Are Infections Just a Trigger of ME/CFS, or an Ongoing Cause of ME/CFS?

[nandixon]

It would be interesting to treat PCS patients with rituximab and see if there are any responders.

Yes, interesting idea. That was also recently proposed in an article I cited on another thread here. The authors stated:

The paradox of chronic neuroinflammation, systemic immune suppression and autoimmunity after traumatic chronic spinal cord injury

.....Although some B cell depleting monoclonal antibodies (e.g., Rituxan®, Ocrelizumab®) fusion proteins or biologicals that regulate B-cell survival factors (e.g., BAFF and APRIL) have or are being tested as therapies for classical forms of autoimmune disease (Mackay, et al., 2003), similar strategies have not been tested in stroke, CNS injury or neurodegenerative disease.

 

[heapsreal]

@heapsreal
I have tried some NK cell function booster supplements myself, and perhaps saw some mild improvements in ME/CFS symptoms, but not significant enough to make me want to continue taking the supplements.

I think it's going to take directly treating infections with abx/avs(effective) and some type of effective immune boosting treatment to really get at things.

I guess we can't even test for whats an active infection and whats not at the moment or if its isolated to specific areas and not picked up on a blood test.

We really need open minded drs who test and treat us all individually .

 

[Tammy]

I guess we can't even test for whats an active infection and whats not at the moment or if its isolated to specific areas and not picked up on a blood test.

I've often wondered about this too. When a person first gets an infection...........the virus is running around in the bloodstream and can be detected via lab tests..............but later can "nest" in different areas where it might not be able to be detected. I think this is a very reasonable possibility.

 

[BurnA]

If the subsequent ME was autoimmune and the autoimmune tendency to over-respond to infection was already there then I agree that a gap would be odd. But if the over-response links in to the anamnestic antibody response at around 15 days post infection then it would still be possible. My suspicion is that some ME is autoimmune and some autoinflammatory but I am only speculating. If so then any rule would apply some times and not others, which makes things so difficult.

If the autoimmune tendency to overrespond was there prior to infection, wouldn't it over respond to any infection ? My understanding is that only ( or certainly mostly ) certain virus types lead to onset or are associated with me/cfs ?

Also, while I believe there may be subsets, what are the chances or is it likely that both an AI and an autoinflammatory disease would have such similar symptoms ? PEM is a unique symptom not observed in other diseases afaik, and could the prevalence of dysautonomia be explained in both types ?
Would people be surprised that two different diseases would have such similar and indistinguishable symptoms ?

 

[BurnA]

Just found this paper, has it been discussed already - couldn't find any reference to it elsewhere.

http://www.jpands.org/hacienda/article24.html

 

[MeSci]

Just found this paper, has it been discussed already - couldn't find any reference to it elsewhere.

http://www.jpands.org/hacienda/article24.html

I couldn't find a thread specifically on that one either, strangely.

There was this thread - just a single post actually - on a similarly-named paper with the same lead author. Also this long list of papers and other references to Garth Nicholson. Seems an interesting chap.

 

[BurnA]

I couldn't find a thread specifically on that one either, strangely.

There was this thread - just a single post actually - on a similarly-named paper with the same lead author. Also this long list of papers and other references to Garth Nicholson. Seems an interesting chap.

And this one.

Systemic Intracellular Bacterial Infections (Mycoplasma, Chlamydia, Borrelia species) in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseasesby Prof. Garth L. Nicolson

"Using the blood of 100 CFS/ME patients and forensic polymerase chain reaction, we found that a majority of patients show evidence of multiple, systemic bacterial and viral infections (Odds Ratio = 18.0, 95% CL 8.5-37.9, P< 0.001) that could play an important role in CFS/ME morbidity.11,79 CFS/ME patients had a high prevalence of one of four Mycoplasma species (Odds Ratio = 13.8, 95% CL 5.8-32.9, P<0.001) and often showed evidence of co-infections with different Mycoplasma species, Chlamydia pneumoniae (Odds Ratio = 8.6, 95% CL 1.0-71.1, P<0.01), and/or active HHV-6 (Odds Ratio = 4.5, 95% CL 2.0-10.2, P<0.001). We found that eight percent of the CFS patients showed evidence of C. pneumoniae and 31% of active HHV-6 infections.11,79 In a separate study, we found that a sizable percentage of CFS/ME patients were infected with Borrelia burgdorferi, and therefore, they were also Lyme disease patients.80"

 

[RYO]

Cell death with presentation of nuclear antigens has been a thread in theories of lupus for at least fifty years. It is not clear that increased cell death is ever the driving stimulus, however. The cell death occurs all the time in all of us and in the lupus like illnesses recognition of the released antigens gets screwed up.

