Lyme is not an 'autoimmune' disease

Friends,

Just thought I'd post this note to let anyone new coming here know that we have protested MedHelp tagging Lyme Disease as an autoimmune disease.

'Autoimmune' means that your own immune system attacks your body by mistake, instead of attacking invading viruses and bacteria.

Lyme, however, is caused by bacteria called Borrelia burgorferi (B. burgdorferi or Bb, for short).

MedHelp has indicated it will fix this error in the website, but it could take a while for reasons I don't know.

There is a possible reason that this error has been made:  there is a split in the medical community over Lyme disease.  The Infectious Disease Society of America (IDSA) takes the position that Lyme is a hard disease to get and an easy one to cure with a couple of weeks of antibiotics; IDSA has held this position for quite a long time.

Contrary to the IDSA position is the International Lyme and Associated Diseases Society (ILADS), which takes into consideration more recent research that shows the Lyme bacteria can and do hide in the body in internal cyst-like areas they create, where antibiotics cannot easily penetrate.  In addition, Lyme bacteria have a very slow reproductive rate that makes them less susceptible to a short course of antibiotics.  When the standard antibiotics given are not capable of breaking into the cysts where the Lyme bacteria are hiding, and when treatment is stopped after a short period of time, Lyme can still be present and continue to give symptoms as before treatment.

When faced with a Lyme patient who has been treated with a short course of antibiotics but is still ill with Lyme symptoms, the IDSA position is that the Lyme was actually cured, and that the continuing symptoms are an over-reaction by the patient's immune system fighting against bacteria that are no longer there, and you are well whether you feel that way or not.  End of treatment.

On the other side, ILADS says that if there are still symptoms, then the disease is not eradicated, and treatment should continue.

Logically, Lyme should be categorized as an infectious disease caused by bacteria, regardless of one's position on allegations of later-developing auto-immunity, but so far the classification has not changed here on the website, although I believe it should.  Just thought you should know.

Welcome to the Lyme wars.

This battle between the IDSA and ILADS

[wonko]

Yes, basically, the medical camp that would deny that we have active infections and deny long-term treatment would label us as having "post-Lyme syndrome," a poorly defined. supposedly autoimmune, disease.  And that's only if you had a CDC positive Lyme test at one point in time.

We do have a lot of symptoms in common with various autoimmune diseases, but as noted above, a key difference is the cause.  Our immune systems are not just firing against our own bodies, but are actively fighting an infection.  An important implication of this different root cause is treatment:  While steroids are often used to control autoimmune attacks, they are contradicted in Lyme disease because they shut down the immune system.  

It is not a simple labeling issue, since our treatment hinges on the acceptance that the infections are persistent and difficult to cure.  If we accept the mislabel of autoimmune, we have no prospect for recovery beyond the IDSA recommended 2-4 weeks of antibiotics.

[wonko]

I've posted this before, but it feels like a good fit here.  From the Columbia University Lyme and Tick-Borne Diseases Research Center Website:

"THE LYME DISEASE CONTROVERSY

The CDC clinical criteria for Lyme Disease which exist for the purpose of monitoring the rate of Lyme disease nationally are quite narrowly defined in order to ensure a high degree of specificity in the diagnosis. These criteria are mainly useful for the early stages and rheumatological presentations of Lyme Disease, such as when a patient appears with an erythema migrans rash, arthritis, a Bell's palsy, or early central neurologic Lyme disease (meningitis or encephalitis). The CDC criteria are not very helpful for helping the clinician to detect late stage neurologic Lyme Disease. For example, the most common manifestation of late neurologic Lyme Disease is cognitive dysfunction (often referred to as "encephalopathy"). A patient who presents with new onset encephalopathy and a positive blood test for Lyme Disease would not be considered by the CDC to be a case of Lyme disease. Although the CDC recognizes that Lyme encephalopathy exists, encephalopathy is not part of the "surveillance case definition". Hence, physicians who rely on the narrow surveillance case criteria of the CDC for clinical diagnosis will fail to diagnose some patients who in fact do have Lyme disease; in these cases, the patient's treatment will either not occur or be delayed. Such delay in treatment may result in an acute treatable illness becoming a chronic less responsive one.

