Why the Government is Suppressing the Lyme Disease Epidemic

Medical topics with questions, information and discussion related to Lyme disease and other tick-borne diseases.
Henry
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by Henry » Fri 9 Jan 2015 19:57

In relation to the other bands, they were among the lowest -- by far. I should add that subsequent studies should that these bands are more likely to be found in patients with a lot of arthritic inflammation. Hardly any at all in patients with neurological symptoms. It should be noted that these are bands vs antigens that are produced (expressed) MAINLY by Borrelia growing on artificial laboratory media and in ticks, not in mammalian hosts. That why they were selected for use in the LYMErx vaccine. However, since their expression is under genetic control, they may always be present in tiny amounts, i.e., amounts sufficient to generate antibodies in the presence of inflammatory cytokines in arthritic patients. I
Last edited by Henry on Fri 9 Jan 2015 20:18, edited 1 time in total.

duncan
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by duncan » Fri 9 Jan 2015 20:05

But also some of the most specific to Bb, yes? If I have five bands IgG positive, and bands 31 and 34 are among them, shouldn't that suggest I have Lyme? If the answer is no, please explain how the answer reflects the greater good of the wider patient population.

Henry
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by Henry » Fri 9 Jan 2015 20:22

It has nothing to do with specificity. What I am saying is that antibodies vs p31 and p34 will react very specifically with laboratory cultivated Borrelia, as well as Borrelia derived from ticks. However, antibodies vs p31 and p34 are not produced in significant amounts -- certainly not in amounts typical for antibodies vs the other bands used to establish the criteria for IgG blots-- in mammalian hosts after infection, except in cases where there is arthritic inflammation and large amounts of inflammatory cytokines are produced. One might always be able to find small amounts of antibodies vs p31 and p34; however, they are not the most predominant types of antibodies produced during infection and hence are not of diagnostic significance.

duncan
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by duncan » Fri 9 Jan 2015 20:31

So what's the problem? If I test positive to b31 or b34, either IgM or IgG, then they should count toward a Lyme diagnosis. Period.

Henry, here's the deal as I see it.

This is an oversimplification, but indulge me for a moment.

If I have 10,000 patients that have three Bb specific IgG bands with or without treatment, but with a full array of symptoms, then I believe we have 10,000 Lyme patients. I have proof of antibody production, and I have proof of continued symptoms - BAM! My sick patients with proof of Bb antibody production trumps your algorithm every time, at least in my book. Do you know why? Because it's about the patients and not the patents. That's what medicine is supposed to be about - the patients.

As I said, a gross oversimplification, but it's the general gist of my non-scientific brain. Also, it will have to do for me for a bit. I hate to hit and run, but I have to hit and run. :)

Henry
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by Henry » Fri 9 Jan 2015 20:47

Look, none of this has anything whatsoever to do with patents, the rights of which have long since expired anyway. It is based solely on probability and statistical considerations, derived from hundreds -- if not thousands -- of comparative studies conducted with well characterized specimens provided by State public health laboratories. I would find it very strange if one had bands vs p31 and p34, and perhaps p41, and NONE vs the other bands that predominate based on extensive frequency distribution analysis . In other words, if you are finding antibodies vs the very minor components, why are you not finding antibodies vs the major, predominant components as well ? That would not make sense. If that is what you are finding, it should be a good reason why the presence of such bands are not judged to be decisive.

duncan
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by duncan » Sat 10 Jan 2015 15:07

Yes, Henry, my allusion to patents was just an off-the-cuff reference to the multimillion dollar Lyme diagnostic market ($500 mill or there abouts?).

And yes, bands 31 and 34 were not all that frequent, but then again those specific bands are more likely to show up in late Lyme disease, and let's face it, not a lot of research being thrown that way these days.

Now. Back to my observation about 3 bands being sufficient to diagnose Lyme. You wield the current 2T like it's the only tool that works. It never was. When Dressler and Steere and company picked it, other combinations were on the table, and were also considered, and each carried with it some validity. These alternatives ranged from a single band to 4 or more. Each, if adopted, would have diagnosed Lyme. The reason they settled in on the current system is because they liked how those numbers played out more in terms of sensitivity and specificity trade-offs in the greater or broader use. In particular, they liked how it reduced the risk of false positives.

