ライフサイエンスコーパス: perfringens

1 ium botulinum, and iota toxin of Clostridium perfringens.

2 um septicum and epsilon-toxin of Clostridium perfringens.

3 agenesis system that works effectively in C. perfringens.

4 s and functions in chicks challenged with C. perfringens.

5 udomonas aeruginosa, and VirR of Clostridium perfringens.

6 reted by the anaerobic bacterium Clostridium perfringens.

7 ntroduced into the sigE and sigK genes of C. perfringens.

8 specific-pathogen-free chicks by Clostridium perfringens.

9 found in the bacterial pathogen Clostridium perfringens.

10 n-encoding genes and the 16S rRNA gene of C. perfringens.

11 rhea and gas gangrene, that are caused by C. perfringens.

12 es, including the human pathogen Clostridium perfringens.

13 ys through which virulence has evolved in C. perfringens.

14 coli, Bacteroides fragilis, and Clostridium perfringens.

15 strong synergy to B. fragilis but not to C. perfringens.

16 Clostridium acetobutylicum, and Clostridium perfringens.

17 a catabolite repressor of sporulation by C. perfringens.

18 oultry dishes were commonly implicated in C. perfringens (63%) and S. aureus (55%) outbreaks, and ric

19 from dogs, cats, and horses was Clostridium perfringens (75, 13, and101 isolates, respectively).

20 The presence and abundance of Clostridium perfringens (8.4%) and Bacteroides dorei (0.9%) in mecon

21 Clostridium perfringens, a human pathogen, is one of the most common

22 ntroduced into the pilT and pilC genes of C. perfringens abolished motility and surface localization

23 0% homology to a sequence within Clostridium perfringens adenosine triphosphate-binding cassette (ABC

24 with a homologous sequence of a Clostridium perfringens adenosine triphosphate-binding cassette tran

25 s CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL) quorum sensing (QS) system.

26 Biotinylated antibodies to C. perfringens alpha toxin bound to streptavidin paramagnet

27 say for identifying and assaying Clostridium perfringens alpha toxin.

28 Given that C. perfringens alpha-toxin cleaves the phosphocholine headg

29 s indicated that all of the isolates were C. perfringens alpha-toxin gene positive and 46 of 48 isola

30 e-active toxins produced by the anaerobic C. perfringens, alpha-toxin (PLC) and perfringolysin O (PFO

31 nM) of epsilon toxin produced by Clostridium perfringens and a prominent food toxin.

32 C. perfringens and B. fragilis provided moderate synergy to

33 e ubiquitous, anaerobic bacteria Clostridium perfringens and Clostridium septicum.

34 llei, Burkholderia pseudomallei, Clostridium perfringens and Entamoeba histolytica.

35 a pore-forming toxin produced by Clostridium perfringens and has been reported to play a major role i

36 afniense, Clostridium novyi, and Clostridium perfringens and increase their activity up to 30-, 5-, a

37 pores of both C-cpe and P-cpe isolates of C. perfringens and provided evidence that proteins encoded

38 nts of the spore germination machinery of C. perfringens and several Bacillus species and the bioinfo

39 esponding genes of 26 strains of Clostridium perfringens and Streptococcus pneumoniae.

40 een the germination of spores of Clostridium perfringens and that of spores of a number of Bacillus s

41 ding a hyaluronidase secreted by Clostridium perfringens, and a C. perfringens hyaluronidase nagI or

42 um hafniense, Clostridium novyi, Clostridium perfringens, and Eggerthella lenta.

43 bacteria, desulfovibrios, type E Clostridium perfringens, and Enterococcus faecalis, whereas the reve

44 urrence of outbreaks caused by B. cereus, C. perfringens, and S. aureus in the United States.

