Why does Kenny De Meirleir diagnose almost every patient with bacterial infections?

[Rossy191276]

Is it your belief that an untreated Lyme infection won't become chronic?

But I think you are also misunderstanding. A Lyme infection may trigger ME, and it may become chronic, but ongoing ME symptoms are not due to Lyme anymore than they're due to ongoing active EBV. I had Lyme, and it may have helped trigger ME. The Lyme was treated after 20 years, and symptoms caused by that have gone away. It has not impacted upon my ME symptoms.

KDM doesn't just see ME patients. He also sees Lyme patients. They have somewhat different symptoms (no PEM, for starters) and a lot of them seem to do much better after antibiotics. Some ME patients have Lyme, some have other chronic infections, and some have no chronic infections. When those ME patients with infections are treated for their infections, they will likely see some improvement. But they will still have ME.

A few will experience side-effects from the antibiotics. This is very unfortunate, but it is a risk of any treatment. But this is why I'm a herx-Nazi when it comes to people ascribing adverse reactions as being a sign of improvement. Unless it's a spirochetal bacteria being treated with something which can kill it, and the symptoms primarily include fever and hypotension, it absolutely is not a Jarisch-Herxheimer reaction. Some adverse reactions should never be pushed through.

Is it your belief that an untreated Lyme infection won't become chronic?

But I think you are also misunderstanding. A Lyme infection may trigger ME, and it may become chronic, but ongoing ME symptoms are not due to Lyme anymore than they're due to ongoing active EBV. I had Lyme, and it may have helped trigger ME. The Lyme was treated after 20 years, and symptoms caused by that have gone away. It has not impacted upon my ME symptoms.

KDM doesn't just see ME patients. He also sees Lyme patients. They have somewhat different symptoms (no PEM, for starters) and a lot of them seem to do much better after antibiotics. Some ME patients have Lyme, some have other chronic infections, and some have no chronic infections. When those ME patients with infections are treated for their infections, they will likely see some improvement. But they will still have ME.

A few will experience side-effects from the antibiotics. This is very unfortunate, but it is a risk of any treatment. But this is why I'm a herx-Nazi when it comes to people ascribing adverse reactions as being a sign of improvement. Unless it's a spirochetal bacteria being treated with something which can kill it, and the symptoms primarily include fever and hypotension, it absolutely is not a Jarisch-Herxheimer reaction. Some adverse reactions should never be pushed through.

Thanks for this summary Valentijn....I am someone who has tested positive to some Lyme tests but associates much more with symptoms I consider to be ME related... I was wondering what other symptoms besides exertion intolerance help you differentiate the 2? Cheers... Rossy

 

[msf]

You are already changing the main subject of the topic.

You started a topic mentioning the fact that KDM almost always finds an infection in his patients : the OMF and many CFS specialists agrees on the fact that Borrelia (or others like EBV) could trigger ME/CFS. You were already criticizing this idea saying it's ''KDM crazy theory'', but it's shared by the vast majority of CFS Doctors and researches, including the OMF.

I was answering to the main subject of your thread. Claiming that only the crazy KDM thinks that way, which is absolutely false.

If it's important to treat your infection with antibiotics or to treat leaky gut with antibiotics, there are every kind of hypothesis and I'm open to everything. I can see the benefits to treat some very active forms of Lyme, as well as I can see reasons to treat leaky gut with antibiotics. You can disagree, and he can make clincal mistakes and bad diagnosis (saying someone is suffering from active Lyme while it's not the case), but it doesn't mean his premise is wrong.

This is what A.B. does: constantly change subjects when someone makes a valid point. That´s why I don´t think it´s worthwhile debating him.

 

[A.B.]

@msf I asked you privately why de Meirleir diagnoses almost everyone with an infection. You responded that you would tell me when the question was made in public where everyone could see your answer. So I made this thread. Feel free to answer and bring the topic back to the original question.

In the meantime I have been contacted by a poster that wished to talk privately. The information given made me think that de Meirleir started believing in an ongoing infection hypothesis after repeatedly hearing about patients feeling better on antibiotics. There is however an alternative explanation for this observation given by Dr Naviaux and Dr Davis which is given here:

https://www.omf.ngo/2016/09/09/upda...-fatigue-syndrome-q-a-with-robert-naviaux-md/

It's a bit long but essentially the idea is that antibiotics affect mitochondria because they're structurally similar to bacteria, that mitochondria have two major roles (energy production and cellular defense), and that they can choose to prioritize on role over another, and that in cases where antibiotics seem to help this might be because they're making mitochondria dedicate more activity to energy production. A similar situation is with antivirals. However Dr Naviaux and Dr Davis also warn of using antibiotics and antivirals when there is no good evidence of an infection since they can cause damage with long term use. They don't appear to consider antibody titers to be good evidence. I remember that Dr Naviaux has commented that changes in antibody levels may simply reflect different ratios of immune cells as result of the illness (or something to that effect, unfortunately I don't remember the source).

