Bullying Borrelia

[Camp Other]

would help, like IGIV and immune modulating drugs which are very specific to the problem underlying chronic immune dysregulation.

If you hold this opinion, then you should support the CDC, IDSA, and NIH, not threaten and 'persecute' them.
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Camp Other wrote:
RitaA may have disagreed with some of what the CDC, IDSA, and NIH has stated at times, but she hasn't to my knowledge threatened them and "persecuted them".

Bagge wrote:
OMG, Ms. Camp! All of this is utterly mind-blowing. It was MuscleCar who clearly stated he is from MI, which as best I recall is indeed part of the United States, as well as North America, and it was he who made the comment to which I referred and discussed with RitaA.

Do not call me Ms. Camp. Thank you. And that remark on another thread about nail polish? Seriously. Enough already.

Second, you addressed RitaA in your last post. I'll drink more coffee just in case I read it wrong, but:

Thanks for the information RitaA. I have access to the same. Yes, you did misunderstand, but that too is understandable.

The first document you listed is dated 2001. A lot has happened since that time. PTLDS is not a theory.

To me, that reads as if you're addressing RitaA. I don't know how else to read it.

I don't have the stamina to address the rest of the chronic misunderstandings, all of which merely go to further evidence the points made by myself and many in the past in that people who are not qualified or otherwise lack the skills to a assess intricate data should not be attempting to do so, else there will be a chronic aka persistent misrepresentations and misunderstandings.
.

I don't think you have addressed a number of the questions and points which members posting here have made.

And I think a number of people here are skilled and qualified to assess intricate data and evaluate its relevance.

[RitaA]

.
My highlights.

Bagge,

It's only because I have these references handy that I'm posting them here. It's difficult for me to tell whether or not you are questioning the autoimmune theory of PTLDS (aka chronic Lyme) that the CDC, NIAID and others support, so please forgive me if I misunderstood your remarks.

MuscleCar55 wrote:

I'm here to tell you that I think chronic Lyme could be autoimmune.

<snip>

Thanks for the information RitaA. I have access to the same. Yes, you did misunderstand, but that too is understandable.

The first document you listed is dated 2001. A lot has happened since that time. PTLDS is not a theory. It's interesting to hear a Lyme patient who is based out of the U.S. say that "chronic Lyme" disease is not due to a persistent infection, but rather an autoimmune disease. My point is that it seems like they are agreeing with the CDC, IDSA, and NIAID, and disagreeing with the ILADS theory. This would make Lyme and PTLDS two different clinical entities, which would likely require two completely different treatment regimens. Lyme disease, being an active infection and responsive to antibiotics, and PTLDS being an autoimmune disease and thus requiring a different treatment regimen. If you hold this opinion, then you should support the CDC, IDSA, and NIH, not threaten and 'persecute' them.
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Hi Bagge,

Note: My highlights (above) are in green to distinguish them from yours (in blue).

And you, apparently, partially misunderstood what I wrote as well. I wasn't suggesting that PTLDS is a theory. It is (as described by the CDC and IDSA) considered a medical syndrome that some people (and especially Lyme disease patients in North America) call "chronic Lyme disease". For many Europeans, chronic Lyme disease is synonymous with an untreated (or treatment-resistant), late stage borrelia infection, so the terminology can indeed be confusing.

The theory (or more correctly, hypothesis *) part comes into play only as it pertains to the possible cause(s) of symptoms that persist for six or more months, and only after two to four weeks of IDSA-recommended antibiotic treatment for Lyme disease. Some (like the NIH, CDC and IDSA) believe the cause of persistent symptoms may be primarily autoimmune. Others (like ILADS and many Lyme disease patients) believe it is a persistent infection that requires a much longer course of antibiotics, although they are willing to consider that autoimmune factors (or other types of immune dysfunction) may also play a role.

As far as quoting from the 2001 article, that was quite deliberate on my part. It was intended to illustrate the fact that researchers still don't have definitive answers regarding the autoimmune theory of PTLDS. A highly-respected source within the Lyme disease establishment (for want of a better word) was quoted, and researchers were hoping to have "useful, and maybe even decisive" answers within a few years. It's now more than a decade later.

Within two or three years, the researchers say, they hope to have some useful, and maybe even decisive, information from this research.

Yes, the recommended treatment for active infections versus post-infectious, autoimmune disorders can be very different (as you pointed out). Immune-suppressing treatments are known to make at least some infections worse, so it's important that doctors know what they are treating. On the other hand, since certain antibiotics are known to have immunomodulatory effects, even folks with autoimmune causes for their persistent symptoms may feel better with long-term antibiotic therapy.

It can be challenging at times to communicate through posts on an internet forum because writing styles differ and assumptions (sometimes incorrect) are therefore made. It's a limitation that we simply have to accept, and hopefully make allowances for at times -- as you and I have done by clarifying what we really meant by our comments.

Edited:

1) * "hypothesis" as opposed to "theory"
2) fixing typo
3) fixing typo (I may also need more coffee)
4) last typo that I'm fixing; please excuse any more
5) inserting quote from the 2001 article
6) who really cares?
7) changing my highlights from blue to green to distinguish them from Bagge's
8) removing a line I had incorrectly inserted in previously quoted material before I totally confuse everyone

[Camp Other]

I have chronic Lyme since holidays at Easton Conn. in 1973 and have an autoimmun disease APLS antipospholidsyndrom
triggered by Lyme disease. No matter what others say.

I'm sorry to hear that.

And yes, this is my point: Some Lyme disease patients do go on to develop autoimmune disorders because of their Lyme disease, and they need separate treatment that differs from antibiotics.

It is just as frustrating for patients in this situation to be acknowledged by society and medical professionals as it is frustrating for those struggling with late stage, persistent Lyme disease (and possibly coinfections).

