Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 I've been following what Fawcett publishes for a couple of years because he vowed to get to the bottom of what was going on with the blots of the vaccinated group that became symptomatic after the Lyme vaccine. You should read some of the papers. It amazed me that they'd actually be so honest as to publish them - showing the solid smeared (blot) bands in some cases that were totally un-readable, and they could not interpret the results because so many bands became reactive. So- their caution to other Drs. is worded something like this: A Lyme vaccine can 'interfere' with a western blot, and create a possible false positive result. I beleive they have shown that the manufacturer of the blot kits does have some bearing on the sensitivity of the tests- which IMO points to poor, non-standardized testing criteria YET AGAIN. As far as I know - they still do not know the true mechanism behind the vaccinated people - post vaccination blots.. and I think they followed some of them for up to 5 years - and some are still testing positive (but they don't tell you how these people are feeling in these papers). Barb > Heres some stuff I didnt know: > > Fawcett, director of the immunology laboratories at the duPont > Hospital for Children in Wilmington, Delaware, and a noted expert on > Lyme disease serology, says he'd observed the ability of the OspA > vaccine to provoke a wide range of Borrelia-specific bands on Western > blots well before the product reached market, as patients involved in > clinical trials appeared for routine Lyme disease tests. Fascinated > by the phenomenon, he coordinated a study of 20 adult volunteers, all > employees of the hospital, who received three vaccine doses each and > submitted blood for analysis. > > As it turned out, the elaborate banding patterns showed up in all but > one subject in Fawcett's experimental group. In fact, the banding was > so robust that 30 days after the second dose of vaccine, the only two > commercial Western blots then approved by the FDA were " rendered > virtually useless for diagnostic purposes. " On one of the FDA- > approved tests, for instance, he found that OspA vaccinees tested > with " antigens covering the whole length of the strip, so that they > were positive for Lyme disease by CDC criteria. These people were so > reactive, " adds Fawcett, " that they often showed 15 to 20 bands, " far > more than the minimum requirement of five. The other FDA-approved > Western blot, he notes, " showed several bands below the OspA region > and one dark gray smear of reactivity at OspA and above. " > > [...] > > Donta says he was alerted to the possibility after the vaccine hit > the market and he began to see, within his own practice, LYMErix > recipients who appeared to have the symptoms of chronic Lyme disease, > most often reported after the third shot. Donta found that these > patients tended to test positive for Lyme bacteria proteins other > than Osp-A on Western blots. Moreover, treating them with > antibiotics, he found most got well, just as he would expect in bona > fide cases of the disease. In a formal study of 50 such patients, 25 > within his own practice, Donta has found the observations hold. > > [...] > > Hogan also notes that " in a study in which 4,087 healthy children > between the ages of 4 and 18 were vaccinated, arthritis was no more > frequent in those who received the vaccine than in those who received > the placebo. " > > > http://www.astralgia.com/magazine/bitterfeud.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 > As far as I know - they still do not know the true mechanism behind > the vaccinated people - post vaccination blots.. and I think they > followed some of them for up to 5 years - and some are still testing > positive (but they don't tell you how these people are feeling in > these papers). A few people suggested in that article that prevailing interpretations could be incorrect, and ALL of the bands could be (at least in part) Ab against various epitopes of OspA. But this article is several years old, and that view doesnt seem to have shaken out AFAIK. Assuming therefore that the possibility above is not correct and the WB bands do in fact correspond to different, well-separated proteins - then for this LYMErix phenomenon to take place, either the immune system would have to have a permanent memory of the association of these various antigens (which would be a spectacular surprise), or the mechanism of this phenomenon would have to involve preexisting asymptomatic infection with Bb, which seems highly likely. Possibly the IS has a mechanism for tolerating highly immunoevasive parasites (which themselves have significant incentives not to harm the host by multiplying too repletely). If such tolerance existed, it would be no surprise for it to be rather " tense " and easily breakable by inoculation with an antigen of the organism in question. In that case one would have to accept the entailment that the inflammatory morbidity was due in particular to activation of the *adaptive* immune system, or