ライフサイエンスコーパス: B. anthracis

1 B. anthracis and other pathogenic B. cereus isolates har

2 B. anthracis carries two copies of the ccdA gene, encodi

3 B. anthracis causes natural infection in humans and anim

4 B. anthracis does not elaborate wall teichoic acids; how

5 B. anthracis does not synthesize these polymers, yet its

6 B. anthracis gneY (BAS5048) and gneZ (BAS5117) encode ne

7 B. anthracis growth was locally controlled for 6 hours.

8 B. anthracis infection also induced a similar enteric ba

9 B. anthracis mutants lacking ltaS1, ltaS2, ltaS3, or lta

10 B. anthracis secretes two NEAT hemophores, IsdX1 and Isd

11 B. anthracis STPK101, a null mutant lacking BA-Stp1 and

12 B. anthracis strains were monitored over time in the pre

13 B. anthracis vesicles formed at the outer layer of the b

14 RS and well below the infective dose of 10(4)B. anthracis cells for inhalation anthrax.

15 A B. anthracis strain lacking the HtrC protease did not ge

16 In the presence of excess CapD, a B. anthracis gamma-glutamyl transpeptidase, the protecti

17 We created a B. anthracis mutant strain altered in lipoproteins by de

18 le of atxA in virulence factor expression, a B. anthracis atxA-null mutant is avirulent in a murine m

19 InhA1 purified from a B. anthracis culture supernatant directly cleaved each o

20 or B. thuringiensis sigP and rsiP genes in a B. anthracis sigP-rsiP-null mutant confers inducible pro

21 The virulence of a B. anthracis strain from which the ccpA gene was deleted

22 We demonstrated that a B. anthracis DeltaexsB mutant unable to synthesize ExsB

23 Here, we present evidence that a B. anthracis S-layer homology (SLH) protein harboring a

24 anthracis protective Ag (PA) together with a B. anthracis edema factor (EF) mutant having reduced ade

25 ved significantly longer than controls after B. anthracis challenge.

26 ole for Nod1/Nod2 in priming responses after B. anthracis aerosol exposure, as mice deficient in Nod1

27 bacterial activity by human NK cells against B. anthracis bacilli within infected autologous monocyte

28 ce, but not FcgammaR-deficient mice, against B. anthracis infection.

29 he mechanism by which MyD88 protects against B. anthracis infection, knockout mice were challenged wi

30 cipate in the innate immune response against B. anthracis and suggest that immune modulation to augme

31 thracis Ames ancestor, the progenitor of all B. anthracis Ames strains.

32 omplexity of germination responses may allow B. anthracis spores to respond to different environments

33 Although B. anthracis has undergone an ecological shift within th

34 mice after infection with the virulent Ames B. anthracis.

35 ore efficient at internalizing S. aureus and B. anthracis compared with E. coli Alveolar macrophages

36 I = CC(50)/MIC) values against S. aureus and B. anthracis for compound 20 were 33 and 66 and for comp

37 iensis that sets it apart from B. cereus and B. anthracis is the production of crystal (Cry) proteins

38 e associated with virulence in B. cereus and B. anthracis, respectively.

39 n virulence regulation between B. cereus and B. anthracis.

40 s upon the uptake of both microparticles and B. anthracis Sterne 34F2 spores.

41 thracis DNA into individual PCR mixtures and B. anthracis CFU into human blood.

42 treptogramin resistance protein, MLSRP), and B. anthracis (sul1), respectively.

43 acillus anthracis, Bordetella pertussis, and B. anthracis (sulfonamide resistance gene, sul1), respec

44 cular link between environmental sensing and B. anthracis pathogenesis.

45 We show that lethal toxin and B. anthracis challenge induce bacteremia as a result of

46 Ps@BNNSs) and conjugated with the mouse anti-B. anthracis Sap antibodies (Ab2); named Au-Pd NPs@BNNSs

47 As B. anthracis is not known to be motile, to be naturally

48 ely detect biological warfare agents such as B. anthracis, emergency responders can implement protoco

49 fficient to render the strain as virulent as B. anthracis Ames.

50 Liquid culture studies with S. aureus , B. anthracis , E. coli , and several other bacterial pat

51 Thus, similar to S. aureus, B. anthracis employs LtaS enzymes to synthesize LTA, an

52 Like several medically important bacteria, B. anthracis lacks glutathione but encodes many genes an

53 antly, in contrast to Sterne, the BaDeltaSET B. anthracis is avirulent in a lethal murine bacteremia

54 moving the focus toward interactions between B. anthracis and lymphoid and epithelial tissues.

