Autoimmune Diseases Caused by Bacteria?

[heapsreal]

Hasn't been mentioned for awhile but abx are said to have some anti inflammatory effects which could explain some symptom improvement? ?

 

[Art Vandelay]

Hasn't been mentioned for awhile but abx are said to have some anti inflammatory effects which could explain some symptom improvement?

Yes, I've definitely found that antibiotics can be anti-inflammatory at higher doses which is why I am using lower dose, pulsed antibiotics (which provoke consistent, generally tolerable Herxheimer reactions in my experience).

 

[justy]

I notice an immediate same day improvement of my breathing problems (air hunger, breathlessness wheezing) with Doxycyline, I think this must be due to its anti inflammatory effect because even tho I have igg pos for cpn I don't think it could affect the infection that quickly. Unfortuantely it caused all over body itching and my GP has said I may be allergic - damn!

Clarithromycin had the same, same day effect on breathing and is also anti inflammatory, but caused a worsening of all neuro symptoms (I presumed a herx) but then caused fast pulse and heart rate so I had to stop that one as well.

 

[Daffodil]

i asked my doctor, who is chief microbiologist at a major institution here. he said that one would have to take mega doses of an antibiotic for its anti inflammatory effects to be significant....

 

[msf]

I don't know if the prof will see this, but this seems like the best place for it. Plus someone else might be able to answer this, there seem to be a few medically-minded people about.

It seems to me that doctors distinguish between auto-immune and infectious diseases based on whether they find certain organisms in the patient that they judge capable of causing chronic disease, but I would like to know if there are any other signs (serological or clinical) that would suggest that the disease is either auto-immune or infectious.

Thanks,

Mark

 

[xrunner]

@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?

I had tests "positive" for Borrelia, Bartonella e CPn. These were sort of confirmed independently by blood microscopy.
Given that I was never bitten by ticks and such tests are not infallible there was certainly a degree of subjectivity in the diagnostic process and before I started on abx I wasn't completely sure myself. However the treatment saved me.
I had on and off treatment for over three years and I started to improve already after the first month of abx. Then had periods of going nowhere interspersed with other improvements. The whole process wasn't linear nor straightforward.

 

[knackers323]

i asked my doctor, who is chief microbiologist at a major institution here. he said that one would have to take mega doses of an antibiotic for its anti inflammatory effects to be significant....

Hi Daffodil did they explain how else people like @justy would see improvement so quickly with the abx?

Justy how long were you on the clarithromycin before you got the herx?

 

[Jonathan Edwards]

It seems to me that doctors distinguish between auto-immune and infectious diseases based on whether they find certain organisms in the patient that they judge capable of causing chronic disease, but I would like to know if there are any other signs (serological or clinical) that would suggest that the disease is either auto-immune or infectious.

Thanks,
Mark

We diagnose an autoimmune disease if we find autoantibodies together with the sort of disease that is specifically associated with that autoantibody. (The chances of having the two coincidentally is generally not a big problem.)

We diagnose an infection if we find an organism alive in a place where it should not be alive. There are other sorts of circumstantial evidence but a definite diagnosis mostly needs finding the organism alive.

There are lots of other differences which can allow a fairly clear distinction if considered in all the details of context. One simple one is that autoimmune disease hardly ever makes a swollen joint go bright red. Redness is almost always infection of a crystal problem like gout. Fever can occur in autoimmunity but lots of autoimmune problems will not be associated with fever above 37 degrees.

One of the most reliable ways to distinguish is by biopsy because the way inflammation forms around an infection tends to be quite different from the way it does in autoimmunity. Cytology can also help - for instance looking at cells in urine can give a good idea if a lupus patient has lupus nephritis or infection.

There is a very long list. Generally speaking it is fairly easy to tell them apart.

 

[Jonathan Edwards]

Somebody asked about formal trials of antibiotics in autoimmunity. I have to admit that I don't know of many outside my own speciality of RA. But RA has been treated with quite a range of antibiotics in trials. Some immunomodulatory relatives of antibiotics do show a benefit - sulphasalazine and doxycycline for instance, but it seems fairly sure that this is not because they are antibiotics. Rifampicin, which is one of the most powerful broad spectrum antibiotics, usually reserved for TB, turned out to have no effect in RA. Up until about 1960 infection was a prominent theory for the cause of RA and I expect penicillins were tried but I do not know the literature - it would probably have been before people published formal trials much and negative trials often do not get published even now. The experience I was referring to was that in the 1970s and 1980s we had large numbers of people with RA who needed antibiotics for extended periods for incidental infections - often staphylococcal or pneumonia - and this never seemed to help the RA.

On the issue of anti-inflammatory properties, a number of tetracycline family drugs do seem to have anti-inflammatory effects at fairly standard doses in some situations but I suspect this has nothing to do with them being antibiotics. I am doubtful that penicillin family drugs have any useful anti-inflammatory properties - I have never heard of it. Anti-malarials can be anti-inflammatory at quite low doses.

 

[msf]

I meant to say things that characterize each kind of disease in general, but you anticipated what I meant anyway.

I remember you saying that antibodies to a disease may in fact be auto-antibodies, but I guess that means that the reverse might be true. Does that mean that auto-immune disease (at least in poorly understood diseases) is a clinical diagnosis (or diagnosis of exclusion), or are there any tests (other than antibodies) that suggest one or the other? You said the inflammation pattern is different, but are the chemical markers of inflammation different?

Thanks,

Mark

 

[Jonathan Edwards]

I meant to say things that characterize each kind of disease in general, but you anticipated what I meant anyway.

