ライフサイエンスコーパス: difficile

1 le, and therefore prevented the growth of C. difficile.

2 e loss of colonization resistance against C. difficile.

3 rategies, reflects the changing biology of C difficile.

4 nes determine vancomycin susceptibility in C difficile.

5 l infections, Pseudomonas infections, and C. difficile.

6 gies to target the most severe strains of C. difficile.

7 ow mucus-associated microbes interact with C difficile.

8 ther gut commensals did not aggregate with C difficile.

9 n Fusobacterium and removal of flagella on C difficile.

10 age and fermentation products produced by C. difficile.

11 are known to block the growth of Clostridium difficile(1), promote hepatocellular carcinoma(2) and mo

12 both) and outpatients (norovirus: 10.7%; C. difficile: 10.5%).

13 cted among inpatients (cases vs controls: C. difficile, 18.8% vs 8.4%; norovirus, 5.1% vs 1.5%; p<0.0

14 was highest among outpatients (AGE: 2715; C. difficile: 285; norovirus: 291) and inpatients >=65 year

15 (21.6% vs 4.5%), development of Clostridium difficile (4.5% vs 1.7%), and incidence density of venti

16 d by the FilmArray GI panel were Clostridium difficile (55.0%), Campylobacter species (20.9%), Salmon

17 and inpatients >=65 years old (AGE: 459; C. difficile: 91; norovirus: 26).

18 d experienced highly variable patterns of C. difficile abundance, where increased shedding over short

19 ecies protecting against hospital-related C. difficile acquisition included Gemmiger spp., Odoribacte

20 were associated with a decreased risk of C. difficile acquisition.

21 ICU MRSA and C. difficile acquisitions per 1000 patients decreased betwe

22 2016 (MRSA acquisitions, 25.4 to 4.1; and C. difficile acquisitions, 11.1 to 3.5), whereas VRE acquis

23 Moreover, it maintained its anti-C. difficile activity after being exposed to SGF and SIF.

24 en substitutions, which afforded new anti-C. difficile agents with ultrapotent activities [MICs as lo

25 nd 2% died; 3 deaths were associated with C. difficile and 1 with norovirus.

26 he activity of aryl-alkyl-lysines against C. difficile and associated pathogens.

27 We observed colocalization of C difficile and F nucleatum in an aggregation assay using

28 a unique interaction of between pathogenic C difficile and F nucleatum in the intestinal mucus layer.

29 rstanding of its genome, the epigenome of C. difficile and its functional impact has not been systema

30 tial degree of the host immune response to C difficile and its pathogenic toxins is a common indicato

31 Gram-positive bacteria including Clostridium difficile and methicillin-resistant Staphylococcus aureu

32 istant bacteria with a virulent strain of C. difficile and monitored colonization and pathogenesis.

33 C. difficile and norovirus were detected year-round with a

34 C. difficile and norovirus were leading AGE pathogens in ou

35 Clostridioides difficile and norovirus were most frequently detected am

36 icin also effectively treated Clostridioides difficile and pan-resistant Acinetobacter baumannii infe

37 level of peptidoglycan N-deacetylation in C. difficile and the consequent resistance to lysozyme.

38 illin-resistant S. aureus, P. aeruginosa, C. difficile, and fungal infections all had high prevalence

39 aureus, Pseudomonas aeruginosa, Clostridium difficile, and fungal infections) in pediatric sepsis pa

40 , the hydrosulphide channel from Clostridium difficile, and the uncharacterized channel from Escheric

41 e, a crucial metabolite for the growth of C. difficile, and therefore prevented the growth of C. diff

42 for development of a mechanistic class of C. difficile antitoxins.

43 matic patients colonized with Clostridioides difficile are at risk of developing C. difficile infecti

44 ively collected data on colonization with C. difficile are largely unavailable.

45 active CDI from asymptomatic carriage of C. difficile are not well understood.

46 e dormant resistant spores of Clostridioides difficile are transformed into metabolically active cell

47 novo resistance development, Clostridioides difficile-associated disease, antibiotic-related toxicit

48 iota interactions in the manifestation of C. difficile-associated disease.

49 e analysis (REA) BI and non-BI strains of C. difficile at study entry.