45 all genes examined from M. gallisepticum, C. perfringens, and S. pneumoniae were under neutral to sta

46 reaks caused by Bacillus cereus, Clostridium perfringens, and Staphylococcus aureus were reported in

47 MPDHs from Campylobacter jejuni, Clostridium perfringens, and Vibrio cholerae.

48 sulfatase-maturating enzyme from Clostridium perfringens (anSMEcpe) catalyzes the two-electron oxidat

49 sequential production of DHDPA and DPA in C. perfringens appears to be catalysed by DHDPA synthase fo

50 logy to pilins in Gram-negative bacteria, C. perfringens appears to have two pilin subunits, PilA1 an

51 These anSME structures from Clostridium perfringens are also the first of an AdoMet radical enzy

52 mon human and livestock pathogen Clostridium perfringens are attributable to a formidable battery of

53 coded alpha-toxin and perfringolysin O by C. perfringens, as well as sporulation by Clostridium botul

54 mal enterotoxin (cpe) gene (C-cpe), while C. perfringens-associated non-food-borne gastrointestinal (

55 tosidase designated E-ABase from Clostridium perfringens ATCC 10543 capable of liberating both the A

56 Although they lack flagella, C. perfringens bacteria can still migrate across surfaces u

57 C. perfringens beta toxin (CPB) is the major virulence dete

58 These results indicate C. perfringens biofilms play an important role in the persi

59 edly control in vitro toxin production by C. perfringens but their importance for virulence has not b

60 Enterococci and C. perfringens, but not E. coli, showed significantly small

61 ith the putative reduced pathogenicity of C. perfringens by BEOs contributed to the reduction in gut

62 tion was introduced into the ccpA gene of C. perfringens by conjugational transfer of a nonreplicatin

63 Thus, CpAL regulates biofilm formation in C. perfringens by increasing levels of certain toxins requi

64 We have previously shown that C. perfringens can glide across an agar surface in long fil

65 t showed that human intestinal strains of C. perfringens can grow by utilizing either glucose or sial

66 Clostridium perfringens can produce up to three different sialidases

67 roduced only during sporulation and since C. perfringens can sporulate in the intestines.

68 ules, which are found throughout numerous C. perfringens carbohydrate-active enzymes.

69 By producing toxins, Clostridium perfringens causes devastating diseases of both humans a

70 Clostridium perfringens causes gas gangrene and gastrointestinal dis

71 vels and the amount of CPB2 produced by a C. perfringens cell and that decreased transcription and/or

72 Significantly, wild-type C. perfringens cells adhered to mouse myoblasts under anaer

73 Escape of C. perfringens cells from phagosomes of macrophage-like J77

74 CPE is produced by sporulating C. perfringens cells in the small intestinal lumen, where i

75 lbicans into "mini-biofilms," which allow C. perfringens cells to survive in a normally toxic environ

76 was purified from extracts of sporulating C. perfringens cells.

77 ex-lytic enzymes (CLEs), and two Clostridium perfringens CLEs, SleC and SleM, degrade cortex PG in vi

78 uster I, including the pathogens Clostridium perfringens, Clostridium botulinum and Clostridium tetan

79 nthracis, Staphylococcus aureus, Clostridium perfringens, Clostridium botulinum, and Clostridium diff

80 tative cell-surface adhesin from Clostridium perfringens comprising an N-terminal adhesin domain foll

81 = .01 for consecutive samples); Clostridium perfringens continued to be more prevalent in NEC cases.

82 ta can be identified in meconium samples; C. perfringens continues to be associated with NEC from the

83 ed Agr-like quorum-sensing (QS) system in C. perfringens controls all toxin production by surveyed ty

84 The C. perfringens cpe gene, encoding CPE, is transcribed from

85 O was shown to be the primary mediator of C. perfringens-dependent cytotoxicity to macrophages.

86 ent with sialidase purified from Clostridium perfringens did (P < 0.05).

87 oxin, which are also important toxins for C. perfringens diseases (enteritis and enterotoxemia) origi

88 The genome of the pathogen Clostridium perfringens encodes two proteins, GerO and GerQ, homolog

89 potential auxiliary virulence factor for C. perfringens enteritis and enterotoxemia.

90 mplicated in the pathogenesis of Clostridium perfringens enteritis.