So an important question is whether de Meirleir drew the incorrect conclusions from his observations, which were compounded by unreliable tests and acceptance of minor alterations of antibodies to pathogens as evidence of a putative low grade infection.

 

[msf]

No, I didn´t. I said I couldn´t see the point in debating you privately, because of the tendency I mentioned before. I didn´t say I would debate you on this subject though, because as one of the first responses noted, this has been covered in detail in other threads. I have also been one of the most active posters on Lyme testing threads over the years, so if you want to know what I think, google it.

 

[msf]

If you want to have a discussion about Yersinia testing, go and read the literature on it (it´s only a small literature, so it´s quite possible to do so, as I know from having done it), and then we can discuss it. I don´t see why I should summarise Pubmed for you in this case, since although I know it is of interest to the two of us, it is of less interest to most people than Lyme is. If anyone wants to ask me a question about Yersinia in good faith though, just PM me with it.

 

[duncan]

@Research 1st everyone is biased and fallible

I'm not sure talking in absolutes is the right way to go, but ok.

All patients and doctors are emotionally attached to their treatments.

Ditto, and quite likely just incorrect.

We need other people and exchange of views to save ourselves from adopting incorrect beliefs.

There it is.

 

[Sidereal]

In a recent document by Naviaux posted around here somewhere he was asked about chronic infections. He said that ruling out infection (and ongoing environmental poisons) was key and that he has the technology to test for presence of actual pathogens as opposed to having to rely on less reliable methods available to office doctors like antibody tests.

 

[duncan]

he has the technology to test for presence of actual pathogens as opposed to having to rely on less reliable methods available to office doctors like antibody tests.

I've no doubt you are recalling this correctly, @Sidereal , but I cannot help but wonder if his claim was not tempered with some limitations. If he could locate Bb reliably each and every time, this would undo the Lyme landscape we've grown to love, and put an end to the Lyme Wars - not to mention erase the uncertainty swirling about other pathogens.

 

[snowathlete]

At the time of this post, Kenny de Meirleir diagnoses one or multiple bacterial infections in nearly every ME/CFS patient he sees and has been doing so for several years. This conclusion is based on my time as member of a forum for patients of de Meirleir where I had the chance to see the diagnoses and treatment plans of other patients.

These diagnoses are in stark contrast to published research which shows no evidence of such high prevalence of bacterial infections in ME/CFS patients.

I have repeatedly asked supporters of de Meirleir to explain this massive discrepancy but have so far not gotten any real answers. I am hoping to finally get some answers in this thread.

If you are a patient of de Meirleir and knew about this discrepancy, why did you choose to trust him?

Edit: some people are challenging the idea that de Meirleir diagnoses one or multiple bacterial infections in nearly every ME/CFS patient. I reviewed 30 cases in the aforementioned forum and in 21 cases the diagnosis was explicitly a bacterial infection (almost always lyme disease). In 7 cases the patients did not disclose the diagnosis but where prescribed antibiotics, in 1 case EBV was diagnosed, and 1 case no diagnosis was made since the patient already had a lyme disease diagnosis from a different doctor.

Do you know how many of these 30 cases were definate (according to the test) bacterial infections and how many were suspected cases without test evidence?

The reason I ask is because when I saw KDM a few years back I was given a diagnosis of, from memory, "probable borrelia" and "probable Bartonella". In fact my Lyme test was negative and my Bartonella test was "grey zone". I did have some non-ME symptoms to suggest Bartonella could be an issue, but no Lyme specific symptoms that I recall.

My impression is that sometimes KDM sees what he thinks are symptoms of bacterial infection and prescribes anti-bacterial treatments without sufficient test evidence. I don't always think that is unreasonable, but I do wonder if this might happen too often.

 

[Twazzle]

In answer to the original question:

He doesn't. He believes ME is an auto-immune disease where ground zero is the gut. The cause of the majority of symptoms for patients is related to the dysfunction in the gut (dysbiosis/ increased permeability/SIBO) as a consequence of this process. Major gut dysfunction has systemic consequences.