50 To detect the phenotype of germinated C. difficile bacteria, we utilize its characteristically hi

51 shown to be unique between F nucleatum and C difficile, because other gut commensals did not aggregat

52 Addition of F nucleatum also enhanced C difficile biofilm formation and extracellular polysaccha

53 f laxatives, more individuals experienced C. difficile blooms.

54 odified cell cytotoxicity assay, isolated C. difficile by anaerobic culture, and performed PCR riboty

55 lonization, as in the case of Clostridioides difficile (C. difficile) infection.

56 ostridioides difficile (formerly Clostridium difficile; C difficile), the leading cause of nosocomial

57 We identified asymptomatic C. difficile carriage among 1897 ICU patients, using rectal

58 Clostridium difficile causes toxin-mediated nosocomial diarrhea and

59 All samples positive for Clostridium difficile (CD) and its toxin were considered.

60 esistant organisms (MDRO) and Clostridioides difficile (CDI) infections seen in ESRD.

61 vulnerable to infection with Clostridioides difficile (CDI).

62 , the samples were tested with PCR (Xpert C. difficile; Cepheid), and chart review was performed.

63 as not found in its entirety in any other C. difficile clade, or indeed, in any other microbial genom

64 passed the activity of vancomycin against C. difficile clinical isolates.

65 lammatory stricture (n = 7), and fulminant C difficile colitis (n = 3).

66 re joins amebic dysentery and Clostridioides difficile colitis as enteric infections profoundly influ

67 umonia, urinary tract infection, Clostridium difficile colitis, sepsis, or death.

68 cture/obstruction, and fulminant Clostridium difficile colitis.

69 nically observed resistance of infants to C. difficile colitis.

70 icrobe-sIgA interactions, greater risk for C difficile colonization and atopic disease in later years

71 ct mucus-associated bacteria would promote C difficile colonization and biofilm formation.

72 of the human gut microbiome, we detected C. difficile colonization and blooms in people recovering f

73 Serological sequelae of infant C. difficile colonization are poorly understood.

74 Influenced by C difficile colonization at 3 months, metabolites propiona

75 Asymptomatic C. difficile colonization is believed to predispose to subs

76 Clostridioides (Clostridium) difficile colonization is common among infants.

77 arrhoeal events trigger susceptibility to C. difficile colonization.

78 tors of the infant gut microbiome, notably C difficile colonization.

79 lic pathway in patients who later acquire C. difficile colonization.

80 differential functions or requirements in C. difficile compared to other spore formers.

81 stool specimens for detection of tcdB in C. difficile, demonstrated acceptable sensitivity and speci

82 of adverse effects (including Clostridioides difficile diarrhea) and contribute to antibiotic resista

83 The most common non-C. difficile diarrheal pathogens in the post-GI PCR cohort

84 Here, we used a murine model of C. difficile disease recurrence to demonstrate that an init

85 tively impacts sporulation, a key step in C. difficile disease transmission, and these results are co

86 ng TcdB toxin, the primary determinant of C. difficile disease.

87 o compare clinical characteristics, Xpert C. difficile/Epi (PCR) cycle threshold (C(T) ), and Singule

88 ne, a covalent conjugate of a distinctive C. difficile fermentation product (isocaproate) and an amin

89 ith Listeria monocytogenes or Clostridioides difficile, followed by treatment with oral ampicillin.

90 Clostridioides difficile (formerly Clostridium difficile; C difficile),

91 s that of spore aggregates and non-viable C. difficile forms, which causes a distinctive high-frequen

92 C. difficile genome analysis showed that 12 genes potential

93 view summarises advances in understanding C. difficile germination and outlines current models of ger

94 Divergent C. difficile germination models have been proposed to expla

95 iodical monitoring included evaluation of C. difficile growth and activity of toxins TcdA and TcdB as

96 The molecular epidemiology of C. difficile has shifted, and this may have implications fo

97 mediating colonization resistance against C. difficile have associated CDI with specific microbial co

98 Here, we identify the C. difficile heme-sensing membrane protein system (HsmRA) a

99 the germination and growth of Clostridioides difficile Here we describe a role for intestinal bile ac

100 infected with a high-virulence strain of C. difficile; however, significant deficits in intestinal n