55 o investigate the early interactions between B. anthracis spores and cutaneous tissue, spores were in

56 d by interorganizational coauthorships, both B. anthracis and Ebola virus research networks expanded

57 ished that the collagen-like regions of both B. anthracis and B. cereus are similarly substituted by

58 A duplex strand-unwinding activities of both B. anthracis and S. aureus helicases without affecting t

59 targets to halt deadly infections caused by B. anthracis and other pathogenic bacteria and suggest n

60 result in lethal infection of C. elegans by B. anthracis.

61 the outcome of LT challenge and infection by B. anthracis spores.

62 additional signaling molecule recognized by B. anthracis for toxin synthesis.

63 The exotoxins secreted by B. anthracis use capillary morphogenesis protein 2 (CMG2

64 lved in inflammation, as being suppressed by B. anthracis.

65 is of macrophages is not a mechanism used by B. anthracis to promote virulence, but rather a protecti

66 Using an experimental model of s.c. B. anthracis infection (an encapsulated nontoxigenic str

67 an and plant pathogens, including B. cereus, B. anthracis, and B. thuringiensis.

68 in the B. cereus group, including B. cereus, B. anthracis, and B. thuringiensis.

69 idase function that is apparent in B. cereus/B. anthracis.

70 In contrast, B. anthracis strains lacking both ltaS1 and ltaS2 were u

71 (LT) and edema toxin (ET) could contribute, B. anthracis cell wall peptidoglycan (PGN), not the toxi

72 itant administration of alpha-GalCer delayed B. anthracis systemic dissemination and prolonged mouse

73 eloped a rapid and sensitive assay to detect B. anthracis bacteremia using a system that is suitable

74 DIC during B. anthracis infection may be related more to components

75 r disruption and vascular dysfunction during B. anthracis infection.

76 shed from an active culture of encapsulated B. anthracis strain Ames in blood.

77 capsule derived from wild-type encapsulated B. anthracis Ames (WT) or a control preparation from an

78 owth of both the fully virulent encapsulated B. anthracis Ames and the non-encapsulated Sterne strain

79 s by acting as a "heme sponge" that enhances B. anthracis replication in iron-starved environments.

80 re identified in single-colony environmental B. anthracis Ames isolates associated with the investiga

81 netic parameters and binding order for every B. anthracis spore germinant pair.

82 vity against intracellular and extracellular B. anthracis.

83 timicrobial susceptibility by 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to

84 array protein (Sap), a unique biomarker for B. anthracis can offer an opportunity for specific detec

85 The tagO gene appears essential for B. anthracis growth and complements the tagO mutant phen

86 Results were available in <4 h for B. anthracis and <6 h for Y. pestis and B. pseudomallei

87 The detection limit for B. anthracis was found to be 50,000 endospores, on the b

88 were markedly higher than those reported for B. anthracis Ames and more like those of the toxigenic b

89 how that gneZ, but not gneY, is required for B. anthracis vegetative growth, rod cell shape, S-layer

90 stem as a new mutational analysis system for B. anthracis.

91 rapid antimicrobial susceptibility test for B. anthracis This method is based on automated digital t

92 ter-based detection cartridge and tested for B. anthracis on a GeneXpert instrument.

93 t requires a 16- to 20-h incubation time for B. anthracis Advances in high-resolution optical screeni

94 ublished 50% lethal dose (LD(50)) values for B. anthracis Ames after aerosol inoculation.

95 e of AtxA1 is identical to that of AtxA from B. anthracis, while the sequences of AtxA1 and AtxA2 are

96 In this work, cAMP from B. anthracis edema toxin (ET) is found to activate the N

97 l enzyme dihydrofolate reductase (DHFR) from B. anthracis.

98 n, enhancer-of-zeste, trithorax protein from B. anthracis (BaSET) methylates human histone H1, result

99 type Ib ribonucleotide reductase (RNR) from B. anthracis in the presence of NADPH and thioredoxin re

100 The purification of soluble SlaP from B. anthracis-cleared lysates did not reveal a specific l

101 ns to exploit host innate defenses to hinder B. anthracis colonization.

