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   --><ref name="Masters">{{cite journal | author=Masters E, Granter S, Duray P, Cordes P | title=Physician-diagnosed erythema migrans and erythema migrans-like rashes following Lone Star tick bites | journal=Arch Dermatol | year=1998 | pages=955-60 | volume=134 | issue=8 | id=PMID 9722725}}</ref>There is currently no diagnostic test available for STARI/Masters, and no official treatment protocol, though antibiotics are generally prescribed.
   --><ref name="Masters">{{cite journal | author=Masters E, Granter S, Duray P, Cordes P | title=Physician-diagnosed erythema migrans and erythema migrans-like rashes following Lone Star tick bites | journal=Arch Dermatol | year=1998 | pages=955-60 | volume=134 | issue=8 | id=PMID 9722725}}</ref>There is currently no diagnostic test available for STARI/Masters, and no official treatment protocol, though antibiotics are generally prescribed.


==Structure and growth==
''B. burgdorferi'' is a highly specialized, motile, two-membrane, spiral-shaped [[spirochete]] ranging from about 9 to 32 [[1 E-6 m|micrometers]] in length. It is often described as [[gram-negative]] and has an outer membrane with [[lipopolysaccharide]] (LPS), though it stains only weakly in the [[Gram stain]]. ''B. burgdorferi'' is a [[microaerophilic]] organism, requiring little oxygen to survive. It lives primarily as an [[extracellular]] pathogen, although it can also hide [[intracellular]]ly (see [[#Mechanisms of persistence|Mechanisms of persistence]] section).
Like other spirochetes such as [[T. pallidum]] (the agent of [[syphilis]]), ''B. burgdorferi'' has an axial filament composed of [[flagella]] which run lengthways between its cell wall and outer membrane. This structure allows the spirochete to move efficiently in corkscrew fashion through [[viscous]] media, such as [[connective tissue]]. As a result, ''B. burgdorferi'' can disseminate throughout the body within days to weeks of infection, penetrating deeply into tissue where the immune system and antibiotics may not be able to eradicate the infection.
''B. burgdorferi'' is very slow growing, with a doubling time of 12-18 hours<ref>Kelly, R. T. (1984). Genus IV. Borrelia Swellengrebel 1907, 582AL. In Bergey's Manual of Systematic Bacteriology, vol. 1, pp. 57–62. Edited by N. R. Krieg & J. G. Holt. Baltimore: Williams & Wilkins.</ref> (in contrast to pathogens such as [[Streptococcus]] and [[Staphylococcus]], which have a doubling time of 20-30 minutes). Since most [[antibiotics]] kill bacteria only when they are dividing, this longer doubling time necessitates the use of relatively longer treatment courses for Lyme disease. Antibiotics are most effective during the [[bacterial growth|growth phase]], which for ''B. burgdorferi'' occurs in four-week cycles.
==Outer surface proteins==
The outer membrane of Borrelia burgdorferi is composed of various unique outer surface [[lipoproteins|proteins]] (Osp) that have been characterized (OspA through OspF). They are presumed to play a role in virulence.
OspA and OspB are by far the most abundant outer surface proteins.
The OspA and OspB genes encode the major outer membrane proteins of the B burgdorferi. The two Osp proteins show a high degree of sequence similarity, indicating a recent evolutionary event. Molecular analysis and sequence comparison of OspA and OspB with other proteins has revealed similarity to the signal [[peptides]] of [[prokaryotic]] [[lipoproteins]].<ref>Bergstrom S. , Bundoc V.G. , Barbour A.G. Molecular analysis of linear plasmid-encoded major surface proteins, OspA and OspB, of the Lyme disease spirochaete Borrelia burgdorferi. Mol. Microbiol. 3 479-486 1989</ref>Virtually all [[spirochetes]] in the midgut of an unfed nymph tick express OspA.
OspC is an [[antigen]]-detection of its presence by the host organism and can stimulate an immune response. While each individual bacterial cell contains just one copy of the gene encoding OspC, populations of ''B. burgdorferi'' have shown high levels of variation among individuals in the gene sequence for OspC.<ref>Girschick, J. and Singh, S.E. Molecular survival strategies of the lyme disease spirochete Borrelia burgdorferi. Sep, 2004. The Lancet Infectious Diseases: Volume 4, Issue 9, September 2004, Pages 575-583.</ref> OspC is likely to play a role in transmission from vector to host, since it has been observed that the protein is only expressed in the presence of mammalian blood or tissue.<ref name=Fikrig> Fikrig, E. and Pal, U. Adaptation of Borrelia burgdorferi in the vector and vertebrate host. Microbes and Infection Volume 5, Issue 7, June 2003, Pages 659-666. PMID 12787742</ref>
The functions of OspD are unknown.
OspE and OspF are structurally arranged in tandem as one transcriptional unit under the control of a common promoter.<ref>Lam TT, Nguyen TP, Montgomery RR, Kantor FS, Fikrig E, Flavell RA. Outer surface proteins E and F of Borrelia burgdorferi, the agent of Lyme disease. Infect Immun. 1994 Jan;62(1):290-8.</ref>
In transmission to the mammaliam host, when the nymphal tick begins to feed, and the spirochetes in the midgut begin to multiply rapidly, most spirochetes cease expressing OspA on their surface. Simultaneous with the disappearance of OspA, the spirochete population in the midgut begins to express a OspC. Upregulation of OspC begins during the first day of feeding and peaks 48 hours after attachment.<ref>Schwan TG, Piesman J.  Temporal changes in outer surface proteins A and C of the Lyme disease-associated spirochete, Borrelia burgdorferi, during the chain of infection in ticks and mice. J Clin Microbiol 2000;38:382-8.</ref>
==Gallery==
==Gallery==


