Burkholderia cenocepacia

From WikiProjectMed
Jump to navigation Jump to search

Burkholderia cenocepacia
Electron micrograph of Burkholderia cepacia
Scientific classification edit
Domain: Bacteria
Phylum: Pseudomonadota
Class: Betaproteobacteria
Order: Burkholderiales
Family: Burkholderiaceae
Genus: Burkholderia
B. cenocepacia
Binomial name
Burkholderia cenocepacia
Vandamme et al. 2003

Burkholderia cenocepacia is a Gram-negative, rod-shaped bacterium that is commonly found in soil and water environments and may also be associated with plants and animals, particularly as a human pathogen.[1] It is one of over 20 species in the Burkholderia cepacia complex (Bcc) and is notable due to its virulence factors and inherent antibiotic resistance that render it a prominent opportunistic pathogen responsible for life-threatening, nosocomial infections in immunocompromised patients, such as those with cystic fibrosis or chronic granulomatous disease.[2] The quorum sensing systems CepIR and CciIR regulate the formation of biofilms and the expression of virulence factors such as siderophores and proteases.[3] Burkholderia cenocepacia may also cause disease in plants, such as in onions[4][5] and bananas.[6] Additionally, some strains serve as plant growth-promoting rhizobacteria.[7]


Within the Burkholderia genus, the Burkholderia cepacia complex contains over 20 related species that cause opportunistic infections and possess antibiotic resistance.[8] Burkholderia cepacia was originally defined as a single species, but it is now one of several species in the Bcc.[9] Although closely related, the species within the Bcc have differing severity of pathogenicity, and B. cenocepacia is one of the most intensively studied due to its higher pathogenicity and antibiotic resistance compared to other species in the complex.[8] Exchange of genetic material between species of the Bcc has resulted in a reticulated phylogeny that presents an obstacle to diagnostic classification at the species-level.[8] Because of this phenotypic overlap between species, previous nomenclature of Bcc species involved genomovar terms, with Burkholderia cenocepacia categorized as genomovar III of the Bcc.[6][10] Within the categorization as genomovar III, there are 4 phylogenetic lineage groups: IIIA, IIIB, IIIC, and IIID.[11] No IIIC isolates have been found in studies on the natural environment, whereas all IIID isolates studied have been in clinical isolates of B. cenocepacia.[12]


The strong environmental protection response of B. cenocepacia is attributed to the biofilm formed by groups of the organism.[13] This biofilm contains exopolysaccharides that strengthen the bacterium's resistance to antibiotics and contribute to the bacteria's virulence. 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 Burkholderia cepacia complex has also created another polysaccharide with one 3-deoxy-d-manno-2-octulosonic acid and three galactose molecules.[14] The biofilm exopolysaccharides act as a barrier to neutrophils from human immune resistance systems, undermining the neutrophil defense action by inhibiting neutrophil chemotaxis and scavenging reactive oxygen species, which are bactericidal products produced by neutrophils to destroy bacteria.[15]


B. cenocepacia's genome consists of three circular chromosomes and one plasmid. Chromosome 1 contains 3.87 Mb, chromosome 2 contains 3.22 Mb, and chromosome 3 contains 0.88 Mb. The plasmid is approximately 0.09 Mb.[16] Chromosome 3 has also been characterized as a large plasmid, or megaplasmid (pC3); unlike chromosomes 2 and 3, it does not contain essential housekeeping genes, instead coding for accessory functions such as virulence and resistance to stress.[17][18] In addition to the multireplicon structure, the genome contains several insertion sequences and can rapidly mutate during infections, which contribute to B. cenocepacia's unique adaptability and ability to acquire diverse catabolic functions.[19][20]