102 To further understand and compare how B. anthracis disseminates from these two different envir

103 ed to provide a comprehensive picture of how B. anthracis alters host physiology.

104 To understand how B. anthracis acquires iron from heme sources, which acco

105 r point-of-care detection rapidly identifies B. anthracis directly from blood with high sensitivity.

106 In B. anthracis and Bacillus subtilis htrC mutants, YpeB wa

107 In B. anthracis, S-layer proteins and BSLs attach via their

108 is-->Ala) amino acid changes for activity in B. anthracis cultures and for protein-protein interactio

109 Expression of ltaS1 or ltaS2 alone in B. anthracis as well as in other microbes was sufficient

110 Thus, lipoprotein biosynthesis in B. anthracis is required for full virulence in a murine

111 icate that ccdA2 encodes the primary CcdA in B. anthracis, active in all three pathways.

112 ate the roles of the two ccdA gene copies in B. anthracis, strains were constructed without each ccdA

113 for the restriction of m6A-containing DNA in B. anthracis remain unidentified, and we suggest that po

114 ficient replication of hemimethylated DNA in B. anthracis.

115 tudy provides the first evidence of DSPKs in B. anthracis that belong to different classes and have d

116 n the question of what additional factors in B. anthracis are responsible for iron uptake from the mo

117 at cwlT was needed for ICEBs1 to function in B. anthracis.

118 identify a novel role for the yceGH genes in B. anthracis Sterne virulence and suggest that C. elegan

119 tes the relationship between SleB, a GSLE in B. anthracis, and YpeB, a protein necessary for SleB sta

120 evidence of recent large-scale gene loss in B. anthracis or for unusual accumulation of nonsynonymou

121 o GBAA_pXO1_0023 is not stably maintained in B. anthracis, whereas the full-size parent pXO1 plasmid

122 etic tools developed for DNA manipulation in B. anthracis (Cre-loxP and Flp-FRT systems) were used to

123 r translocation to enhance H1 methylation in B. anthracis-infected macrophages.

124 These genotypes were identified only in B. anthracis morphotypes isolated from the letters, indi

125 enzymes for the BSH biosynthetic pathway in B. anthracis, which combine to produce alpha-d-glucosami

126 e directly linked to sporulation pathways in B. anthracis and more specifically to the regulation of

127 ns required for the import of petrobactin in B. anthracis.

128 nificant not only to virulence regulation in B. anthracis, but also to analysis of virulence regulati

129 ed by GBAA5330 and GBAA4766 respectively) in B. anthracis iron acquisition and pathogenesis.

130 Our results indicate that toxin secretion in B. anthracis is, at least, partially vesicle-associated,

131 sporulation genes spo0A, spo0B, and spo0F in B. anthracis Sterne resulted in phage resistance with co

132 ortant general disulfide reductase system in B. anthracis is TR1/Trx1 and that Trx1 is the physiologi

133 sm of protein attachment to the cell wall in B. anthracis we investigated the structure, backbone dyn

134 , several Gram-positive pathogens, including B. anthracis, contain genes that encode near iron transp

135 illus and Bacillus-related species including B. anthracis.

136 igate many other Bacillus species, including B. anthracis and even "non-pathogenic" Bacillus subtilis

137 Murine inhalational B. anthracis infections have two portals of entry, the n

138 taining vesicles were also visualized inside B. anthracis-infected macrophages.

139 T) or a control preparation from an isogenic B. anthracis Ames strain that produces only 2% of the ca

140 KBMA B. anthracis-vaccinated animals produced antibodies agai

141 However, like B. anthracis, full virulence of B. cereus G9241 for mice

142 ctivity against Gram-positive pathogens like B. anthracis.

143 mL with a minimum detection limit of 1 pg/mL B. anthracis Sap antigen.

144 sublethal anthrax infections, encounter most B. anthracis in the wet season and can partially booster

145 ening of a library of transposon-mutagenized B. anthracis spores identified a mutant displaying an al

146 We also used mutant B. anthracis strains to determine the effects on BclA gl

147 ples drawn from patients with concurrent non-B. anthracis bacteremia or nonbacteremic controls.

148 Assay specificity was 100% for tests of non-B. anthracis bacterial isolates and patient blood sample

149 e those of the toxigenic but nonencapsulated B. anthracis Sterne.

