Comparative analysis of extracellular enzymes and virulence exhibited by Burkholderia pseudomallei from different sources

Vellasamy, Kumutha Malar; Vasu, Chenthamarakshan; Puthucheary, S. D.; Vadivelu, Jamuna

doi:10.1016/j.micpath.2009.06.003

Cited by 15 publications

(15 citation statements)

References 51 publications

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“…[12], [34], [35], [36], [37], sigma factor [32], [38], quorum sensing [39], reactive nitrogen intermediates [40], O-antigen [41], chaperonin GroEL [42], multidrug effect pump, secondary metabolism functions or drug resistance functions, intracellular stress and motility and chemotaxis [12]. Therefore, these data confirm the previous report from Ulett et al, 2001 that there is no difference in virulence between clinical and environmental isolates.…”

Section: Discussionsupporting

confidence: 88%

Genomic Islands as a Marker to Differentiate between Clinical and Environmental Burkholderia pseudomallei

et al. 2012

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Burkholderia pseudomallei, as a saprophytic bacterium that can cause a severe sepsis disease named melioidosis, has preserved several extra genes in its genome for survival. The sequenced genome of the organism showed high diversity contributed mainly from genomic islands (GIs). Comparative genome hybridization (CGH) of 3 clinical and 2 environmental isolates, using whole genome microarrays based on B. pseudomallei K96243 genes, revealed a difference in the presence of genomic islands between clinical and environmental isolates. The largest GI, GI8, of B. pseudomallei was observed as a 2 sub-GI named GIs8.1 and 8.2 with distinguishable %GC content and unequal presence in the genome. GIs8.1, 8.2 and 15 were found to be more common in clinical isolates. A new GI, GI16c, was detected on chromosome 2. Presences of GIs8.1, 8.2, 15 and 16c were evaluated in 70 environmental and 64 clinical isolates using PCR assays. A combination of GIs8.1 and 16c (positivity of either GI) was detected in 70% of clinical isolates and 11.4% of environmental isolates (P<0.001). Using BALB/c mice model, no significant difference of time to mortality was observed between K96243 isolate and three isolates without GIs under evaluation (P>0.05). Some virulence genes located in the absent GIs and the difference of GIs seems to contribute less to bacterial virulence. The PCR detection of 2 GIs could be used as a cost effective and rapid tool to detect potentially virulent isolates that were contaminated in soil.

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Section: Discussionsupporting

confidence: 88%

Genomic Islands as a Marker to Differentiate between Clinical and Environmental Burkholderia pseudomallei

et al. 2012

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“…[10][11][12]35,[38][39][40] Even strains that originate from the same parental strain exhibit phenotypic diversity, particularly in colony morphology. 17,41 Both arginine deiminase and quorum sensing systems have been suggested to modulate the formation of colonies in response to different environmental conditions.…”

Section: Discussionmentioning

confidence: 99%

“…The filtrates ( 0.45 μm, 100 μL) of the B. pseudomallei culture supernatants (3 mL) grown in LB (Luria broth) at 37 C for 24 hr were used for the detection of extracellular enzyme activity (U/mL). 12 One unit of protease activity was defined as an increase of 0.05 U/hr (540 nm) in a reaction solution (5 mg/mL of azocoll in 0.5 mL of 50 mM PBS, pH 7.5) that was incubated at 37 C for 16 hr. One unit of phospholipase C activity was defined as the amount of enzyme required to produce 1 μM of p-nitrophenol per minute in the reaction solution (20 mM p-nitrophenylphosphorylcholine in 250 mM Tris-HCl, pH 7.0, 60% glycerol (v/v) and 1 mM ZnCl 2 ).…”

Section: Methodsmentioning

confidence: 99%

“…9 The general virulence determinants, such as extracellular enzymes (protease, phospholipase, and catalase), biofilm formation, swarming ability, and lipopolysaccharide (LPS) types of different B. pseudomallei isolates are diverse. [10][11][12] The expression of one or more of these virulence determinants is associated with changes in bacterial colony morphology. [13][14][15][16] In B. pseudomallei, wrinkled and dry colonies are commonly observed in human isolates, and these morphologies are associated with the degree of virulence in BALB/c mice.…”