101 excluding patients from stool testing for C. difficile if they have received laxatives within the pre

102 nst CDI later in life afforded by natural C. difficile immunization events require further investigat

103 e infection (stool specimens positive for C. difficile in a person >=1 year of age with no positive t

104 Efforts to reduce the spread of C. difficile in hospitals have led to the development of ra

105 its the life cycles of various strains of C. difficile in vitro, suggesting that the FDA-approved for

106 o restore colonization resistance against C. difficile in vivo However, the mechanism(s) by which urs

107 C. difficile-induced tissue inflammation and mortality were

108 ons in stool do not differentiate between C. difficile infection (CDI) and asymptomatic carriage.

109 es in the gut microbiota, the severity of C. difficile infection (CDI) and mortality did not differ s

110 Clostridioides difficile infection (CDI) causes serious and sometimes f

111 fer an accurate, stand-alone solution for C. difficile infection (CDI) diagnostics, and further prosp

112 ence, severity, and costs associated with C. difficile infection (CDI) have increased dramatically in

113 Clostridioides difficile infection (CDI) is a major healthcare-associat

114 Clostridioides difficile infection (CDI) is an opportunistic disease th

115 Clostridioides difficile infection (CDI) is associated with increasing

116 ed colonization resistance to Clostridioides difficile infection (CDI) is incompletely understood.

117 Although Clostridioides difficile infection (CDI) is known to involve the disrup

118 Clostridioides difficile infection (CDI) is one of the most common heal

119 vailable diagnostic tests for Clostridioides difficile infection (CDI) lack specificity or sensitivit

120 dstream infection (MDRO-BSI) and Clostridium difficile infection (CDI) rates in the 12 months before

121 Clostridioides difficile infection (CDI) represents a significant burde

122 oides difficile are at risk of developing C. difficile infection (CDI), but the factors associated wi

123 in, are FDA-approved for the treatment of C. difficile infection (CDI), but these therapies still suf

124 ed treatment for all cases of Clostridioides difficile infection (CDI), regardless of disease severit

125 lity of laboratory testing for Clostridiodes difficile infection (CDI), the 2017 Infectious Diseases

126 In patients with Clostridioides difficile infection (CDI), the relationship between clin

127 n with an inactive TcdB fragment prevents C. difficile infection (CDI)-associated pathology.

128 ent of Clostridioides (formerly Clostridium) difficile infection (CDI).

129 the increasing incidence and severity of C. difficile infection (CDI).

130 n is believed to predispose to subsequent C. difficile infection (CDI).

131 ributes to increased rates of Clostridioides difficile infection (CDI).

132 oral vancomycin for fulminant Clostridioides difficile infection (CDI).

133 c oral vancomycin may prevent Clostridioides difficile infection (CDI).

134 e diagnosis and management of Clostridioides difficile infection (CDI).

135 nts are at increased risk for Clostridioides difficile infection (CDI).

136 tation (Tx) is a risk factor for Clostridium difficile infection (CDI).

137 tive for preventing recurrent Clostridioides difficile infection (CDI).

138 ng acute kidney injury (AKI) and Clostridium difficile infection (CDI).

139 Hospital Onset Clostridioides difficile infection (HO-CDI) is a costly problem leading

140 ic use (RR, 1.33; 95% CI, 1.28-1.38), and C. difficile infection (incidence rate ratio, 1.18; 95% CI,

141 R, 1.62; 95% CI, 1.01-2.61; P = .046) and C. difficile infection (OR, 4.01; 95% CI, 2.21-7.59; P < .0

142 nfusion experienced recurrent Clostridioides difficile infection (rCDI) after 9 months (versus actoxu

143 ab reduced rates of recurrent Clostridioides difficile infection (rCDI) versus placebo in MODIFY I/II

144 toxins may protect against recurrence of C. difficile infection (rCDI).

145 ng Infections Program identified cases of C. difficile infection (stool specimens positive for C. dif

146 The estimated national burden of C. difficile infection and associated hospitalizations decr

147 for inhibiting these processes to prevent C. difficile infection and disease recurrence.

148 Rates of Clostridioides difficile infection and ICU and hospital lengths of stay

149 nt to address the unmet needs in treating C. difficile infection and preventing its recurrence.