Other physicians who use a broader more inclusive set of clinical criteria for the diagnosis of Lyme disease will make the diagnosis of Lyme Disease and initiate treatment. The latter group of doctors, by treating some patients for "probable Lyme Disease", will make use of antibiotic responsiveness to confirm their diagnostic impression. These physicians, by erring on the side of not letting a patient with probable Lyme Disease go untreated, will help many patients who otherwise would not get treatment; undoubtedly, however, because of the inclusiveness of their diagnostic approach, these physicians will also treat some patients with antibiotics who do not have Lyme Disease. These physicians would argue that the serious consequences for physical, cognitive, and functional disability associated with chronic Lyme Disease outweigh the risks of antibiotic therapy.

Both sets of doctors are practicing medicine in a reasonable fashion based on the application of certain diagnostic principles, although the therapeutic approaches differ considerably stemming from the narrow vs broad criteria for diagnosis. This is the essence of the medical controversy surrounding chronic Lyme disease. Until medical doctors have a test that definitively identifies the presence or absence of infection (and such a test does not yet exist), the controversy about the diagnosis and treatment of chronic Lyme Disease will continue."

http://www.columbia-lyme.org/patients/controversies.html

[velvetmagnetta]

Please read this very important, ground-breaking research about how the Lyme Disease bacteria react with the immune system even AFTER IT IS DEAD:

http://spirochetesunwound.blogspot.com/2012/11/inflammatory-spirochete-debris-left.html

This is totally unheard of in the medical community as far as I know.  It is a really big deal and gives us a whole new perspective on why those of us with Long-Term Lyme disease (30 years for me) may take antibiotics for many years and still be in more pain than before we even began that dang anti-biotic regimen.

Sure, antibiotics are great - they really do kill off the Lyme disease, but the antibiotics don't clean all of the dead bacteria pieces out of the body.  These pieces have been shown (in the paper that the blog is about) to actually actively REACT with the immune system (the dead bacteria pieces incite a release of cytokines *ouch*).

When the antibiotics get through breaking the Lyme into little dead pieces, you end up with a kind of disseminated Lyme soup that is not only in your joints, but also it has now spread all over your body.

You can't point to where it hurts because it hurts dang all over!

Someone please tell me how we get those left-over pieces out?!?  They are what's causing all the pain and suffering.  Welchol works a little, but it causes much pain.  We need a better way to get those dead bacterial pieces out!

[JackieCalifornia]

Interesting article -- but the second half of the article blows some pretty big holes in the theory presented in the first half, that being that continued symptoms are not continued infection, but are simply reaction to dead, post-treatment bacterial fragments or immune system reaction.

"A critical issue to address is whether the amorphous material left behind following antibiotic treatment inflames the joints.   The authors could not answer this question directly because of the limitations of the mouse model."  Meaning:  because mice are mice and men are men, we can't tell if the junk left behind after treatment actually does inflame the joints.

"Histopathology is unlikely reveal joint inflammation, even in the untreated animals, because laboratory mice do not reliably exhibit joint inflammation so late (4-5 months) during B. burgdorferi infection."  Meaning:  the mouse immune system stops reacting 4-5 months after infection even if the infecting bacteria are still present and alive, so joint inflammation won't happen, and we can't tell if the lack of persisting inflammation is because the bacteria are dead or because the immune system is not reacting any longer.  Side note:  The human immune system reacts the same way to a Lyme infection.

"Instead, the authors conducted a test tube experiment to see whether the deposits had inflammatory potential.  They ground up joint tissue from antibiotic-treated mice in buffer and applied the homogenate to cultured mouse macrophages.  The macrophages responded by producing TNF, a key cytokine that promotes inflammation.  The more tissue that was added, the more TNF that was produced by the macrophages.  In contrast, joint tissue from uninfected mice did not promote TNF production by the macrophages.  Therefore, the deposits had the potential to spark inflammation, even after motile spirochetes were eliminated by antibiotics.  The debris would continue to inflame the tissues even after antibiotics killed all live spirochetes, explaining why symptoms persist in ~10% of Lyme arthritis cases even after antibiotic treatment."

