A Microbial Biorealm page on the genus Borrelia garinii
Higher order taxa
Description and significance
Borrelia garinii is a type of spirochete. Spirochetes are normally thin, approximately 0.1-0.5 micrometers by 5.0-20.0 micrometers. Borrelia garinii is generally characterized to have a spiral shape, to be motile, non-capsulated, and non-sporing. The Borrelia species can be anaerobic or microaerophilic.(10) There are three types of Borrelia that can cause lyme disease: Borrelia burgdorferi, Borrelia afzelii, and Borrelia garinii. (2) In 1982, a man named Burgdofer identified spirochetes within the midsection of an adult deer tick, known as Ixodes dammini, renamed currently to Ixodes scapularis. Another researcher named Barbour, cultured spirochete in Kelly’s medium. Spirochetes have been cultured from blood and tissue samples of patients with erythema migrans, which is a rash associated with Lyme disease, and cerebral spinal fluid of patients with meningoencephalitis, which is a medical condition that resembles meningitis and encephalitis. Jennin and colleagues isolated Borrelia burgdoferi, a spirochete very similar to Borrelia garinii, from ticks and humans in 1984. Not much is known about the Borrelia species. In the future, hopefully new knowledge will be gained from analyzing the genome which will help identify new surface proteins to help possibly prevent, diagnose, and treat Lyme disease.(7)
Borrelia species generally contain 930+/- 20 kbp. (1)Borrelia garinii has one linear chromosome and has a total of 969 genes. Out of these 969 genes, 931 are protein coding genes. Borrelia garinii has one linear chromosome and codes for 869 genes.(6) Like other Borrelia, it also contains one copy each of different types of linear and circular plasmids.(1) Linear plasmids are very rare and have only been detected in two other eubacteria, Streptomyces lividands and Argobacterium turnefaciens. The ends of the Borrelia chromosome and linear plasmids are covalently closed loops. The linear plasmids are approximately 10kb-180kb, while the circular plasmids are approximately 8-40kb. (1) The G-C content of Borrelia species are estimated to be approximately thirty percent of their genome. Borrelia garinii has a G-C content of 28.12%. Some unique properties were found during experiments with Borrelia burgdorferi, which could apply to Borrelia garinii. Borrelia burgodorferi lacks invasion genes, global regulatory systems, toxins, and 2-component signal transduction that can be traced back to a common ancestor. A second unique property of Borrelia burgodorferi is that there is a large amount of duplicated lipoproteins. So far, no functions for the duplicated lipoproteins have been found.(6) The small genome of the Borrelia species suggests that it highly depends on some of the host’s cellular machinery to replicate.(1)
Cell structure and metabolism
Like all the other spirochetes causing Lyme disease, Borrelia garinii has a protoplasm protected by an inner and outer membrane. It also has flagella which are located between the inner and outer membrane. (11) The flagella of the Borrelia species are unique because they are not exposed to the host’s antibodies or tissues. The outer membrane proteins have many genes that are located on plasmids. This is very beneficial to the organism because it can make changes in those proteins; therefore, preventing foreign molecules from entering that could possibly be quite harmful. (2) The Borrelia species lack several metabolic enzymes. The glycolytic enzymes are present, but a few enzymes in the pentose phosphate pathway are missing, such as 6-phosphoglucono lactonase and transaldolase. Most enzymes for lipid metabolism are absent in spirochetes. Since spirochetes lack the ability to synthesize fatty acids, the NADPH requirement is limited.(7)
Borrelia garinii has only been found in ticks in Eurasia, while Borrelia burgdoferi is found in North America and Eurasia. Borrelia garinii and species similar to it have been found in hard ticks such as Ixodes ricinus, Ixodes scapularis, Ixodes pacificus, and Ixodes persulcatus.(6) These ticks then go on to feed on all sorts of mammals, birds, and reptiles. The people that are the most susceptible to getting bit by a tick carrying Borrelia garinii are those that live in rural or suburban places. This is because those areas are generally areas that are wooded and inhabited by deer. Although deer is not the most favorable host for Borrelia garinii, it is sometimes necessary for the ticks to live there to multiply.(7)
Like many other Borrelia species, Borrelia garinii rely on hematophagous arthropods for transmission. Borrelia garinii is usually transferred to avian, rodent hosts, and to humans by Ixodes ricknus, also known as the sheep or forest tick and Ixodes persulcatus, also known as the taiga tick. The seabird tick, Ixodes uriae, carries Borrelia garinii through a silent enzootic cycle in birds. There are two enzootic cycles that exist and as the seabirds migrate, a mixture of the two strains can occur.(7) Ticks generally carry Borrelia garinii within their gut and infect host cells through a bite. On initial contact, the spirochetes are not in the salivary glands or saliva. The spirochetes stay in the intestine and remain there for 24-48 hours. While in the gastro-intestinal section of the tick, Borrelia garinii and other spirochetes do not replicate because of their attachment to epithelial cells. Once the spirochetes make contact with high heat and mammalian blood, the expression of the outer surface proteins change drastically. Borrelia garinii is no longer dormant and begins to spread through the wall of the gut and through the entire tick. The spirochetes infect mammalian cells through the salivary glands of the ticks.(2) Borrelia burgdorferi, a spirochete very similar to Borrelia garinii, binds to human platelets and endothelial cells through beta II b beta 3 and beta v beta 3. Once Borrelia burgdorferi binds to human platelets and endothelial cells, it is transported to the entire body through the blood system. In areas where blood flow is slow, Borrelia species’ movements are generally stopped. This occurs to establish infection to tissues nearby.(12) Between one to three weeks after an infected tick bite, most people end up developing a reaction that causes a flat red rash. Some symptoms that a person could experience after being bit by a tick are a low-grade fever, fatigue, stiff neck, arthritis, and lymphadenopathy. Neurological manifestations are more common with Borrelia garinii, while arthritis occurs mostly in cases dealing with Borrelia burgdorferi.(7)
