Autoimmune Diseases Caused by Bacteria?

[Jonathan Edwards]

Oh, I obviously only know (a bit) about my case, but from what I've read the anti-smooth muscle auto-antibody can be produced as a result of both viral and bacterial infection of the liver.

I don't know of any evidence for anti-smooth muscle antibodies being brought on by infection in humans. I amy have missed this but I doubt it. A lot of these ideas come from inappropriate mouse experiments.

 

[msf]

Thank you for your reply. I really appreciate the chance to ask someone other than a GP these kind of questions.

As I said, I haven't really looked into it, but when I googled Hashimoto's I found this study: http://www.ncbi.nlm.nih.gov/pubmed/11318812

And also this one about Grave's disease: http://www.ncbi.nlm.nih.gov/pubmed/23630351

The second one is a bit dense for me (or maybe it's the other way round), but they seem to be suggesting that this autoimmune disease is a result of molecular mimicry by Yersinia.

I think this touches on your point, that the term autoimmune is used rather loosely.

I don't have the medical knowledge to follow the arguments closely, but it seems to me to statements such as 'there is no evidence for specific immunity against self in Reiter's so it is not an 'autoimmune disease,' might be tautologous. Isn't the reasoning here that because there is an infectious cause in Reiter's, the immune reaction is targeting this, rather than the bodies own cells?

If that is the case, then no disease with an infectious cause can be autoimmune, and therefore as soon as you discover one, you can no longer include it in any discussion/statement about auto-immune diseases.

The same could go for molecular mimicry, if this was proven to be happening in some cases, would they no longer be considered auto-immune diseases?

Re: Reiter's syndrome, I have only read about it where it applies to Y. Enterocolitica infection, and in these cases it has been demonstrated that the immune system is responding to the ongoing presence of Y. Enterocolitica antigens. Would that make it an antibody-mediated response or a T-cell mediated response?

http://ard.bmj.com/content/59/11/914.full

I'm not trying to be difficult, I'm simply trying to make sense of what I read. I would like to be able to rely on doctors to do this for me, but after seeing an infectious disease doc in the NHS, I can only conclude that he has never read any of the Y. Enterocolitica literature. I don't blame him, as I seem to be one in a million in the UK (one report stated that the incidence rate in the UK was 0.1 in 100,000), but it does mean that I feel that I can't just rely on his opinion.

Mark

 

[Jonathan Edwards]

As I said, I haven't really looked into it, but when I googled Hashimoto's I found this study: http://www.ncbi.nlm.nih.gov/pubmed/11318812

And also this one about Grave's disease: http://www.ncbi.nlm.nih.gov/pubmed/23630351

The second one is a bit dense for me (or maybe it's the other way round), but they seem to be suggesting that this autoimmune disease is a result of molecular mimicry by Yersinia.

I don't have the medical knowledge to follow the arguments closely, but it seems to me to statements such as 'there is no evidence for specific immunity against self in Reiter's so it is not an 'autoimmune disease,' might be tautologous. Isn't the reasoning here that because there is an infectious cause in Reiter's, the immune reaction is targeting this, rather than the bodies own cells?

If that is the case, then no disease with an infectious cause can be autoimmune, and therefore as soon as you discover one, you can no longer include it in any discussion/statement about auto-immune diseases.

The same could go for molecular mimicry, if this was proven to be happening in some cases, would they no longer be considered auto-immune diseases?

Re: Reiter's syndrome, I have only read about it where it applies to Y. Enterocolitica infection, and in these cases it has been demonstrated that the immune system is responding to the ongoing presence of Y. Enterocolitica antigens. Would that make it an antibody-mediated response or a T-cell mediated response?

http://ard.bmj.com/content/59/11/914.full

I'm not trying to be difficult, I'm simply trying to make sense of what I read. I would like to be able to rely on doctors to do this for me, but after seeing an infectious disease doc in the NHS, I can only conclude that he has never read any of the Y. Enterocolitica literature. I don't blame him, as I seem to be one in a million in the UK (one report stated that the incidence rate in the UK was 0.1 in 100,000), but it does mean that I feel that I can't just rely on his opinion.

