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Typical Lyme Story, Atypical Victim

Discussion in 'Infections: Lyme, Candida, EBV ...' started by duncan, Jun 26, 2019.

  1. duncan

    duncan Senior Member (Voting Rights)

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    The deliberate mischaracterization of the typical late stage Lyme patient suggests to me that some people know. To be sure, not many. But someone is dragging the collective medical communities' feet on direct testing, and that orchestration has to be for a reason that extends well beyond either frugality or indifference born out of dogma, imo.
     
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  2. chrisb

    chrisb Senior Member (Voting Rights)

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    That's interesting. I would assume that WB would have been one of the youngest to be involved in whatever it was, and that he would only have known about the small part with which he was involved. One would therefore assume that those with first hand knowledge would by now have died. Perhaps there remains some second -hand institutional knowledge.

    I think we can be reasonably certain that WB was not "on a frolic of his own", and that he was under direct control of the head of the laboratory and so accountable up the chain of command. Whoever it was at RML who gave instructions for intervention at the interview must have had greater knowledge than is generally available,
     
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  3. duncan

    duncan Senior Member (Voting Rights)

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    This was organized and conducted over at least two decades. DOD would have vested interests. There'd be cross-elastic benefits from participation to varying degrees, I'd wager, among multiple agencies.

    So my guess is there are some who have inherited this knowledge, and who continue to manage the repercussions of these Cold War machinations.

    Agreed.

    The protection would have to continue, otherwise we'd diagnostically reverse-engineer our way into the truth. That diagnostics have been stonewalled so effectively for so long perhaps represents a testimony either to ineptitude, or to continuing oversight designed to ensure the truth is quelled.

    That indirect diagnostics may actually be getting worse instead of better does not fill me with confidence.
     
    Last edited: Sep 20, 2019
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  4. chrisb

    chrisb Senior Member (Voting Rights)

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    I am now thoroughly confused. The results accompanying that letter from Steere to WB are dated July 1979 and September 1979. The letter is dated April 9 1980. The results are said to show little difference from controls. On wonders about the delay. As the test includes Swiss agent one would assume regular contact between WB and Steere.

    On p132 of the book there is a page of results for Steere's sera dated 18/10/79 said to show a strong positive reaction to Swiss Agent. This just does not make sense. Why would Steere be relying on old tests which seem to be at odds with more recent ones?
     
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  5. duncan

    duncan Senior Member (Voting Rights)

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    LOL. Rheumatologists and infectious diseases are not necessarily a marriage made in Heaven. Perhaps more to the point, was a govt EIS rep the right type to be investigating what might have been a govt-made fire?
     
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  6. chrisb

    chrisb Senior Member (Voting Rights)

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    @duncan Help. I begin to fear for what is left of my sanity, and wonder whether I am mistaken, and need to go back and reread everything.

    Somewhere, in the last couple of months, I have read that WB, Steere and all were initially investigating a disease (or perhaps an undifferentiated group of diseases) in which about 20% of sufferers had the initial rash of ECM. I am sure WB said some of the cases were like spotted fever but without the rash.

    Seemingly, there then followed the formerly undisclosed "false alert" of Swiss Agent and East -side Agent.

    There then follows (in circumstances about which WB finds it necessary to lie to his official biographer) the discovery of Bb, which is tested on rabbits and found to cause an ECM like rash.

    What puzzles me is the start of the Steere et al paper from 1983 which then states that Lyme disease typically begins with the skin lesions of ECM. This is followed by the 1984 Burgdorfer paper in which Lyme and ECM appear to become interchangeable alternatives, the one European, the other American. I would have thought that the use of the word "typical" might be legitimate if referring to 90%, or more, of cases. On this basis 80% of cases of what had been diagnosed as Lyme on a purely clinical basis are now excluded from the diagnosis.

    My reading of the Steere et al paper is that all those tested had ECM.

    I am sure this must have been addressed and discussed over the years. I had not expected to see this apparently fallacious argument set out quite so clearly.

    This is clearly relevant to ME as many of those 80% would no doubt have fallen into the spurious diseases category so loved by eminent psychiatrists.

    Please tell me I am wrong.
     
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  7. duncan

    duncan Senior Member (Voting Rights)

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    When you say ECM you are talking about Erythema Migrans rash, yes, @chrisb ?

    !983 was a watershed year for Lyme papers, and not in a good way.

    So, numbers for the bulls-eye rash are all over the place. It was considered so prevalent and specific to Lyme that to this day the mere appearance of the rash can be used to confirm Lyme diagnostically.