the downstream consequences thereof. Again, Bb may also be an actor in such a putative truce, and may escalate its reproduction in response to vaccine-prompted host aggression against OspA. But it seems more likely that the host is the major actor, as it is a far more sophisticated organism. In my mind, these data I have just now learned about (see top post) virtually exclude the possiblity that the LYMErix illness is mediated by autoimmunity against a native antigen cross-reactive with OspA. It seems odd that most people got sick after the 3rd shot. I know one person had a gradual onset, I wonder if that was the rule? I'd jes about swap my soul for a bunch of before/after quantitative antigen assays on people who got sick from this vaccine. That would reveal a hell of alot. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 I'm sure they have it. But I'm unable to obtain it. The people who got the vacinne tested negative for Lyme by several methods before they got the vaccine. For some reason, the reasearchers - who by their own admission - realize there can be false nagatives - didn't seem to take this into much consideration when testing PRIOR to the vaccinations. Yah- trying to follow this bread crump trail is pretty hard - because there seems to be some elite group quietly doing research on this, and its hard to dig it up. I was in contact with someone in the trials (post vaccine) for a while, and he just stopped emailing me - I think becuase there's a big law suit still going on, and I bet he signed something somehwere along the way. Do you have the full paper showing the post vacinnation blots as one big grey strip? Personally - they really need to keep on this - but I'm not sure if they are or not. It's very interesting to me to follow this. Barb ERIC WROTE in part: I'd jes about swap my soul for a bunch of before/after quantitative antigen assays on people who got sick from this vaccine. That would reveal a hell of alot. > > As far as I know - they still do not know the true mechanism behind > > the vaccinated people - post vaccination blots.. and I think they > > followed some of them for up to 5 years - and some are still testing > > positive (but they don't tell you how these people are feeling in > > these papers). > > A few people suggested in that article that prevailing interpretations > could be incorrect, and ALL of the bands could be (at least in part) > Ab against various epitopes of OspA. But this article is several years > old, and that view doesnt seem to have shaken out AFAIK. > > Assuming therefore that the possibility above is not correct and the > WB bands do in fact correspond to different, well-separated proteins - > then for this LYMErix phenomenon to take place, either the immune > system would have to have a permanent memory of the association of > these various antigens (which would be a spectacular surprise), or the > mechanism of this phenomenon would have to involve preexisting > asymptomatic infection with Bb, which seems highly likely. > > Possibly the IS has a mechanism for tolerating highly immunoevasive > parasites (which themselves have significant incentives not to harm > the host by multiplying too repletely). If such tolerance existed, it > would be no surprise for it to be rather " tense " and easily breakable > by inoculation with an antigen of the organism in question. In that > case one would have to accept the entailment that the inflammatory > morbidity was due in particular to activation of the *adaptive* immune > system, or the downstream consequences thereof. > > Again, Bb may also be an actor in such a putative truce, and may > escalate its reproduction in response to vaccine-prompted host > aggression against OspA. But it seems more likely that the host is the > major actor, as it is a far more sophisticated organism. > > In my mind, these data I have just now learned about (see top post) > virtually exclude the possiblity that the LYMErix illness is mediated > by autoimmunity against a native antigen cross-reactive with OspA. > > It seems odd that most people got sick after the 3rd shot. I know one > person had a gradual onset, I wonder if that was the rule? > > I'd jes about swap my soul for a bunch of before/after quantitative > antigen assays on people who got sick from this vaccine. That would > reveal a hell of alot. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 > I'm sure they have it. > But I'm unable to obtain it. I doubt it... I mean something like the q-RiBb, to directly show you whats up with bacteria as opp to whats up with the host IS. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 ERic, I think it is both mechanisms. It is either dormant or previously unrecognized borrelia infection (which IS widespread--the question is--some of them are not that highly pathogenic and others are. In fact, it may be that you handle repeated tickbites with less pathogenic borrelia until you get a more pathogenic strain that overloads you and you go all out attack and activate them all, AND/OR the coinfections are synergistic in a horrific way, activating everything all at once--maybe bioweaponized to do so?) OR it could also either/or or both/and be autoimmune because of that whtever it was that LF721? That molecular mimicry. