Borrelia burgdorferi

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Borrelia burgdorferi
Borrelia burgdorferi (CDC-PHIL -6631) lores.jpg
Borrelia burgdorferi
Scientific classification e
Domain: Bacteria
Phylum: Spirochaetes
Order: Spirochaetales
Family: Spirochaetaceae
Genus: Borrelia
Species: B. burgdorferi
Binomial name
Borrelia burgdorferi
Johnson et al. 1984 emend. Baranton et al. 1992

Borrelia burgdorferi is a bacterial species of the spirochete class of the genus Borrelia. B. burgdorferi exists in North America and Europe and is the predominant causative agent of Lyme disease. Borrelia species are considered diderm (double-membrane) bacteria rather than Gram positive or negative.[1]


Lyme disease is a zoonotic, vector-borne disease transmitted by the Ixodes tick (also the vector for Babesia); the causative agent is named after the researcher Willy Burgdorfer, who first isolated the bacterium in 1982.[2] B. burgdorferi is one of the few pathogenic bacteria that can survive without iron, having replaced all of its iron-sulfur cluster enzymes with enzymes that use manganese, thus avoiding the problem many pathogenic bacteria face in acquiring iron.[3]

Clinical presentation of Lyme disease may include the characteristic bull's-eye rash and erythema chronicum migrans (a rash which spreads peripherally and spares the central part), as well as myocarditis, cardiomyopathy, arrythmia, arthritis, arthralgia, meningitis, neuropathies, and facial nerve palsy.[4]

Characteristic "bull's-eye" rash of Lyme disease

B. burgdorferi infections have been found in possible association with primary cutaneous B-cell lymphomas (PCBCLs),[5][6] where a review of the primary literature has, as of 2010, noted that most of the PCBLCs examined have been 'unresponsive' to antibiotics;[6]:846 hence, as in case of Chlamydophila psittaci association with ocular adnexal mucosa-associated lymphoid tissue (MALT) lymphoma, the working conclusion was that "if B. burgdorferi is truly associated with PCBCL, then there is wide geographic variability and other factors are probably involved".[6]:846

Borrelia burgdorferi expresses at least seven plasminogen binding proteins for interference of factor H at the activation level. This is part of a complement system evasion strategy that leads to downstream blocking of immune response.[7]


Lyme disease, caused by B. burgdorferi from tick bites consist of three stages starting from initial bite. Stage 1 affects the area around the bite, with a rash or swelling possible. Stage 2 occurs weeks to months after; if l untreated, the bacteria spread through the body affect the heart, bones, and nervous system. Stage 3 occurs years after and chronic arthritis and neurological complications develop.[4]


B. burgdorferi resembles other spirochetes in that it is a highly specialized, motile, two-membrane, spiral-shaped bacterium that lives primarily as an extracellular pathogen. While only 0.2 to 0.3 μm wide, the cell length may exceed 15 to 20 μm.

B. burgdorferi is an anaerobic, motile spirochete with seven to 11 bundled perisplasmic flagella set at each end that allow the bacterium to move in low- and high-viscosity media alike, which is related to its high virulence factor. [8]


B. burgdorferi (B31 strain) was the third microbial genome ever sequenced, following the sequencing of both Haemophilus influenzae and Mycoplasma genitalium in 1995, and its linear chromosome contains 910,725 base pairs and 853 genes.[9] Overall, B. burgdorferi's genome oddly consists of only this one megabase chromosome and a variety of circular and linear plasmids ranging in size from 9 to 62 kilobases.[10] The megabase chromosome, unlike many other eubacteria, seems to have no relation to the bacteria's virulence or contribute to the host-parasite interaction.[9] However, the plasmids prove to be important for B. burgdorferi's virulence and overall protein expression. The sequencing method used was whole genome shotgun. The sequencing project, completed and published in Nature in 1997, was conducted at The Institute for Genomic Research.

See also[edit]

Further reading[edit]

  • Kit Tilly, Patricia A. Rosa & Philip E. Stewart, 2008, "Biology of Infection with Borrelia burgdorferi," Infect. Dis. Clin. North Am. 22(2): pp. 217–234, DOI 10.1016/j.idc.2007.12.013, see [1], accessed 19 June 2015.
  • Velázquez, Encarna, Peix, Álvaro & Gómez-Alonso, Alberto, 2011, "Microorganismos y cáncer: evidencias científicas y nuevas hipótesis", Cirugía Española, vol 89, no. 3, pages 136–144. issn 0009739X; doi 10.1016/j.ciresp.2010.08.006; accessed 16 July 2015. English translation


  1. ^ Samuels DS; Radolf, JD (editors) (2010). "Chapter 6, Structure, Function and Biogenesis of the Borrelia Cell Envelope". Borrelia: Molecular Biology, Host Interaction and Pathogenesis. Caister Academic Press. ISBN 978-1-904455-58-5. 
  2. ^ Burgdorfer W, Barbour AG, Hayes SF, Benach JL, Grunwaldt E, Davis JP (June 1982). "Lyme disease-a tick-borne spirochetosis?". Science 216 (4552): 1317–9. Bibcode:1982Sci...216.1317B. doi:10.1126/science.7043737. PMID 7043737. 
  3. ^ Galdwin, Mark; Trattler, Bill (2009). Spirochetes: Clinical Microbiology Made Ridiculously Simple. MedMaster, Inc. ISBN 978-0-940780-81-1. 
  4. ^ a b "Signs and Symptoms, Lyme Disease". Centers For Disease Control. March 4, 2015. Retrieved 2015-07-16. 
  5. ^ Guidoboni M, Ferreri AJ, Ponzoni M, Doglioni C, Dolcetti R (January 2006). "Infectious agents in mucosa-associated lymphoid tissue-type lymphomas: pathogenic role and therapeutic perspectives". Clinical Lymphoma & Myeloma 6 (4): 289–300. doi:10.3816/CLM.2006.n.003. PMID 16507206. 
  6. ^ a b c Chang, A. H.; Parsonnet, J. (2010). "Role of Bacteria in Oncogenesis" (PDF). Clinical Microbiology Reviews 23 (4): 837–857. doi:10.1128/CMR.00012-10. ISSN 0893-8512. 
  7. ^ Zipfel, P., Hallström, T., & Riesbeck, K. (2013). Human complement control and complement evasion by pathogenic microbes – Tipping the balance. Molecular Immunology, 56(3), 152-160.
  8. ^ Motaleb, Mohammed; Corum, Linda; Bono, James; Elias, Abdallah; Rosa, Patricia; Samuels, D. Scott; Charon, Nyles. "Borrelia burgdorferi periplasmic flagella have both skeletal and motility functions". NCBI. Proceedings of the National Academy of Sciences of the United States of America. Retrieved 10 May 2015. 
  9. ^ a b Fraser CM, Casjens S, Huang WM; et al. (December 1997). "Genomic sequence of a Lyme disease spirochaete, Borrelia burgdorferi". Nature 390 (6660): 580–6. Bibcode:1997Natur.390..580F. doi:10.1038/37551. PMID 9403685. 
  10. ^ Brisson D, Drecktrah D, Eggers CH, Samuels DS (2012). "Genetics of Borrelia burgdorferi". Annual Review of Genetics 46: 515–36. doi:10.1146/annurev-genet-011112-112140. PMC 3856702. PMID 22974303. 

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