Translation:  In a test tube, ground up bits of joint tissue from Lyme-infected (but treated and presumably cured) mice were mixed with a chemical to see if there would be a reaction like the immune system would have in a live mouse that had been treated with antibiotics.  The resulting conclusion of the test tube analysis was that in about 10% of the Lyme-infected mice that had been treated with antibiotics and all the bacteria were presumably dead, there was still an immune-system-type reaction -- although no such reaction would have been expected because the antibiotics should have killed ALL the bacteria and therefore there should be nothing to react to.  In humans, this is called 'post-Lyme syndrome', meaning you were sick, then you were treated, and if you still have symptoms after treatement, it is your over-active immune system reacting to dead bits of Lyme bacteria, NOT that you are still infected with live bacteria.  This is the basis on which standard Lyme treatment is structured:  a couple of weeks of antibiotics and you're good to go, no matter how lousy you feel or that your tests are still positive.  

"The relevance of the deposits to Lyme disease in humans could be questioned because the MyD88-deficient mice did not have a complete immune system."  Meaning:  the mouse test might be invalid because the mice had messed up immune systems that might not react fully, so the results may be wrong.

"The authors addressed this concern in the Discussion by mentioning a recent study that described a TLR1 variant linked to severe inflammation and treatment failure in Lyme arthritis patients."  Meaning:  the docs passed off this issue as unimportant because of a recent study that located a certain aspect of the human immune system that could explain this exception ... but that's just a guess at the moment.

"Although the gene encoding MyD88 has never been examined in Lyme disease patients, it is conceivable that the TLR1 variant or different forms of other immune genes lead to deposits of Borrelia antigen in the joint and other host tissues."  Meaning:  We've never looked at whether this theory applies to humans, having looked only at mice, and it's possible (but not proven) that some variation in the immune systems of various humans could leave little bits of immune-system trash lying around that results in a positive Lyme test.

"The authors also addressed the possibility that the deposits are really biofilms, which generally resist killing by antibiotics.  Biofilms are believed to be populated by persister cells, which are in a nondividing state that allows bacteria to tolerate antibiotics."  Meaning:  Lyme bacteria can create slimy shields in the body that allow Lyme bacteria to hide from the immune system, thus resulting in a continuing Lyme infection despite treatment.  

"According to the authors, if the deposits had harbored persister cells, those cells should have resumed growing when conditions became favorable for growth again.  Because the skin and joints from the treated mice were culture negative and because the skin also tested negative by xenodiagnosis and transplantation assays, the authors quickly dismissed the biofilm hypothesis.  Stricly speaking, the authors are correct.  Persister cells should start multiplying again in fresh culture medium.  However, it's hard to dismiss the biofilm hypothesis completely given the known examples of culture-negative chronic infections associated with biofilms (see this review for one example).  Electron microscopy of the joint tissue could reveal whether these deposits are intact spirochetes or debris."  Meaning:  the study is flawed because it does not take into account the ability of Lyme bacteria to hide from the immune system and from antibiotics, by cloaking themselves in the slimy shields impenetrable to the immune system.  This aspect is understood by Lyme specialists, but not generally by others in the medical community.

"Regardless of their exact nature, deposits of antigen have never been detected within the joints of Lyme arthritis patients.  Allen Steere's group failed to find such deposits in pieces of synovial membrane removed from 26 patients with antibiotic-refractory Lyme arthritis.   The findings of Bockenstedt and colleagues, who detected the deposits in a location outside of the synovial membrane, suggest that Steere's group was looking in the wrong place."  Ah ha ha!  Steere was looking in the wrong place!  Love it.

Steere, you see, is one of the great Lyme deniers and has caused much misery to be inflicted on those with persistent Lyme infection by denying them treatment.  Steere has been a big influence on the treatment standards used by the IDSA (Infectious Disease Society of America) that holds firmly to the belief that a short course of antibiotics is all you need, and if you still have symptoms of Lyme after that, it's your immune system overreacting.

Lyme specialist who lean toward the standards and approaches of ILADS (International Lyme and Associated Diseases Society) recognize the existence of biofilms and the ability of Lyme bacteria to hide from the immune system, and that antibiotics to pierce the slimy shields are needed AND other antibiotics are needed to then kill the exposed Lyme bacteria.