Burkholderia cenocepacia has been found to thrive in primarily microaerophilic conditions, which consist of little to no oxygen.[21] Experimental studies conducted on the growth of B. cenocepacia in environments akin to the human lungs demonstrated the pathogen's increased success in microaerophilic environments over aerophilic settings.[21] In environments with little available iron such as the lungs of a cystic fibrosis patient, Burkholderia cenocepacia secretes siderophores, molecules that bind to iron and transport them to the bacteria.[22] Out of the four types of siderophores produced by the Bcc, B. cenocepacia produces three: ornibactin, pyochelin, and salicylic acid (SA). Ornibactin is the most important iron uptake system and can sustain the bacteria in an iron-deficient environment even without the production of functioning pyochelin or SA.[23]

B. cenocepacia has been demonstrated to colonize an array of ecological niches with diverse lifestyles. The ability to utilize a wide range of carbon sources accompanies the ability of Bcc species to be efficient with plant-growth promotion, bioremediation, and biocontrol.[12][24] High potential of Bcc species, including B. cenocepacia, as a biocontrol of plant-growth promoting agents has been demonstrated; however, the mechanisms that support this are not known.[12] In a bioremediation context, various Bcc strains are suggested to hold high potential to remediate environments contaminated with toxic compounds, including halogenated compounds.[12]

In addition, B. cenocepacia has been found to exist in the rhizosphere, plants, soil, water, and animals.[12] In fact, it was found to have an endophytic lifestyle when recovered from plant material, indicating that it has endosymbiotic characteristics.[12] Burkholderia cenocepacia was the dominant genomovar recovered in a study of bacteria in the rhizosphere of maize in China, pointing to endosymbiotic attributes with plants in soil.[25] However, B. cenocepacia also demonstrated phytopathogenic properties in causing fingertip rot in bananas.[6]

Quorum sensing

One kind of cell-to-cell communication employed by B. cenocepacia is quorum sensing, which is the detection of fluctuations in cell density and usage of this information to regulate functions such as the formation of biofilms. Like other Gram-negative bacteria, B. cenocepacia produces acyl-homoserine lactones (AHLs), signaling molecules that in members of the Burkholderia cepacia complex specifically are encoded by two systems–the CepIR system, which is highly conserved in the Bcc, and the CciIR system.[26] The two AHL-mediated QS systems, CepIR and CciIR, regulate each other; the CepR protein is required for the transcription of the cciIR operon, while the CciR protein represses transcription of cepI. The CciIR system can also negatively regulate the CepIR system through the production of C6-HSL, a type of AHL produced primarily by CciI proteins that inhibits the activity of CepR proteins.[26][27] The bacterium also uses cis-2-dodecenoic acid signals, which are known as Burkholderia diffusible signal factors (BDSF) because they were first identified in Burkholderia cenocepacia.[28]


Burkholderia cenocepacia has the ability to swim and swarm inside the body. It has a polar flagella and produces a surfactant. These characteristics are necessary for the species to have motility in an agar medium. The surfactant produced by Burkholderia cenocepacia allows other pathogenic bacteria in the lungs to have motility. This means that the presence of Burkholderia cenocepacia is necessary for swarms of bacteria to coexist and cooperate in the lungs.[29]


Host evasion by B. cenocepacia-Burkholderia cenocepacia Ptw T4SS is required for subversion of endosomal pathway in host innate immune cells.

Burkholderia cenocepacia is an opportunistic pathogen that commonly infects immunocompromised patients, especially those with cystic fibrosis, and is often lethal.[30] 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."[31] Twenty-four small RNAs were identified using RNA-binding properties of the Hfq protein during the exponential growth phases.[32] sRNAs identified in Burkholderia cenocepacia KC-0 were upregulated under iron depletion and oxidative stress.[33] Burkholderia cenocepacia encodes two RNA chaperone proteins that assist sRNAs in binding to mRNA, Hfq and Hfq2. Both are required for maximum virulence and resistance against stressors such as acidic pH, high temperatures, osmotic stress, and oxidative stress.[34][35] Burkholderia cenocepacia produces a toxin called double-stranded DNA deaminase A (DddA) made by the bacterium that converts DNA base cytosine to uracil.[36] Because uracil, which is not commonly found in DNA, behaves like a thymidine, the enzymes that replicate the cell’s DNA copy it as a thymidine, effectively converting a cytosine in the genome sequence to a thymidine. This has reportedly been used for the first gene-editing of mitochondria – for which a team at the Broad Institute developed a new kind of CRISPR-free base editor, called DdCBE, using the toxin.[37][38][39][40]