[RobertF]

Lupus. 2011 Nov;20(13):1372-7. doi: 10.1177/0961203311414098. Epub 2011 Jul 5.
Antiphospholipid antibodies in patients with purported 'chronic Lyme disease'.
Greco TP Jr, Conti-Kelly AM, Greco TP.
Source
St Mary's Hospital, Department of Medicine, Waterbury, CT, USA. tgreco@stmh.org
Abstract
BACKGROUND:
Antiphospholipid antibody (aPL) positive patients and patients with purported chronic Lyme disease ('CLD') share many clinical features. After identifying significant aPL in sera of several index patients with 'CLD', we performed aPL tests on all patients referred in whom 'CLD' was suspected, diagnosed or treated.

METHODS:
All patients with suspected, diagnosed or treated 'CLD' and reportedly 'positive' Lyme assays were studied. aPL testing included anticardiolipin antibodies (aCL), anti-beta-2-glycoprotein-1 antibodies (anti-β2GP1) and lupus anticoagulant (LAC). Patients were classified into four newly described categories of CLD and data was analyzed.

RESULTS:
One hundred and six patients were evaluated, of whom 82% had neurologic symptoms and 51% rheumatologic symptoms. Eighty-eight of 106 (83%) patients had positive Lyme serologies (enzyme-linked immunosorbent assay [ELISA] 62/106, 58.4%; western blot [WB] 64/106, 60%), while 18/106 (16.9%) were negative or equivocal. aPL was found in all 'CLD' categories. aCL and/or anti-β2GP1 were positive in 85/106 (80%), with aCL present in 69/106 (65%) and anti-β2GP1 present in 69/106 (65%). For all assays, IgM isotypes predominated: WB 55/64 (85%), aCL 63/69 (91%), anti-β2GP1 52/69 (75%), aCL and/or anti-β2GP1 74/85 (87%). Anti-β2GP1 assays occurred in higher titer than aCL: 36/69 (52%) versus 63/69 (91%), p<0.001. Seventeen patients had aPL-related events. Only 12/106 (11.3%) had true post-Lyme syndromes (PLS), category IV, or late Lyme disease (LLD). Most patients had been treated for Lyme: 82/106 (79%).

CONCLUSION:
aPL occurs frequently in patients with 'CLD'. IgM anti-β2GP1, IgM aCL and IgM WB were frequently found. Documented PLS or LLD was uncommon. The role of aPL in patients with 'CLD' needs further investigation.

Comment in
Antiphospholipid antibodies in patients with persistent Lyme disease symptoms. [Lupus. 2012]

[RitaA]

Hi RobertF,

I'm sure you're already familiar with the following article, however other folks might not be.

http://ard.bmj.com/content/62/5/388.full.pdf

Ann Rheum Dis 2003;62:388–393

REVIEW

Antiphospholipid antibodies and infections

R A Asherson, R Cervera

Many infections have been found to be associated with antiphospholipid antibodies (aPL), although a pathogenic role for these antibodies has not usually been obvious except in a few isolated cases. Two types of aPL have been referred to as “autoimmune” and “infectious” types. This distinction, however, has subsequently been found not to be absolute.

[snip]

This has led to the hypothesis that perhaps infections may be a “trigger” for the induction of pathogenic aPL in certain predisposed subjects. The b2GPI induced by infections may bind to “self” aPL thus forming an immunogenic complex against which aPL are then produced.15 What constitutes this predisposition is unknown at this time, but clearly genetic factors might have a significant role. The antibodies produced by infectious “triggers” are therefore heterogeneous in their dependency on b2GPI, and a minority may resemble the “autoimmune” type. Viruses and microbial agents may induce autoimmune disease by several differing mechanisms. The mechanism which concerns the production of aPL and indeed the APS is known as “molecular mimicry”.16–18

• Table 1 Infections in which aPL have been detected
  
  1. Viral
  
  Hepatitis C
  EBV
  HIV
  CMV
  Parvovirus B19
  Adenovirus
  Varicella
  Vaccinia
  Mumps
  Rubella
  HTLV-1
  
  2. Bacterial
  
  Leprosy
  Tuberculosis
  M pneumoniae, M penetrans
  Salmonella
  Staphylococci, streptococci
  Coxiella burnetii (Q fever)
  Bacterial endocarditis
  
  3. Spirochaetal
  
  Syphilis
  Leptospirosis
  Lyme disease (Borrelia burgdorferi)
  4. Parasitic
  
  Malaria
  Kala azar
  Toxoplasmosis

[the full article follows]

It might be even be worthwhile creating a separate thread called something like "Borrelia Infections and Antiphospholipid Antibodies", so others could learn from your personal experiences. No pressure intended -- it's just an idea.

[Lorima]

My question is still pending. Did Henry write his way into a narrative cul-de-sac, and then get hv808ct to take over, while Henry disappeared?

In any case, here is my question, yet again.

{Repeating my question}

Lorima:  Steere's work focuses on arthritis because he is a rheumatologist by training and practically all of his grant support is from the NIAMD. Most -- if not all -- Lyme disease researchers know that the serology in patients with Lyme induced arthritis is strikingly different and not typical of that seen in patients with late Lyme disease or neuroborreliosis. This is most likely due to the rather strong inflammatory response in the arthritic joints of such patients. I think Steere has been quite careful in confining his views to that pathology.

I don't see that "Steere has been quite careful in confining his views to that pathology", at all. To the contrary, I think he has vigorously and successfully sought to extend his diagnostic scheme, which he formulated based on his arthritis patients, to the whole field of LD. I can document this in detail, but it is so well-known that I am surprised you would question it. What makes you think Steere has been careful in this way?