ライフサイエンスコーパス: C. perfringens

1 C. perfringens and B. fragilis provided moderate synergy

2 C. perfringens beta toxin (CPB) is the major virulence d

3 C. perfringens EtfA was expressed in and purified from E

4 C. perfringens is an underrecognized but frequently obse

5 C. perfringens is responsible for a wide spectrum of dis

6 C. perfringens lacks flagella but possesses type IV pili

7 C. perfringens sleC spores did not germinate completely

8 C. perfringens spores are thought to be the important in

9 C. perfringens spores lacking GerO were defective in ger

10 C. perfringens survival in the presence of mouse periton

11 C. perfringens type A strains producing C. perfringens e

12 C. perfringens type C isolates, which cause rapidly fata

13 C. perfringens, an opportunistic pathogen, was specifica

14 nvestigate genotypic relationships among 139 C. perfringens isolates from 74 flocks.

15 A C. perfringens strain with etfA inactivated is blocked i

16 e secreted by Clostridium perfringens, and a C. perfringens hyaluronidase nagI or nagK pseudogene wer

17 levels and the amount of CPB2 produced by a C. perfringens cell and that decreased transcription and

18 ight regulate the pathogenicity of CN3685, a C. perfringens type C strain.

19 arrying a chromosomal cpe gene) and F4969 (a C. perfringens type A non-food-borne GI disease isolate

20 s, we investigated whether the cpe gene of a C. perfringens food poisoning isolate can be expressed a

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

22 genetic element near the dcm sequences of a C. perfringens plasmid.

23 out mutants in both SM101 (a derivative of a C. perfringens type A food poisoning isolate carrying a

24 ota toxin genes, to several different type A C. perfringens isolates.

25 esults allow the following conclusions about C. perfringens spore germination: (i) SleC is essential

26 ing the production of NanI, which may affect C. perfringens growth, adhesion, and toxin binding in vi

27 Biofilms afforded C. perfringens protection from environmental stress, inc

28 ding of Ib was inhibited by antisera against C. perfringens type E or Clostridium spiroforme culture

29 e of macrophages in the host defense against C. perfringens infections is still unknown.

30 are among the most plasmid dependent of all C. perfringens isolates for virulence, as they usually c

31 . albicans into "mini-biofilms," which allow C. perfringens cells to survive in a normally toxic envi

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

33 ontal transfer of a common cpe plasmid among C. perfringens type A strains.

34 rane-active toxins produced by the anaerobic C. perfringens, alpha-toxin (PLC) and perfringolysin O (

35 Enterococci and C. perfringens, but not E. coli, showed significantly sm

36 Mucolytic bacteria in general and C. perfringens in particular were selected when enteral

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

38 le in the core genomes of poultry-associated C. perfringens isolates, a concept with both epidemiolog

39 omology to pilins in Gram-negative bacteria, C. perfringens appears to have two pilin subunits, PilA1

40 rfringens type A food poisoning is caused by C. perfringens isolates carrying a chromosomal cpe gene,

41 nificantly reduce the impact of NE caused by C. perfringens on broilers.

42 al gastrointestinal (GI) illnesses caused by C. perfringens type A isolates, including C. perfringens

43 iarrhea and gas gangrene, that are caused by C. perfringens.

44 ns of food-borne-disease outbreaks caused by C. perfringens.

45 The same four sigma factors are encoded by C. perfringens genomes, and two (SigE and SigK) have pre

46 nscriptional regulation of CPE expression by C. perfringens food poisoning isolates.

47 , when activated in a dysregulated manner by C. perfringens alpha toxin, may contribute to localized

48 encoded alpha-toxin and perfringolysin O by C. perfringens, as well as sporulation by Clostridium bo

49 de for the alpha and beta toxins produced by C. perfringens.

50 ortedly control in vitro toxin production by C. perfringens but their importance for virulence has no

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

52 gene, which encodes a sialidase secreted by C. perfringens, in the M. alligatoris genome.

53 ader sequence necessary for its secretion by C. perfringens is absent.

54 is a catabolite repressor of sporulation by C. perfringens.