It is initiated by a major immune response which can often be bacterial - Lyme for instance, but can also be viral ie an enterovirus or EBV. Usually the initial triggering infection is no longer active and whilst care must be taken to make sure that the original infection does not reactivate, it usually does not need proactive treatment and fixing the gut is his priority. This is not always the case however and some do have active infections which need immediately taking care of. I believe in the past he may have been more inclined to immediately focus on possible infections for a wider cross-section of his patients however I think his view has changed as the research has moved on.

Just to be clear - he does not believe Lyme is the cause of ME. Borellia is the initiating organism in a large subset of patients, but it is not the ongoing cause of symptoms in most patients. When he has said previously that a huge proportion of sufferers have the borellia organism, this is not the same as saying that Lyme is causing their ME.

I've only been sick just over year and am already getting bored of all of the criticism that KDM gets on these pages. Whilst some former patients do have genuine grievances (which given he is the most in demand ME doc in the world and sees a huge amount of patients, is unfortunately to be expected from time to time) - most of this stems from sufferers who have never seen him. In a disease where standard medicine has completely failed to provide any effective treatments for patients over 30+ years - criticizing someone who has gone against the grain isn't logical. KDM was one of the first doctors to focus on the gut and most research/development in ME seems now seems to be focusing on that area.

Rituximab is clearly an interesting development and I believe does fits in with KDM's view of the disease although I am not informed enough to be in a position to be able to explain why. Rituximab is clearly not a long term answer though given pretty much everyone relapses.

.

 

[msf]

You should repost that in every KDM thread.

 

[A.B.]

He doesn't. He believes ME is an auto-immune disease where ground zero is the gut.

Nobody treats an autoimmune disease with a ton of antibiotics and uses borrelia tests to diagnose it. In a presentation by him from 2014 he presented ME/CFS as late stage lyme disease, which unambiguously refers to a chronic infection.

This behaviour of denying what is obviously occurring is rather bizarre I have to say.

 

[Valentijn]

Nobody treats an autoimmune disease with a ton of antibiotics and uses borrelia tests to diagnose it.

Some antibiotics have additional effects on the immune system, beyond killing bacteria. Perhaps it's the right answer for the wrong reason.

 

[dadouv47]

One study found that 42/42 fibromyalgia patients—that's 100%—had SIBO. No equivalent study has been done in ME/CFS but we do know that the gut biome is disturbed and that LPS-provoked autoimmunity may play a role in the aetiology.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1754959/

Not proving that this apply to ME/CFS patients, but it's not delusional to think that a lot ME/CFS patients suffers from leaky gut/SIBO as well.

PS : adding what I said previously, he prescribes more antibiotics for leaky gut than for Lyme.

 

[msf]

Nobody treats an autoimmune disease with a ton of antibiotics and uses borrelia tests to diagnose it. In a presentation by him from 2014 he presented ME/CFS as late stage lyme disease, which unambiguously refers to a chronic infection.

This behaviour of denying what is obviously occurring is rather bizarre I have to say.

You seem to be jumping to conclusions, as usual. The slide says that 95% of patients with ME have late-stage lyme disease. That does not necessarily imply that they are the same. In fact, it is perfectly in keeping with what Twazzle has said (and I noticed you ignored all the other valid points he/she made, as you are wont to do). What late-stage Lyme disease is a controversial issue, and as Twazzle noted, KDM´s view on this may have changed since then.

BUT, and even if it was the case that KDM still views these patients as having an active Lyme infection, ME AND LATE STAGE LYME WOULD ONLY BE THE SAME IF EVERYONE WITH LATE STAGE LYME ALSO HAD ME. Now, do you have a slide where KDM claims that?

This is a fairly simple logical formula (if I was in charge, it would be taught at secondary school), so I will assume that brain fog prevented you from applying it yourself.

 

[msf]

Here is the formula for you, in question form: if all As are B, are all Bs necessarily A?

 

[msf]

Anyway, I did say I wasn´t going to debate you on this, I just thought you needed a little help with the logic of your argument.

 

[A.B.]

You seem to be jumping to conclusions, as usual. The slide says that 95% of patients with ME have late-stage lyme disease. That does not necessarily imply that they are the same. In fact, it is perfectly in keeping with what Twazzle has said (and I noticed you ignored all the other valid points he/she made, as you are wont to do). What late-stage Lyme disease is a controversial issue, and as Twazzle noted, KDM´s view on this may have changed since then.

BUT, and even if it was the case that KDM still views these patients as having an active Lyme infection, ME AND LATE STAGE LYME WOULD ONLY BE THE SAME IF EVERYONE WITH LATE STAGE LYME ALSO HAD ME. Now, do you have a slide where KDM claims that?

My private source gave me this transcript of the talk where these slides were shown: de Meirleir proposes the idea that ME/CFS is a chronic borrelia infection.