Mark

Some good questions, Mark.
The sentence you mention is intended to be a tautology - or if you like a clarification of what autoimmune means (if it means anything useful).

The real problem is that immune reactions do not 'target' anything. Antibodies will bind to what they bind to. That might be self or bacterium or both but if it is both it is not 'targeting' either one or the other - just binding. The misconception that is so widespread is given away by the sentence in the Graves' paper: 'How TSAbs arise from early precursor B cells has not been established. ' This is nonsense because we know that all antibodies arise from B cells by random gene shuffling, nothing to do with 'targeting anything'. The immune system throws up antibodies at random and the problem comes if it forgets to delete one that reacts to self. There is no need to say that the antibody was made because of an infection and then cross reacted. Whatever mistake the immune system made not to delete it has nothing to do with there being an infection.

The other paper probably shows that if you have an autoantibody - as in Hashimoto's then if you look at almost any bacterium, which will have maybe 1000 proteins with 100 epitopes on each protein to recognise then you will almost certainly find some epitope that cross reacts with the autoantibody. But this gives no evidence that the autoantibody is there because you had the infection - for the reason above.

I realise that this can be very confusing and seem backwards but it is standard textbook immunology. But because it is counterintuitive most immunologists do not understand it. I have a very eminent immunology friend who is the world authority on certain types of autoimmune disease who still does not get it (in fact there are dozens, though they may not all be friends!).

In short, cross reactivity provides no evidence that there is a causal connection between meeting one antigen and having the other as self. There is a much more plausible explanation for autoantibodies. But that does not mean that it is impossible - so an infectious cause might lead to autoimmunity - because the antibody is not 'targeting' either one or the other. There are potential ways in which having the bacterial antigen presented in a particular way could make it easier to make the mistake of not deleting the B cell, although the vast bulk of epidemiological evidence does not suggest this happens often.

So we don't have a problem with crossing off diseases where there is cross reactivity.

When there is Yersinia infection you make an immune response to Yersinia with both B and T cells recognising Yersinia. But the Reiter's response seems to be some sort of general hyperactivity of T cells triggered by this with no indication that any particular T cells are more active than others - what you might call a 'rent-a-crowd' disease. The T cells are just any old T cells come along for the party. Once they start talking they won't go home.

The paper on antibiotics relates to treatment during the acute infection. As far as I know infection beyond a matter of several weeks is not an issue. The Reiter syndrome goes on without there being any Yersinia there. So after several months there is probably no point using antibiotics, although if none have been had it may be worth a course to make sure the bacterium has gone.

This is all very complex stuff known to a very small number of academic rheumatologists - maybe a dozen in each of a ten Western countries. Infectious disease specialists probably know little or nothing about it.

 

[Strawberry]

Since often times when people with cold/flu get over the virus, they get a bacterial infection (say sinus infection), could it just be possible then that these people that responded to antibacterials just had a bacterial response to an underlying virus? And once on antibiotics the body was then properly able to respond to the virus? Which then led to the remission?

 

[Daffodil]

Some good questions, Mark.
The sentence you mention is intended to be a tautology - or if you like a clarification of what autoimmune means (if it means anything useful).

The real problem is that immune reactions do not 'target' anything. Antibodies will bind to what they bind to. That might be self or bacterium or both but if it is both it is not 'targeting' either one or the other - just binding. The misconception that is so widespread is given away by the sentence in the Graves' paper: 'How TSAbs arise from early precursor B cells has not been established. ' This is nonsense because we know that all antibodies arise from B cells by random gene shuffling, nothing to do with 'targeting anything'. The immune system throws up antibodies at random and the problem comes if it forgets to delete one that reacts to self. There is no need to say that the antibody was made because of an infection and then cross reacted. Whatever mistake the immune system made not to delete it has nothing to do with there being an infection.