150 The ability of B. anthracis to cause anthrax is attributed to the plasm

151 ce of toxin did not influence the ability of B. anthracis to traffic to draining lymph nodes, but sys

152 contrast to other bacteria, O-acetylation of B. anthracis peptidoglycan is combined with N-deacetylat

153 iple inputs and may reflect an adaptation of B. anthracis to changing iron reservoirs during an infec

154 enome-wide expression microarray analysis of B. anthracis parental and sinR mutant strains indicated

155 Using kinetic analysis of B. anthracis spores germinated with inosine and L-alanin

156 lity shift assays revealed direct binding of B. anthracis SinR to promoter DNA from strongly regulate

157 sed at the same time in sporulating cells of B. anthracis and immediately colocalize to high-molecula

158 ile protection against a lethal challenge of B. anthracis Ames strain spores in rabbits.

159 unological pathway leading to the control of B. anthracis infection, a finding that might lead to imp

160 No report is available for the detection of B. anthracis by using atxA an anthrax toxin activator ge

161 fer an opportunity for specific detection of B. anthracis in culture broth.

162 developed a rapid protocol for detection of B. anthracis on clinical swabs.

163 immunosensor for ultrasensitive detection of B. anthracis Sap antigen.

164 t was found to provide enhanced detection of B. anthracis Sterne strain (34F2) spores relative to the

165 netic approach to search for determinants of B. anthracis chain length, we identified mutants with in

166 r developing species-specific diagnostics of B. anthracis spores and thus targeted therapeutic interv

167 the host environment alter dissemination of B. anthracis depending on the site of initial colonizati

168 at BslO effects a non-random distribution of B. anthracis chain lengths, implying that all septa are

169 crucial landmark dictating the emergence of B. anthracis, the evolution of this species and its clos

170 Protein assembly in the envelope of B. anthracis requires S-layer homology domains (SLH) wit

171 s were used to detect LTA in the envelope of B. anthracis strain Sterne (pXO1(+) pXO2(-)) vegetative

172 ar material within the cell wall envelope of B. anthracis.

173 the genetic background for the evolution of B. anthracis virulence, we obtained high-redundancy geno

174 In extracts of B. anthracis, Trx1 was responsible for almost all of the

175 Among the virulence factors of B. anthracis is the S-layer-associated protein BslA, whi

176 th very high similarities to the sap gene of B. anthracis.

177 to vegetative growth, neither germination of B. anthracis spores nor the formation of spores in mothe

178 ents that stimulate premature germination of B. anthracis spores, greatly simplifying decontamination

179 es of PrkD and PrkG and affect the growth of B. anthracis cells, indicating a possible role of these

180 om BaPGN-treated cells altered the growth of B. anthracis Sterne, and this effect was blocked by LT,

181 unable to bind iron could inhibit growth of B. anthracis.

182 itable tools for the rapid identification of B. anthracis.

183 hat culture is not reliable for isolation of B. anthracis from swabs at >/= 7 days.

184 patA1 and patA2 affect the chain lengths of B. anthracis vegetative forms and perturb the deposition

185 The majority of B. anthracis spores in the lung were tightly associated

186 hrax meningitis is a common manifestation of B. anthracis infection, has high mortality, and requires

187 aring model predictions with measurements of B. anthracis spores made after one of the 2001 anthrax l

188 Here we propose a new "jailbreak" model of B. anthracis dissemination which applies to the dissemin

189 ens, elicits protection in a murine model of B. anthracis infection.

190 n inhalational and cutaneous mouse models of B. anthracis infection.

191 ding site, and in vivo, surface molecules of B. anthracis spores promoted GALT development.

192 An FtsX mutant of B. anthracis known to be resistant to the antimicrobial

193 ed approximately 5,000 transposon mutants of B. anthracis Sterne for decreased virulence.

194 ine IL-15 and the protective antigen (PA) of B. anthracis into the Wyeth vaccinia virus.

195 y modifying the general secretory pathway of B. anthracis to transport large amounts of Sap and EA1.

196 have previously shown that peptidoglycan of B. anthracis can induce the production of proinflammator

197 We conclude that peptidoglycan of B. anthracis is initially bound by an unknown extracellu

198 report a novel mechanism for phagocytosis of B. anthracis spores.

199 sicle preparations confirmed the presence of B. anthracis toxin components.

200 s anthracis NrdF and the redox properties of B. anthracis NrdI.