Revision as of 19:06, 17 August 2015

Borrelia burgdorferi
Scientific classification
Kingdom: Bacteria
Phylum: Spirochaetes
Class: Spirochaetes
Order: Spirochaetales
Genus: Borrelia
Species: B. burgdorferi
Binomial name
Borrelia burgdorferi

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This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Lyme disease.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Template:Seealso

Main article: Lyme disease microbiology

Overview

Borrelia burgdorferi is species of bacteria of the spirochete class of the genus Borrelia. B. burgdorferi is predominant in North America, but also exists in Europe, and is the agent of Lyme disease. It is a zoonotic, vector-borne disease transmitted by ticks and is named after the researcher Willy Burgdorfer who first isolated the bacterium in 1982. B. burgdorferi is one of the few pathogenic bacteria that can survive without iron, having replaced all of its iron-sulphur cluster enzymes with enzymes that use manganese, thus avoiding the problem many pathogenic bacteria face in acquiring iron. B. burgdorferi infections have been linked to non-Hodgkin lymphomas.[1]

Organism

Borrelia burgdorferi the causative agent of Lyme disease (borreliosis). Magnified 400 times.

Lyme disease, or Lyme borreliosis, is caused by Gram negative spirochetal bacteria from the genus Borrelia, which has at least 37 known species, 12 of which are Lyme related, and an unknown number of genomic strains. Borrelia species known to cause Lyme disease are collectively known as Borrelia burgdorferi sensu lato.

Borrelia are microaerophillic and slow-growing—the primary reason for the long delays when diagnosing Lyme disease—and have been found to have greater strain diversity than previously estimated.[2] The strains differ in clinical symptoms and/or presentation as well as geographic distribution.[3]

Except for Borrelia recurrentis (which causes louse-borne relapsing fever and is transmitted by the human body louse), all known species are believed to be transmitted by ticks.[4]

Species and Strains

Until recently it was thought that only three genospecies caused Lyme disease (borreliosis): B. burgdorferi sensu stricto ( the predominant species in North America, but also present in Europe); B. afzelii; and B. garinii (both predominant in Eurasia). To date the complete genome of B. burgdorferi sensu stricto strain B31, B. afzelii strain PKo and B. garinii strain PBi is known. B. burgdorferi strain B31 was derived by limited dilutional cloning from the original Lyme-disease tick isolate derived by Alan Barbour. There are over 300 species or strains of Borrelia world wide with apx 100 in the U.S. and it is unknown how many cause lyme like sickness, but many of them may.