The other paper probably shows that if you have an autoantibody - as in Hashimoto's then if you look at almost any bacterium, which will have maybe 1000 proteins with 100 epitopes on each protein to recognise then you will almost certainly find some epitope that cross reacts with the autoantibody. But this gives no evidence that the autoantibody is there because you had the infection - for the reason above.

I realise that this can be very confusing and seem backwards but it is standard textbook immunology. But because it is counterintuitive most immunologists do not understand it. I have a very eminent immunology friend who is the world authority on certain types of autoimmune disease who still does not get it (in fact there are dozens, though they may not all be friends!).

In short, cross reactivity provides no evidence that there is a causal connection between meeting one antigen and having the other as self. There is a much more plausible explanation for autoantibodies. But that does not mean that it is impossible - so an infectious cause might lead to autoimmunity - because the antibody is not 'targeting' either one or the other. There are potential ways in which having the bacterial antigen presented in a particular way could make it easier to make the mistake of not deleting the B cell, although the vast bulk of epidemiological evidence does not suggest this happens often.

So we don't have a problem with crossing off diseases where there is cross reactivity.

When there is Yersinia infection you make an immune response to Yersinia with both B and T cells recognising Yersinia. But the Reiter's response seems to be some sort of general hyperactivity of T cells triggered by this with no indication that any particular T cells are more active than others - what you might call a 'rent-a-crowd' disease. The T cells are just any old T cells come along for the party. Once they start talking they won't go home.

The paper on antibiotics relates to treatment during the acute infection. As far as I know infection beyond a matter of several weeks is not an issue. The Reiter syndrome goes on without there being any Yersinia there. So after several months there is probably no point using antibiotics, although if none have been had it may be worth a course to make sure the bacterium has gone.

This is all very complex stuff known to a very small number of academic rheumatologists - maybe a dozen in each of a ten Western countries. Infectious disease specialists probably know little or nothing about it.

Hi Jonathan. I wanted to ask how you would explain my improvements on antibiotics...do you think they were targeting translocated bacteria from the gut? I did show severely low secretory IgA...I think that is mucosal IgA.

My CD8 is always high but no one can find a virus....

Thanks

 

[Jonathan Edwards]

Hi Jonathan. I wanted to ask how you would explain my improvements on antibiotics...do you think they were targeting translocated bacteria from the gut? I did show severely low secretory IgA...I think that is mucosal IgA.

My CD8 is always high but no one can find a virus....

Thanks

It is never any good trying to draw conclusions from a single case of getting better associated with taking a treatment - that is the whole reason for the controlled trials industry. People with diseases of fluctuating severity will always seem to get better when taking treatments some of the time because they take the treatment when they are worst and the condition stabilises. As I have said in the context of studying the value of trials or lab tests or anything one can never be sure about an individual case but we know from looking at lots of cases that you cannot draw any reliable conclusions from individual people getting better on a treatment I am afraid.

I thought my nighttime stomach pains definitely improved on diloxanide furoate after I discovered I had Entamoeba coli but four years later the stomach pains were back just the same, with no new visit to an endemic area. I was quite convinced at the time, but human beings are very easily convinced of these things!!

 

[A.B.]

People with diseases of fluctuating severity will always seem to get better when taking treatments some of the time because they take the treatment when they are worst and the condition stabilises

I suspect that the decision to start a new treatment or lab tests is often made when the worst has already passed because during the trough of the symptom cycle they just don't have the mental and physical energy for problem solving.

PS: I'm very curious: why does autoimmunity cause fluctuating symptoms?

 

[msf]

Thanks for the clarification, although I'm still not entirely sure I understand it all (at least I'm in good company then). I need to ask my sister how it all works again, it is very counter-intuitive as you say.

I realise that using words like 'targeting' is imprecise when it comes to the natural world, I should have said responding.

I would just like to clear a couple of things up.

