ライフサイエンスコーパス: pseudomallei

1 g. PenA in B. cepacia complex and PenI in B. pseudomallei).

2 hemical associations with the presence of B. pseudomallei.

3 idase (GPx) of PMNs after exposed to live B. pseudomallei.

4 h as Francisella tularensis and Burkholderia pseudomallei.

5 about secretion systems of B. mallei and B. pseudomallei.

6 base with corresponding information about B. pseudomallei.

7 the Gram-negative soil bacillus Burkholderia pseudomallei.

8 y results guided soil sampling to isolate B. pseudomallei.

9 into a frequently overlooked reservoir of B. pseudomallei.

10 open a new avenue for the pathogenesis of B. pseudomallei.

11 tribution of NOD2 to the host response to B. pseudomallei.

12 th the NOD2 ligand, muramyl dipeptide, or B. pseudomallei.

13 ed against intraperitoneal challenge with B. pseudomallei.

14 tes when challenged with a lethal dose of B. pseudomallei.

15 ing severe Gram-negative sepsis caused by B. pseudomallei.

16 ethal challenge with B. thailandensis and B. pseudomallei.

17 d by the flagellated saprophyte Burkholderia pseudomallei.

18 nates were elevated in mice infected with B. pseudomallei.

19 elop chronic, subclinical infections with B. pseudomallei.

20 ctional characterization of BPSS2242 from B. pseudomallei.

21 mice infected via the aerosol route with B. pseudomallei.

22 by the environmental bacterium Burkholderia pseudomallei.

23 ard-rectifier K(+) channel from Burkholderia pseudomallei.

24 erall, 195 of 653 samples (29.7%) yielded B. pseudomallei.

25 em against reactive carbonyl compounds in B. pseudomallei..

26 /c mice to various amounts of aerosolized B. pseudomallei 1026b to determine lethality.

27 CT(E479) is another CDI toxin domain from B. pseudomallei 1026b.

28 ns were Escherichia coli (28%), Burkholderia pseudomallei (11%), Klebsiella pneumoniae (9%), and Stap

29 ngi, MB bottles improved the detection of B. pseudomallei (27% [MB] versus 8% [F]; P < 0.0001), with

30 sonance (NMR) spectroscopy, we found that B. pseudomallei 4095a and 4095c OPS antigens exhibited subs

31 Gram-negative sepsis caused by Burkholderia pseudomallei, a "Tier 1" biothreat agent and the causati

32 fungal infections and for infection with B. pseudomallei, a common cause of septicemia in Thailand.

33 Burkholderia pseudomallei, a facultative intracellular bacterium, cau

34 Burkholderia pseudomallei, a highly pathogenic bacterium that causes

35 h the highly virulent bacterium Burkholderia pseudomallei, a particularly antimicrobial-resistant pat

36 ic evidence of repeated reintroduction of B. pseudomallei across countries bordered by the Mekong Riv

37 ve shown that BipC was capable of delayed B. pseudomallei actin-based motility.

38 helial cells (IECs), we demonstrated that B. pseudomallei adheres, invades, and forms multinucleated

39 for the rapid in vivo diversification of B. pseudomallei after inoculation and systemic spread.

40 cells following infection with Burkholderia pseudomallei, an intracellular bacterial pathogen and th

41 pestis, Francisella tularensis, Burkholderia pseudomallei and Acinetobacter baumannii, with a view to

42 Burkholderia pseudomallei and B. mallei are bacterial pathogens that

43 In contrast, B. pseudomallei and B. mallei BimA mimic host Ena/VASP acti

44 mono- and disaccharidic fragments of the B. pseudomallei and B. mallei CPS repeating unit is reporte

45 hes and contribute to the pathogenesis of B. pseudomallei and B. mallei.

46 PL as a critical virulence determinant of B. pseudomallei and B. thailandensis, further highlighting

47 g exopolysaccharide produced by Burkholderia pseudomallei and bacteria of the B. cepacia complex is d

48 The global distribution of B. pseudomallei and burden of melioidosis, however, remain

49 ted from the pathogenic species Burkholderia pseudomallei and Burkholderia mallei and from less-patho

50 Burkholderia pseudomallei and Burkholderia mallei are potential biote

51 the closely related pathogenic Burkholderia pseudomallei and Burkholderia mallei.

52 ultative intracellular bacteria Burkholderia pseudomallei and Burkholderia thailandensis.