Antibiotic resistance

The structural factors that contribute to the antibiotic resistance of B. cenocepacia include: an impermeable outer membrane, an efflux pump mechanism, and the production of a beta-lactamase.[41] This microbe challenges infection prevention as it is resistant to some disinfectants and antiseptics. It can survive on surfaces, including human skin and mucosal surfaces for an extended period of time.[42]


Virulence in Burkholderia cenocepacia is widely attributed to biofilm formation, siderophore production, and QS signaling - each of which affect how the species adapts in various environmental conditions.[22] B. cenocepacia's ability to adapt to host environments contributes to chronic opportunistic infections and bacterial persistence.[19] Several strains are noted as "epidemic strains" due to increased transmission capability and patient-to-patient transmission.[12] The ET12 strain was found to have a "cable pilus," which enables greater adhesion of bacteria to epithelial cells.[12]

In human airway epithelial cells, the invasion pathway utilized by the BC-7 strain of B. cenocepacia is largely the result of the strain's biofilm formation.[43] In general, both environmental and clinical strains of B. cenocepacia are able to form biofilms; however, the ability to do so is greater in clinical strains.[44] The H111 strain of Burkholderia cenocepacia forms biofilms on pea roots, for example.[45] Quorum signaling (QS) affects the ability of B. cenocepacia to develop biofilms, in addition to the motility abilities.[46] In addition, quorum signaling controls a variety of cellular processes, such as extracellular proteases, polygalacturonase, and the production of siderophores.[46]

Cystic fibrosis

Burkholderia cenocepacia is one of over twenty bacteria in the Burkholderia cepacia complex (Bcc), and among these species, it is a dominant bacteria associated with cystic fibrosis. B. cenocepacia has such high transmissibility that it has spread across continents, including Europe and Canada, between cystic fibrosis patients at epidemic levels.[22] Patients with cystic fibrosis are threatened most by opportunistic pathogens.[22] Based on the distribution of Bcc species in sample cystic fibrosis patient populations, B. cenocepacia claims between 45.6% and 91.8% of all infections caused by the Bcc complex.[22] Compared to other infectious agents found in cystic fibrosis patients, the Bcc complex demonstrates the greatest association with increased morbidity and mortality.[47] Compared to other species in the Bcc complex, B. cenocepacia was shown to possibly accelerate BMI decline and FEV1 (forced expiration) at the greatest rate, leading to worse prognoses for cystic fibrosis patients.[47] The Bcc complex consists of genomovars, which are species characterized to be phylogenetically close, though distinct from each other.[48] In cystic fibrosis infections, it is common for only one of the known nine genomovars to induce an infection.[48] Overall, in patients with cystic fibrosis, the genomovar status of the Bcc has a significant influence on the success of clinical interventions, as well as the temporal progression of the condition.[49]



Given the opportunistic nature of the Bcc complex and B. cenocepacia, the severity of respiratory infections is considered to be a significant conflict for applications in biotechnology.[12]


To increase soil health, plant-growth promoting rhizobacteria (PGPR) are used in the agricultural industry to create bio-organic fertilizers.[50] A current challenge is identifying which bacterial species are optimal at stimulating plant growth in bio-organic fertilizers. Creating bio-organic fertilizers has been increasingly successful with the use of plant-growth promoting rhizobacteria mixed with organic substrates.[50] B. cenocepacia has various PGPR traits like phosphate solubilization that make it well-suited to promote growth. With the addition of solid-state fermentation technology, creating bio-organic fertilizers was highly successful by incorporating B. cenocepacia with high protein content agricultural wastes.[50]