1.) You seem to be saying that you can never prove that an auto-immune disease is responding to an infectious cause, but surely a strong correlation between auto-antibodies and foreign antigens in hundreds of patients would suggest. Or does this come back to the tautalogy, in that if you proved it it would no longer be an auto-antibody, and therefore no longer an auto-immune disease.

2.) From the Y. E. reactive arthritis article: In experimental yersinia triggered arthritis in Lewis rats it was noted that the earlier ciprofloxacin treatment was started, the better were the results.13 This might also be the case in humans and might explain the positive effect in our patients with a disease duration of 1.9 years, which is much shorter than that (4.9 years) in the Finnish study,8 in which no effect was seen.

If 1.9 years is considered to be the acute phase, then when does it become chronic? I realise (as the authors did) that this study needs to be replicated with more patients, but there are lots of accounts in the literature of individual patients responding after long-term antibiotic treatment of Y.E.

Mark

 

[Jonathan Edwards]

I realise that using words like 'targeting' is imprecise when it comes to the natural world, I should have said responding.

No,actually you shouldn't. That would be just as bad. Antibody genesis is never a response - it is a preprogrammed random process. Antibodies bind, that's all. They do not target or respond. What seems like a response is the tendency of binding to encourage more synthesis of the same antibody by clonal expansion - which for autoimmunity can also be seen as a failure of veto of this expansion. It really is counterintuitive.

I would just like to clear a couple of things up.

1.) You seem to be saying that you can never prove that an auto-immune disease is responding to an infectious cause, but surely a strong correlation between auto-antibodies and foreign antigens in hundreds of patients would suggest.

If autoimmunity was due to infection it would be easy to prove. You would find the autoimmunity appearing in people who just been infected - so you might expect epidemics. You do get epidemics in Reiter's (that was how he discovered it) but not for autoimmune diseases, with the possible exception of MS and that may not be exactly autoimmune. Moreover, you could show that eradicating the infection stopped any further autoimmunity.

I am not aware that any autoimmune disease has even been reliably shown to correlate with infection. The fact that Hashimoto's patients had antibodies that bind to a Yersinia protein does not mean that any of them ever met Yersinia. If the protein cross-reacts with thyroglobulin the antibodies will bind to both. But the suggestion of a causal role in the authors' abstract is completely unjustified.

2.) From the Y. E. reactive arthritis article: In experimental yersinia triggered arthritis in Lewis rats it was noted that the earlier ciprofloxacin treatment was started, the better were the results.13 This might also be the case in humans and might explain the positive effect in our patients with a disease duration of 1.9 years, which is much shorter than that (4.9 years) in the Finnish study,8 in which no effect was seen.

If 1.9 years is considered to be the acute phase, then when does it become chronic? I realise (as the authors did) that this study needs to be replicated with more patients, but there are lots of accounts in the literature of individual patients responding after long-term antibiotic treatment of Y.E.

Mark

A human infection with Yersinia lasts about a fortnight as far as I know. I am not sure rats are much help here. The earlier you give antibiotics I guess the less forceful the immune reaction is that generates the long term Reiter picture - which as I said is not a'chronic phase if infection'. The infection is long gone in all cases. I guess that the degree of the triggering process during the brief infection may correlate with how long the reaction pase lasts and how bad it is.

 

[Jonathan Edwards]

I suspect that the decision to start a new treatment or lab tests is often made when the worst has already passed because during the trough of the symptom cycle they just don't have the mental and physical energy for problem solving.

PS: I'm very curious: why does autoimmunity cause fluctuating symptoms?

We would expect autoimmune disease to fluctuate if it is due to the effects of autoantibodies because the immune system has a mechanism for ensuring that no one antibody type expands at the expanse of all other antibody types. There always has to be a mix of different antibody species even if they bind to the same antigen. Moreover, B cell clones do not last for ever. So there is almost certainly a constant roll over of different clones all making slightly different antibodies. If different antibodies have different abilities to cause trouble - maybe because they bind from the left side rather than the right and get in the way of something else (or not) - then you would expect things to go up and down. In fact there are rules for antibodies that if they get 'too good' at binding they may get vetoed, as much as if they are not good enough. Since there is a constant re-editing of antibody species it seems likely that there is a constant drifting back and forth of just how troublesome a bunch you have.