91 Domain I of Clostridium perfringens enterotoxin (cCPE) binds to the second extra

92 cytotoxic C-terminal fragment of Clostridium perfringens enterotoxin (cCPE) is a natural ligand for c

93 Clostridium perfringens enterotoxin (CPE) action starts when the tox

94 C. perfringens type A strains producing C. perfringens enterotoxin (CPE) cause human food poisoning

95 Clostridium perfringens enterotoxin (CPE) causes food poisoning and

96 Clostridium perfringens enterotoxin (CPE) causes the gastrointestina

97 Clostridium perfringens enterotoxin (CPE) causes the symptoms of a v

98 Clostridium perfringens enterotoxin (CPE) has a unique mechanism of

99 Clostridium perfringens enterotoxin (CPE) has recently been shown to

100 Clostridium perfringens enterotoxin (CPE) induces cytolysis very rap

101 Clostridium perfringens enterotoxin (CPE) is a major cause of food p

102 Clostridium perfringens enterotoxin (CPE) is a pore-forming toxin wi

103 Clostridium perfringens enterotoxin (CPE) is responsible for causing

104 Clostridium perfringens enterotoxin (CPE) is the etiological agent o

105 respectively, for the cytotoxic Clostridium perfringens enterotoxin (CPE), in this study we investig

106 However, many EN strains also express C. perfringens enterotoxin (CPE), suggesting that CPE could

107 that CPB2 could be an accessory toxin in C. perfringens enterotoxin (CPE)-associated AAD/SD.

108 .g., Claudin-4) as receptors for Clostridium perfringens enterotoxin (CPE).

109 and -3 serve as the receptor for Clostridium perfringens enterotoxin (Cpe).

110 similar cytotoxicity-enhancing effects on C. perfringens enterotoxin and beta toxin, which are also i

111 ntially plasmid-encoded toxins, including C. perfringens enterotoxin and beta2 toxin, encoded by the

112 Clostridium perfringens enterotoxin causes the gastrointestinal (GI)

113 ue to sporulation-dependent production of C. perfringens enterotoxin encoded by the cpe gene.

114 Clostridium perfringens enterotoxin is a common cause of food-borne

115 CPE (Clostridium perfringens enterotoxin) is the major virulence determin

116 s botulinum neurotoxins (BoNTs), Clostridium perfringens epsilon toxin (ETX), staphylococcal enteroto

117 Clostridium perfringens epsilon toxin belongs to the aerolysin-like

118 studies showed that NanI could potentiate C. perfringens epsilon toxin cytotoxicity by enhancing the

119 f single membrane receptors, the Clostridium perfringens epsilon-toxin (CPepsilonT) receptors that ar

120 The Clostridium perfringens epsilon-toxin causes a severe, often fatal i

121 The Clostridium perfringens epsilon-toxin is responsible for a severe, o

122 alizing monoclonal antibodies against the C. perfringens epsilon-toxin.

123 habitants: Bacteroides fragilis, Clostridium perfringens, Escherichia coli, Klebsiella pneumoniae, an

124 C. perfringens EtfA was expressed in and purified from Esch

125 cherichia coli, enterococci, and Clostridium perfringens) exhibited biphasic decay patterns in all mi

126 Clostridium perfringens food poisoning is caused by type A isolates

127 by SM101, a transformable derivative of a C. perfringens food-poisoning strain.

128 anaerobic gram-positive pathogen Clostridium perfringens forms biofilms.

129 t + 120 mg/kg BEOs), were challenged with C. perfringens from days 14 to 20 and were killed on day 21

130 Clostridium perfringens gas gangrene is characterized by rapid tissu

131 f morbidity and mortality associated with C. perfringens gas gangrene.

132 he same four sigma factors are encoded by C. perfringens genomes, and two (SigE and SigK) have previo

133 complex of an inactive (D220N) variant of C. perfringens GH125 enzyme in complex with 1,6-alpha-manno

134 A published complex of Clostridium perfringens GH125 enzyme with a nonhydrolyzable 1,6-alph

135 is necessary for efficient sporulation in C. perfringens, glucose-mediated catabolite repression of s

136 the production of NanI, which may affect C. perfringens growth, adhesion, and toxin binding in vivo.

137 me sequences of three strains of Clostridium perfringens have been completed and we identified gene p

138 ecreted by Clostridium perfringens, and a C. perfringens hyaluronidase nagI or nagK pseudogene were d

139 racis, Campylobacter jejuni, and Clostridium perfringens IMPDHs.

140 caused by an experimental infection with C. perfringens in a murine model of gas gangrene.

141 thods are not suitable to detect Clostridium perfringens in formalin-fixed, paraffin-embedded tissue

142 observations support a potential role for C. perfringens in NMO pathogenesis.

143 itive exclusion agent to control Clostridium perfringens in poultry.