I remember you saying that antibodies to a disease may in fact be auto-antibodies, but I guess that means that the reverse might be true. Does that mean that auto-immune disease (at least in poorly understood diseases) is a clinical diagnosis (or diagnosis of exclusion), or are there any tests (other than antibodies) that suggest one or the other? You said the inflammation pattern is different, but are the chemical markers of inflammation different?

Thanks,

Mark

Mostly the diagnosis of autoimmune disease as specifically autoimmune comes with a positive antibody test. In RA, for instance you can be pretty confident before you see an antibody, but it might turn out to be psoriatic arthritis looking very similar (which is not autoimmune). There are a few diseases that look to be autoimmune despite no autoantibody. Narcolepsy is one. The link to DR, which is involved in T cells helping B cells, makes it very likely. MS is an interesting example because there are antibodies in the wrong place but it is not clear that they are autoantibodies.

I did not say much about chemical markers because they tend not to distinguish very well. A raised CRP tends to indicate infection if the only relevant autoimmune option is not one that raises CRP (like scleroderma and some forms of lupus).

 

[Daffodil]

Hi Daffodil did they explain how else people like @justy would see improvement so quickly with the abx?

Justy how long were you on the clarithromycin before you got the herx?

Hi knackers. i did ask these questions but he just says he has no idea why.

After 21 years of this utter hell, if antibiotics give me relief, i guess i have to be OK with not knowing why.

What is concerning is that fact that antibiotics themselves can further damage gut flora and incite autoimmune disease ....so who knows if I might develop some other disease later on from taking antibiotics...?

I am unable to tolerate probiotics.

 

[acer2000]

FWIW I have felt better on Antibiotics as well. I have also seen my IL-8 go down in response to both Doxycycline and Azithromycin. Of course, nobody seems to know why my IL-8 is so high to begin with, so its not clear why this is.

I wonder if PANDAS can be considered an autoimmune disease that is triggered by bacteria (strep)? Or Rheumatic Fever?

Also, Dr. Edwards, what do you make of persistently elevated CD4 T Cells?

 

[Jonathan Edwards]

FWIW I have felt better on Antibiotics as well. I have also seen my IL-8 go down in response to both Doxycycline and Azithromycin. Of course, nobody seems to know why my IL-8 is so high to begin with, so its not clear why this is.

I wonder if PANDAS can be considered an autoimmune disease that is triggered by bacteria (strep)? Or Rheumatic Fever?

Also, Dr. Edwards, what do you make of persistently elevated CD4 T Cells?

PANDAS and rheumatic fever do not seem to be autoimmune diseases because nobody, as far as I know, has found an antibody or T cell reaction against self the stands up to scrutiny. Rheumatic fever looks like a delayed immune complex reaction over a week or so, presumably with bacterial antigen still the basis of the complex (not self). The long term effects are likely to be due to scarring. There is a mouse model of PANDAS that seems to get anti-complement antibody. This would be autoimmune strictly speaking, but it may be a transient effect like transient rheumatoid factor with acute infection - which as far as we know causes no disease itself. The difference with true autoimmune disease is that there is long term production of autoantibody that causes tissue damage.

So although it was rheumatic fever that kicked off the interest in autoimmunity in the 1960s it is probably not autoimmune.

A high CD4 T cell count might seem to be a good thing since CD4 T cells are useful! But in reality circulating lymphocyte counts are of very little significance. The circulation is just a traffic zone. It says nothing about what is going on in the lymphoid tissue. It is only relevant if levels are very very low - indicating no useful cells, or very very high, indicating a leukaemia (but then they are abnormal cells and hardly ever T cells).

 

[msf]

'Rheumatic fever looks like a delayed immune complex reactionover a week or so, presumably with bacterial antigen still the basis of the complex (not self).'

Would this be your tentative description for Reiter's disease too? I just looked at what you wrote about it again, and I've noticed that Reactive Arthritis/Reiter's seems to include two T-cell playgrounds in terms of symptoms: GALT and MALT.

Also, have there been any suggestions for why T-cell mediated auto-immune disease occurs? Is it defined by the absence of antibodies, or is there something specific about the behaviour of T-cells in this kind of disease?

I promise to stop asking questions after this.

Mark

 

[msf]

I mean't definition, not description.

 

[msf]

Sorry, I read what you wrote again and you already said it was a non-specific over-reactivity, so scratch that question.

 

[Jonathan Edwards]

Sorry, I read what you wrote again and you already said it was a non-specific over-reactivity, so scratch that question.

No problem. Reiter's would not be immune complex if it is T cell mediated. Immune complexes are bound by antibody. And that fits because Reiter's does not look like an immune complex disease. Immune complex problems unfold over hours or days and rarely last much more than a week. They tend to produce problems in joints, kidney, pericardium, lung, brain and a skin rash that is erythematous (pink or red from dilated blood vessels but not scaly). Small complexes produce what looks more like RA. Large complexes produce what looks more like lupus. Rheumatic fever lesions look like some sort of hybrid form. In Reiter's you get the T cell domain pattern and the skin lesions are, like psoriasis, flaky or keratotic. The joint problems are probably a knock on effect from ligament inflammation.

 

[msf]

I know I promised, but I can't resist as this is my worst symptom - what causes the ligament inflammation? And is there anything that can be done to treat it in patients with Reiter's?

 

[knackers323]

Hi knackers. i did ask these questions but he just says he has no idea why.

After 21 years of this utter hell, if antibiotics give me relief, i guess i have to be OK with not knowing why.

I wonder what explanation @Jonathan Edwards has for this?