53 l cases and the presence of environmental B. pseudomallei and combine this in a formal modelling fram

54 A bipC TTSS-3-deficient strain of B. pseudomallei and complemented strains were generated to

55 hogenic, select-agent-excluded strains of B. pseudomallei and covalently linked to carrier proteins.

56 sis results from infection with Burkholderia pseudomallei and is associated with case-fatality rates

57 Melioidosis is caused by Burkholderia pseudomallei and is predominantly seen in tropical regio

58 that is caused by the bacterium Burkholderia pseudomallei and is underreported in many countries wher

59 ionally interchangeable between Burkholderia pseudomallei and its relatives B. mallei, B. oklahomensi

60 Mice were intranasally infected with live B. pseudomallei and killed after 24, 48, or 72 hours for ha

61 ce were intranasally infected with viable B. pseudomallei and killed after 24, 48, or 72 hours for ha

62 tranasally infected with viable Burkholderia pseudomallei and killed after 24, 48, or 72 hrs for harv

63 Thailand was co-cultured with B. pseudomallei and production of IL-10 and IFN-gamma detec

64 VgrG5 facilitates intercellular spread by B. pseudomallei and related species following injection acr

65 upon subsequent infection with Burkholderia pseudomallei and Salmonella enterica HMBA treatment was

66 The global distribution of B. pseudomallei and the burden of melioidosis, however, rem

67 d to investigate cross-reactivity between B. pseudomallei and the related Burkholderia species associ

68 The human pathogen Burkholderia pseudomallei and the related species Burkholderia thaila

69 tic C-terminal regions from the Burkholderia pseudomallei and Xanthamonas campestris p.v.

70 cases, and the presence of environmental B. pseudomallei, and combine this in a formal modelling fra

71 ignificant protection from challenge with B. pseudomallei, and protection was associated with a signi

72 No coworkers had detectable anti-B. pseudomallei antibody, whereas seropositive results amon

73 B. mallei and B. pseudomallei are closely related genetically; B. mallei

74 urkholderia cepacia complex and Burkholderia pseudomallei are opportunistic human pathogens.

75 Burkholderia mallei and B. pseudomallei are the causative agents of glanders and me

76 Due to the potential malicious use of B. pseudomallei as well as its impact on public health in r

77 gates of antigen-induced immunity against B. pseudomallei as well as provide valuable insights toward

78 25 x 25 m) should be sufficient to detect B. pseudomallei at a given location if samples are taken at

79 ltured soil from a rice field in Laos for B. pseudomallei at different depths on 4 occasions over a 1

80 Burkholderia spp. that includes Burkholderia pseudomallei, B. mallei, and B. thailandensis.

81 This global survey of the QS regulons of B. pseudomallei, B. thailandensis, and B. mallei serves as

82 is showed similar LPS ladder patterns for B. pseudomallei, B. thailandensis, and B. mallei, these pat

83 pidly recognizing isolates suspicious for B. pseudomallei, be able to safely perform necessary rule-o

84 Burkholderia pseudomallei (Bp) and Burkholderia mallei (Bm) are Tier-

85 Burkholderia pseudomallei (Bp) and Burkholderia mallei (Bm), the etio

86 Burkholderia pseudomallei (Bp) is the causative agent of the infectio

87 terial infections, particularly Burkholderia pseudomallei (Bp), the causative agent of melioidosis in

88 , antibiotic-resistant pathogen Burkholderia pseudomallei (BP).

89 Burkholderia pseudomallei (Bpm) is a bacterial pathogen that causes M

90 Burkholderia pseudomallei, Burkholderia thailandensis, and Burkholder

91 ve cell mediated immune responses against B. pseudomallei, but may also moderate the pathological eff

92 allei evolved from an ancestral strain of B. pseudomallei by genome reduction and adaptation to an ob

93 tested for evidence of prior exposure to B. pseudomallei by indirect hemagglutination assay.

94 ction induced by flagellin or heat-killed B. pseudomallei by TLR5(1174C)>T genotype in healthy subjec

95 ith the gram-negative bacterium Burkholderia pseudomallei can result in melioidosis, a life-threateni

96 B. pseudomallei carries a putative cyclophilin B gene, ppiB

97 Burkholderia mallei and B. pseudomallei cause glanders and melioidosis, respectivel

98 The environmental bacterium Burkholderia pseudomallei causes an estimated 165,000 cases of human

99 m and potential biothreat agent Burkholderia pseudomallei causes melioidosis, an often fatal infectio