At present, diagnostic tests are based only on B. burgdorferi sensu stricto (the only species used in the U.S.), B. afzelii, and B. garinii.

Emerging Genospecies

  • B. valaisiana was identified as a genomic species from Strain VS116, and named B. valaisiana in 1997.[5] It was later detected by Polymerase chain reaction (PCR) in human cerebral spinal fluid (CSF) in Greece.[6] B. valaisiana has been isolated throughout Europe, as well east Asia.[7]

Newly discovered genospecies have also been found to cause disease in humans:

  • B. lusitaniae [8] in Europe (especially Portugal), North Africa and Asia.
  • B. bissettii [9][10] in the U.S. and Europe.

Additional B. burgdorferi sensu lato genospecies suspected of causing illness, but not confirmed by culture, include B. japonica, B. tanukii and B. turdae (Japan); B. sinica (China); and B. andersonii (U.S.). Some of these species are carried by ticks not currently recognized as carriers of Lyme disease.

The B. miyamotoi spirochete, related to the relapsing fever group of spirochetes, is also suspected of causing illness in Japan. Spirochetes similar to B. miyamotoi have recently been found in both I. ricinus ticks in Sweden and I. scapularis ticks in the U.S.[13][14]

B. lonestari

Apart from this group of closely related genospecies, additional Borrelia species of interest include B. lonestari, a spirochete recently detected in the Amblyomma americanum tick (Lone Star tick) in the U.S.[15] B. lonestari is suspected of causing STARI (Southern Tick-Associated Rash Illness), also known as Masters disease in honor of its discoverer Ed Masters. The illness follows a Lone Star tick bite and clinically resembles Lyme disease, but sufferers usually test negative for Lyme.[16]There is currently no diagnostic test available for STARI/Masters, and no official treatment protocol, though antibiotics are generally prescribed.

Structure and growth

B. burgdorferi is a highly specialized, motile, two-membrane, spiral-shaped spirochete ranging from about 9 to 32 micrometers in length. It is often described as gram-negative and has an outer membrane with lipopolysaccharide (LPS), though it stains only weakly in the Gram stain. B. burgdorferi is a microaerophilic organism, requiring little oxygen to survive. It lives primarily as an extracellular pathogen, although it can also hide intracellularly (see Mechanisms of persistence section).

Like other spirochetes such as T. pallidum (the agent of syphilis), B. burgdorferi has an axial filament composed of flagella which run lengthways between its cell wall and outer membrane. This structure allows the spirochete to move efficiently in corkscrew fashion through viscous media, such as connective tissue. As a result, B. burgdorferi can disseminate throughout the body within days to weeks of infection, penetrating deeply into tissue where the immune system and antibiotics may not be able to eradicate the infection.

B. burgdorferi is very slow growing, with a doubling time of 12-18 hours[17] (in contrast to pathogens such as Streptococcus and Staphylococcus, which have a doubling time of 20-30 minutes). Since most antibiotics kill bacteria only when they are dividing, this longer doubling time necessitates the use of relatively longer treatment courses for Lyme disease. Antibiotics are most effective during the growth phase, which for B. burgdorferi occurs in four-week cycles.

Outer surface proteins

The outer membrane of Borrelia burgdorferi is composed of various unique outer surface proteins (Osp) that have been characterized (OspA through OspF). They are presumed to play a role in virulence.

OspA and OspB are by far the most abundant outer surface proteins.