Section: Introductionmentioning

confidence: 99%

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Alteration of the Phenotypic and Pathogenic Patterns of Burkholderia pseudomallei that Persist in a Soil Environment

Chen

Shieh

Goldsmith³

et al. 2014

The American Society of Tropical Medicine and Hygiene

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Abstract. Melioidosis is caused by the soil-borne pathogen Burkholderia pseudomallei. To investigate whether the distinct phenotypic and virulent characteristics result from environmental adaptations in the soil or from the host body, two pairs of isogenic strains were generated by passages in soil or mice. After cultivation in soil, the levels of 3-hydroxytetradecanoic acid, biofilm formation, flagellar expression, and ultrastructure were altered in the bacteria. Uniformly fatal melioidosis developed as a result of infection with mouse-derived strains; however, the survival rates of mice infected with soil-derived strains prolonged. After primary infection or reinfection with soil-derived strains, the mice developed a low degree of bacterial hepatitis and bacterial colonization in the liver and bone marrow compared with mice that were infected with isogenic or heterogenic mouse-derived strains. We suggest that specific phenotypic and pathogenic patterns can be induced through infection with B. pseudomallei that has been cultured in different (soil versus mouse) environments.

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“…PLC activity was determined through the breakdown of pNPPC. The reaction was prepared as described previously but with minor modifications: a 20 mM solution of pNPPC was prepared in 0.25 M Tris-HCl buffer (pH 7.0) containing 60% glycerol (v/v) and 1 mM zinc chloride (44,65). The reaction was initiated by the addition of 10 ll supernatant to 190 ll of reaction reagent and the A 440 measured after 5 h incubation at 310 K.…”

Section: Plc Assaymentioning

confidence: 99%

DisarmingBurkholderia pseudomallei: Structural and Functional Characterization of a Disulfide Oxidoreductase (DsbA) Required for VirulenceIn Vivo

Ireland

McMahon²,

Marshall³

et al. 2014

Antioxidants & Redox Signaling

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Aims: The intracellular pathogen Burkholderia pseudomallei causes the disease melioidosis, a major source of morbidity and mortality in southeast Asia and northern Australia. The need to develop novel antimicrobials is compounded by the absence of a licensed vaccine and the bacterium's resistance to multiple antibiotics. In a number of clinically relevant Gram-negative pathogens, DsbA is the primary disulfide oxidoreductase responsible for catalyzing the formation of disulfide bonds in secreted and membrane-associated proteins. In this study, a putative B. pseudomallei dsbA gene was evaluated functionally and structurally and its contribution to infection assessed. Results: Biochemical studies confirmed the dsbA gene encodes a protein disulfide oxidoreductase. A dsbA deletion strain of B. pseudomallei was attenuated in both macrophages and a BALB/c mouse model of infection and displayed pleiotropic phenotypes that included defects in both secretion and motility. The 1.9 Å resolution crystal structure of BpsDsbA revealed differences from the classic member of this family Escherichia coli DsbA, in particular within the region surrounding the active site disulfide where EcDsbA engages with its partner protein E. coli DsbB, indicating that the interaction of BpsDsbA with its proposed partner BpsDsbB may be distinct from that of EcDsbA-EcDsbB. Innovation: This study has characterized BpsDsbA biochemically and structurally and determined that it is required for virulence of B. pseudomallei. Conclusion: These data establish a critical role for BpsDsbA in B. pseudomallei infection, which in combination with our structural characterization of BpsDsbA will facilitate the future development of rationally designed inhibitors against this drug-resistant organism. Antioxid. Redox Signal. 20,[606][607][608][609][610][611][612][613][614][615][616][617]

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Comparative analysis of extracellular enzymes and virulence exhibited by Burkholderia pseudomallei from different sources

Cited by 15 publications

References 51 publications

Genomic Islands as a Marker to Differentiate between Clinical and Environmental Burkholderia pseudomallei

Genomic Islands as a Marker to Differentiate between Clinical and Environmental Burkholderia pseudomallei

Alteration of the Phenotypic and Pathogenic Patterns of Burkholderia pseudomallei that Persist in a Soil Environment

DisarmingBurkholderia pseudomallei: Structural and Functional Characterization of a Disulfide Oxidoreductase (DsbA) Required for VirulenceIn Vivo

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