is strictly anaerobic, it survives in aerobic

206 Clostridium difficile is the cause of antibiotics-associated diarrhe

207 Clostridium difficile is the most common hospital acquired pathogen

208 Clostridium difficile is the most commonly reported nosocomial patho

209 Clostridium difficile is the most important enteropathogen involved

210 Clostridium difficile is the principal cause of nosocomial infectiou

211 Clostridium difficile (Peptoclostridium difficile) is a common health care-associated infection

212 Although cultured C. difficile isolates can be reliably subtyped by various m

213 le-genome sequencing (WGS) of consecutive C. difficile isolates from 6 English hospitals over 1 year

214 C. difficile isolates from these patients then were analyze

215 IC values of the anthelmintics against 16 C. difficile isolates of defined PCR-ribotype.

216 ences from 4045 national and international C difficile isolates.

217 e, we hypothesized that Alr2 could affect C. difficile l-alanine-induced spore germination in a defin

218 alth service and predisposing to Clostridium difficile, methicillin-resistant Staphylococcus aureus i

219 cus sequence typing for identification of C. difficile NAP1 and found "very good" agreement at 97.9%

220 mples identified by PCR and qPCR and five C. difficile-negative diarrhea controls were studied.

221 c neurons of human patients with Clostridium difficile or ulcerative colitis.

222 During a C. difficile outbreak, a strain from this clade was found t

223 ial community that preferentially targets C. difficile outgrowth and toxicity, a finding consistent w

224 Despite the importance of sporulation to C. difficile pathogenesis, the molecular mechanisms control

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

226 Clostridium difficile PCR ribotype 265 (toxin A negative, B positive

227 Clostridium difficile (Peptoclostridium difficile) is a common healt

228 primary efficacy end point was absence of C. difficile-positive diarrhea during an 8-week follow-up p

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

230 AIMS: Nosocomial infections with Clostridium difficile present a considerable problem despite numerou

231 tomatic carriers or progression of latent C. difficile present on admission to active infection.

232 C. difficile produces two large toxins, TcdA and TcdB, whic

233 Here we show C. difficile proteins CD2537 and CD3392 are functional subs

234 ys) and explained 72% of the variation in C. difficile rates.

235 rs on ventilator-associated pneumonia and C. difficile remain unclear.

236 at spoIIQ or spoIIIAH deletion mutants of C. difficile result in anomalous engulfment, and that disru

237 h 869 episodes with diarrhea but negative C. difficile results.

238 ive TcdA epitope sequences across several C. difficile ribotypes and homologous repeat sequences with

239 cile infection through dysbiosis, epidemic C difficile ribotypes characterised by multidrug resistanc

240 evenly split sublineages (SL1 and SL2) of C. difficile RT017 that contain multiple independent clonal

241 es in late-stage clinical development for C. difficile, S. aureus, and P. aeruginosa Basic, preclinic

242 everal potential pathogens (e.g. Clostridium difficile, Salmonella, and Escherichia coli) that do not

243 n led to resolution of recurrent Clostridium difficile, significantly decreased recurrent UTI frequen

244 h consequently enables toxigenic Clostridium difficile species to proliferate and cause infection.

245 e sixth most highly expressed gene during C. difficile spore formation, a previous study reported tha

246 1b, was found to be a potent inhibitor of C. difficile spore germination and poorly permeable in a Ca

247 C. difficile spore germination is triggered in response to

248 These results suggest that C. difficile spores can respond to a diverse set of amino a

249 2 has little to no role in germination of C. difficile spores in rich medium.

250 - and d-serine are also co-germinants for C. difficile spores.

251 HAIs), including those caused by Clostridium difficile, Staphylococcus aureus, Pseudomonas aeruginosa

252 exposure of the prior room occupant, and C. difficile status of the prior room occupant increase ris

253 investigate the role of selenoproteins in C. difficile Stickland metabolism and found that a TargeTro

254 in protected animals when challenged with C. difficile strain 630.

255 Clostridium difficile strain BI/NAP1/027 is associated with increase

256 Clostridium difficile strains within the hypervirulent clade 2 are r

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

258 tate sustained clinical cure by prolonging C difficile suppression and supporting gut microbiota reco

259 nd a subfragment of toxin A from Clostridium difficile (TcdA-A2).

260 Clostridium difficile TcdB (2366 amino acid residues) is an intracel

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

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

263 C. difficile test utilization decreased upon implementation

264 Outcome measures included C. difficile test utilization, HO-CDI incidence, oral vanco

265 d as a positive result on a long-term care C difficile test without a positive result in the prior 8

266 CDI), defined as a person with a positive C. difficile test without a positive test in the prior 8 we

267 DI should be considered prior to ordering C. difficile testing and must be taken into account when in

268 nical bioinformatics resources to prevent C. difficile testing of stools from patients without clinic

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

270 entified from the human pathogen Clostridium difficile The crystal structure shows that the protein a

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

272 Efforts to control C difficile through antibiotic stewardship should account

273 on also significantly reduces adhesion of C. difficile to Caco-2 intestinal epithelial cells but does

274 pores were able to reduce the adhesion of C. difficile to mucus-producing intestinal cells.

275 eum, Salmonella typhimurium, and Clostridium difficile) to quantify, expand, and characterize microbe

276 oglobulin A, and immunoglobulin G against C. difficile toxin A were depressed in aged mice, and vanco

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

278 ab, a human monoclonal antibody, binds to C. difficile toxin B (TcdB), reducing recurrence presumably

279 Our study reveals a unique mechanism of C. difficile toxin neutralization by a monoclonal antibody,

280 Clostridium difficile toxin was subsequently detected in his stools,

281 CDT, the third C. difficile toxin, is a binary actin-ADP-ribosylating toxi

282 e pathogen produces three protein toxins: C. difficile toxins A (TcdA) and B (TcdB), and C. difficile

283 2 trial testing monoclonal antibodies to C. difficile toxins A and B for preventing CDI recurrence (

284 The C. difficile toxins contribute directly to CDI-associated l

285 itative methods for detection of Clostridium difficile toxins provide new tools for diagnosis and, po

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

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

288 illance tool to identify varying rates of C. difficile transmission between institutions and therefor

289 mptomatic TS+/FT- and TS+/FT+ patients in C. difficile transmission in 2 UK regions.

290 Accurate tracking of Clostridium difficile transmission within healthcare settings is key

291 tomatic TS+/FT- patients were a source of C. difficile transmission, although they accounted for less

292 Toxigenic C. difficile was detected in 6.0% (27/451) after a median c

293 sion was defined as possible if toxigenic C. difficile was detected in contacts, as probable if the i

294 C. difficile was identified in 4.1% pantoprazole patients a

295 C. difficile was isolated from stool specimens in 432 (10.9

296 toxigenic, predominantly nonhypervirulent C. difficile, was low and no outbreaks were recorded over a

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

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

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

300 such as Cryptosporidiumspp. and Clostridium difficile, were detected with the GPP.