 

[msf]

I meant the immune system is responding, not the antibodies. Obviously, Wikipedia can be wrong, but: Following activation with antigen, B cells begin to proliferate rapidly. In these rapidly dividing cells, the genes encoding the variable domains of the heavy and light chains undergo a high rate of point mutation, by a process called somatic hypermutation (SHM). SHM results in approximately one nucleotide change per variable gene, per cell division. As a consequence, any daughter B cells will acquire slight amino acid differences in the variable domains of their antibody chains. This suggests that the whole process is a response to an antigen. On the subject of ASMA, I quote from the NHS website: 'Low titres of anti-smooth muscle antibodies are also associated with infectious diseases giving hypogammaglobulinaemia. Lower levels (usually) are also found in connective tissue diseases and chronic infections.

http://southtees.nhs.uk/services/pathology/tests/smooth-muscle-antibody/

The study I posted was of Y. Enterocolitica in humans, not rats. I realise that you are not an infectious disease doc, but I find it strange that doctors in general believe that Tuberculosis can become chronic, and Lyme can (if it hasnt been treated with 2 weeks of doxy at any point), but that no other bacterial infections can become chronic.

The study I quoted found persisting Y.E antigens, and suggested that they also found whole bacteria in the gut. I think this is a contentious area, but the continuing existence of Y.E. antigens in these cases isn't, as far as I know.

Mark









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[Jonathan Edwards]

I meant the immune system is responding, not the antibodies. Obviously, Wikipedia can be wrong, but: Following activation with antigen, B cells begin to proliferate rapidly. In these rapidly dividing cells, the genes encoding the variable domains of the heavy and light chains undergo a high rate of point mutation, by a process called somatic hypermutation (SHM). SHM results in approximately one nucleotide change per variable gene, per cell division. As a consequence, any daughter B cells will acquire slight amino acid differences in the variable domains of their antibody chains. This suggests that the whole process is a response to an antigen.

The problem is that the person writing the wikipedia article has fallen into the usual trap of thinking that making an antibody species is a 'response to antigen'. They forgot to say that before activation with antigen the B cell has an antibody - activation does not cause the B cell to think of an antibody, it already has one. What is true is that once activated B cells will undergo further mutation to 'fine tune' their antibodies to improve binding, but unless the B cell had an antibody that bound to the antigen in the first place it would never be activated because activation occurs through binding of a copy of the same antibody on the B cell surface to an antigen!

So the process of coming to have an antibody to a particular antigen is NOT a response to the antigen - if you think it through it cannot be because there is no way the antigen can tell the B cell what antibody it should have, although I admit that the presence of antigen encourages the B cell to change to what might be a better version. It also encourages bulk production of the antibody, that is for sure.

The real problem is that if you take this simple idea that antigen causes genesis of antibody you then fall into the trap of proposing the entirely redundant idea that infection has to trigger antibodies to self. Since self is already there you do not need anything to trigger anyway. Whatever mistake gets around the anti-self veto must occur if autoantibody is made. If that mistake occurs then self is quite enough to encourage B cell proliferation.

On the subject of ASMA, I quote from the NHS website: 'Low titres of anti-smooth muscle antibodies are also associated with infectious diseases giving hypogammaglobulinaemia. Lower levels (usually) are also found in connective tissue diseases and chronic infections.

http://southtees.nhs.uk/services/pathology/tests/smooth-muscle-antibody/

I am not sure that whoever writes sites for Teeside pathology services is a very good guide. Nevertheless, it is true that a lot of autoantibodies associated with autoimmune diseases crop up at lower levels in a few normal people and also rather more often in people who have other autoimmune diseases or infections. This is generally regarded as 'noise' that may relate to mild generalised facilitation of B cell clonal expansion in various situations that never really amounts to anything significant. You get the same thing with almost any antibody you can measure. There are lots of reasons. (One may be concomitant rheumatoid factor (anti-IgG Fc) production which occurs in lots of these situations. Rheumatoid factor antibodies can 'amplify' the apparent levels of other antibodies in tests.)