I may have a very wayward view on things, but for 25 years I've been looking at people with chronic fatigue syndrome, and eventually people say, whenever I get antibiotics from my doctor, I feel better for a week or two. And that hasn't been said to me once, but hundreds of times. And then you think that a microorganism may play a role in this disease. And in recent years, it became clearer and clearer that something had to be behind this. Now, if you take the criteria of Chronic Fatigue Syndrome of both the ICC criteria and the Fukuda criteria and you take that group and you do three to four different Lyme tests, also the LTT test, then you see that more than 95% of the group I see is actually Borrelia positive. And there is two or three percent who have too few lymphocytes to actually perform a normal LTT test. That is, it comes back false-negative, because if we do it again with three times more lymphocytes, it's positive. So that means we are far above 95% of people who have, uhm, a diagnosis of ME/CFS, which is actually not a diagnosis but a description, that may eventually have a chronic Borrelia infection. (...)

 

[Twazzle]

Nobody treats an autoimmune disease with a ton of antibiotics and uses borrelia tests to diagnose it. In a presentation by him from 2014 he presented ME/CFS as late stage lyme disease, which unambiguously refers to a chronic infection.

This behaviour of denying what is obviously occurring is rather bizarre I have to say.

You're putting 2+2 together and getting 5. The abx he presrcibes these days are mostly for SIBO - rifaxmin/vancomycin etc. These do not have an effect on pathogens however they allow the immune system to stop reacting to the excess lipopolysaccharides.

The presentaiton you quoted is 3/4 years old and his opinion has evolved although he does still believe Lyme plays a role in a lot of patients either as the initiaing organism, or in some cases as a cause of ongoing symptoms.

I put a more detailed explanation in another thread:

• According to KDM, the core of the problem in the vast majority of his patients lies in the intestines. ME/CFS is a gut disease which is initiated by a severe infection (often Lyme, but not always. Yersinia is another common one) that causes a sequential chain of events to happen in the intestines that results in a self perpetuating illness.
• During my first follow up appointment in April he showed me pictures of the cross section of the guts of ME sufferers - it was filled with purple blobs that looked like raisins/grapes. These are inflammatory cells/dentritic cells which have migrated to the gut from the rest of the body during the initial infection (in my case borellia invaded the intestinal lining).
• These cells cause major inflammation and an increase in intestinal permeability and this is the reason why most ME sufferers have pain in the abdomen when pressed in a certain area. Normal healthy people do not have this pain.
• Once this mechanism has occurred we enter a vicious cycle - the dendritic cells in the swollen gut affect immune system homeostasis and we quickly develop dysbiosis and SIBO. LPS from the overgrowth of gram negative bacteria in the small intestines perpetuate the inflammation and the dentritic cells continue to be activated, causing further immune dysfunction.

SIBO/increased leaky gut/translocated LPS as the consequence of the immune dysregulation is the first domino to fall, setting off our cascade of symptoms. LPS is highly toxic to the body and when translocated causes a huge amount of systemic inflammation. Specifically:

• High sCD14 - the body's IGA response to LPS
• High PGE2 (which then causes a Th2 shift - which is responsible for the reactivation of EBV, poor viral defence, high nagalase) etc)
• A significant increase in nitric oxide (part of the body's immune response to a bacterial infection). This results in a major upregulation of the NO/OONO cycle which causes mitochondrial problems/fatigue.
• A big increase in body toxicity resulting in low glutathione/methylation problems etc compounding mitochondrial problems.
• A major amount of neuroinflammation. LPS causes an increase in IDO which results in the massive increase of the breakdown on tryptophan in the brain into quinolinic acid (often leaving sufferers depressed). The inflammation messes up the signalling of the HPA axis, so ACTH is not produced in large enough amounts. The adrenal glands then do not get the signal to produce cortisol. This causes more fatigue, orthostatic hypotension etc.

High ammonia is also a result of the SIBO. Ammonia contributes to most of the above problems.

The goal of KDM’s treatment is to attempt to break the cycle which is happening in the intestines by correcting the dysbiosis using pulsed antibiotics/probiotics. In continually removing the source of the inflammation (the excess LPS caused by the SIBO), the immune system over time will allowed a chance to normalise and eventually be able to take care of the problem itself.

This is easier said than done however as the SIBO comes back very quickly after the course of antibiotics, especially in sufferers who have been sick for a long time as the biofilms are better established/there is usually greater degree of inflammation & tight junction breakdown

 

[msf]

Please read that again, A.B., and try not jumping to conclusions this time.

Hint: The word you need to pay attention to is ´may´