The OspA and OspB genes encode the major outer membrane proteins of the B burgdorferi. The two Osp proteins show a high degree of sequence similarity, indicating a recent evolutionary event. Molecular analysis and sequence comparison of OspA and OspB with other proteins has revealed similarity to the signal peptides of prokaryotic lipoproteins.[18]Virtually all spirochetes in the midgut of an unfed nymph tick express OspA.

OspC is an antigen-detection of its presence by the host organism and can stimulate an immune response. While each individual bacterial cell contains just one copy of the gene encoding OspC, populations of B. burgdorferi have shown high levels of variation among individuals in the gene sequence for OspC.[19] OspC is likely to play a role in transmission from vector to host, since it has been observed that the protein is only expressed in the presence of mammalian blood or tissue.[20]

The functions of OspD are unknown.

OspE and OspF are structurally arranged in tandem as one transcriptional unit under the control of a common promoter.[21]

In transmission to the mammaliam host, when the nymphal tick begins to feed, and the spirochetes in the midgut begin to multiply rapidly, most spirochetes cease expressing OspA on their surface. Simultaneous with the disappearance of OspA, the spirochete population in the midgut begins to express a OspC. Upregulation of OspC begins during the first day of feeding and peaks 48 hours after attachment.[22]

Gallery

References

  1. ↑ Guidoboni M, Ferreri AJ, Ponzoni M, Doglioni C, Dolcetti R (2006). "Infectious agents in mucosa-associated lymphoid tissue-type lymphomas: pathogenic role and therapeutic perspectives". Clinical lymphoma & myeloma. 6 (4): 289–300. PMID 16507206.
  2. ↑ Bunikis J, Garpmo U, Tsao J, Berglund J, Fish D, Barbour AG (2004). "Sequence typing reveals extensive strain diversity of the Lyme borreliosis agents Borrelia burgdorferi in North America and Borrelia afzelii in Europe" (PDF). Microbiology. 150 (Pt 6): 1741–55. PMID 15184561.
  3. ↑ Ryan KJ, Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
  4. ↑ Felsenfeld O (1971). Borrelia: Strains, Vectors, Human and Animal Borreliosis. St. Louis: Warren H. Green, Inc.
  5. ↑ Wang G, van Dam AP, Le Fleche A; et al. (1997). "Genetic and phenotypic analysis of Borrelia valaisiana sp. nov. (Borrelia genomic groups VS116 and M19)". Int. J. Syst. Bacteriol. 47 (4): 926–32. PMID 9336888.
  6. ↑ Diza E, Papa A, Vezyri E, Tsounis S, Milonas I, Antoniadis A (2004). "Borrelia valaisiana in cerebrospinal fluid". Emerging Infect. Dis. 10 (9): 1692–3. PMID 15503409.
  7. ↑ Masuzawa T (2004). "Terrestrial distribution of the Lyme borreliosis agent Borrelia burgdorferi sensu lato in East Asia". Jpn. J. Infect. Dis. 57 (6): 229–35. PMID 15623946.
  8. ↑ Collares-Pereira M, Couceiro S, Franca I, Kurtenbach K, Schafer SM, Vitorino L, Goncalves L, Baptista S, Vieira ML, Cunha C (2004). "First isolation of Borrelia lusitaniae from a human patient" (PDF). J Clin Microbiol. 42 (3): 1316–8. PMID 15004107.
  9. ↑ Postic D, Ras NM, Lane RS, Hendson M, Baranton G (1998). "Expanded diversity among Californian borrelia isolates and description of Borrelia bissettii sp. nov. (formerly Borrelia group DN127)" (PDF). J Clin Microbiol. 36 (12): 3497–504. PMID 9817861.