BUT LET'S BE CLEAR HERE: A person can be infected with Lyme and not be 2T positive.

For example, I might have IgG bands 18, 21 and 93 only positive, and not satisfy the CDC 2T criteria but still have Lyme, as those bands are fairly specific to Bb, correct? Three bands, yes?

To be CDC 2T negative is not necessarily the same as not having Lyme. The bands at play matter. That the numbers of 2 or more IgM and 5 or more IgG were settled on was simply a function of averages that held true for more people - it was not an absolute for telling whether someone had Lyme or did not.

This is why I wrote that I prefer diagnostic support along with symptoms, but that I did not believe that the 2T system was definitive by any stretch, and lesser amounts of bands could also indicate active infection.
Last edited by duncan on Sat 10 Jan 2015 15:43, edited 1 time in total.

Henry
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by Henry » Sat 10 Jan 2015 15:43

Yes, I have seen statements that bands 31 and 34 are more likely to show up in late Lyme disease. However, I have yet to see any data to support such a claim. I find it hard to believe that, during infection, antibody would be produced against minor components, but not against the most abundant components representing the remainder of the CDC IgG Western blot criteria. That does make sense at all, and contradicts basic immunology.

Now, what about your EM rash that doesn't seem to go away despite recommended antibiotic therapy? Although I have never heard of such a thing, I couldn't resist the temptation to contact a physician who has vast experience treating patients with Lyme disease. He told me that in all his many years of experience, he only saw one case of an EM rash that would not go away with antibiotic treatment; upon further examination, it proved to be a pseudo-EM rash.

So, based on what you've told me, I must conclude that you do not have Lyme disease, but some other medical condition that won't improve as long as you are treated as though you have Lyme disease. You've been doing this for how many years? Don't you think it is about time you quit "beating that dead horse" and consider other possibilities? Believe me, I'm trying to help you, Duncan.
Last edited by Henry on Sat 10 Jan 2015 15:47, edited 1 time in total.

duncan
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by duncan » Sat 10 Jan 2015 15:45

:shock:

Henry, are you ok?

Henry
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by Henry » Sat 10 Jan 2015 16:41

I'm perfectly fine.

dlf
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Re: Why the Government is Suppressing the Lyme Disease Epide

Post by dlf » Sat 10 Jan 2015 16:49

Henry wrote:
Yes, I have seen statements that bands 31 and 34 are more likely to show up in late Lyme disease. However, I have yet to see any data to support such a claim. I find it hard to believe that, during infection, antibody would be produced against minor components, but not against the most abundant components representing the remainder of the CDC IgG Western blot criteria. That does make sense at all, and contradicts basic immunology.
You might look at this study. It only included seropositive patients and noted that could be a limitation in the findings. At the time though not all of these patients fulfilled the CDC criteria, only 47 of the 54 did. Too bad they didn't post more information about the complete band profiles for all the patients tested. The references for bands 31 and 34 being more likely to show up in late Lyme though are included. You might want to look at those too.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3122515/

