quote:
Originally posted by laserred:
Hi Everyone,I'm confused....why did/would an (Problem hereID doc dx me) with Fibro in Jan '05....when there was a recent confirmed WB dx of Lyme from August '04 right there in my records?
I was referred to him, as well as a (Problem here Rhuemy) (Dec '04)after my GP rx'd Doxy 100mg bid for 3 months.
I am now seeing a LLMD, but just curious as to "What was up with that?"
I even asked him...and his reply was, "Well, I think something else is going on here". 
I wasn't aware of the ID docs dx until I requested my records for the LLMD, and read it before turning them over to the LLMD.
Anyone see any reasoning with that?
Thanks for any thoughts on this,
-laserred-
Quack quack ID Rhuemy docs in general are lost when it comes to lyme.LLMD is the way
``Regarding Lyme disease, there are two camps in the medical community. Camp A says that it is strictly a bacterial problem, and we don't want to look at any autoimmune aspects. Camp B says that Lyme is easily treatable and, after that, it is an autoimmune problem; but we don't want to try anything to fix it.''
``There is a basis for a third theory.
I still think that Lyme spirochetes cause some of our neurological problems by eating the myelin off our nerve cells. But in January, 2002, I completed reading "Germs" by Judith Miller and others; and now I think a major component of the attack may be similar to autoimmune disease, but it should be called something like "camouflage" disease.
Among many horrible pieces of information, Miller describes the work of the Russian germ warrior Sergei Popov who has defected to the U.S. Popov's most ingenious trick was to snip out the gene for myelin from a human (or other, e.g. mouse) chromosome, and insert it into a virus, for example smallpox, which the Russians made by the ton after signing the 1972 treaty outlawing germ warfare (hopefully without Popov's insertion).
When exposed to Popov's chimera, the test animals (mice) would develop the viral disease. Those that did not die then developed a one hundred percent fatal multiple sclerosis. Popov also inserted the gene into bacteria which gave the same sequence of events.
In a moment of inspiration, Popov discovered he could infect a bacteria such as plague (the black death) with a virus such as smallpox that contained the gene for making myelin. Now he had a 3-wave weapon: Some of the people exposed to the plague bacteria would survive with antibiotic treatment. On dying, the bacteria would release the virus causing, for example, a second wave of smallpox. Those who survived the smallpox would then die of MS.
How does it work? Apparently the body recognizes the microbe with the myelin on its cell wall and produces antibodies for the myelin. These antibodies then attack the myelin in our nerve cells. Because the antibodes are diluted by attacking the host's nerve cells, the microbe has improved its chance of survival.
Could some microbes have developed this talent for picking up host "surface" genes naturally? It would be a most useful adaptation because the host would be firing indiscriminately at the microbe and its own tissues, reducing the probabilty that the microbe would be hit. The microbe has camouflaged itself.
Of course, it would be of little use to a spirochete living in the cartilage of a knee joint to absorb a gene for making myelin, but it would be most useful for it to absorb a gene for making collagen. Such a microbe would also be camouflaged, and the victim would develop arthritis because of his body's indiscriminate attempt to kill the microbe.''
Commentator 1 wrote:
`` "Blebbing" is fascinating, kind of like a jet dropping flares to attract the incoming missles. The blebs are left wherever they were dropped and should be able to continue an antigen response.
This is a play on what you're talking about: ''
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ARTICLE from The Scientist, Vol:10, #14, pg.13, July 8, 1996, 1996, By Karen Hopkin
Read the article
``Searching The Surface
... Many researchers believe that the secret to B. burgdorferi's infectivity and inflammatory capacity lies in the interaction of its surface proteins with the host's immunological system.
Yale researcher Stephen Barthold, a veterinarian and professor of comparative medicine who developed the first mouse model of Lyme disease, studies the expression of B. burgdorferi surface proteins throughout various stages of the spirochete's life cycle.
He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. "It's using some sort of stealth-bomber-type mechanism," he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins.
Explains Barbour: "It's like a bacterial Star Wars defense program," in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack ...''
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ARTICLE from Infection 2001 Dec;29):315-9, By Brorson O, Brorson SH, Henriksen TH, Skogen PR, Schoyen R., Dept. of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway.
Read the article
``Association between multiple sclerosis and cystic structures in cerebrospinal fluid.
BACKGROUND: The aim of the study was to search for infectious agents in the cerebrospinal fluid of patients with multiple sclerosis (MS).
PATIENTS AND METHODS: cerebrospinal fluid from ten patients with the diagnosis relapsing remitting MS and from five controls without MS were examined by transmission electron microscopy, dark field microscopy, interference contrast microscopy and UV-microscopic examination of acridine orange staining (AO). All cerebrospinal fluid samples from patients and controls were cultured.
RESULTS: Cystic structures were observed in cerebrospinal fluid of all ten patients by AO and transmission electron microscopy. dark field miscroscopy revealed eight cyst-positive patients out of nine. One of five control persons had such structures in the cerebrospinal fluid; this person had suffered from erythema migrans. Spirochete or rod-like structures emerged after culturing two of the MS patient cerebrospinal fluid samples and these structures could be propagated.
CONCLUSION: A significant association of cerebrospinal fluid cysts and MS was identified in this small study among residents in a coastal area of southern Norway. The cysts could be of spirochetal origin. Our study may encourage other researchers to study larger patient groups.''
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ARTICLE from APMIS 2001 May;109(5):383-8, Gruntar I, Malovrh T, Murgia R, Cinco M., Institute of Microbiology and Parasitology, Veterinary Faculty, Ljubljana, Slovenia. [email protected]
Read the article
``Conversion of Borrelia garinii cystic forms to motile spirochetes in vivo.
Cystic forms (also called spheroplasts or starvation forms) and their ability to reconvert into normal motile spirochetes have already been demonstrated in the Borrelia burgdorferi sensu lato complex.
The aim of this study was to determine whether motile Borrelia garinii could develop from cystic forms, not only in vitro but also in vivo, in cyst-inoculated mice.
The cysts prepared in distilled water were able to reconvert into normal motile spirochetes at any time during in vitro experiments, lasting one month, even after freeze-thawing of the cysts. Motile spirochetes were successfully isolated from 2 out of 15 mice inoculated intraperitoneally with cystic forms, showing the infectivity of the cysts.
The demonstrated capacity of the cysts to reconvert into motile spirochetes in vivo and their surprising resistance to adverse environmental conditions should lead to further studies on the role and function of these forms in Lyme disease.''
[This message has been edited by treepatrol (edited 10 March 2005).]
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