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 P.S. --remember the OspC paper you posted a while back. One interpretation is that certain OspC's only cause a rash, ie are not highly pathogenic. This could skew all treatment results. Could be those who took 2 weeks of abx with a lowpathogenic strain looked cured becuase it would've never progressed. I believe this is likely. THere is high variance of OspC expression. > > > As far as I know - they still do not know the true mechanism > behind > > > the vaccinated people - post vaccination blots.. and I think they > > > followed some of them for up to 5 years - and some are still > testing > > > positive (but they don't tell you how these people are feeling in > > > these papers). > > > > A few people suggested in that article that prevailing > interpretations > > could be incorrect, and ALL of the bands could be (at least in > part) > > Ab against various epitopes of OspA. But this article is several > years > > old, and that view doesnt seem to have shaken out AFAIK. > > > > Assuming therefore that the possibility above is not correct and > the > > WB bands do in fact correspond to different, well-separated > proteins - > > then for this LYMErix phenomenon to take place, either the immune > > system would have to have a permanent memory of the association of > > these various antigens (which would be a spectacular surprise), or > the > > mechanism of this phenomenon would have to involve preexisting > > asymptomatic infection with Bb, which seems highly likely. > > > > Possibly the IS has a mechanism for tolerating highly immunoevasive > > parasites (which themselves have significant incentives not to harm > > the host by multiplying too repletely). If such tolerance existed, > it > > would be no surprise for it to be rather " tense " and easily > breakable > > by inoculation with an antigen of the organism in question. In that > > case one would have to accept the entailment that the inflammatory > > morbidity was due in particular to activation of the *adaptive* > immune > > system, or the downstream consequences thereof. > > > > Again, Bb may also be an actor in such a putative truce, and may > > escalate its reproduction in response to vaccine-prompted host > > aggression against OspA. But it seems more likely that the host is > the > > major actor, as it is a far more sophisticated organism. > > > > In my mind, these data I have just now learned about (see top post) > > virtually exclude the possiblity that the LYMErix illness is > mediated > > by autoimmunity against a native antigen cross-reactive with OspA. > > > > It seems odd that most people got sick after the 3rd shot. I know > one > > person had a gradual onset, I wonder if that was the rule? > > > > I'd jes about swap my soul for a bunch of before/after quantitative > > antigen assays on people who got sick from this vaccine. That would > > reveal a hell of alot. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 Thats a good theory. With syphilis most people never get anything beyond the chancre, which resolves. Its wise to bear in mind that this could be totally a function of the strain. However, I dont see how this bears on LYMErix. There, it appears very likely that what we're seeing is some sort of destablization of an asymptomatic infection. I will need to look into it more to see if there is anything statistically significant going on there at all in the first place, as far as people getting sick form the vaccine. Apparantly certain studies say otherwise, but I shoooore dont take those at face value. > P.S. --remember the OspC paper you posted a while back. One > interpretation is that certain OspC's only cause a rash, ie are not > highly pathogenic. This could skew all treatment results. Could be > those who took 2 weeks of abx with a lowpathogenic strain looked > cured becuase it would've never progressed. > > I believe this is likely. THere is high variance of OspC expression. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 I agree. But who knows what kind of asymptomatic infection. Maybe having our immune system attacking ospA all over the place makes the spirochetes crazy as if they were in the tick gut, and who knows what they start expressing. They do NOT expect ospA in the human > > P.S. --remember the OspC paper you posted a while back. One > > interpretation is that certain OspC's only cause a rash, ie are not > > highly pathogenic. This could skew all treatment results. Could be > > those who took 2 weeks of abx with a lowpathogenic strain looked > > cured becuase it would've never progressed. > > > > I believe this is likely. THere is high variance of OspC expression. > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 OspA is expressed in the human. Possibly a whole whole lot simpler than any of this is an allergy-like hypersensitivity mechanism, ie an adaptive immune system respone that is gone hog wild, yet fails to