  1. O'Grady EP, Sokol PA (2011-12-09). "Burkholderia cenocepacia differential gene expression during host-pathogen interactions and adaptation to the host environment". Frontiers in Cellular and Infection Microbiology. 1: 15. doi:10.3389/fcimb.2011.00015. PMC 3417382. PMID 22919581.
  2. Lauman P, Dennis JJ (July 2021). "Advances in Phage Therapy: Targeting the Burkholderia cepacia Complex". Viruses. 13 (7): 1331. doi:10.3390/v13071331. PMC 8310193. PMID 34372537.
  3. Scoffone VC, Chiarelli LR, Makarov V, Brackman G, Israyilova A, Azzalin A, et al. (September 2016). "Discovery of new diketopiperazines inhibiting Burkholderia cenocepacia quorum sensing in vitro and in vivo". Scientific Reports. 6 (1): 32487. doi:10.1038/srep32487. PMC 5007513. PMID 27580679.
  4. da Silva PH, de Assunção EF, da Silva Velez L, Dos Santos LN, de Souza EB, da Gama MA (December 2021). "Biofilm formation by strains of Burkholderia cenocepacia lineages IIIA and IIIB and B. gladioli pv. alliicola associated with onion bacterial scale rot". Brazilian Journal of Microbiology. 52 (4): 1665–1675. doi:10.1007/s42770-021-00564-6. PMC 8578472. PMID 34351603.
  5. Jacobs JL, Fasi AC, Ramette A, Smith JJ, Hammerschmidt R, Sundin GW (May 2008). "Identification and onion pathogenicity of Burkholderia cepacia complex isolates from the onion rhizosphere and onion field soil". Applied and Environmental Microbiology. 74 (10): 3121–3129. Bibcode:2008ApEnM..74.3121J. doi:10.1128/AEM.01941-07. PMC 2394932. PMID 18344334.
  6. 6.0 6.1 6.2 Lee YA, Chan CW (February 2007). "Molecular Typing and Presence of Genetic Markers Among Strains of Banana Finger-Tip Rot Pathogen, Burkholderia cenocepacia, in Taiwan". Phytopathology. 97 (2): 195–201. doi:10.1094/PHYTO-97-2-0195. PMID 18944375.
  7. You M, Fang S, MacDonald J, Xu J, Yuan ZC (March 2020). "Isolation and characterization of Burkholderia cenocepacia CR318, a phosphate solubilizing bacterium promoting corn growth". Microbiological Research. 233: 126395. doi:10.1016/j.micres.2019.126395. PMID 31865096. S2CID 209445961.
  8. 8.0 8.1 8.2 Wang H, Cissé OH, Bolig T, Drake SK, Chen Y, Strich JR, et al. (October 2020). "A Phylogeny-Informed Proteomics Approach for Species Identification within the Burkholderia cepacia Complex". Journal of Clinical Microbiology. 58 (11): e01741–20. doi:10.1128/JCM.01741-20. PMC 7587091. PMID 32878952.
  9. Tavares M, Kozak M, Balola A, Sá-Correia I (June 2020). "Burkholderia cepacia Complex Bacteria: a Feared Contamination Risk in Water-Based Pharmaceutical Products". Clinical Microbiology Reviews. 33 (3): e00139–19. doi:10.1128/CMR.00139-19. PMC 7194853. PMID 32295766.
  10. Lipuma JJ (November 2005). "Update on the Burkholderia cepacia complex". Current Opinion in Pulmonary Medicine. 11 (6): 528–533. doi:10.1097/01.mcp.0000181475.85187.ed. PMID 16217180. S2CID 19117513.
  11. Vandamme P, Holmes B, Coenye T, Goris J, Mahenthiralingam E, LiPuma JJ, Govan JR (March 2003). "Burkholderia cenocepacia sp. nov.--a new twist to an old story". Research in Microbiology. 154 (2): 91–96. doi:10.1016/S0923-2508(03)00026-3. PMID 12648723.
  12. 12.0 12.1 12.2 12.3 12.4 12.5 12.6 12.7 12.8 Vial L, Chapalain A, Groleau MC, Déziel E (January 2011). "The various lifestyles of the Burkholderia cepacia complex species: a tribute to adaptation". Environmental Microbiology. 13 (1): 1–12. doi:10.1111/j.1462-2920.2010.02343.x. PMID 20880095.