201 etA (Bacillus exosporium-targeted protein of B. anthracis).

202 p and EA1 (Eag), the two S-layer proteins of B. anthracis, but not for the secretion of S-layer-assoc

203 of over half of all the secreted proteins of B. anthracis.

204 model parameters (e.g., release quantity of B. anthracis spores, risk of illness, spore setting velo

205 ed that the SETS yielded greater recovery of B. anthracis from 1-day-old swabs; however, reduced viab

206 The collagen-like region of B. anthracis is known to be densely substituted by unusu

207 plays a prominent role in the replication of B. anthracis in hematogenous environments.

208 pid, extensive, and efficient replication of B. anthracis in host tissues makes this pathogen an exce

209 ils in the dLNs, leading to the restraint of B. anthracis dissemination.

210 We investigated the roles of B. anthracis capsule and toxins in the pathogenesis of i

211 re, we report the detection of a simulant of B. anthracis (B. globigii) alone and in a mixture with a

212 globigii (Bg), which serves as a simulant of B. anthracis (or anthrax) and which possesses a peptidog

213 -LD(50) challenge with aerosolized spores of B. anthracis Ames strain.

214 Moreover, spores of B. anthracis were significantly better at persisting in

215 XO2-61 (or pXO1-118) inhibits sporulation of B. anthracis in a BA2291-dependent manner, and pXO2-61 e

216 This strain of B. anthracis can potentially serve as a preferred host f

217 A mutant strain of B. anthracis deficient in the BshA glycosyltransferase f

218 s hypothesis, we engineered three strains of B. anthracis Sterne, each marked with a different fluore

219 s in growth characteristics among strains of B. anthracis, which is considered to be a clonal organis

220 Ebola virus but contracted for the subset of B. anthracis research that did not involve possession of

221 tripped the PDGA capsule from the surface of B. anthracis Pasteur within 5 min.

222 tic pathway is required for the virulence of B. anthracis in guinea pigs.

223 The mature cell wall of B. anthracis is resistant to digestion by CwlT, indicati

224 uctural role in stabilizing the cell wall of B. anthracis.

225 alone exhibited little sporicidal effect on B. anthracis spores, while treatment with H(2)O(2) or Na

226 e likely to have significant implications on B. anthracis pathogenesis and microbial manipulation of

227 imicrobial chemicals, H(2)O(2) and NaOCl, on B. anthracis spores.

228 sion of host transcription as well as proper B. anthracis growth, making it a potentially unique viru

229 e end, all 27 test set samples including six B. anthracis strains were identified correctly.

230 and dynamic range were determined by spiking B. anthracis DNA into individual PCR mixtures and B. ant

231 s rapidly, subsequent and frequent sublethal B. anthracis infections cause maturation of anti-anthrax

232 matured less well in response to subsequent B. anthracis peptidoglycan (Ba PGN) exposure, with reduc

233 emoglobin directly at the bacterial surface, B. anthracis secretes IsdX1 to capture heme in the extra

234 esign of inhibitors that specifically target B. anthracis and other microbial IMPDH enzymes.

235 Our findings demonstrate that B. anthracis has evolved to use LT and ET to induce host

236 esults of the present study demonstrate that B. anthracis lrgAB and clhAB(2) play important roles in

237 We found that B. anthracis and C. tetani epitopes were the most promis

238 We have shown previously that B. anthracis Sterne is capable of blood-brain barrier (B

239 Our results show that B. anthracis LT blunts signaling through Tie-2, thereby

240 Previous work has shown that B. anthracis spores use germination (Ger) receptors to r

241 Together, the results suggest that B. anthracis spores have special properties that promote

242 The B. anthracis regulon includes homologues of some B. subt

243 The B. anthracis SinR protein also negatively regulates tran

244 ary for sensing beta-lactam antibiotics, the B. anthracis sigP and rsiP gene products are not suffici

245 ch are necessary for SLH domains to bind the B. anthracis SCWP.

246 er reaction and 10 CFU/ml blood for both the B. anthracis Sterne and V1B strains.

247 by specific detection of Sap secreted by the B. anthracis in culture broth just after 1h of growth.

248 ce proteins attached to the cell wall by the B. anthracis Sortase A ((Ba)SrtA) enzyme.