eliminate the offending organisms. In that case we would exist in a mild state of anaphylaxis. Thats what most spiorchetologists cite as the probable mechanism of tertiary syphilis - but since no one ever *wrote or investigated anything about it* that I can find since a 100-yr-old paper by Warthin which I cant get yet, nor can I find any precedent for a microbial antigen causing such a thing (tho I havent really studied paucibacillary leprosy), I thought this view was just a bunch of crap at least as far as tertiary syphilis goes. This LYMErix stuff makes me totally reconsider that. A similar theory has been expressed regarding sarc - as a sort of systemic acne, caused by Proprionibacterim acnes and other spp. If that is the case, some sort of desensitization immunotherapy, if do- able, might be just the ticket for us, provided we could trust innate immunity to keep our little buddies in check. I read American Indians *ate* poison ivy to avoid the hapten-mediated dermatitis it causes, BUT I dont know if thats true. But yes, I think the bugs detecting antibody aggression against OspA, and responding by proliferation, is one possibility, elaborate tho it may be. OspA is an integral membrane protein and thus spans the membrane, so conformational changes caused by antibody binding a specific epitope might be communicated into the periplasm. But I'm not sure the Abs wouldnt have to be identical to produce an identical conformational change, and I'm not sure all Abs which strongly bind a given epitope are identical. Or, possibly, there could be a thing more like the CRASPS, which are theorized to be tethered proteins that sort of reach over to wherever complement has bound in order to cleave it. Such a protein which could recognize an antibody and register its presence would sure be extremely sophisticated - and would have to have some way to avoid being itself bound by antibody, which would jam it up. > I agree. > But who knows what kind of asymptomatic infection. Maybe having our > immune system attacking ospA all over the place makes the spirochetes > crazy as if they were in the tick gut, and who knows what they start > expressing. They do NOT expect ospA in the human > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 If just sensitization why would abx " cure " the vaccine victims. Who knows. Lets just kill the bug! > > I agree. > > But who knows what kind of asymptomatic infection. Maybe having our > > immune system attacking ospA all over the place makes the > spirochetes > > crazy as if they were in the tick gut, and who knows what they start > > expressing. They do NOT expect ospA in the human > > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 > If just sensitization why would abx " cure " the vaccine victims. By reducing the presence of antigens (Bb infection) to which the hypersensitivity is directed. Thing is, I'm not sure there is, yet, an actual demonstration that Tp's numbers are reduced when tert syphilis is treated! Only tiny numbers of organisms have actually been seen in the disease (tho no one has looked properly AFAIK), and small numbers of keets which are probably Tp have been seen after successful treatment! If tert syphilis is truly an iummune hyperreactivity, its hard to see why it wouldnt sort of continue. As for why those Tp survive abx, no one knows - seeing as they are very poorly transmissable in experiments, IMO its possible they have an extremely slow-growth genotype. Other thing is, shouldnt this hyperreactivity be demonstrable in vitro using spirochetal antigens and white cells from sickies? In fact I think the negation of this has been demonstrated. > Who knows. > Lets just kill the bug! Yeah, let me know when you figure that out... Quote Link to comment Share on other sites More sharing options...
Guest guest Posted August 4, 2005 Report Share Posted August 4, 2005 You ought to talk to Lynn Margulis about all this. > > If just sensitization why would abx " cure " the vaccine victims. > > By reducing the presence of antigens (Bb infection) to which the > hypersensitivity is directed. > > Thing is, I'm not sure there is, yet, an actual demonstration that > Tp's numbers are reduced when tert syphilis is treated! Only tiny > numbers of organisms have actually been seen in the disease (tho no > one has looked properly AFAIK), and small numbers of keets which are > probably Tp have been seen after successful treatment! If tert > syphilis is truly an iummune hyperreactivity, its hard to see why it > wouldnt sort of continue. As for why those Tp survive abx, no one > knows - seeing as they are very poorly transmissable in experiments, > IMO its possible they have an extremely slow-growth genotype. > > Other thing is, shouldnt this hyperreactivity be demonstrable in > vitro using spirochetal antigens and white cells from sickies? In > fact I think the negation of this has been demonstrated. > > > > Who knows. > > Lets just kill the bug! > > Yeah, let me know when you figure that out... Quote Link to comment Share on other sites More sharing options...
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