144 We successfully detected and genotyped C. perfringens in tissue sections from two autopsy cases.

145 ne, which encodes a sialidase secreted by C. perfringens, in the M. alligatoris genome.

146 we observed that in suspension cultures, C. perfringens induces aggregation of C. albicans into "min

147 amics of host microbiota in responding to C. perfringens infection.

148 f macrophages in the host defense against C. perfringens infections is still unknown.

149 ial synergistic toxin interactions during C. perfringens intestinal infections and support a possible

150 Clostridium perfringens iota-toxin consists of two separate proteins

151 Clostridium perfringens is a Gram-positive anaerobic pathogen of hum

152 Clostridium perfringens is a Gram-positive, anaerobic spore-forming

153 -content gram-positive bacteria, of which C. perfringens is a member.

154 Clostridium perfringens is a ubiquitous and versatile pathogenic bac

155 r sequence necessary for its secretion by C. perfringens is absent.

156 Clostridium perfringens is an anaerobic Gram-positive pathogen that

157 Clostridium perfringens is an anaerobic, Gram-positive bacterium tha

158 Clostridium perfringens is an important human and animal pathogen th

159 C. perfringens is an underrecognized but frequently observe

160 Clostridium perfringens is capable of producing up to 15 toxins, inc

161 y for phospholipase C (PLC) from Clostridium perfringens is developed based on the reversible interac

162 events in the mother cell compartment of C. perfringens is not the same as that in B. subtilis and C

163 ecrotic enteritis (NE) caused by Clostridium perfringens is one of the most detrimental infectious di

164 C. perfringens is responsible for a wide spectrum of diseas

165 Clostridium perfringens is the cause of several human diseases, incl

166 Clostridium perfringens is the most common cause of clostridial myon

167 Clostridium perfringens is the third most frequent cause of bacteria

168 ies suggested that cpb2-positive Clostridium perfringens isolates are associated with gastrointestina

169 e among the most plasmid dependent of all C. perfringens isolates for virulence, as they usually carr

170 stigate genotypic relationships among 139 C. perfringens isolates from 74 flocks.

171 yping and phenotyping of 23 cpb2-positive C. perfringens isolates from horses with GI disease (referr

172 ts the first sequence-based comparison of C. perfringens isolates recovered in clinical cases of PG a

173 No PG-associated and NE-associated C. perfringens isolates shared the same sequence type or cl

174 However, cpb2 genes from nonporcine C. perfringens isolates were not always expressed, at least

175 in the core genomes of poultry-associated C. perfringens isolates, a concept with both epidemiologica

176 l defense mechanism against CPB-producing C. perfringens isolates.

177 rovirus and toxigenic strains of Clostridium perfringens, Klebsiella oxytoca, Staphylococcus aureus,

178 C. perfringens lacks flagella but possesses type IV pili (T

179 challenged by the glycosylating Clostridium perfringens large cytotoxin (TpeL toxin) that is devoid

180 tical and reproducible means of subtyping C. perfringens libraries from specific epidemiological or p

181 gies may be possible for the treatment of C. perfringens-mediated myonecrosis.

182 ainst myonecrotic disease was specific to C. perfringens-mediated myonecrosis; buprenorphine did not

183 We have recently shown that strains of C. perfringens move across the surface of agar plates by a

184 Therefore, C. perfringens mutants lacking PFO and PLC were examined fo

185 activity on human substrates of Clostridium perfringens NagJ, a close homologue of human O-GlcNAcase

186 e able to identify inhibitors of Clostridium perfringens neuraminidase present in a root extract of t

187 C. difficile was codetected with Clostridium perfringens, norovirus, sapovirus, parechovirus, and ane

188 es, but only in three bacterial (Clostridium perfringens, Oenococcus oeni, and Leuconostoc mesenteroi

189 icantly reduce the impact of NE caused by C. perfringens on broilers.

190 fringolysin O (PFO), secreted by Clostridium perfringens, only binds to membranes containing substant

191 us outbreaks (median, 87%), but rarely in C. perfringens outbreaks (median, 9%).

192 rted action of alpha-toxin and PFO during C. perfringens pathogenesis.

193 investigations into the genetic basis of C. perfringens pathogenicity have focused on toxins and oth

194 o the transfer protein TcpC from Clostridium perfringens plasmid pCW3 (G+).