Borrelia garinii is known to be a spirochete that is very active in causing Lyme disease in Europe, but it so far has not been found to cause Lyme disease in North America. Therefore, a study was done to test to see if Borrelia garinii is present in seabird ticks on the Atlantic Coast of North America. In this research, 261 Ixodes uriae ticks were examined by polyclonal antiborrelial fluorescent antibody. Many ticks were dissected, and then the midguts of the ticks were screened for spirochetes through the previous method mentioned. DNA was extracted from the ticks that contained Borrelia and then the DNA was amplified. The researchers found that out of the many different ticks they analyzed, spirochetes were found only in ticks from Gull Island, Newfoundland. 9 out of 22 adult ticks and 1 out of 39 nymphal ticks carried spirochetes. The finding of Borrelia garinii in Gull Island, Newfoundland, confirms that this particular species is present in seabird nesting sites on the Atlantic Coast of North America. This research is important for the prevention of Lyme disease because Borrelia garinii is now known to be in the presence of Borrelia burgdorferi, which could possibly lead to the introduction of Borrelia garinii into North America.(8)
Another very important research that was done in 2006, tested the effects of a coinfection of Borrelia burgdorferi and Borrelia garinii on Lyme Borreliosis. Ixodes ricknus ticks and mice can be coinfected. Therefore, mice were used in this experiment to test the effects. Mice coinfected showed signs of more paw swelling and arthritis. However, there was a larger number of Borrelia burgdorferi in the coinfected mice than in mice infected with just Borrelia burgdorferi. Also, there was a fewer number of Borrelia garinii in the coinfected mice than in mice infected with only Borrelia garinii. The researchers first purchased the mice from a laboratory and infected the 6 week old mice with spirochetes that were grown at an optimal temperature of 33 degrees. Cultures using blood containing viable spirochetes were analyzed. DNA was also extracted from the tissues and PCR was used to amplify the sequence. After much experimentation, the researchers concluded that the coinfection resulted in a more severe form of Lyme disease.(13)
A large part of doing research is finding better ways to prevent or treat a disease. A research article was published April 17, 2007 about the interactions of Borrelia garinii and human dendritic cells. The researchers used cDNA microarrays during this research and it showed that the enzyme CD38, which is crucial in dendritic cell chemotaxis and migration to lymph nodes was upregulated by lipopolysaccharide(LPS), but not by Borrelia garinii. PCR showed that the expression of CCR7 was much greater when activated by lipopolysaccharide than by Borrelia garinii. These results suggested to the researchers that Borrelia garinii has a large effect on dendritic cells by hindering the upregulation of some important molecules in dendritic cell migration to lymph nodes. This in turn, affects the immune response to Lyme borreliosis. (14)
1. Ed. Saier, Milton H., and Jorge Garcia-Lara. The Spriochetes: Molecular and Cellular Biology. United Kingdom: Norfolk, 2001
2. Schaechter, Moselia, N. Cary Engleberg, Berry I. Eisenstein, Gerald Medoff. Mechanisms of Microbial Disease: third ed.. 1998
4. Baranton, G., Postic, D., Saint Girons, I., Boerlin, P., Piffaretti, J.C., Assous, M., and Grimont, P.A. "Delineation of Borrelia burgdorferi sensu stricto, Borrelia garinii sp. nov., and group VS461 associated with Lyme borreliosis." Int. J. Syst. Bacteriol. (1992) 42:378-383.
5. Ed. Shaw, Karen Joy. Pathogen Genomics. Totowa, New Jersey: Humana Press, 2003.
6. Ed. Craig, Alister and Artur Scherf. Antigenic Variation. London, United Kingdom: Elsevier Ltd, 2003.
7. Rahn, Daniel and Janine Evans. Lyme Disease. Philadelphia, PA: American College of Physicians, 1998.
8. Smith RP, Muzaffar SB, Lavers J, Lacombe EH, Cahill BK, Lubelczyk CB, et al. Borrelia garinii in seabird ticks (Ixodes uriae), Atlantic Coast, North America. Emerg Infect Disease. 2006 Dec. Available from http://www.cdc.gov/ncidod/EID/vol12no12/06-0446.htm
9. De la Maza, Luis M. Color Atlas of Medical Bacteriology. Washington, D.C.: ASM Press, 2004.
10. Elliott, Tom. Medical Microbiology and Infection. Malden Mass., Oxford: Blackwell Pub., 2007
11. Ed. Gray, J.S., O. Kahl, R.S. Lane, and G. Stanek. Lyme Borreliosis. Oxon, UK; New York: Cabi Pub., 2002.
12. Ginsburg, Howard S. Ecology and environmental mangagement of Lyme Disease. New Brunswick, N.J.: Rutgers University Press, 1993.
13. Hovius, Joppe W.R., Li X, Ramamoorthi N, van Dam A, Barthold S, van der Poll T, Speelman P, and Fikrig E. Coinfection with Borrelia burgdorferi sensu stricto and Borrelia garinii alters the course of murine Lyme borreliosis. 2006 Dec. Available from http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17328756&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
14. Hartiala P, Hytonen J, Pelkonen J, Kimppa K, West A, Penttinen M, Suhonen J, Lahesmaa R, and Viljanen M. Transcriptional response of human dendritic cells to Borrelia garinii- defective CD38 and CCR7 expression detected. 2007 April 17. Available from http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17440035&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Edited by Kimberly Tong, student of Rachel Larsen and Kit Pogliano