  10. ↑ Maraspin V, Cimperman J, Lotric-Furlan S, Ruzic-Sabljic E, Jurca T, Picken RN, Strle F (2002). "Solitary borrelial lymphocytoma in adult patients". Wien Klin Wochenschr. 114 (13–14): 515–23. PMID 12422593.
  11. ↑ Richter D, Postic D, Sertour N, Livey I, Matuschka FR, Baranton G (2006). "Delineation of Borrelia burgdorferi sensu lato species by multilocus sequence analysis and confirmation of the delineation of Borrelia spielmanii sp. nov". Int J Syst Evol Microbiol. 56 (Pt 4): 873–81. PMID 16585709.
  12. ↑ Foldvari G, Farkas R, Lakos A (2005). "Borrelia spielmanii erythema migrans, Hungary". Emerg Infect Dis. 11 (11): 1794–5. PMID 16422006.
  13. ↑ Scoles GA, Papero M, Beati L, Fish D (2001). "A relapsing fever group spirochete transmitted by Ixodes scapularis ticks". Vector Borne Zoonotic Dis. 1 (1): 21–34. PMID 12653133.
  14. ↑ Bunikis J, Tsao J, Garpmo U, Berglund J, Fish D, Barbour AG (2004). "Typing of Borrelia relapsing fever group strains". Emerg Infect Dis. 10 (9): 1661–4. PMID 15498172.
  15. ↑ Varela AS, Luttrell MP, Howerth EW, Moore VA, Davidson WR, Stallknecht DE, Little SE (2004). "First culture isolation of Borrelia lonestari, putative agent of southern tick-associated rash illness" (PDF). J Clin Microbiol. 42 (3): 1163–9. PMID 15004069.
  16. ↑ Masters E, Granter S, Duray P, Cordes P (1998). "Physician-diagnosed erythema migrans and erythema migrans-like rashes following Lone Star tick bites". Arch Dermatol. 134 (8): 955–60. PMID 9722725.
  17. ↑ Kelly, R. T. (1984). Genus IV. Borrelia Swellengrebel 1907, 582AL. In Bergey's Manual of Systematic Bacteriology, vol. 1, pp. 57–62. Edited by N. R. Krieg & J. G. Holt. Baltimore: Williams & Wilkins.
  18. ↑ Bergstrom S. , Bundoc V.G. , Barbour A.G. Molecular analysis of linear plasmid-encoded major surface proteins, OspA and OspB, of the Lyme disease spirochaete Borrelia burgdorferi. Mol. Microbiol. 3 479-486 1989
  19. ↑ Girschick, J. and Singh, S.E. Molecular survival strategies of the lyme disease spirochete Borrelia burgdorferi. Sep, 2004. The Lancet Infectious Diseases: Volume 4, Issue 9, September 2004, Pages 575-583.
  20. ↑ Fikrig, E. and Pal, U. Adaptation of Borrelia burgdorferi in the vector and vertebrate host. Microbes and Infection Volume 5, Issue 7, June 2003, Pages 659-666. PMID 12787742
  21. ↑ Lam TT, Nguyen TP, Montgomery RR, Kantor FS, Fikrig E, Flavell RA. Outer surface proteins E and F of Borrelia burgdorferi, the agent of Lyme disease. Infect Immun. 1994 Jan;62(1):290-8.
  22. ↑ Schwan TG, Piesman J. Temporal changes in outer surface proteins A and C of the Lyme disease-associated spirochete, Borrelia burgdorferi, during the chain of infection in ticks and mice. J Clin Microbiol 2000;38:382-8.
  23. ↑ 23.00 23.01 23.02 23.03 23.04 23.05 23.06 23.07 23.08 23.09 23.10 23.11 23.12 23.13 23.14 23.15 23.16 23.17 23.18 23.19 23.20 23.21 23.22 23.23 23.24 23.25 23.26 23.27 23.28 23.29 23.30 23.31 23.32 23.33 23.34 23.35 23.36 23.37 23.38 23.39 23.40 23.41 23.42 23.43 "Public Health Image Library (PHIL)".

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