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

56 which codes for beta-glucuronidase; E. coli-C. perfringens shuttle vectors carrying the fusions were

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

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

59 ed carriage of the tpeL gene among different C. perfringens strains, detecting this toxin gene in som

60 lation of sporulation varies among different C. perfringens strains.

61 d only in the mother cell compartment during C. perfringens sporulation.

62 ential synergistic toxin interactions during C. perfringens intestinal infections and support a possi

63 ncerted action of alpha-toxin and PFO during C. perfringens pathogenesis.

64 2+) and DPA into the developing spore during C. perfringens sporulation.

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

66 rrying sequences for the gene (cpe) encoding C. perfringens enterotoxin (CPE), were unable to express

67 od poisoning, is produced by enterotoxigenic C. perfringens type A isolates when these bacteria sporu

68 nsformants and the naturally enterotoxigenic C. perfringens NCTC 8239 were similar and that this mess

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

70 Although they lack flagella, C. perfringens bacteria can still migrate across surface

71 demonstrated that tissue destruction follows C. perfringens phospholipase C (PLC)-induced, platelet g

72 Sporulation is critical for C. perfringens type A food poisoning since spores contri

73 oxin) is the major virulence determinant for C. perfringens type-A food poisoning, the second most co

74 ative sigma factors, which are essential for C. perfringens sporulation.

75 s a potential auxiliary virulence factor for C. perfringens enteritis and enterotoxemia.

76 alternative sigma factors are necessary for C. perfringens sporulation, but only SigE, SigF, and Sig

77 uity of the patient's bowel was negative for C. perfringens.

78 eins and Ca-DPA release are not required for C. perfringens spore germination.

79 perfringens isolates may be responsible for C. perfringens type A food poisoning versus CPE-associat

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

81 However, the importance of SigF and SigG for C. perfringens sporulation or CPE production had not yet

82 a toxin, which are also important toxins for C. perfringens diseases (enteritis and enterotoxemia) or

83 A 4.0-kb DNA fragment from C. perfringens NCTC 8798 that contains the nanE and nanA

84 , from the genomic DNA library prepared from C. perfringens ATCC10543.

85 Upon its release from C. perfringens spores, CPE binds to its receptor, claudi

86 tream and downstream flanking sequences from C. perfringens food poisoning isolate NCTC 8239, or a 1.

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

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

89 Less than 5% of the global C. perfringens population apparently carries the cpe gen

90 the diarrheal and cramping symptoms of human C. perfringens type A food poisoning.

91 These findings implicate C. perfringens TFP in the ability of C. perfringens to a

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

93 mutagenesis system that works effectively in C. perfringens.

94 hways through which virulence has evolved in C. perfringens.

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

96 ribosomal methylase B (ermB) gene - found in C. perfringens and C. difficile.

97 ption and translation of the spoIIID gene in C. perfringens were not affected by mutations in sigE an

98 regulating the expression of other genes in C. perfringens.

99 n, suggesting an auxiliary role for GerAA in C. perfringens spore germination.

100 r poultry dishes were commonly implicated in C. perfringens (63%) and S. aureus (55%) outbreaks, and

101 eron and that transcription of the operon in C. perfringens is inducible by the addition of sialic ac

102 ureus outbreaks (median, 87%), but rarely in C. perfringens outbreaks (median, 9%).

103 valent cation transporters play some role in C. perfringens spore germination.

104 pA is necessary for efficient sporulation in C. perfringens, glucose-mediated catabolite repression o

105 tment in which enterotoxin is synthesized in C. perfringens.

106 ified Agr-like quorum-sensing (QS) system in C. perfringens controls all toxin production by surveyed

107 lture, providing the first evidence that, in C. perfringens, this system can control production of pl

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

109 etic component that explains the variance in C. perfringens strain virulence by assessing patterns of

110 by C. perfringens type A isolates, including C. perfringens type A food poisoning and non-food-borne

111 otentially plasmid-encoded toxins, including C. perfringens enterotoxin and beta2 toxin, encoded by t

112 These results indicate C. perfringens biofilms play an important role in the pe

113 Ingested C. perfringens vegetative cells sporulate in the intesti

114 rs carrying the fusions were introduced into C. perfringens by electroporation.

115 lucuronidase (gusA) gene and introduced into C. perfringens.