    Turns out, though, it may not occur as frequently as researchers once maintained. Worse, there's this pesky STARI mess down in the midwest US which also has an EM rash, but which, according to the CDC, is NOT Lyme. So, does that mean having the EM is not diagnostic of Lyme if you live in an area where there are LoneStar ticks (the tick vector which purportedly transmits STARI)?

    Anyway, not as many people get the rash as leading Lyme researchers once thought.
     
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  8. chrisb

    chrisb Senior Member (Voting Rights)

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    @duncan

    yes, its the erythema chronicum migrans rash. That's interesting. I am sire though that I have seen WB write something which seemed to suggest that they knew that only about 2o5 of the patients they were initially investigating had the rash. I shall have to try and find it and see when it was written.

    I am sure that the rash has been viewed as specific since 1983. What I am wondering is whether it was regarded as specific before they had a test for something that caused the rash. What would be interesting to know is whether they retested all the sera which they had used for the Swiss agent testing, before they knew that Bb seemed to cause the rash.

    Something that is surprising me about the Swiss agent testing is that they do not seem to have run identical tests, on the Lyme sera, for East-side agent alongside those for Swiss Agent. In my amateurish way, knowing nothing of microbiology, I would have thought that would have been fundamental. I suppose misconceptions may be based purely on the artefacts of the evidence which has come down to us.
     
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  9. duncan

    duncan Senior Member (Voting Rights)

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    I am not having a particularly good brain day, so forgive me if I am wrong, but I want to say that researchers somewhere in Europe tied the rash into what eventually was labeled Lyme many years before. Many years. I'm not talking about ACA either, I'm talking EM.

    I could be misremembering, though. :(

    Did they retest the Swiss Agent sera...OH! I see where you're going with this! Why did WB think the Swiss Agent was the cause if he knew it didn't cause the rash?! Maybe he didn't know at that point about the rash being tied to the infection?

    Here's a question for you: Did all the sera that had Bb and caused Lyme also have the Swiss Agent? Were there any sera that came from Lyme patients that did not have the Swiss Agent? I don't recall.

    Here's another, this one theoretical: Could it take the tandem of Bb and the Swiss Agent to make the case impervious to abx?

    Ultimately it should not matter. Rickettsia and Borrelia are both supposed to be curable with various abx protocols. But 20% of pople who get sick with at least Bb do not get better.
     
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  10. chrisb

    chrisb Senior Member (Voting Rights)

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    There are so many odd features. It never becomes clear in the official narrative at what point WB recalls that he knew all along that ECM was thought to be caused by a spirochete and that he , WB, had attended a lecture at which this was mentioned, I think it was in Ohio, in 1949. His memory seems to have worked in an unusual manner for so able a man.

    I don't think we know the answer to those questions. Who knows what there might have been in the records which Newby says are missing? Without them little can be said.

    I am not even convinced that WB knew the answer - merely that he was not at liberty to disclose everything that he did know. What is needed is the sort of access and funding that went into the Amerithrax case. Don't hold your breath.
     
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  11. chrisb

    chrisb Senior Member (Voting Rights)

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    How do you feel about coincidences? I must admit to being largely unconvinced by them and accept them only when other explanations can be ruled out.

    We already have one. In 1978 WB takes a sabbatical tick hunting with his friend Aeshclimann from Neuchatel. He comes back with the "Swiss agent" rickettsia almost identical to the East side agent. Supposedly he was looking for the cause of a Q fever like illness.

    What is claimed to be the first case of Lyme arthritis outside the US was reported, by doctors from Lausanne on October 10 1981, to have occurred at Payerne, Vaud, Switzerland in August 1979. This lies just across the lake from Neuchatel.

    Br Med J (Clin Res Ed). 1981 Oct 10; 283(6297): 951–952.
    doi: 10.1136/bmj.283.6297.951-a
    PMCID: PMC1507214
    PMID: 6793189
    Lyme arthritis appearing outside the United States: a case report from Switzerland.
    J C Gerster, S Guggi, H Perroud, and R Bovet

    Within a month of the publication of that paper WB discovers his spirochete.

    It all seems very odd. Who knows what to make of it all?
     
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  12. duncan

    duncan Senior Member (Voting Rights)

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    Kris Newby?

    In all seriousness, I also do not hold store with coincidence. It's a small, small world, especially when it comes to biological agents.
     
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  13. duncan

    duncan Senior Member (Voting Rights)

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    I am a bit confused by this article, @chrisb. WB discovered the cause of Lyme arthritis in the US around 1980, right? That was from Benach's ticks from Long Island, New York. The spirochetes from that batch of ticks would have been what we today call Bb sensu stricto. We now know the causative agents of Lyme in Europe, historically speaking, are B afzellii and B garinii - neither of which is strongly associated with Lyme arthritis, if I recall correctly. So, did the US exports back in the late 70's include a new species of spirochete?

