ライフサイエンスコーパス: B. cepacia

1 B. cepacia DBO1 AntDO (designated AntDO-3C) is a three-c

2 B. cepacia isolates recovered from 606 CF patients recei

3 B. cepacia strains were determined by polymerase chain r

4 l and environmental sources and included 107 B. cepacia complex strains, 23 Burkholderia gladioli str

5 s that included 69 Pandoraea sp. strains, 24 B. cepacia complex strains, 6 Burkholderia gladioli stra

6 During this period, 28 B. cepacia isolates were obtained from clinical specimen

7 IS1363 was used to probe a collection of 943 B. cepacia complex isolates, representing all nine genom

8 he misidentification of a Pandoraea sp. as a B. cepacia complex isolate.

9 not flagellin-deficient strain PAK/fliC or a B. cepacia fliC mutant, activated the NF-kappaB reporter

10 Host defense against B. cepacia and C. violaceum is critically dependent in v

11 Although all B. cepacia complex species were found, some were rarely

12 ty was demonstrated in LPS extracts from all B. cepacia strains tested, with one environmental strain

13 bactin, a siderophore produced by nearly all B. cepacia strains, can induce P. aeruginosa PA4467.

14 zymes may play an important role in allowing B. cepacia to evade host defence.

15 in this study, we suggest a role that allows B. cepacia to thwart the immune response and a model of

16 late clinical isolates of P. aeruginosa, and B. cepacia.

17 isogenic flagellin-free strains PAK/fliC and B. cepacia BC/fliC.

18 e available, B. mallei, B. pseudomallei, and B. cepacia, are predicted to contain only the first two

19 Patients with arthropathy, B. cepacia infection, or younger age derive no aggregate

20 As B. cepacia is currently being developed as a biocontrol

21 several isolates presumptively identified as B. cepacia by clinical microbiology laboratories were in

22 culture isolates presumptively identified as B. cepacia.

23 The species most frequently misidentified as B. cepacia was Burkholderia gladioli.

24 stered cases were initially misidentified as B. cepacia, and available isolates from 4 of these cases

25 two to seven isolates were misidentified as B. cepacia.

26 account for differences in virulence between B. cepacia genomovars.

27 In vitro, both B. cepacia and C. violaceum were sensitive to H(2)O(2) a

28 e penetration of host epithelial barriers by B. cepacia, contributing to establishment of infection a

29 and sometimes invasive infections caused by B. cepacia suggest that the organism possesses mechanism

30 t the distinct invasion pathways employed by B. cepacia may account for differences in virulence betw

31 at dietary intake on the day of infection by B. cepacia can make a significant difference in long-ter

32 Infection by B. cepacia poses a great risk to cystic fibrosis patient

33 The level of epithelial cell invasion by B. cepacia in the A549 model was relatively low compared

34 Colonization of the lungs of a CF patient by B. cepacia can lead not only to a decline in respiratory

35 ndicating that ornibactin can be produced by B. cepacia and detected by P. aeruginosa when the two sp

36 late is an important siderophore produced by B. cepacia complex isolates, and both extrinsic salicyla

37 e autophagy allows Burkholderia cenocepacia (B. cepacia) to survive and replicate in DeltaF508 macrop

38 In the second outbreak, two consecutive B. cepacia infection/colonization cases were seen in the

39 rosis (CF) patient sputum samples containing B. cepacia genomovar I, Burkholderia multivorans, B. cep

40 in-producing but not an ornibactin-deficient B. cepacia strain, indicating that ornibactin can be pro

41 r this enzyme, while non-phthalate-degrading B. cepacia strains have only a single gene.

42 cate that DBO1 and other phthalate-degrading B. cepacia strains have two dissimilar genes for this en

43 ed that recA-based PCR could reliably detect B. cepacia complex organisms to concentrations of 10(6)

44 ndependently by culture and by PCR to detect B. cepacia.

45 enge, but numbers of organisms for different B. cepacia strains varied.

46 the product-size patterns used to type each B. cepacia isolate.

47 rains is a new observation for this emerging B. cepacia complex pathogen and suggests that certain st

48 to enable separation of strains of all five B. cepacia complex genomovars.

49 ent over previously published PCR assays for B. cepacia.

50 s were obtained to evaluate risk factors for B. cepacia acquisition.

51 putum samples that were culture positive for B. cepacia either prior or subsequent to this study.

52 mples from 100 CF patients were screened for B. cepacia complex infection by selective culturing and

53 wo primer pairs were putatively specific for B. cepacia.