150 events that follow primary and recurrent C. difficile infection and provide a compelling inverse cor

151 kine responses are associated with severe C. difficile infection and support a key role for intestina

152 The symptoms of C. difficile infection are caused by the activity of three

153 crobiota, using the recurrent Clostridioides difficile infection as a prototype disease.

154 Efforts to prevent Clostridioides difficile infection continue to expand across the health

155 ate of the burden of hospitalizations for C. difficile infection decreased by 24% (95% CI, 0 to 48),

156 adjusted estimate of the total burden of C. difficile infection decreased by 24% (95% CI, 6 to 36) f

157 national burden of health care-associated C. difficile infection decreased by 36% (95% CI, 24 to 54),

158 factors, the host immune response during C. difficile infection greatly influences disease severity.

159 ples showed that a subset of patients with C difficile infection harbored high levels of Fusobacteriu

160 uggest that CDT increases the severity of C. difficile infection in some of the most problematic clin

161 The number of cases of C. difficile infection in the 10 U.S. sites was 15,461 in 2

162 days after the assessment and Clostridiodes difficile infection in the 90 days after the assessment.

163 Colitis caused by Clostridium difficile infection is a growing cause of human morbidit

164 C. difficile infection is dependent on the secretion of one

165 forts are reducing the national burden of C. difficile infection is unclear.

166 Clostridioides difficile infection of the colon leads to severe inflamm

167 ents and results in over 400,000 cases of C. difficile infection per year.

168 ciation test of the reduction in Clostridium difficile infection recurrence in patients treated with

169 mpact of aging on immune responses during C. difficile infection remains to be well described.

170 The estimated national burden of C. difficile infection was 476,400 cases (95% confidence in

171 ocyte response in aged mice during severe C. difficile infection was accompanied by a simultaneous in

172 Clostridioides difficile infection was diagnosed by an independent PCR

173 e national burden of community-associated C. difficile infection was unchanged.

174 months old) were rendered susceptible to C. difficile infection with the antibiotic cefoperazone and

175 nents of the primary outcome, Clostridioides difficile infection, and antibiotic-related adverse effe

176 s posing the highest risk for Clostridioides difficile infection, and azithromycin (pediatrics only)

177 er gastrointestinal bleeding, Clostridioides difficile infection, and ICU and hospital lengths of sta

178 eights to estimate the national burden of C. difficile infection, first recurrences, hospitalizations

179 cohort study of patients with Clostridioides difficile infection, the use of oral vancomycin did not

180 ed for IL-17 production were resistant to C. difficile infection, whereas elimination of gammadelta T

181 ammadelta T cells in host defense against C. difficile infection.

182 d mouse model to assess susceptibility to C. difficile infection.

183 ttractive therapeutic target for managing C. difficile infection.

184 ular and cytokine immune responses during C. difficile infection.

185 e development of effective agents against C. difficile infection.

186 d with higher antibiotic use and rates of C. difficile infection.

187 te to host susceptibility and severity of C. difficile infection.

188 persistence in a murine model of relapse C. difficile infection.

189 in the case of Clostridioides difficile (C. difficile) infection.

190 pyuria was associated with postoperative C. difficile infections (aOR, 1.7; 95% CI, 1.2-2.4); risk w

191 ence of primary and recurring Clostridioides difficile infections (CDI), which evade current treatmen

192 Clostridium difficile infections (CDIs) are a growing health concern

193 Clostridioides difficile infections (CDIs) are among the most prevalent

194 sed commonly for treatment of Clostridioides difficile infections (CDIs), although prospective safety

195 is a key predisposing factor for Clostridium difficile infections (CDIs), which cause intestinal dise

196 Recurrent Clostridioides difficile infections (rCDI) are a global public health t

197 ients with multiple recurrent Clostridioides difficile infections (rCDI) are treated with fecal micro

198 Staphylococcus aureus (MRSA) and Clostridium difficile infections declined across the UK National Hea

199 C. difficile infections have mortality rates of 6 to 30% an

200 n FMT treatment for recurrent Clostridioides difficile infections.

201 o dampen the inflammatory tissue damage in C difficile infections.