100 Infection with Burkholderia pseudomallei causes the disease melioidosis, which often

101 Biochemical analysis of three B. pseudomallei CdiA-CTs revealed that each protein possess

102 ivity of detection and recovery of viable B. pseudomallei cells from small volumes (0.45 ml) of urine

103 with B. pseudomallei Next, we found that B. pseudomallei-challenged TLR5-deficient (Tlr5(-/-) ) mice

104 nclude Acinetobacter baumannii, Burkholderia pseudomallei, Chlamydia trachomatis, Escherichia coli, K

105 Deficiency of Nrf2 improved B. pseudomallei clearance by macrophages, whereas Nrf2 acti

106 fection caused by the bacterium Burkholderia pseudomallei Clinical diagnosis of melioidosis can be ch

107 AhpC is virtually invariant among global B. pseudomallei clinical isolates, a Cambodian isolate vari

108 ularensis, Burkholderia mallei, Burkholderia pseudomallei, Clostridium botulinum, Brucella melitensis

109 % to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to conventional methods.

110 anthracis, Yersinia pestis, or Burkholderia pseudomallei Conventional susceptibility tests require 1

111 pernatants of B. pseudomallei MSHR668 and B. pseudomallei DeltagspD grown in rich and minimal media.

112 A B. pseudomallei DeltappiB (BpsDeltappiB) mutant strain demo

113 The B. pseudomallei DeltarelA DeltaspoT mutant displayed a defe

114 Mutational analysis of wild-type B. pseudomallei demonstrated that ceftazidime resistance wa

115 The FCR method showed greater B. pseudomallei detection sensitivity than conventional uri

116 ides new insights into global patterns of B. pseudomallei dissemination, most notably the dynamic nat

117 Detection of B. pseudomallei DNA or recovery of the pathogen by culture

118 ice treated with doxycycline survived and B. pseudomallei DNA was not amplified from the lungs or spl

119 We demonstrate that B. pseudomallei down-regulation of ELT-2 targets is associa

120 The bsa locus of Burkholderia pseudomallei encodes several proteins that are component

121 Importantly, the viability of B. pseudomallei encountered dicarbonyl toxicity was enhance

122 ams targeting both at-risk individuals in B. pseudomallei endemic regions as well as CF patients.

123 than the 30 cm currently recommended for B. pseudomallei environmental sampling.

124 o encompass strong CD4 T cell epitopes in B. pseudomallei-exposed individuals and in HLA transgenic m

125 B. pseudomallei expresses three serologically distinct LPS

126 The B. pseudomallei flagellar protein FliC is strongly seroreac

127 B. pseudomallei FliC contained several peptide sequences wi

128 T cell hybridomas against an immunogenic B. pseudomallei FliC epitope also cross-reacted with orthol

129 We assessed B. pseudomallei FliC peptide binding affinity to multiple H

130 or clinical sample positive for Burkholderia pseudomallei from 2001 to 2012.

131 Taken together, isolation of B. pseudomallei from a soil sample and high seropositivity

132 The diversity of B. pseudomallei from Myanmar and divergence within our glob

133 aerosolized clinical isolate of Burkholderia pseudomallei from Thailand.

134 enes may be remnants of the QS network in B. pseudomallei from which this host-adapted pathogen evolv

135 ecies: B. thailandensis, B. gladioli, and B. pseudomallei Furthermore, we show that absence of protei

136 t of in vitro and in vivo models to study B. pseudomallei gastrointestinal infection.

137 Pseudomallei group Burkholderia are emerging pathogens w

138 Pseudomallei group Burkholderia species are facultative

139 disease caused by the bacterium Burkholderia pseudomallei, has a wide spectrum of clinical manifestat

140 ed to prepare highly purified recombinant B. pseudomallei Hcp1 and TssM proteins.

141 Human OECs killed >90% of the B. pseudomallei in a CPS I-independent manner and exhibited

142 display markedly impaired phagocytosis of B. pseudomallei In conclusion, these data suggest that TLR5

143 However, culture of B. pseudomallei in environmental samples is difficult and l

144 measured NF-kappaB activation induced by B. pseudomallei in human embryonic kidney-293 cells transfe

145 , phylogeography and potential origins of B. pseudomallei in Myanmar.

146 ysicians to provide treatment specific to B. pseudomallei In our study, we adapted host gene expressi

147 tis and B. pseudomallei One exception was B. pseudomallei in the presence of ceftazidime, which requi

148 A and Bp340DeltabcaB mutants to wild-type B. pseudomallei in vitro demonstrated similar levels of adh

149 d diabetic individuals infected with live B. pseudomallei in vitro showed lower free glutathione (GSH

150 althy individuals and improved killing of B. pseudomallei in vitro.

