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Borrelia burgdorferi
Borrelia burgdorferi as viewed via darkfield microscopy.
Scientific classification
Kingdom: Bacteria Phylum: Spirochaetes Class: Spirochaetes Order: Spirochaetales Family: Spirochaetaceae Genus: Borrelia Species: B. burgdorferi
Binomial name
Borrelia burgdorferi Johnson RC et al 1984

Borrelia burgdorferi is a gram negative spirochete bacteria and the causative agent of Lyme disease,^[1] its most commonly transmitted to humans through an infected tick bite. Typical symptoms include fever, headache, fatigue, and a characteristic skin rash called erythema migrans that usually blooms from the bite mark. If left untreated, infection can spread to joints, the heart, and the nervous system. Paralysis of one or both sides of the face may occur. This paralysis is known as Bell's Palsy and treatment often requires antibiotics. This bacteria is microaerophillic and slow-growing—the primary reason for the long delays when diagnosing Lyme disease. There are a large number of sub-species which differ in clinical symptoms and/or presentation as well as geographic distribution.^[2]

The life-cycle of B. burgdorferi is complex, requiring ticks, rodents, and deer at various points. Mice are the primary reservoir for the bacteria; Ixodes ticks then transmit the B. burgdorferi infection to deer.^[1],[3]

The life-cycle concept encompassing reservoirs and infections in multiple hosts has recently been expanded to encompass forms of the spirochete which differ from the motile corkscrew form, and these include cystic forms spheroplast-like, straighted non-coiled bacillary forms which are immotile due to flagellin mutations and granular forms coccoid in profile. The model of Plasmodium species Malaria with multiple parasitic profiles demonstrable in various host insects and mammals is the textbook model for a similarly complex proposed Borrelia spirochete life cycle. ^{[4] [5] [6]}

Controversially, some in the medical community believe Borrelia bacterium infections can also occur like other blood borne illnesses, including congenital, transfusion, and sexual. While patients have Borrelia infection-like symptoms, they may be missing the characteristic erythema migrans, leading many mainstream doctors to resist diagnosing Lyme disease.

Common misdiagnoses include depression and chronic fatigue syndrome. Despite credible symptoms, after many blood samples do not grow the bacterium in a lab culture, some labs use unapproved and unverified assays with mixed results, and because the CDC continues to insist that tick bites are the cause, then mainstream medicine remains skeptical. Some believe that the cyst form can lay dormant for months or years, and is easily missed in typical blood tests, and why normal cultures fail.

Contents 1 Molecular Biology and Survial Strategies 2 References 3 Borellia burgdorferi as component of CVBD 4 External links

As it is an obligate parasite, B. burgdorferi relies on its host’s metabolism for survival- but is capable of surviving outside of a host.It was for the first time cultivated outside a mammal in 1981 in a modified Kelly medium.^[7] B. burgdorferi has the ability to survive in mammalian or avian blood and tissue as well as the tick gut and salivary glands. Because both temperature and pH levels differ significantly from one host environment to another, B. burgdorferi must continually adapt to extreme environmental fluctuations.^[8]

The genomic organization of B. burgdorferi is atypical in that its genome is composed of one linear chromosome (most species of bacteria have a circular chromosome) and 21 circular and linear extra-chromosomal plasmids (the highest number of plasmids observed in a bacterial species).^[9]

Evidence indicates that the plasmid genes, which comprise 40% of the organism’s entire genome, encode functions specific to the Borrelia genus.^[9] Thus, many of the products of plasmid genes are likely necessary to the survival B. burgdorferi in its own environmental niche. The selective advantages of partitioning essential genes into a large array of plasmids is unknown, and B. burgdorferi is the only organism of its kind known to have such a dispersive genome.^[9]

A relatively large portion (about 8%) of B. burgdorferi’s coding genome consists of genes encoding lipoproteins.^[9] This diversity of lipoproteins allows the organism to alter its surface structure in response to changes in the host environment and assists in evasion of the host immune system.^[9] It has been observed that changes in temperature and pH and detection of host factors in B. burgdorferi’s surroundings induce changes in expression of certain lipoproteins.^[9] For example, outer surface protein C (OspC) is a lipoprotein that is differentially expressed in B. burgdorferi according to environmental influences.^[9] 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.^[9]

OspC also provides an example of functional polymorphism in B. burgdorferi. ^[10] OspC is an antigen- detection of its presence by the host organism can stimulate an immune response.^[10] 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.^[10] Through several molecular mechanisms, such as genetic recombination, B. burgdorferi populations are able to maintain the diversity of the OspC locus.^[10] This ability to sustain variability in the morphology of OspC is a selective adaptation, because host immune responses are not effective against some variants of OspC.^[10]

1. ^ ^{a b} Johnson RC (1996). Leptospira. In: Barron's Medical Microbiology (Barron S et al, eds.), 4th ed., Univ of Texas Medical Branch. (via NCBI Bookshelf) ISBN 0-9631172-1-1. 
2. ^ Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0-8385-8529-9. 
3. ^ Karlen A (2000). Biography of a Germ. Pantheon. ISBN 0-375-40199-7. 
4. ^ Macdonald AB. A life cycle for Borrelia spirochetes? Med Hypotheses. 2006;67(4):810-8. PMID 16716532
5. ^ {http://www.springerlink.com/(25j1zenolti2w445sfabub55)/app/home/contribution.asp?referrer=parent&backto=issue,14,21;journal,43,237;linkingpublicationresults,1:103905,1}
6. ^ {http://www.lymeinfo.net/medical/LDAdverseConditions.pdf
7. ^ http://www.medscape.com/viewarticle/424737_4
8. ^ Byram, R., Grimm, D., Rosa, P.A, Stewart, P.E. and Tilly, K. The plasmids of Borrelia burgdorferi: essential genetic elements of a pathogen. Plasmid Volume 53, Issue 1, January 2005, Pages 1-13. PMID 15631949
9. ^ ^{a b c d e f g h} 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
10. ^ ^{a b c d e} 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. PMID 15336225

CVBD stands for Canine Vector-borne Diseases. This covers diseases caused by pathogens transmitted by ectoparasites as ticks, fleas, sand flies or mosquitoes.

Other diseases caused by ectoparasites:

• Leishmania
• Bartonella
• Babesia
• Dirofilaria
• Ehrlichia
• Anaplasma

• Borrelia burgdorferi B31 at Genome Project
• CDC Home page for Lyme disease
• of the Borrelia burgdoferi strain