  13. Alshraiedeh NH, Higginbotham S, Flynn PB, Alkawareek MY, Tunney MM, Gorman SP, et al. (June 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
  14. Chiarini L, Cescutti P, Drigo L, Impallomeni G, Herasimenka Y, Bevivino A, et al. (August 2004). "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. PMID 15463903.
  15. Bylund J, Burgess LA, Cescutti P, Ernst RK, Speert DP (February 2006). "Exopolysaccharides from Burkholderia cenocepacia inhibit neutrophil chemotaxis and scavenge reactive oxygen species". The Journal of Biological Chemistry. 281 (5): 2526–2532. doi:10.1074/jbc.M510692200. PMID 16316987. 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
  16. O'Grady EP, Sokol PA (2011). "Burkholderia cenocepacia differential gene expression during host-pathogen interactions and adaptation to the host environment". Frontiers in Cellular and Infection Microbiology. 1: 15. doi:10.3389/fcimb.2011.00015. PMC 3417382. PMID 22919581.
  17. Agnoli K, Frauenknecht C, Freitag R, Schwager S, Jenul C, Vergunst A, et al. (February 2014). "The third replicon of members of the Burkholderia cepacia Complex, plasmid pC3, plays a role in stress tolerance". Applied and Environmental Microbiology. 80 (4): 1340–1348. doi:10.1128/AEM.03330-13. PMC 3911052. PMID 24334662.
  18. Agnoli K, Schwager S, Uehlinger S, Vergunst A, Viteri DF, Nguyen DT, et al. (January 2012). "Exposing the third chromosome of Burkholderia cepacia complex strains as a virulence plasmid". Molecular Microbiology. 83 (2): 362–378. doi:10.1111/j.1365-2958.2011.07937.x. PMID 22171913. S2CID 12668288.
  19. 19.0 19.1 Loutet, Slade A.; Valvano, Miguel A. (October 2010). "A Decade of Burkholderia cenocepacia Virulence Determinant Research". Infection and Immunity. 78 (10): 4088–4100. doi:10.1128/IAI.00212-10. ISSN 0019-9567. PMC 2950345. PMID 20643851.
  20. Lessie, T. G.; Hendrickson, W.; Manning, B. D.; Devereux, R. (1996-11-01). "Genomic complexity and plasticity of Burkholderia cepacia". FEMS Microbiology Letters. 144 (2–3): 117–128. doi:10.1111/j.1574-6968.1996.tb08517.x. ISSN 0378-1097. PMID 8900054. S2CID 46192579. Archived from the original on 2022-12-01. Retrieved 2023-02-14.
  21. 21.0 21.1 Coutinho CP, de Carvalho CC, Madeira A, Pinto-de-Oliveira A, Sá-Correia I (July 2011). Payne SM (ed.). "Burkholderia cenocepacia phenotypic clonal variation during a 3.5-year colonization in the lungs of a cystic fibrosis patient". Infection and Immunity. 79 (7): 2950–2960. doi:10.1128/IAI.01366-10. PMC 3191963. PMID 21536796.
  22. 22.0 22.1 22.2 22.3 22.4 Drevinek P, Mahenthiralingam E (July 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.
  23. Visser MB, Majumdar S, Hani E, Sokol PA (May 2004). "Importance of the ornibactin and pyochelin siderophore transport systems in Burkholderia cenocepacia lung infections". Infection and Immunity. 72 (5): 2850–2857. doi:10.1128/IAI.72.5.2850-2857.2004. PMC 387874. PMID 15102796.
  24. Mahenthiralingam E, Baldwin A, Dowson CG (June 2008). "Burkholderia cepacia complex bacteria: opportunistic pathogens with important natural biology". Journal of Applied Microbiology. 104 (6): 1539–1551. doi:10.1111/j.1365-2672.2007.03706.x. PMID 18217926. S2CID 23275498.