151 protective immunity against B. mallei and B. pseudomallei, including antigen discovery.

152 the highly pathogenic bacterium Burkholderia pseudomallei, indicating that therapeutic dose and metab

153 B. pseudomallei induced lower monocyte-normalized levels of

154 ells transfected with TLR5 and found that B. pseudomallei induced TLR5(1174C)- but not TLR5(1174T)-de

155 gnatures obtained from microarray data of B. pseudomallei-infected cases to develop a real-time PCR d

156 The unfavorable outcome of B. pseudomallei infection after HO-1 induction was associat

157 e demonstrated enhanced susceptibility to B. pseudomallei infection compared with wild type mice as e

158 eins, but its role in the pathogenesis of B. pseudomallei infection is not well understood.

159 tes effective protective immunity against B. pseudomallei infection remains incomplete.

160 Their roles in B. pseudomallei infection were investigated in vitro using

161 sights into the host defense responses to B. pseudomallei infection within an intact host, we analyze

162 er explore the role of the OM response to B. pseudomallei infection, we infected human olfactory ensh

163 ontribute to the pathogenesis observed in B. pseudomallei infection.

164 r biliverdin, ferrous iron, and CO during B. pseudomallei infection.

165 susceptibility of diabetic individuals to B. pseudomallei infection.

166 investigated the role of tetraspanins in B. pseudomallei infection.

167 induced protective immunity against acute B. pseudomallei infection.

168 nternalization and membrane fusion during B. pseudomallei infection.

169 ct on the host response against pulmonary B. pseudomallei infection.

170 d infection induced weight loss following B. pseudomallei infection.

171 We tested blood from 33 patients with B. pseudomallei infections and 29 patients with other bacte

172 ified calprotectin as a lead biomarker of B. pseudomallei infections and examined correlations betwee

173 mising antivirulence target to both treat B. pseudomallei infections and increase antibiotic efficacy

174 ost-B. mallei interactions and 2,286 host-B. pseudomallei interactions.

175 st CD9 and CD9-EC2 significantly enhanced B. pseudomallei internalization, but MAb against CD81 and C

176 and that type 1 fimbria is important for B. pseudomallei intestinal adherence, and we identify a new

177 th American isolates with introduction of B. pseudomallei into the Americas between 1650 and 1850, pr

178 Furthermore, we show that B. pseudomallei invades fibroblasts and keratinocytes and s

179 Burkholderia pseudomallei is a CDC tier 1 select agent that causes me

180 Burkholderia pseudomallei is a Gram-negative bacterium and the causat

181 Burkholderia pseudomallei is a Gram-negative intracellular bacterium

182 Burkholderia pseudomallei is a Gram-negative soil bacterium that infe

183 Burkholderia pseudomallei is a tier 1 select agent and the causative

184 Burkholderia pseudomallei is a tier 1 select agent, and the causative

185 B. pseudomallei is an encapsulated bacterium that can infec

186 Overall, we showed that B. pseudomallei is an enteric pathogen and that type 1 fimb

187 Burkholderia pseudomallei is an intracellular bacterium and the causa

188 relatives with very different lifestyles: B. pseudomallei is an opportunistic pathogen, B. thailanden

189 B. pseudomallei is classed as a tier 1 select agent by the

190 alkyl hydroperoxidase reductase (AhpC) of B. pseudomallei is strongly immunogenic for T cells of 'hum

191 Burkholderia pseudomallei is the causative agent of melioidosis chara

192 Burkholderia pseudomallei is the causative agent of melioidosis, a di

193 Burkholderia pseudomallei is the causative agent of melioidosis, an i

194 negative intracellular pathogen Burkholderia pseudomallei is the causative agent of melioidosis, an i

195 Burkholderia pseudomallei is the causative agent of melioidosis.

196 Burkholderia pseudomallei is the causative agent of the tropical dise

197 by the Gram-negative bacterium Burkholderia pseudomallei, is a frequent cause of pneumosepsis in Sou

198 Melioidosis, caused by Burkholderia pseudomallei, is a potentially lethal infection with no

199 idosis, caused by the bacterium Burkholderia pseudomallei, is an often severe infection that regularl

200 ith the environmental bacterium Burkholderia pseudomallei, is being recognised increasingly frequentl

201 ioidosis, an infectious disease caused by B. pseudomallei, is diabetes mellitus.