The study I posted was of Y. Enterocolitica in humans, not rats. I realise that you are not an infectious disease doc, but I find it strange that doctors in general believe that Tuberculosis can become chronic, and Lyme can (if it hasnt been treated with 2 weeks of doxy at any point), but that no other bacterial infections can become chronic.

The study I quoted found persisting Y.E antigens, and suggested that they also found whole bacteria in the gut. I think this is a contentious area, but the continuing existence of Y.E. antigens in these cases isn't, as far as I know.

Mark

You said Lewis rats and gave a reference, but no matter. I don't think there is anything strange about doctors thinking TB is chronic but not some other things. This is not a matter of belief. It is a matter of centuries of pathology. In the nineteenth and early twentieth century people with TB and typhoid carriers went on infecting other people for years. We know these are chronic infections. I am prepared to believe that Yersinia infection might hang around but for all the other causes of Reiter's (salmonella, shigella, chlamydia) we see the Reiter's appear AFTER the infection - and very often after the infection has been cleared with treatment. Studies showing bacterial antigens hanging around have been reported sporadically for decades and we know that bits of antigen can hang around on dendritic cells in spleen or peripheral tissues for ages in any situation. But that is a long way from saying there are live proliferating organisms present. As I say, this might be the case for Yersinia but I have not heard of that and it would not fit with what we know about Reiter's in other situations

Reiter's itself does not look like an infective process histopathologically. The fascinating thing about these diseases is that there are four types - one for each T cell 'playground' - one for gut associated lymphoid tissue or GALT (Crohn's/UC arthritis), one for skin associated T cells (psoriatic arthritis), one for mucosa-associated lymphoid tissue or MALT (Reiter's) and one for T cells that go everywhere else (Ankylosing spondylitis). And for MALT the T cells appear to get overexcited anywhere in their domain regardless of where the original infection was - i.e. conjunctiva, urethra, mouth. The only strange things are that nail bed and enthesis tissue are affected in all four diseases and Reiter's ;eaks over into the skin domain with keratoderma blenorrhagica.

I don't think there is any need to postulate chronic infection here. Any spond is genetically programmed with no infection trigger.









I[/QUOTE]

 

[msf]

Sorry, I forgot to put quote marks in, the bit about the rats was part of the quote from the study about humans where they found both antigens and antibodies (and maybe bacteria) persisting in cases of Y.E. reactive arthritis.

I am glad you are willing to consider that some (Y.E. at least) bacterial infections might become chronic, but then you say that there is no need for such a hypothesis. I would suggest that there is a need to investigate all aspects of any disease that we do not fully understand, and do not have any treatments for.

Once again, I appreciate the time you've taken to respond, and I've learnt a lot from your replies.

One final question that I can't find the (short) answer to online: has autoimmune disease ever been observed in animals? I appreciate there are problems with an animal model, but surely the basic processes would be the same, in terms of antibodies and T-cells and so on.

Mark

 

[msf]

Oh, and I just pasted the first link I found on ASMA and infection.

Here is a research paper where they talk about the apperance of ASMA antibodies in viral and bacterial infection:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1145947/

 

[Jonathan Edwards]

One final question that I can't find the (short) answer to online: has autoimmune disease ever been observed in animals? I appreciate there are problems with an animal model, but surely the basic processes would be the same, in terms of antibodies and T-cells and so on. Mark

Yup. There was a really smart vet called David Bennett who used to lecture on autoimmune disease in dogs. He had this neat idea of covering up the faces of the dogs he showed on his slides to protect their anonymity! My memory is the lupus and RA are particularly common in King Charles Spaniels. The trouble is that if you think it is hard getting informed consent for research from patients it is way harder getting consent from owners to allow research on their oh-so-goregous puppies. And you cannot breed autoimmune disease into real pets - only nasty little things like mice and rats.

