posted
I have read Cure Unknown, but I still have some scientific questions:
Could somebody explain to me the hypothesis or theory of why some people develope nueropathy and myalgia and others develop arthritus as a result of a borrelia pathogen?
Is this a species/genospecies variation or a subspecies/strain variation?
Is there a species/genospecies and/or subspecies/strain that is suspected of causing neuropathy and myalgia and not arthritus?
Is there a species/genospecies and/or subspecies/strain that is suspected of causing a negative ELISA and WB result?
Is there a species/genospecies and/or subspecies/strain that is suspected of being resistant to antibiotics and being chronic?
Has anyone ever experienced electric shock sensations in their chest as a common neuropathy?
Are the tests for genospecies other than b. burgdorferi different? For example, those used in europe. It could be theoretically possible that Americans are infected with these.
What are the more sophisticated biomarker tests that the IOM conference panel stated should be used to succeed 20th century WB and ELISA technology?
Thank you
Posts: 136 | From arlington, VA | Registered: Jun 2010
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onbam
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To my knowledge, the test cannot tell us what Borrelia species we have. We may be infected with organisms that don't have all that much in common with the B31 Bbsl. , etc.
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TF
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Regarding why some develop lyme arthritis and some don't, I understand that the theory is that it is based on the person's genetic predisposition. If you are predisposed to arthritis, then lyme will give you lyme arthritis.
I could be wrong on this, but I thought I read that people with this gene got lyme arthritis when they got the lyme vaccine. In fact, I think I read that this may be why it was taken off the market, even though this is not the official reason given by the manufacturer.
I remember reading that in selecting the bands that would make up a CDC "positive" test, the IDSA panel selected those that would most likely be positive for someone exhibiting lyme arthritis symptoms.
I never had any type of arthritis symptoms and I had undiagnosed lyme for 10 years. I have never had any type of arthritis symptom in my life, either.
So, I don't think I have the gene. Still, I got a positive result on the LabCorp lyme test.
The following quote regarding 20 strains of lyme disease is, to me, one of the most important pieces of information I got from the book:
p. 342 tells how Ben Luft, infectious disease specialist and Daniel Dykhuizen, evolutionary biologist, working together at Stony Brook went out into the field collecting ticks and analyzing Borrelia. A few years later, they had a graduate student travel the Eastern seaboard as far north as New Hampshire and south through the Carolinas collecting ticks infected with B. burgdorferi spirochetes. p.343 �The Borrelia were duly isolated and compared for differences in their genes.
Eventually the researchers focused on twenty strains, each with a different version of the changeable OspC. Working with those twenty strains, Luft learned that six didn�t infect humans and ten caused only a rash. Only four of the twenty could leave the skin to invade other tissue like the heart and joints or the brain. The most virulent of the strains turned out to be the prototypical B31, the version of B. burgdorferi � ultimately isolated by Burgdorfer and Barbour at the Rocky Mountain labs in 1981.�
The implications are profound. One of the most important is that if just four strains of the twenty cause disseminated infection, then the roster of rash-based studies on the treatment of early Lyme disease, conducted from the 1980s to the present, would have to be reassessed. Take a moment to ponder the simple math: It would be impossible to accept results based on the assumption that 100 percent of Lyme rashes can cause invasive disease when a significant percent cannot. Some of the classic studies claim very high cure rates for early infection; yet if the causative strain were of the rash-only variety, then even orange juice would be a �cure.� Are recommended treatment protocols truly curing most of those with early, invasive borreliosis? Or has noise from rash-only strains obscured less rosy results?� (p. 344)
So, the lyme strains that can only cause a rash are probably what is making doctors believe that they are "curing" lyme disease with 30 days of doxy. That is confounding the picture of this disease greatly and to our detriment.
Sorry, I have never researched any of your science questions. If you find the answers, however, I would be VERY interested in reading them.
As stated in the above quote, one of the 20 strains was found to be the most virulent. I would like to know if that strain causes the ALS presentation which has the absolute worst outcome of them all.
Posts: 9931 | From Maryland | Registered: Dec 2007
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posted
I'm not sure we can say the inefctious agent is borrelia for sure. Who knows what the infectious agent may be. It could be borrelia, and borrelia is the most likely candidate because it is the only known candidate that would explain this. However, it is theoretically possible that there is an unknown bacteria causing this. Perhaps even it is Borrelia, but another species than the one causing arthritus.
I think the key thing is to get people with the same symptoms together.
Additionally, the many diseases with unknown caues should focus on infectious disease as the likely cause, rather than endless genetic research from government funding that goes nowhere and pays research salaries that don't depend on results.
That is why it is important to have seperation of science and government, which we don't have.
Posts: 136 | From arlington, VA | Registered: Jun 2010
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onbam
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If you have the time, here's a very good explanation of symptom variability and how the testing criteria were skewed so that all but the arthritic cases would be missed:
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