202 d by the Gram-negative bacillus Burkholderia pseudomallei, is difficult to cure.

203 Melioidosis, caused by Burkholderia pseudomallei, is endemic in northeastern Thailand and No

204 prove when the infecting agent, Burkholderia pseudomallei, is rapidly detected and identified by labo

205 n/immunity protein complex from Burkholderia pseudomallei isolate E479.

206 uate 69 independent colonies of Burkholderia pseudomallei isolated from seven body sites of a patient

207 Twelve Burkholderia pseudomallei isolates collected over a 32-month period f

208 We used whole genome sequences of 469 B. pseudomallei isolates from 30 countries collected over 7

209 esent the first whole-genome sequences of B. pseudomallei isolates from Myanmar: nine clinical and se

210 B. pseudomallei isolates from the property's groundwater su

211 We observed that primary clinical B. pseudomallei isolates with mucoid and nonmucoid colony m

212 Burkholderia pseudomallei isolates with shared multilocus sequence ty

213 ations outside the OA subset in Burkholderia pseudomallei K96243 for comparison.

214 computationally derived information about B. pseudomallei K96243.

215 nvolved in LPS synthesis was performed in B. pseudomallei K96243.

216 expressed during macrophage infection by B. pseudomallei K96243.

217 sis we have identified 8 putative Ltgs in B. pseudomallei K96243.

218 O-releasing molecule CORM-2 increases the B. pseudomallei load in macrophages and mice.

219 B. pseudomallei locus tags within the full text and tables

220 h a combination of CPS2B1 and recombinant B. pseudomallei LolC, rather than with CPS2B1 or LolC indiv

221 Thus, our data suggest that the B. pseudomallei-mediated induction of HO-1 and the release

222 ith the Gram-negative bacterium Burkholderia pseudomallei (melioidosis) are associated with high mort

223 Following exposure to B. pseudomallei, mice lacking the lectin-like domain of thr

224 y proteins present in the supernatants of B. pseudomallei MSHR668 and B. pseudomallei DeltagspD grown

225 The secretion profiles of B. pseudomallei MSHR668 and its T2SS mutants were noticeabl

226 hepatic compartments upon infection with B. pseudomallei Next, we found that B. pseudomallei-challen

227 ter low-dose inoculation with aerosolized B. pseudomallei, Nod2-deficient mice showed impaired clinic

228 Although unrelated in sequence, the two B. pseudomallei nuclease domains share similar folds and ac

229 ound magnesium ions in the active site of B. pseudomallei OLD in a geometry that supports a two-metal

230 r B. anthracis and <6 h for Y. pestis and B. pseudomallei One exception was B. pseudomallei in the pr

231 Our studies indicate that B. pseudomallei OPS undergoes antigenic variation and sugge

232 ing with clinical isolates suspicious for B. pseudomallei or clinical specimens from suspected melioi

233 B. cenocepacia, Burkholderia multivorans, B. pseudomallei, or Burkholderia mallei develop O-glycan-sp

234 Recent genomic studies showed that B. pseudomallei originated in Australia and spread to Asia,

235 causative agent of melioidosis, Burkholderia pseudomallei Passive-transfer experiments also revealed

236 rulence with roles in different stages of B. pseudomallei pathogenesis, including extracellular and i

237 determine its role(s) in the virulence of B. pseudomallei pathogenesis.

238 n reduced the survival of intramacrophage B. pseudomallei Pharmacological administration of cobalt pr

239 ngs indicate functional redundancy of the B. pseudomallei phospholipases in virulence.

240 nces in our understanding of the disease, B. pseudomallei poses a significant health risk, especially

241 lei proteins, and new information for 281 B. pseudomallei proteins associated with 5 secretion system

242 ived a lethal inhalational challenge with B. pseudomallei Remarkably, 70% of the survivors had no cul

243 sults and decrease the number of negative B. pseudomallei reports that are currently observed from ur

244 h kinetics or the levels of bacteremia of B. pseudomallei represent the next-generation of diagnostic

245 Finally, we also showed that B. pseudomallei requires a functional T6SS for full virulen

246 ic mechanisms of action for B. mallei and B. pseudomallei secretion system proteins inferred from the

247 virulence attenuation experiments for 61 B. pseudomallei secretion system proteins.

248 e, Wong et al. (2015) show that Burkholderia pseudomallei senses host cytosolic glutathione, a low-mo

249 a role in virulence in either the BCC or B. pseudomallei Since many of these TCS are involved in vir

250 mediated NF-kappaB activation induced by B. pseudomallei stimulation of HEK293 cells.