249 In contrast, the B. anthracis lcpB3 variant displayed reduced cell size a

250 parvum IMPDH inhibitors was examined for the B. anthracis enzyme and compared with those of three bac

251 In this study, we identified the B. anthracis lcpD mutant, which displays increased chain

252 upon concentration of the protein inside the B. anthracis cells.

253 malian substrates but also by modulating the B. anthracis secretome itself.

254 ontrast to hitherto characterized NrdIs, the B. anthracis NrdI is stable in its semiquinone form (Nrd

255 were sequenced and compared with that of the B. anthracis Ames ancestor, the progenitor of all B. ant

256 strains indicated limited convergence of the B. anthracis and B. subtilis SinR regulons.

257 s well as BslO near the septal region of the B. anthracis envelope.

258 Here the transmembrane topologies of the B. anthracis GerH(A), GerH(B), and GerH(C) proteins are

259 In solving the crystal structure of the B. anthracis siderophore biosynthesis protein B (AsbB),

260 gene immediately downstream of secA2 on the B. anthracis chromosome, is also a determinant of chain

261 Here, we report the effect of InhA1 on the B. anthracis secretome.

262 dily form biofilms, we hypothesized that the B. anthracis sinIR regulon is distinct from that of B. s

263 In stark contrast to the B. anthracis CoADR, the BaCoADR-RHD isoform does not cat

264 inkage units tethers pyruvylated SCWP to the B. anthracis envelope, thereby enabling S-layer assembly

265 erminal domain having some similarity to the B. anthracis septum site-determining protein MinD and a

266 This B. anthracis bshA locus (BA1558) has been identified in

267 molecular mechanisms of PHB contribution to B. anthracis sporulation and provide valuable insight in

268 nd therapeutic avenues for humans exposed to B. anthracis.

269 and can partially booster their immunity to B. anthracis.

270 ibute to sensitizing MyD88-deficient mice to B. anthracis and that MyD88 plays a protective role agai

271 (SNP) previously reported to be specific to B. anthracis was detected in some B. cereus strains.

272 on 1139, was identified as being specific to B. anthracis, which is a biothreat agent with high morta

273 ficient mice had increased susceptibility to B. anthracis and anthrax lethal toxin but not to edema t

274 e challenged with nonencapsulated, toxigenic B. anthracis or with anthrax toxins.

275 However, besides toxins, B. anthracis expresses effector proteins, whose role in

276 Deltasap mutant in trans with the wild-type B. anthracis sap or the sap gene from either of two diff

277 Unlike B. anthracis, much of the increased virulence gene expre

278 the disease pathophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mut

279 ted antimicrobial effects against vegetative B. anthracis bacilli.

280 er in their efficiency of recovery of viable B. anthracis cells.

281 portantly, lethal toxin produced by virulent B. anthracis blocked activation of protein kinases, p38

282 IL-1-dependent host protection from virulent B. anthracis.

283 ntratracheal spore challenge by the virulent B. anthracis Ames strain.

284 terized defined purH mutants of the virulent B. anthracis Ames strain.

285 Swabs were spiked with virulent B. anthracis cells, and the methods were compared for th

286 is most lethal and of greatest concern when B. anthracis is weaponized.

287 We propose a model whereby B. anthracis LCPs promote attachment of SCWP precursors

288 Here, we investigated whether B. anthracis impacts the function of colonic B-1 cells t

289 vide new insight into the mechanism by which B. anthracis triggers sepsis during a critical stage of

290 thrax; however, the mechanisms through which B. anthracis-derived factors contribute to the pathology

291 ta-lactamase activity, suggesting that while B. anthracis contains the genes necessary for sensing be

292 EF in liver lysates from mice infected with B. anthracis Sterne 34F2.

293 IgM MAb to A/JCr mice lethally infected with B. anthracis strain Sterne had no significant effect on

294 induced genes in a macrophage infected with B. anthracis.

295 survival following intranasal infection with B. anthracis spores in our studies but significantly inc

296 Acute infection with B. anthracis Sterne and the DeltaLF mutant resulted in d

297 ere completely protected from infection with B. anthracis strain Sterne, which suggested that a polyc

298 that weeks after intranasal inoculation with B. anthracis spores, substantial amounts of spores could

299 ng of Cry5B-expressing B. thuringiensis with B. anthracis can result in lethal infection of C. elegan

300 accumulation of toxic amounts of haem within B. anthracis.