202 SI), urinary tract (UTI), and Clostridioides difficile infections.

203 The effects of increased C. difficile inoculum, and pre-exposure to simulated gastri

204 While the knowledge on gut microbiota - C. difficile interactions has improved over the years, the

205 Clostridium difficile is a Gram-positive bacterium with an S-layer c

206 Clostridioides difficile is a Gram-positive, pathogenic bacterium and a

207 Clostridioides (formerly Clostridium) difficile is a Gram-positive, spore-forming anaerobe and

208 Clostridioides difficile is a Gram-positive, spore-forming, anaerobic b

209 Clostridioides (formerly Clostridium) difficile is a leading cause of healthcare-associated in

210 The S-layer in C. difficile is constructed mainly of S-layer protein A (Sl

211 isturbances, our results help explain why C. difficile is frequently detected as a co-infecting patho

212 ic bacteria, a lack of N-deacetylation in C. difficile is not linked to a decrease in virulence.

213 Spore germination in C. difficile is regulated by the detection of bile salt ger

214 Clostridioides difficile is the leading cause of diarrhea in hospitaliz

215 Clostridioides difficile is the leading cause of healthcare-associated

216 Clostridioides difficile is the leading cause of nosocomial infections

217 Clostridioides difficile is the most common cause of healthcare-associa

218 Although Clostridium difficile is widely considered an antibiotic- and hospit

219 f this plasmid to a vancomycin-susceptible C difficile isolate decreased its susceptibility to vancom

220 C. difficile isolates from VRE swabs, and from C. difficile

221 ot result in a consistent decrease in the C. difficile life cycle in vivo, it was able to attenuate a

222 for intestinal eosinophils in mitigating C. difficile-mediated disease severity.

223 ed with toxigenic (TCD) and non-toxigenic C. difficile (NTCD), respectively.

224 re stool collection) and a positive stool C. difficile nucleic acid amplification test were enrolled.

225 esses, factors that are conserved only in C. difficile or the related Peptostreptococcaceae family ar

226 holerae, Salmonella enterica, Clostridioides difficile, or Streptococcus pyogenes, multiple highly co

227 , and pathogen-microbiota interactions in C. difficile pathogenesis, as well as the impact of host-mi

228 on to suggesting a role for bile acids in C. difficile pathogenesis, these findings provide a framewo

229 -2013, we evaluate stool toxin levels and C. difficile PCR ribotypes.

230 The C. difficile peptidoglycan is largely N-deacetylated on its

231 ents were included if they had a positive C. difficile polymerase chain reaction (PCR) performed on a

232 fficile isolates from VRE swabs, and from C. difficile-positive stool samples, were genome sequenced.

233 Infection with BI strains of C. difficile predicted poor outcomes in the MODIFY I/II tri

234 Here, we confirmed that ursodiol inhibits C. difficile R20291 spore germination and outgrowth, growth

235 o restore colonization resistance against C. difficile remains unknown.

236 ent with trends across the United States, C. difficile RT106 was the second-most prevalent molecular

237 -acetylglucosamine utilizers that impedes C. difficile's access to these mucosal sugars and impairs p

238 l virulence has been long recognized, and C. difficile sortase B (Cd-SrtB) has become an attractive t

239 hage information, we screened Clostridioides difficile-specific phages and identified antibacterial e

240 The C. difficile spore assembly pathway also exhibits notable d

241 derstanding of the mechanisms controlling C. difficile spore formation and germination and describes

242 Assessment of C. difficile spore germination typically requires measureme

243 As mice exposed to avirulent C. difficile spores ingested increasing quantities of laxat

244 The recalcitrance of C. difficile spores to currently available treatments and c

245 C. difficile status was assessed by GDH EIA and real-time P

246 serve that the host age and the infecting C. difficile strain influenced the severity of disease asso

247 to assess bezlotoxumab's efficacy against C. difficile strains associated with increased rates of mor

248 C difficile strains were found to coaggregate with F nucle

249 tory activity across multiple Clostridioides difficile strains while preserving the microbiome to dev

250 iotic cefoperazone and then infected with C. difficile strains with varied disease-causing potentials

251 Indeed, against certain C. difficile strains, NCK-10 was more active than vancomyci

252 ug/ml), exhibited potent activity against C. difficile strains.

253 inary toxin (CDT)-producing hypervirulent C. difficile strains.