  25. Zhang L, Xie G (January 2007). "Diversity and distribution of Burkholderia cepacia complex in the rhizosphere of rice and maize". FEMS Microbiology Letters. 266 (2): 231–5. doi:10.1111/j.1574-6968.2006.00530.x. PMID 17233735.
  26. 26.0 26.1 Suppiger A, Schmid N, Aguilar C, Pessi G, Eberl L (July 2013). "Two quorum sensing systems control biofilm formation and virulence in members of the Burkholderia cepacia complex". Virulence. 4 (5): 400–409. doi:10.4161/viru.25338. PMC 3714132. PMID 23799665.
  27. O'Grady EP, Viteri DF, Malott RJ, Sokol PA (September 2009). "Reciprocal regulation by the CepIR and CciIR quorum sensing systems in Burkholderia cenocepacia". BMC Genomics. 10 (1): 441. doi:10.1186/1471-2164-10-441. PMC 2753556. PMID 19761612.
  28. Wang M, Li X, Song S, Cui C, Zhang LH, Deng Y (February 2022). Alexandre G (ed.). "The cis-2-Dodecenoic Acid (BDSF) Quorum Sensing System in Burkholderia cenocepacia". Applied and Environmental Microbiology. 88 (4): e0234221. doi:10.1128/aem.02342-21. PMC 8863054. PMID 34985987.
  29. Morin C, Landry M, Groleau MC, Déziel E (August 2022). Tamaki H (ed.). "Surface Motility Favors Codependent Interaction between Pseudomonas aeruginosa and Burkholderia cenocepacia". mSphere. 7 (4): e0015322. doi:10.1128/msphere.00153-22. PMC 9429929. PMID 35862793.
  30. Csávás M, Malinovská L, Perret F, Gyurkó M, Illyés ZT, Wimmerová M, Borbás A (January 2017). "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
  31. Drevinek P, Mahenthiralingam E (July 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.
  32. Ramos CG, Grilo AM, da Costa PJ, Leitão JH (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. PMID 23142676.
  33. Ghosh S, Dureja C, Khatri I, Subramanian S, Raychaudhuri S, Ghosh S (December 2017). "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. PMID 29099689.
  34. Ramos CG, Sousa SA, Grilo AM, Feliciano JR, Leitão JH (April 2011). "The second RNA chaperone, Hfq2, is also required for survival under stress and full virulence of Burkholderia cenocepacia J2315". Journal of Bacteriology. 193 (7): 1515–1526. doi:10.1128/JB.01375-10. PMC 3067662. PMID 21278292.
  35. Sousa SA, Feliciano JR, Pita T, Guerreiro SI, Leitão JH (January 2017). "Burkholderia cepacia Complex Regulation of Virulence Gene Expression: A Review". Genes. 8 (1): 43. doi:10.3390/genes8010043. PMC 5295037. PMID 28106859.
  36. de Moraes MH, Hsu F, Huang D, Bosch DE, Zeng J, Radey MC, Simon N, Ledvina HE, Frick JP, Wiggins PA, Peterson SB, Mougous JD (January 2021). "An interbacterial DNA deaminase toxin directly mutagenizes surviving target populations". eLife. 10. doi:10.7554/eLife.62967. PMC 7901873. PMID 33448264.
  37. "The powerhouses inside cells have been gene-edited for the first time". New Scientist. 8 July 2020. Archived from the original on 14 July 2020. Retrieved 12 July 2020.
  38. Mok BY, de Moraes MH, Zeng J, Bosch DE, Kotrys AV, Raguram A, et al. (July 2020). "A bacterial cytidine deaminase toxin enables CRISPR-free mitochondrial base editing". Nature. 583 (7817): 631–637. Bibcode:2020Natur.583..631M. doi:10.1038/s41586-020-2477-4. PMC 7381381. PMID 32641830.