116 al transfer of a nonreplicating plasmid into C. perfringens, which led to inactivation of the ccpA ge

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

118 nsistent with NanI sialidase being the major C. perfringens sialidase when produced, FP and Db strain

119 ases and chromosomal cpe isolates cause most C. perfringens type A food poisoning cases.

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

121 suggest that many, if not all, cpe-negative C. perfringens isolates (including type B isolates, whic

122 s were also detected in several cpe-negative C. perfringens isolates carrying plasmids but not in typ

123 when transformed into naturally cpe-negative C. perfringens isolates.

124 8239, were electroporated into cpe-negative C. perfringens type A, B, and C isolates.

125 However, cpb2 genes from nonporcine C. perfringens isolates were not always expressed, at le

126 ium spiroforme culture supernatants, but not C. perfringens types C or D.

127 modules, which are found throughout numerous C. perfringens carbohydrate-active enzymes.

128 plicate C. perfringens TFP in the ability of C. perfringens to adhere to and move along muscle fibers

129 The ability of C. perfringens to regulate its exosialidase activity, la

130 s may be important factors in the ability of C. perfringens to survive in host tissues when bacterial

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

132 ous investigations into the genetic basis of C. perfringens pathogenicity have focused on toxins and

133 omise, and capillary leak characteristics of C. perfringens gas gangrene.

134 widely variable across a large collection of C. perfringens strains.

135 sents the first sequence-based comparison of C. perfringens isolates recovered in clinical cases of P

136 tal events in the mother cell compartment of C. perfringens is not the same as that in B. subtilis an

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

138 Escape of C. perfringens cells from phagosomes of macrophage-like

139 utation was introduced into the ccpA gene of C. perfringens by conjugational transfer of a nonreplica

140 found to be identical to the CPE0329 gene of C. perfringens strain 13, whose product was labeled as a

141 oxin-encoding genes and the 16S rRNA gene of C. perfringens.

142 s introduced into the pilT and pilC genes of C. perfringens abolished motility and surface localizati

143 e introduced into the sigE and sigK genes of C. perfringens.

144 on-based studies that showed rapid growth of C. perfringens on mucin-based substrates.

145 st to assist epidemiologic investigations of C. perfringens outbreaks.

146 r spores of both C-cpe and P-cpe isolates of C. perfringens and provided evidence that proteins encod

147 A total of 48 isolates of C. perfringens were obtained from different stages of th

148 onents of the spore germination machinery of C. perfringens and several Bacillus species and the bioi

149 PFO was shown to be the primary mediator of C. perfringens-dependent cytotoxicity to macrophages.

150 e developed an oral challenge mouse model of C. perfringens type D enterotoxemia.

151 this study we developed two mouse models of C. perfringens type C-induced lethality.

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

153 ens, or isogenic, toxin-deficient mutants of C. perfringens.

154 XbaI) were evaluated with a select panel of C. perfringens strains.

155 mportant contributors to the pathogenesis of C. perfringens type B infections in domestic animals.

156 l new model for studying the pathogenesis of C. perfringens type D infections.

157 d with the putative reduced pathogenicity of C. perfringens by BEOs contributed to the reduction in g

158 h inducible expression of PilA1 and PilA2 of C. perfringens were constructed.

159 d cpb genes, which indicated the presence of C. perfringens type C.

160 e due to sporulation-dependent production of C. perfringens enterotoxin encoded by the cpe gene.

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

162 content is essential for full resistance of C. perfringens spores to moist heat, UV radiation, and c

163 irst showed that human intestinal strains of C. perfringens can grow by utilizing either glucose or s

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

165 sis (PFGE) method for molecular subtyping of C. perfringens isolates to aid in epidemiologic investig

166 h PFO and PLC were necessary for survival of C. perfringens in mouse muscle tissue.

167 causes the gastrointestinal (GI) symptoms of C. perfringens type A food poisoning and CPE-associated

168 for causing the gastrointestinal symptoms of C. perfringens type A food poisoning, the second most co

169 Fs) known to mediate conjugative transfer of C. perfringens plasmid pCW3.

170 ategies may be possible for the treatment of C. perfringens-mediated myonecrosis.

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

172 ntial for cortex hydrolysis and viability of C. perfringens spores.

