Burkholderia cenocepacia

Burkholderia cenocepacia is a species of Gram-negative bacteria that is common in the environment, can form a biofilm with itself,[1] is resistant to many antibiotics[2] and may cause disease in plants.

Electron micrograph of Burkholeria cepacia

Burkholderia cenocepacia
Scientific classification
Kingdom:
Bacteria
Phylum:
Proteobacteria
Class:
Betaproteobacteria
Order:
Burkholderiales
Family:
Burkholderiaceae
Genus:
Burkholderia
Species:
B. cenocepacia
Binomial name
Burkholderia cenocepacia
Vandamme et al. 2003

Pathogenicity

It is an opportunistic pathogen and human infections are common in patients with cystic fibrosis and chronic granulomatous disease, and are often fatal.[3] In cystic fibrosis, it can cause "cepacia syndrome" which is characterized by a rapidly progressive fever, uncontrolled bronchopneumonia, weight loss, and in some cases, death. A review of B. cenocepacia in respiratory infections of cystic fibrosis patients stated that "one of the most threatening pathogens in [cystic fibrosis] is Burkholderia cenocepacia, a member of a bacterial group collectively referred to as the Burkholderia cepacia complex (Bcc)".[4] Twenty-four Small RNAs were identified using RNA binding properties of the Hfq protein during the exponential growth phases.[5] sRNAs identified in Burkholderia cenocepacia KC-0 were upregulated under iron depletion and oxidate stress.[6]

See also: Burkholderia thailandensis sRNA

Taxonomy

Originally defined as B. cepacia, the group has now been split into nine species,[7] and B. cenocepacia is one of the most intensively-studied.[8]

Microbiology

In addition, the strong environmental protection response of B. cenocepacia is attributed to the biofilm formed by groups of the organism.[2] This biofilm contains exopolysaccharides (abbreviated EPS) that strengthen the bacterium's resistance to antibiotics. It is made up of a highly branched polysaccharide unit with one glucose, one glucuronic acid, one mannose, one rhamnose, and three galactose molecules. This species in the Bcc has also created another polysaccharide with one 3-deoxy-d-manno-2-octulosonic acid and three galactose molecules.[9] The biofilm exopolysaccharides acted as a barrier to neutrophils from human immune resistance systems, undermining the neutrophil defense action by inhibiting chemotaxis and reducing the production of reactive oxygen species.[10]

References
  1. Magdolna Csavas; Lenka Malinovska; Florent Perret; Milan Gyurko; Zita Tunde Illyes; Michaela Wimmerova; Aniko Borbas (14 November 2016). "Tri- and tetravalent mannoclusters cross-link and aggregate BC2L-A lectin from Burkholderia cenocepacia". Carbohydrate Research. Elsevier. 437: 1–8. doi:10.1016/j.carres.2016.11.008. hdl:2437/239138. PMID 27871013. Burkholderia cenocepacia is a Gram-negative bacterium with the ability to form a biofilm
  2. Nida H. Alshraiedeh; Sarah Higginbotham; Padrig B. Flynn; Mahmoud Y. Alkawareek; Michael M. Tunney; Sean P. Gorman; William G. Graham; Brendan F. Gilmore (22 April 2016). "Eradication and phenotypic tolerance of Burkholderia cenocepacia biofilms exposed to atmospheric pressure non-thermal plasma". International Journal of Antimicrobial Agents. 47 (6): 446–450. doi:10.1016/j.ijantimicag.2016.03.004. PMID 27179816. B. cenocepacia can spread from person to person and exhibits intrinsic broad-spectrum antibiotic resistance
  3. Magdolna Csavas; Lenka Malinovska; Florent Perret; Milan Gyurko; Zita Tunde Illyes; Michaela Wimmerova; Aniko Borbas (14 November 2016). "Tri- and tetravalent mannoclusters cross-link and aggregate BC2L-A lectin from Burkholderia cenocepacia". Carbohydrate Research. Elsevier. 437: 1–8. doi:10.1016/j.carres.2016.11.008. hdl:2437/239138. PMID 27871013. It is recognized as an opportunistic human pathogen causing lung infections in immunocompromised individuals, especially in cystic fibrosis patients, with significant mortality and morbidity
  4. P. Drevinkek; E. Mahenthiralingam (2010). "Burkholderia cenocepacia in cystic fibrosis: epidemiology and molecular mechanisms of virulence". Clinical Microbiology and Infection. 16 (7): 821–830. doi:10.1111/j.1469-0691.2010.03237.x. PMID 20880411. Retrieved 6 January 2017.
  5. Ramos, Christian G.; Grilo, André M.; da Costa, Paulo J. P.; Leitão, Jorge H. (February 2013). "Experimental identification of small non-coding regulatory RNAs in the opportunistic human pathogen Burkholderia cenocepacia J2315". Genomics. 101 (2): 139–148. doi:10.1016/j.ygeno.2012.10.006. ISSN 1089-8646. PMID 23142676.
  6. Ghosh, Suparna; Dureja, Chetna; Khatri, Indu; Subramanian, Srikrishna; Raychaudhuri, Saumya; Ghosh, Sagarmoy (2017-11-03). "Identification of novel small RNAs in Burkholderia cenocepacia KC-01 expressed under iron limitation and oxidative stress conditions". Microbiology. 163 (12): 1924–1936. doi:10.1099/mic.0.000566. ISSN 1465-2080. PMID 29099689.
  7. Lipuma J (2005). "Update on the Burkholderia cepacia complex". Curr Opin Pulm Med. 11 (6): 528–33. doi:10.1097/01.mcp.0000181475.85187.ed. PMID 16217180.
  8. Mahenthiralingam E, Vandamme P (2005). "Taxonomy and pathogenesis of the Burkholderia cepacia complex". Chron Respir Dis. 2 (4): 209–17. doi:10.1191/1479972305cd053ra. PMID 16541604.
  9. Chiarini, Luigi; Cescutti, Paola; Drigo, Laura; Impallomeni, Giuseppe; Herasimenka, Yury; Bevivino, Annamaria; Dalmastri, Claudia; Tabacchioni, Silvia; Manno, Graziana; Zanetti, Flavio; Rizzo, Roberto (2004-08-01). "Exopolysaccharides produced by Burkholderia cenocepacia recA lineages IIIA and IIIB". Journal of Cystic Fibrosis. 3 (3): 165–172. doi:10.1016/j.jcf.2004.04.004. ISSN 1569-1993. PMID 15463903.
  10. Johann Bylund; Lee-Anna Burgess; Paola Cescutti; Robert K. Ernst; David P. Speert (29 November 2005). "Exopolysaccharides from Burkholderia cenocepacia Inhibit Neutrophil Chemotaxis and Scavenge Reactive Oxygen Species" (PDF). The Journal of Biological Chemistry. 281 (5): 2526–2532. doi:10.1074/jbc.M510692200. PMID 16316987. Retrieved 6 January 2017. We showed that EPS from a clinical B. cenocepacia isolate interfered with the function of human neutrophils in vitro; it inhibited chemotaxis and production of reactive oxygen species (ROS), both essential components of innate neutrophil-mediated host defenses
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