Autoimmune diseases can also be manufactured in mice by genetic engineering but the cause there is the engineering - not what it is in humans, so these diseases tell you nothing about the cause in humans, although they can help to understand the pathways.

Cats get something a bit like human type I diabetes but it often goes away and diabetes has lots of causes other than autoimmunity.

On the T cell disease side there is a lot of work on the role of HLA-B in diseases in rats that look a lot like Reiter's and ank spond. They suggest that you do not necessarily need any specific infection - that B27 alters some sort of threshold that allows overactivity of T cells anyway. But it is a while since I read about that stuff.

 

[msf]

Very interesting, I would then ask if there has ever been an experiment to engineer auto-immune disease in germ-free mice, but I guess you would need human subjects to convince everyone.

Any volunteers?

 

[msf]

That was a joke, by the way - you'd obviously have to use germ-free humans.

 

[knackers323]

Hi Jonathan,
There's truth in what you say about antibiotics but what would you say to Dr Wheldon who treated his wife MS and probably saved her life with an antibiotic protocol. From the little I read, mostly on forums, it doesn't work for everybody but for some people abx seem to help.
Perhaps here also we're dealing with different underlying diseases.

PS: I myself recovered from being housebound to having a decent life (no more pain, pem and insomnia) thanks to three years (on and off) multiple antibiotics when most consultants strongly advised against that and one even said to me I was totally mad in taking antibiotics.

I was also not aware of any big study's or reports of autoimmune patients unsuccessfully trying antibiotics.

@xrunner @Daffodil @Art Vandelay how long did it take to see improvement? So you had no test results that indicated infection, you just took it on a hunch?

Daffodil you think it may have been treating gut dysbiosis? Have any of you ever tested for gut dysbiosis or bacterial infections via PCR?

 

[Art Vandelay]

@xrunner @Daffodil @Art Vandelay how long did it take to see improvement? So you had no test results that indicated infection, you just took it on a hunch?

@knackers323 it was mostly a hunch rather than based on any definitive test result. I do have positive tests for Chlamydia Pneumonia and Lyme as well as some tests that may indicate inflammation and infection (including high ferritin levels, high 1,25 vit. D etc. Unfortunately I'm in Australia so we are limited in which tests can be done.).

I didn't respond very well to high dose antibiotics so I tried the Marshall Protocol instead. I got extremely strong Herxheimer reactions within a few weeks of starting the Protocol. I felt worse for the first two years of the Protocol due to the constant Herxing but that arguably could be due to the fact that my doctor at the time had me on inappropriate doses of the main medication and hurried me onto higher doses of antibiotics before I was ready.

 

[Daffodil]

I was also not aware of any big study's or reports of autoimmune patients unsuccessfully trying antibiotics.

@xrunner @Daffodil @Art Vandelay how long did it take to see improvement? So you had no test results that indicated infection, you just took it on a hunch?

Daffodil you think it may have been treating gut dysbiosis? Have any of you ever tested for gut dysbiosis or bacterial infections via PCR?

hi knackers. I think I may have mentioned this above, but I most certainly do have leaky gut and yes, it is very possible the antibiotics were addressing translocated bacteria...in fact, one researcher believes that this is what happened.

I am still very ill because I stopped the antibiotic protocol for quite some time. I hope to start it again. It was very hard on my GI system.

I have had all kinds of PCR testing for bacteria, at the best labs (Igenex, MDL, etc). Nothing was ever found, except for a positive Borrelia ELISPOT LTT. Also, I had slightly IgG antibody elevation of C. Pneum. long after taking antibiotics; never before.
xox