Borrelia garinii
A Microbial Biorealm page on the genus Borrelia garinii
Classification
Higher order taxa
Kingdom: Bacteria
Phylum: Spirochaete
Class: Spirochaetes
Order: Spirochaetales
Family: Spirochaetaceae
Genus:Borrelia
Species
garinii
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.(11) 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.(8)
Genome structure
Borrelia species generally contain 930+/- 20 kbp. (1)Borrelia garinii has one linear chromosome and codes for 869 genes.Borrelia garinii 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.(7) 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. One being 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.(7) 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. The flagellas of the Borrelia species are unique because the flagellas 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. (Schaechter) The Borrelia species lack several metabolic enzymes. The glycolytic enzymes are present, but are missing a few in the pentose phosphate pathway. Such enzymes are the 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.
Ecology
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. 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.
Pathology
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. The ticks generally carry Borrelia garinii within its gut and it then infects host cells through a tick 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. 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. Between one to three weeks after a 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.
Current Research
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.
Enter summaries of the most recent research here--at least three required
References
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. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi db=genome&cmd=Retrieve&dopt=Overview&list_uids=495
6. Ed. Shaw, Karen Joy. Pathogen Genomics. Totowa, New Jersey: Humana Press, 2003.
7. Ed. Craig, Alister and Artur Scherf. Antigenic Variation. London, United Kingdom: Elsevier Ltd, 2003.
8. Rahn, Daniel and Janine Evans. Lyme Disease. Philadelphia, PA: American College of Physicians, 1998.
9. 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
10. De la Maza, Luis M. Color Atlas of Medical Bacteriology. Washington, D.C.: ASM Press, 2004.
11. Elliott, Tom. Medical Microbiology and Infection. Malden Mass., Oxford: Blackwell Pub., 2007
12. Ed. Gray, J.S., O. Kahl, R.S. Lane, and G. Stanek. Lyme Borreliosis. New York: Plenum Press, 1994.
Edited by Kimberly Tong, student of Rachel Larsen and Kit Pogliano
