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]


As a tick-transmitted bacteria, Borrelia burgdorferi must first infect a non-human host reservoir, such as a deer or mice.[2] This host reservoir must be a vertebrate that is able to maintain and to grow the pathogen within its blood.[2] The tick, Ixodes, then, must acquire the pathogen through blood feeding and maintain the pathogen, until it can pass it off onto another host reservoir or to a human.[2] The process of infection involves an adult tick re-injecting the host's blood back into its system, transmitting the disease along with it. This is also known as coxal fluid.[3] In order for a successful infection, the vertebrate host reservoir must cultivate enough bacteria that can be circulated throughout the blood, so that B. burgodorferi can be transmitted through Ixodes blood feeding.[2] Additionally, the bacteria itself must withstand the molting and life cycle of the Ixodes tick and successfully transinfect a host for B. Burgdorferi to spread to humans.[2]

Anaplasmosis and babesiosis are also common tick borne pathogens that infect humans similarly to Borrelia burgdorferi.[4] Consequently, it is possible for an Ixodes tick to coinfect a host with either two or all other diseases. When a host is coinfected, the combined effects of the diseases act synergistically, often proving to cause worse symptoms than a single infection alone[4] Coinfected humans tend to present with a more severe manifestation of Lyme disease. In addition, they tend to acquire a wider arrange of secondary symptoms, such as influenza-like symptoms.[4] More studies and research must be done to determine the synergistic effect of co-infection and its effect on the human body.


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.[5] 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.[6]

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

B. burgdorferi infections have been found in possible association with primary cutaneous B-cell lymphomas (PCBCLs),[7][8] where a review of the primary literature has, as of 2010, noted that most of the PCBLCs examined have been 'unresponsive' to antibiotics;[8]: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".[8]:846


Lyme disease is caused by B. burgdorferi, transmitted to the host from tick bites. Progression of the disease follows from 3 stages.

Stage 1[edit]

Stage 1 affects the area around the bite, with a rash or swelling possible. The pathophysiology of Borrelia Burgdorferi in humans starts with an infected tick bite. After the pathogen is transmitted, it will acclimate to the mammalian conditions. Borrellia Burgdorferi will change its glycoproteins and proteases on its plasma membrane to facilitate its dissemination throughout the blood.[9] While infecting, B. Burgdorferi will express proteins that will interact with endothelial cells, platelets, chondrocytes, and the extracellular matrix.[9] This interaction inhibits proper function of the infected areas, leading to the pathological manifestations of Lyme disease. In response, the host will emit an inflammatory response to fight off the infection.[9]

Stage 2[edit]

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[edit]

Stage 3 occurs years after and chronic arthritis and neurological complications develop.[6]

Variation of Severity[edit]

So far, there are three factors that may contribute to the severity of the clinical manifestation of Lyme Disease. The presence of ribosomal spacers, plasmids, and the outer surface protein C (OspC) are indicators of the severity of the infection.[9] Additionally, humans, themselves, vary in their response to the infection.[9] The variation in response leads to different clinical manifestations and different infections to different organs.


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.[10]

Borrelia burgdorferi, also, 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.[11]


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.[12]


B. burgdorferi (B31 strain) was the third microbial genome ever sequenced, following the sequencing of both Haemophilus influenzae and Mycoplasma genitalium in 1995. Its linear chromosome contains 910,725 base pairs and 853 genes.[13] 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. Overall, B. burgdorferi's genome oddly consists of one megabase chromosome and a variety of circular and linear plasmids ranging in size from 9 to 62 kilobases.[2] The megabase chromosome, unlike many other eubacteria, has no relation to neither the bacteria's virulence nor to the host-parasite interaction.[13] The virulence and overall protein expression can be explained by present plasmids.

Thirteen distinct genomic classifications of Lyme disease bacteria have been identified worldwide. These include but are not limited to B. burgdorferi sensu stricto, B. afzelii, B. garinii, B. valaisana, B. Lusitaniae, B. andersoni, 25015, DN127, CA55, 25015, HK501, B. Miyamotoi, and B. Japonica.[14] Many of these genomic groups are country or continent specific. For example, without migration, B. Japonica is only prevalent in the eastern hemisphere.[14]

The genomic variations have direct implications on the clinical symptoms of tick borne Lyme disease. For example, B. burgdorferi senso stricto’s tick borne Lyme disease may manifest itself into arthritis-like symptoms.[14] In contrast, B. garinii’s tick borne Lyme disease may manifest itself into an infection of the central nervous system.[14]