Bottom line:  I would revisit the assumption that you are just dealing with trash left over in your body after the Lyme party.  I would see a Lyme specialist and get diagnosed and treated.  If you need help finding such a doc, let us know -- we are glad to help.  

[jx28]

As a follow on to the above, you may find this review article to be of interest:

http://www.futuremedicine.com/doi/full/10.2217/fmb.12.92

Spirochetal ‘debris’ versus persistent infection in chronic Lyme disease: from semantics to science

Apologies if it has already been posted elsewhere!

[JackieCalifornia]

Thanks for posting this!  Stricker is one of the well-known LLMDs, no secret there -- so I don't hesitate to mention his name in the open.

The whole article is interesting, about the ins and outs of how Lyme research is funded and approached -- and how the politics of Lyme has ... 'infected' it all.

Here's the final paragraph of the article:

"Scientific knowledge depends upon the free marketplace of ideas and on public trust. We can no longer afford to empower dogmatic researchers who ignore contradictory findings and pursue their favorite lines of research, leading to dead ends. Nor can we afford to continue to erode public trust by using research to pursue political ends. It is time to establish a scientific agenda that stimulates funding for research on the mechanisms of B. burgdorferi persistence and eradication of persistent infection in Lyme disease."

Hurray!

[Ricobord]

Eloquent quote from Stricker!  Thanks for posting that.

[velvetmagnetta]

Yeah, but what if it is all just left-over bits of Lyme debris making us so sick?

You seem rather passionate that the answer to why some of us stay sick even after years of antibiotic treatment has to be complicated.  Maybe it doesn't.  Maybe it's as simple as clearing out all that debris.  Remember, this debris is not just innocuous trash - it is immune-system reactive.  In other words, even though it is already dead, it invokes an immune response in the body - inflammation, flu-like symptoms, etc.  So, it is rather dangerous and extremely painful.  The only good thing about it is that it is not reproducing.

Look, Jackie, I have read all the internet Lyme information you have.  After all, I have been laying in bed in horrible pain for 5 years with just my laptop for company.  I've been to not one but 3 Lyme-Literate doctors who all tried to help me.

I was pretty darn sick 5 years ago when I found out I'd had Lyme disease for the past 30 years.  That's when I first began antibiotic treatment for it.  6 weeks in I got so sick I cannot even describe the immense amount of pain I was in.  At the time, I was told it was this so-called Herxheimer reaction to the bacteria die-off and if I just got through that, I would feel better.  Well, 3 years go by, then 5 years, and I'm not feeling any better - just worse and worse and worse.  A true Herxheimer reaction lasts only a few days to a couple of weeks.  What I was and am feeling does not even resemble a Herxheimer reaction.  I now believe that idea is completely false and there is something else entirely going on.

Maybe the disease takes on a whole new meaning if you have it for 30 years, but all I know is that I tried just about everything and felt like absolute crap.  This is what makes me think there might be some other mechanism at work here.  Something terrible happened to me after taking those antibiotics that i still haven't been able to come back from.

That's why when I read about Bockenstedt's mouse research bells went off in my head.  It fit everything that happened to me!  The Lyme disease was pretty bad when it was alive - I couldn't swallow, couldn't play guitar any more, and had a very hard time walking.  But this was NOTHING compared with what happened to me after I tried to kill it off!!!!!

SO much pain all the time all the time I mean ll the time!  What could explain that?  What was different before as compared to after I took antibiotics.  The Lyme bacteria is actually not that hard to kill off.  Antibiotics kill it very quickly.  (of course there are always the unsubstantiated claims of cyst forms and hiding and all that) but in any animal study, it has been shown that the Lyme bacteria dies off just fine within a matter of days once the antibiotic reached high enough levels in the blood stream.

So, please.  Before you go trashing a real scientist for being a scientist (yes, her results are limited to mice and in particular immune-deficient mice) please consider what the research is trying to tell us.  Ms. Bockenstedt will be the first to tell you not to take her research outside it's limited scope - as she told me when I wrote to her her with much enthusiasm.  But this is not a weakness but a strength in scientific studies.  I can't tell you how many of the "scientific" papers I find online that don't even have a control group!

I mean doing any research without a control group - you wouldn't know what to compare your results with!  Do you know what a control group is?