Stem cell transplantation, as you know, is not really a treatment in its own right, but merely a way of keeping a person alive after giving them lethal chemotherapy. The treatment is cytotoxic drugs of sufficient power to wipe out the immune system as a whole. I know of no case of this being used in ME. The closest we have is the chemotherapy regimens used in the lymphoma cases Fluge and Mella documented, whose ME got better. The only autoimmune disease where this sort of approach really makes any sense is lupus, I think, because some cases have such a poor prognosis otherwise. In RA it does not better than rituximab. What I think is needed is a way of ablating the immune system without using things like alkylating agents. What is not quite clear is which cells need killing better than we can do at present. We can kill T cells with anti-CD52 and B cells with anti-CD20 but not plasma cells. There are a lot of unanswered questions.

There are physicians in Chicago (NorthWestern) who are performing non ablative stem cell transplants for CIDP and MS. Many patients successfully treated.

 

[Jonathan Edwards]

There are physicians in Chicago (NorthWestern) who are performing non ablative stem cell transplants for CIDP and MS. Many patients successfully treated.

Do you have a reference for that? My understanding is that you cannot even harvest stem cells unless you give cyclophosphamide. And I cannot see what value there would be in just taking stem cells out and putting them back. If they are allogeneic stem cells one would expect them to be killed pretty much at once by an allogeneic response that had not been suppressed.

 

[Jonathan Edwards]

Do you have a reference for that? My understanding is that you cannot even harvest stem cells unless you give cyclophosphamide. And I cannot see what value there would be in just taking stem cells out and putting them back. If they are allogeneic stem cells one would expect them to be killed pretty much at once by an allogeneic response that had not been suppressed.

From what I picked up first off this looks like Richard Burt, who is close to Anne Traynor, who I know from lupus work. They seem to be using high dose cyclo and anti-thymocyte globulin to ablate.

 

[heapsreal]

Referring back to the title of this thread, i cant help but think its an ongoing infection. I have been back on valcyte 4 weeks and have noticed improvements . The chronic headaches from shingles has gone and i have had one incident where i was pushed to my physical limits at work and finished sore and tired as any unfit person would , but no pem.

Than later yesterday afternoon i went for a half hour walk, which was nothing compared to me 5 days earlier where i had to hike into some very hilly terrain to a guy who had fallen from a waterfall. These jobs dont happen every day that's for sure . Getting out was worse as its was 4km all up hill. I honestly didnt think i was going to recover from it. 4km in the bush is like 12km on the flat.

A few months back i would easily get pem from activities of much less .

 

[MeSci]

Referring back to the title of this thread, i cant help but think its an ongoing infection. I have been back on valcyte 4 weeks and have noticed improvements . The chronic headaches from shingles has gone and i have had one incident where i was pushed to my physical limits at work and finished sore and tired as any unfit person would , but no pem.

Than later yesterday afternoon i went for a half hour walk, which was nothing compared to me 5 days earlier where i had to hike into some very hilly terrain to a guy who had fallen from a waterfall. These jobs dont happen every day that's for sure . Getting out was worse as its was 4km all up hill. I honestly didnt think i was going to recover from it. 4km in the bush is like 12km on the flat.

A few months back i would easily get pem from activities of much less .

Crikey - your work sounds strenuous!

 

[heapsreal]

Crikey - your work sounds strenuous!

Once in a blue fit this happens .

I have just noticed inklings of improvement and this big hike really tested me.

While im on valcyte and minimal pem, it might be a chance to improve fitness, but always cautious of pem and crashes while plugging in rest days.

 

[RYO]

From what I picked up first off this looks like Richard Burt, who is close to Anne Traynor, who I know from lupus work. They seem to be using high dose cyclo and anti-thymocyte globulin to ablate.