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

174 ts similar cytotoxicity-enhancing effects on C. perfringens enterotoxin and beta toxin, which are als

175 sts concerning the association of particular C. perfringens toxinotypes (type A to E) with gastrointe

176 ignificant association between CPB2-positive C. perfringens isolates and diarrhea in piglets.

177 notyping and phenotyping of 23 cpb2-positive C. perfringens isolates from horses with GI disease (ref

178 notyping and phenotyping of 29 cpb2-positive C. perfringens isolates from pigs with GI disease (pig G

179 that distinct subpopulations of cpe-positive C. perfringens isolates may be responsible for C. perfri

180 to compare the genotypes of 43 cpe-positive C. perfringens isolates obtained from diverse sources.

181 sion is necessary for these two cpe-positive C. perfringens type A human disease isolates to cause GI

182 factor in GI diseases involving cpe-positive C. perfringens type A isolates.

183 current study by examining 34 cpe-positive, C. perfringens fecal isolates from North American cases

184 us studies showed that NanI could potentiate C. perfringens epsilon toxin cytotoxicity by enhancing t

185 inal defense mechanism against CPB-producing C. perfringens isolates.

186 CPE-producing C. perfringens isolates have also recently been associat

187 C. perfringens type A strains producing C. perfringens enterotoxin (CPE) cause human food poison

188 amples from NEC infants not carrying profuse C. perfringens revealed an overabundance of a Klebsiella

189 e determined and compared with the published C. perfringens strain 13 genome.

190 involvement of AbrB repression in regulating C. perfringens sporulation.

191 biota can be identified in meconium samples; C. perfringens continues to be associated with NEC from

192 s produced only during sporulation and since C. perfringens can sporulate in the intestines.

193 Some C. perfringens isolates also produce the newly discovere

194 CPE is produced by sporulating C. perfringens cells in the small intestinal lumen, wher

195 se was purified from extracts of sporulating C. perfringens cells.

196 Indeed, wild-type and spoVA C. perfringens spores germinated similarly with a mixtur

197 Strikingly, C. perfringens was overrepresented in NMO (p = 5.24 x 10

198 ractical and reproducible means of subtyping C. perfringens libraries from specific epidemiological o

199 Given that C. perfringens alpha-toxin cleaves the phosphocholine he

200 Here we show that C. perfringens produces TFP and moves with an unusual fo

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

202 These results suggest that C. perfringens type A and C strains that cause human foo

203 Recent studies suggest that C. perfringens type A food poisoning is caused by C. per

204 ecent epidemiological studies suggested that C. perfringens isolates carrying the gene encoding CPB2

205 The C. perfringens cpe gene, encoding CPE, is transcribed fr

206 utralizing monoclonal antibodies against the C. perfringens epsilon-toxin.

207 h as CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL) quorum sensing (QS) syste

208 e A isolates carry the cpe gene encoding the C. perfringens enterotoxin.

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

210 Biotinylated antibodies to C. perfringens alpha toxin bound to streptavidin paramag

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

212 ded strong synergy to B. fragilis but not to C. perfringens.

213 dynamics of host microbiota in responding to C. perfringens infection.

214 against myonecrotic disease was specific to C. perfringens-mediated myonecrosis; buprenorphine did n

215 Significantly, wild-type C. perfringens cells adhered to mouse myoblasts under an

216 ed on animals infected with either wild-type C. perfringens, or isogenic, toxin-deficient mutants of

217 l in sheep, goats, and mice using a virulent C. perfringens type D wild-type strain (WT), an isogenic

218 s were injected together with killed, washed C. perfringens further substantiated these tissue-destru

219 ates indicated that all of the isolates were C. perfringens alpha-toxin gene positive and 46 of 48 is

220 G+C-content gram-positive bacteria, of which C. perfringens is a member.

221 a chromosomal enterotoxin gene (cpe), while C. perfringens type A isolates responsible for non-food-

222 osomal enterotoxin (cpe) gene (C-cpe), while C. perfringens-associated non-food-borne gastrointestina

223 n of morbidity and mortality associated with C. perfringens gas gangrene.

224 tor responsible for symptoms associated with C. perfringens type A food poisoning, is produced by ent

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

226 mics and functions in chicks challenged with C. perfringens.

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