  39. McRae M (10 July 2020). "For The First Time, Scientists Find a Way to Make Targeted Edits to Mitochondrial DNA". Science Alert. Archived from the original on 10 August 2022. Retrieved 14 February 2023.
  40. Mok BY, de Moraes MH, Zeng J, Bosch DE, Kotrys AV, Raguram A, et al. (July 2020). "A bacterial cytidine deaminase toxin enables CRISPR-free mitochondrial base editing". Nature. 583 (7817): 631–637. Bibcode:2020Natur.583..631M. doi:10.1038/s41586-020-2477-4. PMC 7381381. PMID 32641830.
  41. You M, Fang S, MacDonald J, Xu J, Yuan ZC (March 2020). "Isolation and characterization of Burkholderia cenocepacia CR318, a phosphate solubilizing bacterium promoting corn growth". Microbiological Research. 233: 126395. doi:10.1016/j.micres.2019.126395. PMID 31865096. S2CID 209445961.
  42. Loeven NA, Perault AI, Cotter PA, Hodges CA, Schwartzman JD, Hampton TH, Bliska JB (October 2021). "The Burkholderia cenocepacia Type VI Secretion System Effector TecA Is a Virulence Factor in Mouse Models of Lung Infection". mBio. 12 (5): e0209821. doi:10.1128/mBio.02098-21. PMC 8546862. PMID 34579569.
  43. Schwab U, Leigh M, Ribeiro C, Yankaskas J, Burns K, Gilligan P, et al. (August 2002). "Patterns of epithelial cell invasion by different species of the Burkholderia cepacia complex in well-differentiated human airway epithelia". Infection and Immunity. 70 (8): 4547–4555. doi:10.1128/IAI.70.8.4547-4555.2002. PMC 128168. PMID 12117967.
  44. Savoia D, Zucca M (June 2007). "Clinical and environmental Burkholderia strains: biofilm production and intracellular survival". Current Microbiology. 54 (6): 440–444. doi:10.1007/s00284-006-0601-9. PMID 17457645. S2CID 35624527.
  45. Kjelleberg S, Givskov M (2007). The biofilm mode of life : mechanisms and adaptations. Wymondham: Horizon Bioscience. ISBN 978-1-904933-33-5. OCLC 153550538. Archived from the original on 2023-06-30. Retrieved 2023-02-14.
  46. 46.0 46.1 Eberl L (April 2006). "Quorum sensing in the genus Burkholderia". International Journal of Medical Microbiology. Quorum sensing in human pathogens. 296 (2–3): 103–110. doi:10.1016/j.ijmm.2006.01.035. PMID 16490397.
  47. 47.0 47.1 Courtney JM, Dunbar KE, McDowell A, Moore JE, Warke TJ, Stevenson M, Elborn JS (June 2004). "Clinical outcome of Burkholderia cepacia complex infection in cystic fibrosis adults". Journal of Cystic Fibrosis. 3 (2): 93–98. doi:10.1016/j.jcf.2004.01.005. PMID 15463892.
  48. 48.0 48.1 Anselmo MA, Lands LC (January 2008). "Chapter 60 - Overview". In Taussig LM, Landau LI (eds.). Pediatric Respiratory Medicine (Second ed.). Philadelphia: Mosby. pp. 845–857. doi:10.1016/b978-032304048-8.50064-5. ISBN 978-0-323-04048-8.
  49. Jones AM, Dodd ME, Govan JR, Barcus V, Doherty CJ, Morris J, Webb AK (November 2004). "Burkholderia cenocepacia and Burkholderia multivorans: influence on survival in cystic fibrosis". Thorax. 59 (11): 948–951. doi:10.1136/thx.2003.017210. PMC 1746874. PMID 15516469.
  50. 50.0 50.1 50.2 Bibi F, Ilyas N, Arshad M, Khalid A, Saeed M, Ansar S, Batley J (March 2022). "Formulation and efficacy testing of bio-organic fertilizer produced through solid-state fermentation of agro-waste by Burkholderia cenocepacia". Chemosphere. 291 (Pt 3): 132762. doi:10.1016/j.chemosphere.2021.132762. PMID 34740700. S2CID 242072559.

External links