254 l damage or inflammation that Clostridioides difficile subverts, enabling continued growth.

255 re tested for non-toxigenic and toxigenic C. difficile (TCD).

256 rformance characteristics of the Revogene C. difficile test (Meridian Bioscience, Cincinnati, OH, USA

257 sence of the tcdB gene using the Revogene C. difficile test, and results were compared with those of

258 The Revogene C. difficile test, using clinical stool specimens for detec

259 was to assess the performance of various C. difficile tests and to compare clinical characteristics,

260 of the toxin B (tcdB) gene from toxigenic C. difficile The Revogene instrument is a new molecular pla

261 difficile (formerly Clostridium difficile; C difficile), the leading cause of nosocomial antibiotic-a

262 Unlike other bacteria, Clostridium difficile, the major human pathogen responsible for anti

263 tial clinical lead for the development of C. difficile therapeutics but also highlights dramatic drug

264 From Monoclonal Antibodies for C. difficile Therapy II, no participants (n = 0/69) with a

265 ta from MODIFY (Monoclonal Antibodies for C. difficile Therapy) I and II (NCT01241552 and NCT01513239

266 acetate promotes host innate responses to C. difficile through coordinate action on neutrophils and I

267 and how they may relate to recovery from C. difficile through FMT therapy.

268 n potentially target the cell membrane of C. difficile to minimize relapse in the recovering patient.

269 e results define a mechanism exploited by C. difficile to repurpose toxic heme within the inflamed gu

270 al for the bacterial pathogen Clostridioides difficile to transmit infection.

271 tentially driving decreased sensitivity of C difficile to vancomycin treatment.

272 the receptor-binding site in Clostridioides difficile toxin B (TcdB), which binds the human receptor

273 Recent data indicate that Clostridioides difficile toxin concentrations in stool do not different

274 The C. difficile toxin has an enzymatic component, termed CDTa,

275 Rho-modifying toxins, including Clostridium difficile toxins A and B.

276 unoassay for the detection of Clostridioides difficile toxins in stool.

277 (eAbs) against Clostridioides (Clostridium) difficile toxins may protect against recurrence of C. di

278 Ultrasensitive assays for detection of C. difficile toxins provide measurements of disease-specifi

279 sporogenes decreased the activity of both C. difficile toxins TcdA and TcdB.

280 s: toxin A (TcdA), toxin B (TcdB) and the C. difficile transferase toxin (CDT)(2).

281 s toxin A (TcdA), toxin B (TcdB), and the C. difficile transferase toxin (CDT).

282 n disease (diverticular disease, Clostridium difficile) undergoing major abdominal surgery.

283 testinal pathogens, including Clostridioides difficile, use mucus-derived sugars as crucial nutrients

284 Work in the last decade has revealed that C. difficile uses a distinct mechanism for sensing and tran

285 a comprehensive DNA methylome analysis of C. difficile using 36 human isolates and observe a high lev

286 ows a strategy for improved production of C. difficile vaccine candidate in E. coli by using restrict

287 US adults of an investigational bivalent C. difficile vaccine that contains equal dosages of genetic

288 The C. difficile vaccine was safe, well tolerated, and immunoge

289 Data on MRSA, C. difficile, vancomycin-resistant Enterococcus (VRE), and

290 tested positive for a pathogen other than C. difficile versus 49 patients (27%) in the post-GI PCR co

291 cterial toxin TcdB is a major Clostridioides difficile virulence factor that contributes to inflammat

292 C difficile was found to colonize and form biofilms on MUC

293 From 2559 randomized participants, C. difficile was isolated from 1588 (67.2%) baseline stool

294 The successful growth of C. difficile was most significantly correlated with the dec

295 d interrupted week-long periods in which C. difficile was undetectable.

296 itis caused by infection with Clostridioides difficile, we coinfected mice that were colonized with a

297 Using the pathogen Clostridioides difficile, we show that infection disrupts murine intest

298 l samples of patients tested positive for C. difficile were analyzed by assessing alpha and beta dive

299 ure of HypD from the pathogen Clostridioides difficile with Hyp bound in the active site.

300 treated with clindamycin and infected with C difficile with the addition of human MUC2-coated coversl