Clin Vaccine Immunol. 2011 May;18(5):767-71. doi: 10.1128/CVI.00002-11. Epub 2011 Mar 16.
Anti-Borrelia burgdorferi antibody profile in post-Lyme disease syndrome.
Chandra A1, Wormser GP, Marques AR, Latov N, Alaedini A.
Author information
1Department of Neurology and Neuroscience, Weill Cornell Medical College, Cornell University, New York, New York, USA.
Abstract
Patients with post-Lyme disease syndrome (PLDS) report persistent symptoms of pain, fatigue, and/or concentration and memory disturbances despite antibiotic treatment for Lyme borreliosis. The etiopathogenesis of these symptoms remains unknown and no effective therapies have been identified. We sought to examine the antiborrelia antibody profile in affected patients with the aim of finding clues to the mechanism of the syndrome and its relationship to the original spirochetal infection. Serum specimens from 54 borrelia-seropositive PLDS patients were examined for antibodies to Borrelia burgdorferi proteins p18, p25, p28, p30, p31, p34, p39, p41, p45, p58, p66, p93, and VlsE by automated immunoblotting and software-assisted band analysis. The presence of serum antibodies to the 31-kDa band was further investigated by examination of reactivity against purified recombinant OspA protein. Control specimens included sera from 14 borrelia-seropositive individuals with a history of early localized or disseminated Lyme disease who were symptom free (post-Lyme healthy group), as well as 20 healthy individuals without serologic evidence or history of Lyme disease. In comparison to the post-Lyme healthy group, higher frequencies of antibodies to p28 (P < 0.05), p30 (P < 0.05), p31 (P < 0.0001), and p34 (P < 0.05) proteins were found in the PLDS group. Assessment of antibody reactivity to recombinant OspA confirmed the presence of elevated levels in PLDS patients (P < 0.005). The described antiborrelia antibody profile in PLDS offers clues about the course of the antecedent infection in affected patients, which may be useful for understanding the pathogenic mechanism of the disease.

DISCUSSION
The controversy surrounding PLDS is partially caused by our limited knowledge about the etiology and pathology of the syndrome. A potential source of information about PLDS, namely, the specificity of the immune response to B. burgdorferi in affected patients, has not been systematically characterized before. The availability of serum specimens from 54 seropositive patients fulfilling strict criteria for PLDS provided the opportunity to examine the respective antiborrelia antibody profiles in detail. The data in this report suggest that a defined pattern of antibody reactivity to borrelial antigens in PLDS may exist and offer novel clues about the etiopathogenesis of the syndrome and its relationship to the original spirochetal infection.

We can consider some possibilities that would explain the observed antiborrelia antibody response in PLDS and help in understanding its significance and pathogenic relevance to the syndrome. First, it is important to note that the apparently higher overall antiborrelia antibody response in PLDS was not evenly distributed toward the various B. burgdorferi immunodominant proteins. We observed higher-than-expected frequencies of antibody reactivity to p28, p30, p31, and p34 protein bands in the patient group than in the post-early Lyme healthy group, while the frequencies of antibody reactivity to p18, p25, p39, and p45 were either comparable or slightly higher in the post-early Lyme healthy group. Previous studies have shown that IgG antibodies to p25, p39, and p45 are generated early in Lyme disease, whereas antibodies against p30, p31, and p34 are more frequent in later stages of infection (2, 8, 14, 19, 22). The IgG antibody response to p31 (OspA), a protein whose expression by the B. burgdorferi spirochete diminishes in the early stage of the infection, is particularly rare during this phase but becomes more common in late Lyme disease (1, 2, 9, 15). Accordingly, the observed antibody profile, especially the significantly higher antibody reactivity toward the p31 band on WB and toward the recombinant OspA protein on ELISA in the PLDS group, may be indicative of a longer-than-assumed course of active infection in affected patients. This may have been caused by a delay in the start of the appropriate course of antibiotic treatment and/or an undocumented repeat infection(s) in many PLDS patients. This finding would be in line with previous studies indicating that delayed treatment is associated with increased post-Lyme disease symptoms (20).

<snip>

A second limitation of our study may be perceived to be the exclusion of seronegative patients. In this study, we chose to focus specifically on patients and post-Lyme healthy control subjects who were seropositive by whole-cell ELISA. This was done in order to ensure that all samples in the comparison had the minimal detectable antiborrelia antibody response necessary for subsequent analyses. Obviously, our findings and conclusions in this report do not extend to the seronegative subpopulation. It should be noted that in the original clinical trial that provided the specimens examined in this study (16), in which there was simultaneous recruitment of both seropositive and seronegative subjects, nearly 40% of the subjects were, in fact, seronegative. The absence of an antiborrelia antibody response in many PLDS patients points to the heterogeneity of the population under study but does not diminish the significance of the reported findings. Closer examination of the immune response in seronegative PLDS patients, including the antigen specificity of antiborrelia antibodies as a function of time since infection, needs to be done in future prospective studies.


Henry, can't you tell when duncan is yanking your chain?

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