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 udomonas aeruginosa, and VirR of Clostridium perfringens.

5 reted by the anaerobic bacterium Clostridium perfringens.

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

7 specific-pathogen-free chicks by Clostridium perfringens.

8 found in the bacterial pathogen Clostridium perfringens.

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

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

11 es, including the human pathogen Clostridium perfringens.

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

13 coli, Bacteroides fragilis, and Clostridium perfringens.

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

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

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

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

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

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

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

21 0% homology to a sequence within Clostridium perfringens adenosine triphosphate-binding cassette (ABC

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

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

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

25 say for identifying and assaying Clostridium perfringens alpha toxin.

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

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

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

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

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

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

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

33 s- forming bacteria - most often Clostridium perfringens and Escherichia coli.

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

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

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

37 replication of bacteria, such as Clostridium perfringens and Salmonella enterica serovar Typhimurium.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 show that Clostridium perfringens beta-toxin (CPB) binds platelet endothelial

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

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

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

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

61 ivity against the human pathogen Clostridium perfringens By combining in vivo and in vitro approaches

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

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

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

65 Clostridium perfringens can produce up to three different sialidases

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

67 ssociated with responses against Clostridium perfringens, Candida albicans, and Bacteroides vulgatus

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

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

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

76 Sequential Eimeria maxima and C. perfringens challenges significantly induced NE, severe

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 ogenic bacterial sialidases from Clostridium perfringens (CpNanI) and Vibrio cholerae.

86 against human pathogens such as Clostridium perfringens, define two hairpin domains giving this sact

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

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

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

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

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

92 mplicated in the pathogenesis of Clostridium perfringens enteritis.

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

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

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

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

97 Clostridium perfringens enterotoxin (CPE) causes food poisoning and

98 Clostridium perfringens enterotoxin (CPE) causes the gastrointestina

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

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

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

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

103 Clostridium perfringens enterotoxin (CPE) is a pore-forming toxin th

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

105 Clostridium perfringens enterotoxin (CPE) is responsible for causing

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

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

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

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

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

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

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

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

114 Clostridium perfringens enterotoxin causes the gastrointestinal (GI)

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

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

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

118 Clostridium perfringens epsilon toxin belongs to the aerolysin-like

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

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

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

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

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

124 occus aureus, Bacillus subtilis, Clostridium perfringens, Escherichia coli), except Enterococcus faec

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

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

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

128 Clostridium perfringens food poisoning is caused by type A isolates

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

130 anaerobic gram-positive pathogen Clostridium perfringens forms biofilms.

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

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

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

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

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

136 ), at as low as 50 uM, inhibited 82.8% of C. perfringens growth in Tryptic Soy Broth (P < 0.05).

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

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

139 njection of formalin-fixed whole cells of C. perfringens HN13 (a laboratory strain) and JGS4143 (chic

140 racis, Campylobacter jejuni, and Clostridium perfringens IMPDHs.

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

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

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

144 itive exclusion agent to control Clostridium perfringens in poultry.

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

146 Mechanism studies revealed that C. perfringens induced (P < 0.05) elevated expression of in

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

148 ecrotic enteritis (NE) caused by Clostridium perfringens infection has reemerged as a prevalent poult

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

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

151 Interestingly, DCA reduced C. perfringens invasion into ileum (P < 0.05) without alter

152 Clostridium perfringens iota-toxin consists of two separate proteins

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

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

155 Clostridium perfringens is a leading cause of food-poisoning and cau

156 Clostridium perfringens is a ubiquitous and versatile pathogenic bac

157 Clostridium perfringens is an anaerobic Gram-positive pathogen that

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

159 Clostridium perfringens is an important human and animal pathogen th

160 C. perfringens is an underrecognized but frequently observe

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

162 No effective vaccine against C. perfringens is currently available.

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

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

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

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

167 Clostridium perfringens is the third most frequent cause of bacteria

168 forming toxin (PFT) produced by Clostridium perfringens, is responsible for the pathogenesis of ente

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

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

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

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

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

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

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 n chicken experiment, oral challenge with C. perfringens JGS4143 lead to 22% survival, whereas co-gav

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

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

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

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

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

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

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

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 ease-associated bacteria such as Clostridium perfringens, Ruminococcus gnavus, and Klebsiella pneumon

208 The human pathogenic bacterium Clostridium perfringens secretes an enterotoxin (CpE) that targets c

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

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

211 C. perfringens sleC spores did not germinate completely wit

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

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

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

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

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

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

218 C. perfringens spores lacking GerO were defective in germin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

239 Many Clostridium perfringens strains produce NanI as their major sialidas

240 Clostridium perfringens strains produce severe diseases, including m

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

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

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

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 iserum screen of mutants generated from a C. perfringens transposon-mutant library, here we identifie

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

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

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

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

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

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

263 Clostridium perfringens type A isolates carrying an enterotoxin (cpe

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

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

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

267 ulture confirmed the presence of Clostridium perfringens type A.

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

269 Clostridium perfringens type B causes enteritis and enterotoxemia in

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

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

272 Clostridium perfringens type C isolates cause enteritis necroticans

273 Clostridium perfringens type C isolates cause enterotoxemias and ent

274 Clostridium perfringens type C isolates, which cause enteritis necro

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

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

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

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

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

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

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

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

283 Clostridium perfringens type D enterotoxemias have significant econo

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

285 Clostridium perfringens type D isolates are important in biodefense

286 Clostridium perfringens type D isolates cause enterotoxemia in sheep

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

288 Clostridium perfringens type D strains cause enterotoxemia and enter

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

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

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

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

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

294 Ingested C. perfringens vegetative cells sporulate in the intestinal

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

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

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

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

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

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