Additionally, the genomic variations of Borrelia burgodrferi contribute to varying degrees of infection and dissemination.[15] Each genomic group has varying antigens on its membrane receptor, which are specific to the infection of the host. One such membrane receptor is the surface protein OspC.[15] The OspC surface protein is shown to be a strong indicator of the identification of genomic classification and the degree of dissemination.[15] Varying number of OspC loci are indications and determinants for the variations of Borrelia burdorferi.[15] The surface protein is also on the forefront of current vaccine research for Lyme disease via Borrelia.[16]

Balanced Selection[edit]

Balanced selection is the process by which various alleles are kept within the gene pool at unexpected frequencies. Two major models that control the selection balance of B.burgdorferi is negative frequency-dependent selection and multiple-niche polymorphism[17]. These models may explain how B. burdorferi have diversified, and how selection may have affected the distribution of the B. burdorferi variants, or the variation of specific traits of the species, in certain environments.

Negative-Frequency Dependent Selection[edit]

In negative frequency-dependent selection, rare and uncommon variants will have a selective advantage over variants that are very common in an environment.[17] For B. burgdorferi, low-frequency variants will be advantageous because potential hosts will not have a built immunological response to the variants specific OspC outer protein.[17]

Multiple-niche Polymorphism[edit]

Ecological niches are all of the variables in an environment, such as the resources, competitors, and responses, that contribute to the organism's fitness. Multiple-niche polymorphism states that diversity is maintained within a population due to the varying amount of possible niches and environments.[17] Therefore, the more various niches the more likelihood of polymophrism and diversity. For B. burgdorferi, varying vertebrae niches, such deer and mice, can affect the overall balancing selection for variants.[17]

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. ^ a b c d e f 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. 
  3. ^ Burgdorfer, Willy; Hayes, Stanley F.; Corwin, Dan (1989-09-01). "Pathophysiology of the Lyme Disease Spirochete, Borrelia burgdorferi, in Ixodid Ticks". Review of Infectious Diseases 11 (Supplement 6): S1442–S1450. doi:10.1093/clinids/11.Supplement_6.S1442. ISSN 1058-4838. 
  4. ^ a b c Swanson, Stephen J.; Neitzel, David; Reed, Kurt D.; Belongia, Edward A. (2006-10-01). "Coinfections Acquired from Ixodes Ticks". Clinical Microbiology Reviews 19 (4): 708–727. doi:10.1128/CMR.00011-06. ISSN 0893-8512. PMC 1592693. PMID 17041141. 
  5. ^ 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. 
  6. ^ a b "Signs and Symptoms, Lyme Disease". Centers For Disease Control. March 4, 2015. Retrieved 2015-07-16. 
  7. ^ 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. 
  8. ^ 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. 
  9. ^ a b c d e Weis, Janet (2011). "Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes: Workshop Report.". The National Academies: 97–101. 
  10. ^ Galdwin, Mark; Trattler, Bill (2009). Spirochetes: Clinical Microbiology Made Ridiculously Simple. MedMaster, Inc. ISBN 978-0-940780-81-1. 
  11. ^ 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.
  12. ^ 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. 
  13. ^ 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. 
  14. ^ a b c d Habálek, Z.; Halouzka, J. (1997-12-01). "Distribution of Borrelia burgdorferi sensu lato genomic groups in Europe, a review". European Journal of Epidemiology 13 (8): 951–957. doi:10.1023/A:1007426304900. ISSN 0393-2990. 
  15. ^ a b c d Theisen, M.; Borre, M.; Mathiesen, M. J.; Mikkelsen, B.; Lebech, A. M.; Hansen, K. (1995-06-01). "Evolution of the Borrelia burgdorferi outer surface protein OspC.". Journal of Bacteriology 177 (11): 3036–3044. ISSN 0021-9193. PMC 176990. PMID 7768799. 
  16. ^ Embers, Monica E.; Narasimhan, Sukanya (2013-02-12). "Vaccination against Lyme disease: past, present, and future". Frontiers in Cellular and Infection Microbiology 3. doi:10.3389/fcimb.2013.00006. ISSN 2235-2988. PMC 3569838. PMID 23407755. 
  17. ^ a b c d e Samuels, D. Scott (2010-01-01). Borrelia: Molecular Biology, Host Interaction and Pathogenesis. Horizon Scientific Press. ISBN 9781904455585. 

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