195 known to mediate conjugative transfer of C. perfringens plasmid pCW3.

196 tcp genes, which can mediate conjugative C. perfringens plasmid transfer.

197 A dcm gene, which is often present near C. perfringens plasmid-borne toxin genes, was identified up

198 Spores of Clostridium perfringens possess high heat resistance, and when these

199 Clostridium perfringens possesses at least two functional quorum sen

200 The gram-positive anaerobe Clostridium perfringens produces a large arsenal of toxins that are

201 Here we show that C. perfringens produces TFP and moves with an unusual form

202 Biofilms afforded C. perfringens protection from environmental stress, includ

203 acetyl sialic acid--but not from Clostridium perfringens resulted in an increase in RN6390 and ALC135

204 MazF-cd expression in E. coli or Clostridium perfringens resulted in growth arrest.

205 les from NEC infants not carrying profuse C. perfringens revealed an overabundance of a Klebsiella OT

206 ructure of ligand-free NanE from Clostridium perfringens reveals a modified triose-phosphate isomeras

207 Infusion of Clostridium perfringens sialidase to the injury site markedly increa

208 stent with NanI sialidase being the major C. perfringens sialidase when produced, FP and Db strains h

209 C. perfringens sleC spores did not germinate completely wit

210 ent cation transporters play some role in C. perfringens spore germination.

211 s and Ca-DPA release are not required for C. perfringens spore germination.

212 suggesting an auxiliary role for GerAA in C. perfringens spore germination.

213 lts allow the following conclusions about C. perfringens spore germination: (i) SleC is essential for

214 C. perfringens spores are thought to be the important infec

215 Indeed, wild-type and spoVA C. perfringens spores germinated similarly with a mixture o

216 C. perfringens spores lacking GerO were defective in germin

217 ntent is essential for full resistance of C. perfringens spores to moist heat, UV radiation, and chem

218 Upon its release from C. perfringens spores, CPE binds to its receptor, claudin,

219 al for cortex hydrolysis and viability of C. perfringens spores.

220 ever, the importance of SigF and SigG for C. perfringens sporulation or CPE production had not yet be

221 ternative sigma factors are necessary for C. perfringens sporulation, but only SigE, SigF, and SigK a

222 ve sigma factors, which are essential for C. perfringens sporulation.

223 nly in the mother cell compartment during C. perfringens sporulation.

224 and DPA into the developing spore during C. perfringens sporulation.

225 Ca-DPA uptake by developing spores during C. perfringens sporulation.

226 olvement of AbrB repression in regulating C. perfringens sporulation.

227 However, the viability of C. perfringens spoVA spores was 20-fold lower than the viab

228 etermined and compared with the published C. perfringens strain 13 genome.

229 he carbonic anhydrase (Cpb) from Clostridium perfringens strain 13, the only carbonic anhydrase encod

230 nd to be identical to the CPE0329 gene of C. perfringens strain 13, whose product was labeled as a hy

231 The complete genome sequences of Clostridium perfringens strain ATCC 13124, a gas gangrene isolate an

232 Analyses of a cpb deletion mutant of C. perfringens strain HN13 showed that Cpb is strictly requ

233 for other LCTs and for TpeL production by C. perfringens strain JIR12688.

234 c component that explains the variance in C. perfringens strain virulence by assessing patterns of ge

235 A C. perfringens strain with etfA inactivated is blocked in l

236 Clostridium perfringens strains (type A) isolated from an integrated

237 Although C. perfringens strains form biofilm-like structures, the re

238 Many Clostridium perfringens strains produce NanI as their major sialidas

239 Clostridium perfringens strains produce severe diseases, including m

240 carriage of the tpeL gene among different C. perfringens strains, detecting this toxin gene in some t

241 ion of sporulation varies among different C. perfringens strains.

242 ely variable across a large collection of C. perfringens strains.

243 C. perfringens survival in the presence of mouse peritoneal

244 These findings implicate C. perfringens TFP in the ability of C. perfringens to adhe

245 ic acid using neuraminidase from Clostridium perfringens that cleaves sialic acid monomers with an al

246 ently identified LCT produced by Clostridium perfringens that has received relatively limited study.