Please read her research a little more closely before you go and criticize what you so obviously don't understand.  The way she found the immune-reactive debris was through an imaging technique that allowed for the subject to be alive while being scanned in 3 dimensions.  

She was trying to find out if, in fact, Lyme is as resilient and they say.  So she prepared a generation of mice without the ability to kill off Lyme disease naturally (immune-deficient) all the while keeping some who were normal (this is the control group).  She then infected both populations with Lyme bacteria whose genes had been spliced with a green fluorescing protein.  This is Lyme disease with some genes that glow green.

Then, after several months, she applied common antibiotics - here is where yet another control group comes in - The antibiotics were applied to the normal infected mice and the immune-deficient mice.  She then imaged them using an awesome technique that allowed for the mice to be alive during imaging!

This is just amazing.  What she found was that in both normal and immune deficient mice, the bacteria had been killed off in the first 18 days of antibiotic treatment.  This is to be expected with antibiotics - they do work fast.  But she found something else that she would explore further in a later study:

Even though she found no whole motile spirochetes, she found a sort of green fluorescing soup concentrated mostly in the mouse knee and ear areas.  And this green goo she would later find was definitely causing an immune system reaction.

These mice were infected for only a few months - I can only imagine how much Lyme goo I have all over my body after 30 YEARS of infection!

Please.  Don't knock science for being too scientific!

[JackieCalifornia]

You are entitled to your opinions as I am to mine.  What I am knocking is not 'science for being too scientific' (whatever that means), but the willful ignorance that the IDSA and their fellow travelers engage in.  

You say:  "Antibiotics kill [Lyme] very quickly.  (of course there are always the unsubstantiated claims of cyst forms and hiding and all that)"

You might want to rethink your 'of course' assumptions about Lyme versus its ability to hide in areas of low blood flow, its cystic forms, and related issues -- all of which get in the way of treatment effectiveness, as treatment is decreed by the IDSA/CDC.  

After you've suffered from Lyme for 30 years without getting well, you might want to reconsider your touching faith in the IDSA positions.   You say, "3 years go by, then 5 years, and I'm not feeling any better - just worse and worse and worse.  A true Herxheimer reaction lasts only a few days to a couple of weeks.  What I was and am feeling does not even resemble a Herxheimer reaction."  I would agree that you don't seem to be Herxing.  So .... find a new doc with a new view.  Were you taking just doxy?  I wouldn't be surprised.  It doesn't deal with the cystic form of Lyme, nor coinfections.  If you're hurting and doxy isn't kicking the ailment, then there's something wrong with the treatment and/or the diagnosis.

You say, "I can't tell you how many of the 'scientific' papers I find online that don't even have a control group!"  Hon, you ARE the control group for the IDSA, only they aren't bothering to do the work to progress against Lyme.

Walk on the wild side.  See an LLMD; read 'Cure Unknown.'  What have you got to lose at this point, after 30 years of misery?  Not to put too fine a point on it:  I'm well; and you're not.  And think about co-infections, which the IDSA-types are often not interested in.

If you need help finding an LLMD, let us know.  We're happy to help.  

[leilajax]

OMG, it is all so very confusing!  No wonder many of us starting treatment are still unsure of what is wrong with us.  I posted about how scared I was that my lymph problem was cancer, but mystery diagnosis petrifies me!  Especially concerning is the fact that Lyme and autoimmune disorders mimic each other, leaving mainstream doctors baffled with how to treat.  I am so glad that my doctor is concerned and caring enough to insist that I stay on the doxy and suppressing his urge to give me a steroid until after my lymphectomy.  Sure, pathology probably isn't going to show Lyme just like my blood (however, I will ask if my lymph node contained "green goo";) when they take it out.), but it will rule out some other things.  I am unwrapping the layers of my disease like an onion, a giant stinky rotten onion, but I am focused on getting to the healthy core!  Leaving no leaf unturned, I plan to see 2 different LLMD's, stay with my Hopkins intern, my hospital endocrinologist and rheumatologist and my newest addition an acupuncturist.  Why not, right?  I'd give my pain an 8 today, not an 11 like 2 days ago, can you tell?  There is a tinge of hope in there somewhere:)

[leilajax]

Ok, an 8.5, but still a giant improvement!