Yes, Richard Burt is running clinical trials. I know of several patients who have undergone successful treatment. One patient in particular has concomitant Lupus. This person was able to reduce their medications to just 5-10 mg of prednisone. This patient also received Rituxan in addition to cyclo and ATG.
https://clinicaltrials.gov/ct2/show/NCT00278629

 

[Mel9]

And this one.

Systemic Intracellular Bacterial Infections (Mycoplasma, Chlamydia, Borrelia species) in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseasesby Prof. Garth L. Nicolson

"Using the blood of 100 CFS/ME patients and forensic polymerase chain reaction, we found that a majority of patients show evidence of multiple, systemic bacterial and viral infections (Odds Ratio = 18.0, 95% CL 8.5-37.9, P< 0.001) that could play an important role in CFS/ME morbidity.11,79 CFS/ME patients had a high prevalence of one of four Mycoplasma species (Odds Ratio = 13.8, 95% CL 5.8-32.9, P<0.001) and often showed evidence of co-infections with different Mycoplasma species, Chlamydia pneumoniae (Odds Ratio = 8.6, 95% CL 1.0-71.1, P<0.01), and/or active HHV-6 (Odds Ratio = 4.5, 95% CL 2.0-10.2, P<0.001). We found that eight percent of the CFS patients showed evidence of C. pneumoniae and 31% of active HHV-6 infections.11,79 In a separate study, we found that a sizable percentage of CFS/ME patients were infected with Borrelia burgdorferi, and therefore, they were also Lyme disease patients.80"

Does this mean that one could divide ME -CFS onto sub groups relating to the pathogen isolated?

 

[Jonathan Edwards]

And this one.

Systemic Intracellular Bacterial Infections (Mycoplasma, Chlamydia, Borrelia species) in Neurodegenerative (Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Alzheimer's) and Behavioral (Autistic Spectrum Disorders) Diseasesby Prof. Garth L. Nicolson

"Using the blood of 100 CFS/ME patients and forensic polymerase chain reaction, we found that a majority of patients show evidence of multiple, systemic bacterial and viral infections (Odds Ratio = 18.0, 95% CL 8.5-37.9, P< 0.001) that could play an important role in CFS/ME morbidity.11,79 CFS/ME patients had a high prevalence of one of four Mycoplasma species (Odds Ratio = 13.8, 95% CL 5.8-32.9, P<0.001) and often showed evidence of co-infections with different Mycoplasma species, Chlamydia pneumoniae (Odds Ratio = 8.6, 95% CL 1.0-71.1, P<0.01), and/or active HHV-6 (Odds Ratio = 4.5, 95% CL 2.0-10.2, P<0.001). We found that eight percent of the CFS patients showed evidence of C. pneumoniae and 31% of active HHV-6 infections.11,79 In a separate study, we found that a sizable percentage of CFS/ME patients were infected with Borrelia burgdorferi, and therefore, they were also Lyme disease patients.80"

This looks like a paper but I actually think it is a pseudopaper. It is not published anywhere as far as I can see. The presentation of the data looks as if it has been made up along the way. There are lots of P>0.001 attached to no actual numbers! I am fairy sure it is just an advert.

 

[Marco]

@Jonathan Edwards

If you hover over the graph and right click you can ask Google to search for the image (something I only discovered recently).

 

[Jonathan Edwards]

@Jonathan Edwards

If you hover over the graph and right click you can ask Google to search for the image (something I only discovered recently).

It wasn't the graphs I was worried about - although the bizarre standard error bars made my eyebrows rise a bit too. The text has P values without telling us what they refer to. This is not how you present real data.

 

[Marco]

It wasn't the graphs I was worried about - although the bizarre standard error bars made my eyebrows rise a bit too. The text has P values without telling us what they refer to. This is not how you present real data.

But the graph will bring you to the article (what there is of it) which is presumably all the detail we're likely to get :

http://www.townsendletter.com/April2008/systemicintracel0408.htm

 

[Jonathan Edwards]

But the graph will bring you to the article (what there is of it) which is presumably all the detail we're likely to get :

http://www.townsendletter.com/April2008/systemicintracel0408.htm

I was working from that article, rather than the post.