54 athogenic Burkholderia cenocepacia (formally B. cepacia genomovar III) isolates, and determined its c

55 We cloned and hyperexpressed a gene from B. cepacia strain 71 that encodes the homologue of P. ae

56 other lipopeptide toxins, the hemolysin from B. cepacia was surface active and lowered the surface te

57 to (i) more reliably amplify these loci from B. cepacia complex species, (ii) amplify these same loci

58 this hemolytic activity and is secreted from B. cepacia J2315, a representative of the virulent and h

59 this gene for growth on phthalate thus gives B. cepacia an advantage over other phthalate-degrading b

60 Four patients grew B. cepacia from the blood, with the organism being the s

61 Hepatic B. cepacia burden was similar in the two genotypes, but

62 n, the 16S primer pair putatively identified B. cepacia in seven patients whose sputa were culture ne

63 accuracies of these systems for identifying B. cepacia ranged from 43 to 86%, with the Remel system

64 the same species as zmpA and was detected in B. cepacia, B. cenocepacia, B. stabilis, B. ambifaria, a

65 expression of beta-lactamases (e.g. PenA in B. cepacia complex and PenI in B. pseudomallei).

66 The invasion phenotype in B. cepacia may be an important virulence factor for CF i

67 esence or absence of pathogenic potential in B. cepacia strains proposed for environmental release.

68 These organisms include B. cepacia, Burkholderia sp. other than B. cepacia, and

69 eas overexpression of p62 leads to increased B. cepacia intracellular growth.

70 ages confirmed the presence of intracellular B. cepacia and showed that intracellular bacteria were c

71 Intraperitoneal B. cepacia challenge (4.0 x 10(3) to 4.0 x 10(5) organis

72 esence of putative transmissibility markers (B. cepacia epidemic strain marker [BCESM] and cable pili

73 All systems misidentified B. cepacia complex.

74 pacia genomovar I, Burkholderia multivorans, B. cepacia genomovar III, Burkholderia stabilis, and Bur

75 y based on 16S and 23S rRNA gene analysis of B. cepacia ATCC 25416 (genomovar I) was useful in identi

76 se results warrant a multicenter analysis of B. cepacia complex-infected patients with genomovar-typi

77 The clinical course of B. cepacia infections is variable, but approximately 20%

78 al data, numbers of organisms in cultures of B. cepacia from multiple sites were higher for p47(phox)

79 investigation of the global epidemiology of B. cepacia complex genomovar III, the species most commo

80 that p62 differentially dictates the fate of B. cepacia infection in WT and DeltaF508 macrophages.

81 the largest chromosome within the genome of B. cepacia complex strains and, in contrast to the findi

82 or the rapid detection and identification of B. cepacia complex genomovars directly from sputum.

83 ostic method for the rapid identification of B. cepacia in sputum samples of CF patients.

84 To determine the influence of B. cepacia complex genomovar type on transplant outcome,

85 r characterize the mechanisms of invasion of B. cepacia, we screened a transposon-generated mutant li

86 tility are required for full invasiveness of B. cepacia.

87 y demonstrated that a CF clinical isolate of B. cepacia, strain J2315, can invade and survive within

88 An environmental isolate of B. cepacia, strain J2540, was also examined for its abil

89 Various environmental isolates of B. cepacia are, however, capable of degrading environmen

90 r 150 nonfermenters including 58 isolates of B. cepacia recovered from respiratory secretions from CF

91 tween clinical and environmental isolates of B. cepacia with regard to their virulence characteristic

92 ifferent agars designed for the isolation of B. cepacia complex varied considerably in their inhibiti

93 and medical implications of the isolation of B. cepacia from CF patients, accurate identification of

94 ests that they are not sufficient markers of B. cepacia virulence or transmissibility.

95 flowthrough fraction of the growth medium of B. cepacia strain 71 enriched with the azurin and cytoch

96 in were examined by use of a murine model of B. cepacia infection.

97 nd characterization of a nonmotile mutant of B. cepacia with reduced invasiveness due to disruption o

98 may contribute to the inflammatory nature of B. cepacia infection in CF patients, both by promoting i

99 lectrophoresis analysis of a large number of B. cepacia genomovar III isolates (including isolates be

100 ut the virulence factors and pathogenesis of B. cepacia, although the persistent and sometimes invasi

101 important determinant in the pathogenesis of B. cepacia.

102 iginal vented FAN medium for the recovery of B. cepacia and yeasts, especially C. albicans and C. neo

103 length of exposure, or FEV1 and the risk of B. cepacia acquisition.

104 var III patients were at the highest risk of B. cepacia complex-related mortality (5 of 12 versus 0 o

105 atory molecules, we investigated the role of B. cepacia LPS in neutrophil activation processes.

106 invasion and intracellular sequestration of B. cepacia in CF are persistence of infection in the fac

107 tation evaluation were not a major source of B. cepacia complex strains that infected our resident CF

108 highly transmissible and virulent strain of B. cepacia (J2315) was found to increase neutrophil surf

109 e filtrates of clinically derived strains of B. cepacia are hemolytic.