251 The genome of B. pseudomallei strain 1026b encodes nine putative trimeric

252 en reading frame Bp1026b_II1054 (bcaA) in B. pseudomallei strain 1026b is predicted to encode a class

253 ted to intranasal challenge with virulent B. pseudomallei strain 1026b.

254 ing mutant MM36 compared to the wild-type B. pseudomallei strain 1026b.

255 , we created a relA spoT double mutant in B. pseudomallei strain K96243, which lacks (p)ppGpp-synthes

256 ct Agent-excluded purM deletion mutant of B. pseudomallei (strain Bp82) and then subjected to intrana

257 tagenesis and secretion experiments using B. pseudomallei strains engineered to express T6SS-5 in vit

258 immunity against challenge with wild-type B. pseudomallei, suggesting that the genes identified in ou

259 CPS I improved B. pseudomallei survival in vivo and triggered multiple cyt

260 , these findings show a role for CPS I in B. pseudomallei survival in vivo following inhalation infec

261 he first in-depth characterization of the B. pseudomallei T2SS secretome.

262 e on GSH and PMN functions in response to B. pseudomallei that may contribute to the susceptibility o

263 al infectious disease caused by Burkholderia pseudomallei that results in high mortality.

264 DNA from eight strains of B. pseudomallei that were spiked into synthetic urine at lo

265 gen and culture filtrate [CF] antigen) of B. pseudomallei The ELISAs were evaluated using serum sampl

266 tanding of adaptive immunity to Burkholderia pseudomallei, the causative agent of melioidosis that is

267 Burkholderia pseudomallei, the causative agent of melioidosis, has co

268 Burkholderia pseudomallei, the causative agent of melioidosis, is an

269 The LPS structure of B. pseudomallei, the causative agent of melioidosis, is hig

270 Burkholderia pseudomallei, the causative agent of melioidosis, is rec

271 Burkholderia pseudomallei, the causative agent of melioidosis, posses

272 Burkholderia pseudomallei, the etiologic agent of melioidosis, causes

273 Burkholderia pseudomallei, the etiologic agent of melioidosis, is a C

274 Burkholderia pseudomallei, the etiologic agent of melioidosis, is an

275 cretion system proteins for B. mallei and B. pseudomallei, their pathogenic mechanisms of action, and

276 During infection with Burkholderia pseudomallei, tissue-type plasminogen activator-deficien

277 We report the capacity of B. pseudomallei to enter, efficiently replicate in, and med

278 We used aerosol delivery of B. pseudomallei to establish respiratory infection in mice

279 infected with either high or low doses of B. pseudomallei to generate either acute, chronic, or laten

280 a is involved in the initial adherence of B. pseudomallei to IECs, although the impact on full virule

281 /-)) mice were intranasally infected with B. pseudomallei to induce severe pneumosepsis (melioidosis)

282 ancient and more recent dissemination of B. pseudomallei to Myanmar and elsewhere in Southeast Asia

283 suggest that the original introduction of B. pseudomallei to Myanmar was not a recent event.

284 urkholderia species and compare those for B. pseudomallei to those for the other seven species.

285 Degradation of ELT-2 requires the B. pseudomallei type III secretion system.

286 standing into the molecular mechanisms of B. pseudomallei virulence and dormancy.

287 to cell, indicating ppiB is essential for B. pseudomallei virulence.

288 eature of the transcriptional response to B. pseudomallei was a progressive increase in the proportio

289 B. pseudomallei was associated with a high soil water conte

290 piric use of antibiotics not specific for B. pseudomallei was associated with increased risk of death

291 ression was up-regulated by ten-fold when B. pseudomallei was cultured under high salt concentration.

292 Burkholderia pseudomallei was first isolated from the environment of

293 A higher prevalence of B. pseudomallei was found at soil depths greater than the 3

294 Burkholderia pseudomallei was isolated from soil collected in the nei

295 heptan capsular polysaccharide (CPS) from B. pseudomallei was purified, chemically activated, and cov

296 ogenase/oxidoreductase (SDR) in Burkholderia pseudomallei, was identified and its expression was up-r

297 Separate from the BCC is Burkholderia pseudomallei, which is the causative agent of melioidosi

298 Comparing B. pseudomallei wild-type with plc mutants revealed that pl

299 roteins exported by these systems provide B. pseudomallei with a growth advantage in vitro and in viv

300 notably the dynamic nature of movement of B. pseudomallei within densely populated Southeast Asia.