247 Clostridium perfringens, the most broadly distributed pathogen in na

248 For example, Clostridium perfringens, the species with the highest value of S, ca

249 re, providing the first evidence that, in C. perfringens, this system can control production of plasm

250 cate C. perfringens TFP in the ability of C. perfringens to adhere to and move along muscle fibers in

251 at NanI is important for the adherence of C. perfringens to enterocyte-like cells, NanI sialidase is

252 The ability of C. perfringens to regulate its exosialidase activity, large

253 ttributed to norovirus; however, Clostridium perfringens toxicoinfection was subsequently confirmed.

254 exist in Agr-like QS system regulation of C. perfringens toxin production.

255 unique for producing the two most lethal C. perfringens toxins, i.e., epsilon-toxin and beta-toxin.

256 These results suggest that C. perfringens type A and C strains that cause human food-b

257 ses the gastrointestinal (GI) symptoms of C. perfringens type A food poisoning and CPE-associated non

258 Clostridium perfringens type A food poisoning is the second most com

259 Sporulation is critical for C. perfringens type A food poisoning since spores contribut

260 causing the gastrointestinal symptoms of C. perfringens type A food poisoning, the second most commo

261 CPE production in SM101, a derivative of C. perfringens type A food-poisoning strain NCTC8798.

262 Clostridium perfringens type A isolates carrying an enterotoxin (cpe

263 C. perfringens type A strains producing C. perfringens ente

264 Clostridium perfringens type A strains producing enterotoxin (CPE) c

265 glucosylating toxins produced by Clostridium perfringens type A, B, and C strains.

266 ulture confirmed the presence of Clostridium perfringens type A.

267 Clostridium perfringens type B and type C isolates, which produce be

268 Clostridium perfringens type B causes enteritis and enterotoxemia in

269 rtant contributors to the pathogenesis of C. perfringens type B infections in domestic animals.

270 he important veterinary pathogen Clostridium perfringens type B is unique for producing the two most

271 Clostridium perfringens type C isolates cause enteritis necroticans

272 Clostridium perfringens type C isolates cause enterotoxemias and ent

273 Clostridium perfringens type C isolates, which cause enteritis necro

274 C. perfringens type C isolates, which cause rapidly fatal d

275 t regulate the pathogenicity of CN3685, a C. perfringens type C strain.

276 Clostridium perfringens type C strains are the only non-type-A isola

277 The ability of Clostridium perfringens type C to cause human enteritis necroticans

278 is study we developed two mouse models of C. perfringens type C-induced lethality.

279 Previous studies showed that Clostridium perfringens type D animal disease strain CN3718 uses Nan

280 Clostridium perfringens type D causes disease in sheep, goats, and o

281 eveloped an oral challenge mouse model of C. perfringens type D enterotoxemia.

282 Clostridium perfringens type D enterotoxemias have significant econo

283 ew model for studying the pathogenesis of C. perfringens type D infections.

284 Clostridium perfringens type D isolates are important in biodefense

285 Clostridium perfringens type D isolates cause enterotoxemia in sheep

286 We evaluated the contribution of ETX to C. perfringens type D pathogenicity in an intraduodenal cha

287 Clostridium perfringens type D strains cause enterotoxemia and enter

288 n sheep, goats, and mice using a virulent C. perfringens type D wild-type strain (WT), an isogenic ET

289 the primary virulence factor of Clostridium perfringens type D, causes mortality in livestock, parti

290 Clostridium perfringens type E isolates produce iota-toxin, which is

291 n) is the major virulence determinant for C. perfringens type-A food poisoning, the second most commo

292 ated hydrolysis catalyzed by the Clostridium perfringens unsaturated glucuronyl hydrolase of glycosid

293 Ingested C. perfringens vegetative cells sporulate in the intestinal

294 alpha/beta-type SASP, Ssp2, from Clostridium perfringens was expressed at significant levels in B. su

295 Strikingly, C. perfringens was overrepresented in NMO (p = 5.24 x 10(-8

296 nducible expression of PilA1 and PilA2 of C. perfringens were constructed.

297 on and translation of the spoIIID gene in C. perfringens were not affected by mutations in sigE and s

298 A total of 48 isolates of C. perfringens were obtained from different stages of the b

299 ncreases in genus Sutterella and Clostridium perfringens when compared to healthy dogs.

300 transfer of a nonreplicating plasmid into C. perfringens, which led to inactivation of the ccpA gene