User talk:Cheungd

Hello!

What's up David, this is Krishna! — Preceding unsigned comment added by Krish707 (talk • contribs) 07:09, 28 August 2015 (UTC)[reply]

Welcome!

Hello, Cheungd, and welcome to Wikipedia! My name is Ian and I work with the Wiki Education Foundation; I help support students who are editing as part of a class assignment.

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If you have any questions, please don't hesitate to contact me on my talk page. Ian (Wiki Ed) (talk) 15:54, 28 August 2015 (UTC)[reply]

Hello

Hi David! This is Ada from Evolutionary Class!Daisuke 780 (talk) 20:27, 29 August 2015 (UTC)[reply]

Wikipedia Citations

Hello! Below you will find some article references for my Wikipedia Assignment: tick borne disease evolution of Borrelia burgdorferi.

Please feel free to add any comments regarding my chosen articles in the comment section below. Please specify the article in your comment.

References:

Fraser, C.M, Casjens, S. 1997. Genomic Sequence of a Lyme disease spirochaete, Borrelia burgdorferi. Nature. 390: 580-586.

Reference: http://www.nature.com/nature/journal/v390/n6660/full/390580a0.html

Ramamoorthi, N. 2005. The Lyme disease agent exploits a tick protein to infect the mammalian host. Nature. 436: 573-577.

Reference: http://www.nature.com/nature/journal/v436/n7050/abs/nature03812.html

Hoen, A.G, Margos, G. 2009. Phylogeography of Borrelia burgdorferi in the eastern United States reflects multiple independent Lyme disease emergence events. Proceedings of the National Academy of Sciences of the United States of America. 106: 15013-15018.

Reference: http://www.pnas.org/content/106/35/15013.full

Parola, P. 2001. Ticks and Tickborne Bacterial diseases in humans: an emerging infectious threat. Clinical Infectious Diseases. 32: 987-928.

Reference: http://cid.oxfordjournals.org/content/32/6/897.short

Ogden, N.H, Feil, E.J. 2015. Evolutionary Aspect of an emerging Lyme Disease in Canada. Applied and Environmental Microbiology. 81: 1-27.

Hodzic, Emir. 2015. Lyme Borreliosis: is there a preexisting (natural) variation in antimicrobial susceptibility among Borrelia burgdorferi strains. Bosnian Journal of Basic Medical Sciences. 15: 1-13.

You should move these to the talk page of the study species so that more users will come across them and can comment on them! Also, are there any popsci articles you might be able to cite?Evol&Glass (talk) 19:04, 21 September 2015 (UTC)[reply]

Update 9.27.15

Made an edit to this page: https://en.wikipedia.org/wiki/Borrelia_burgdorferi using the Fraser reference. Fraser, C.M, Casjens, S. 1997. Genomic Sequence of a Lyme disease spirochaete, Borrelia burgdorferi. Nature. 390: 580-586. Reference: http://www.nature.com/nature/journal/v390/n6660/full/390580a0.html

Borrelia burgdorferi

Hi there. I added some comments to the talk page of Borrelia burgdorferi article in response to your query. I moved your comments to the bottom of the talk page since that's where new comments are supposed to go. Also, remember to sign the end of each new post on the talk page with four tildes (~~~~) before you click on "Save page" so that we know who wrote them and when. The four tildes are automatically converted to the current time and your user name. You can quickly add four tildes by clicking on the special button located near the bottom right-hand corner of the editing window. CatPath (talk) 18:20, 29 September 2015 (UTC)[reply]

10/19/15

Infection

As a tick transmitted bacteria, Borrelia burgdorferi must first infect a non-human host reservoir, such as a deer or mice. This host reservoir must be a vertebrate that is able to maintain and to grow the pathogen within its blood. 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. 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. Additionally, the bacteria itself must withstand the molting and life cycle of the Ixodes tick and successfully transfect a host for B. Burgdorferi to spread to humans.

Anaplasmosis and babesiosis are also common tick borne pathogens that infect humans similarly to Borrelia burgdorferi. 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. 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. More studies and research must be done to determine the synergistic effect of coinfection and its effect on the human body.

Genetics

Through combined worldwide data, such as from countries like the United States, Japan, and Europe, researchers have developed at least thirteen genomic groups to classify the Lyme disease bacteria, Borrelia burgdorferi sensu lato. 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. Many of these genomic groups are country or continent specific. For example, the strain, B. Japonica, was first isolated in Japan and appears to be a prevalent morphology of B. burdorferi sensu lato on the eastern hemisphere, but virtually non-existent in the western hemisphere, without the influence of migration. Thus, geographic isolation and genetic drift proves to be a source of the bacteria’s heterogenic nature.

Consequently, the genomic differences 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. In contrast, B. garinii’s tick borne Lyme disease may manifest itself into an infection of the central nervous system.

Another consequence of Borrelia burgodrferi’s polymorphism is its varying degree of infection and dissemination. 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. The OspC surface protein poses to be a strong indicator of the polymorphism type and the degree of dissemination. Varying number of OspC loci are indications and determinants for the various polymorphs. The surface protein is also on the forefront of current vaccine research for Lyme disease via Borrelia.

References: Theisen M, Borre M. 1995. Evolution of the Borrelia burgdorferi Outer Surface protein OspC. Journal of Bacteriology. 177: 3036-3044.

Swanson S.J, Neitzel D.2006. Coinfections Acquired from Ixodes Ticks. Clinical Microbiology Reviews. 19: 708-727.

Embers M.E, Narasimhan S. 2013. Vaccination against Lyme disease: past, present, and future. Frontiers in Cellular and Infection Microbiology. 3: 6.

Hubalek Z. 1997. Distribution of Borrelia burgdorferi sensu lato genomic groups in Europe, a review. European Journal of Epidemiology. 13: 951-957.

Bruno J.F, Qiu W. 2008. Wide Distribution of a High Virulence Borrelia burgdorferi Clone in Europe and North America. Emerging Infectious Diseases. 14: 1097-1104.

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