    It's certainly possible it migrated over with birds or whatever.

    I feel like I am forgetting something.

    Btw, great find - it would have to be about a case in Switzerland....
     
    Last edited: Oct 11, 2019
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  14. chrisb

    chrisb Senior Member (Voting Rights)

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    1 November 1981 is given as the date of WB's discovery of Bb.

    In the 1984 paper this is what WB says about retesting the Swiss material:

    One of our subsequent research objectives was to determine whether I. ricinus, the
    incriminated vector of ECM in Europe, was also a carrier of spirochetes. Evidence
    that this was the case was obtained from smears prepared in 1978 from nymphal
    ticks at the University of Neuchatel in Switzerland, where I spent several months
    conducting a tick/rickettsial survey in various parts of that country. Of 135 smears
    of ticks collected in the Seewald forest on the Swiss Plateau, where according to
    medical authorities ECM had occurred in the past, 23 (17 percent) contained spirochetes
    that tinctorially and morphologically appeared similar to those detected in L
    dammini.


    Seewald forest is about 50 miles due east of Payerne.
     
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  15. duncan

    duncan Senior Member (Voting Rights)

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    So the timing dovetails with the case study of Lyme arthritis. But when did it first arrive in Europe? Why didn't he nail it as a causative agent possibility back in '78? So they got it was a tick vector. No biggee. Even Steere suspected that early on. But you see spirochetes, you know there's an association in I ricinus and EM - how do you miss the tie-in? Certainly this would explain how he was so nimbly able to put 2 + 2 together in '81.

    I don't know. I think he knew back in '78. He had to have seen this paper. He grew up not too far from there. More to the point, ticks and spirochetes were his thing.

    I'd be surprised he didn't know well before that.
     
    Last edited: Oct 11, 2019
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  16. chrisb

    chrisb Senior Member (Voting Rights)

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    I think that he at least suspected by 1978, and probably knew by 1979. There has to be a reason for his claiming to not be interested in Lyme before discovering his spirochete. The official story is implausible. Even if it be true, it is still implausible.
     
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  17. chrisb

    chrisb Senior Member (Voting Rights)

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    Incidentally, I found the reference to only 20% of patients with Lyme having initially suffered from ECM. On p192 of Bitten, Newby writes when discussing Steere:

    The first step was to develop a definition of the disease based upon its symptoms. The common denominator among their patient cohort was an intermittent swelling of joints, what appeared to be a novel type of arthritis. the second most prevalent symptom, noted in about 20% of cases, was an expanding red bull's eye rash. The researchers also noted flu-like symptoms (malaise, fatigue, chills, fever, head ace, stiff neck, backache, muscle aches, and, occasionally, cardiac and neurological problems

    The authority for this is not cited and I shall have to fine it. Presumably it is one of Steere's papers from around 1978. Somehow that morphed into a disease typically starting with the bull's eye rash.

    There is something else that puzzles me on p188. Describing the testing of the ticks for his spotted fever paper with Bernavh it says

    Rickettsia testing for this study was done at Long Island hospitals and at New York State and Nassau county health departments. The lab personnel weren't rickettsia experts, and they used a not that accurate anti-body test….

    If this is an accurate description, one could be forgiven for thinking that WB did not wish to know the answer with any greater certainty.
     
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  18. duncan

    duncan Senior Member (Voting Rights)

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    Strikingly low incidence compared to what the official line is today. The 20% number comports more with the ILADS folk.

    Except what he had been doing for a living for the preceeding 25 years...:)
     
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  19. chrisb

    chrisb Senior Member (Voting Rights)

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    The recent paper by Benach and Barbour on another thread contains the link to the archived Burgdorfer papers at Utah.

    This letter from WB to Jenkins and Fort Detrick might be thought illuminating. In discussing simultaneous infection of Dermacentor andersoni with Colorado tick fever and Rickettsia rickettsia organisms WB writes

    "It will be interesting to see whether there actually exists an interference between these two agents,"
    https://uvu.contentdm.oclc.org/digital/collection/Burgdorfer/id/65/rec/199

    Newby mentions this in the book but it is chilling to see the original.


    EDIT letter dated 6 January 1959
     
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  20. chrisb

    chrisb Senior Member (Voting Rights)

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    It does seem that the missing research papers and correspondence with Steere and others are included in the papers at Utah. WB seems to have been making some sort of point in withholding them from the National Archive. The archivists at Utah would have had more time with the papers than |Newby.

    These papers also clear up a point made earlier about the inclusion of Davis as an author of the Science paper. Material was received from him on 30 Nov 1981. The only mildly surprising feature is therefor that his contribution received no mention.
     
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