110 but insufficient to discriminate strains of B. cepacia genomovars I and III and B. stabilis.

111 nses, and (ii) that environmental strains of B. cepacia may have considerable inflammatory potential

112 horesis confirmed that one of two strains of B. cepacia recovered from the nebulizer of a third patie

113 now report that several clinical strains of B. cepacia secrete cytotoxic factors that allow macropha

114 roles in the ability of virulent strains of B. cepacia to evade the host immune response and cause p

115 reliable tool for epidemiological studies of B. cepacia isolates from nosocomial outbreaks.

116 e the invasion and intracellular survival of B. cepacia J2315, a highly transmissible clinical isolat

117 Thirty-one B. cepacia complex isolates belonging to five of the sev

118 ption of B. ambifaria, was absent from other B. cepacia complex species.

119 tion sequences identified in AC1100 or other B. cepacia isolates.

120 The majority (36 of 56) of our B. cepacia complex-infected CF patients harbor isolates

121 As expected, panresistant B. cepacia patients had a lower 1-yr survival (50% versu

122 The mechanisms that permit B. cepacia to cause bacteremia are not yet known but pro

123 uring identified 19 samples with presumptive B. cepacia complex infection, which was corroborated by

124 Burkholderia multivorans is a prominent B. cepacia complex (BCC) species causing infection in pe

125 The original species B. cepacia has been split into eight genetic species (ge

126 lude B. cepacia, Burkholderia sp. other than B. cepacia, and infrequently encountered environmental s

127 ntracellular growth assays demonstrated that B. cepacia J2315 was able to enter, survive, and replica

128 These findings indicate (i) that B. cepacia LPS may contribute to the inflammatory nature

129 The B. cepacia gene is the most recent addition to a growing

130 The B. cepacia isolate produces low levels of octanoyl-HSL.

131 ese species, collectively referred to as the B. cepacia complex, differ in their epidemiology and pat

132 he rRNA operon, to specifically identify the B. cepacia complex in a PCR.

133 -yr survival were significantly lower in the B. cepacia complex cohort.

134 primers for detection of each species of the B. cepacia complex in sputum samples.

135 urkholderia pseudomallei and bacteria of the B. cepacia complex is described.

136 conclusion, analysis of the recA gene of the B. cepacia complex provides a rapid and robust nucleotid

137 Successful amplification of the B. cepacia complex recA gene from cystic fibrosis (CF) p

138 ed the abilities of different species of the B. cepacia complex, including a strain from the ET12 lin

139 Each of the B. cepacia complex-related deaths was caused by a unique

140 logenetically closely related species of the B. cepacia complex.

141 rains representative of the diversity of the B. cepacia complex.

142 ws its redistribution and recruitment to the B. cepacia vacuole, mediating the acquisition of the aut

143 ere assessed to determine species within the B. cepacia complex and examined for the presence of puta

144 by light and electron microscopy, all three B. cepacia strains tested circumvented the mechanical ba

145 ) and had a higher mortality attributable to B. cepacia (50% versus 0%, p < 0.01) compared with panre

146 OS(-/-) and wild-type mice were resistant to B. cepacia challenges of at least 10(6) organisms per mo

147 nt genomic-based methods can be used to type B. cepacia genomovar III isolates depending on the situa

148 Transplanted adults with B. cepacia, arthropathy, or a 5-year predicted survival

149 l isolates of P. aeruginosa, as well as with B. cepacia, suggesting that the more severe clinical out

150 20% of patients, pulmonary colonization with B. cepacia leads to cepacia syndrome, a fatal fulminatin

151 ents whose nebulizers were contaminated with B. cepacia did not yield the organism.

152 data suggest that CF patients infected with B. cepacia complex and referred for lung transplantation

153 Fifty percent of patients were infected with B. cepacia complex genomovar III, 38% with B. multivoran

154 solates from referred patients infected with B. cepacia complex isolates prior to referral.

155 multivorans, 11 patients (65%) infected with B. cepacia genomovar III-A, and 4 patients (23%) infecte

156 ar III-A, and 4 patients (23%) infected with B. cepacia genomovar III-B.

157 rient intake and tolerance of infection with B. cepacia, a bacterial pathogen of rising importance in

158 e clinical isolates of P. aeruginosa or with B. cepacia cannot be explained by differences in the ear

159 , were infected pre- or postoperatively with B. cepacia complex.

160 months in those infected preoperatively with B. cepacia complex compared with those not infected (33%

161 predicted survival of less than 50% without B. cepacia or arthropathy have improved survival.

162 s with low 5-year predicted survival without B. cepacia infection should receive priority for lung tr