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Discussion about Armin labs (Split Thread).

Biarritz13

Senior Member
Messages
699
Location
France
I really don't know. It is difficult to say, since the LTT measures the Th cells response, while the IgA is a response by B cells. Moreover, the IgA is against P. aeruginosa LPS, while the LTT would show a reaction agaist a surface protein of P. aeruginosa, which is OprG.

Thx. And for the Western Blot, can it have a cross reactivity to something also?
 

paolo

Senior Member
Messages
198
Location
Italy
Thx. And for the Western Blot, can it have a cross reactivity to something also?

Yes, it can. This is the reason why you need a certain number of positive bands in order to be sure of the specificity of the immune response against Borrelia burgdorferi.
 
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Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
Hello...Firstly thank you to everyone who contributes to this forum... It has been so informative to read your insights! My question relates to something I am surprised that hasn't been spoken more about (at least that I've seen)...

A criticism of the LTT has been:

"It is often criticized that the detected T-cell reactivity is not specific to borreliosis but simply a general T-cell
reactivity of patients with other inflammatory diseases."

I have read widely that it seems ME/CFS patients have a very high positive rate on the LTT test...Of course it would make sense that it is higher given that Lyme could lead to ME/CFS...But is it possible that ME/CFS itself results in false positives without having a lyme infection?

For example- I have seen the following quotes on various forum threads:

"What's also interesting is the possibility that the false positive rate for the LTT in ME/CFS patients might be higher than it is in healthy individuals. If that's true, I think it might suggest an underlying problem in some ME/CFS patients that could be mediated by memory T-cells."

Also here is comment from Dr Edwards: "I personally suspect that a subset of ME is likely to be due to the sort of non-specific T cell overreactivity you see in Reiter's syndrome."

Personally, I have tested positive to LTT tests from 2 different labs (Armin + Australian Biologics) but I am seronegative on 3 different Western Blots (with band 41 the only band ever positive once which i have now read is quite common without having lyme)...In the study of LTT testing they reported that only 2.2% of the 1500 cases was seronegative and LTT positive...

My clinical picture is classic severe ME/CFS- extreme exertion intolerance, PEM, cyclical, extreme ANS disregulation, other neural symptoms, and much more.... But from a lyme perspective this can be seen as chronic lyme...(I realise I could also have both)...I have been doing antibiotic/herb combo treatment for lyme for 3 months...

But it seems to me that if ME/CFS spikes T Cell reactivity my positive results may be due to ME/CFS...What are peoples' current thoughts on whether ME/CFS without Lyme is causing/can cause False positives on the Armin LTT?

Thank you in advance for your insights!
 

paolo

Senior Member
Messages
198
Location
Italy
@Rossy191276 As mentioned above, I have proposed a cross-reaction between a T cell epitope from B. burgdorferi OspC and a T cell epitope fom Pseudomonas aeruginosa OprG (see this post from my blog, skip brief introduction in Italian).

As serum concentration of IgA against lipopolysaccharides from P. aeruginosa and other enterobacteria has been found to be significantly greater in ME/CFS patients than in normal volunteers (Maes, et al., 2007), this could explain the high rate of positive LTTs for Lyme disease in PWME.

My hypothesis applies only to those LTTs which use full length OspC from Borrelia burgdorferi sensu stricto. And it is only a hypothesis!
 
Last edited:

Valentijn

Senior Member
Messages
15,786
I have read widely that it seems ME/CFS patients have a very high positive rate on the LTT test...Of course it would make sense that it is higher given that Lyme could lead to ME/CFS...But is it possible that ME/CFS itself results in false positives without having a lyme infection?
They weren't using ME patients when they validated the test. Those were samples which had a known positive or negative result from the standard two-tier test.
 

dadouv47

Senior Member
Messages
745
Location
Belgium
@Rossy191276 As mentioned above, I have proposed a cross-reaction between a T cell epitope from B. burgdorferi OspC and a T cell epitope fom Pseudomonas aeruginosa OprG (see this post from my blog, skip brief introduction in Italian).

As serum concentration of IgA against lipopolysaccharides from P. aeruginosa and other enterobacteria has been found to be significantly greater in ME/CFS patients than in normal volunteers (Maes, et al., 2007), this could explain the high rate of positive LTTs for Lyme disease in PWME.

My hypothesis applies only to those LTTs which use full length OspC from Borrelia burgdorferi sensu stricto. And it is only a hypothesis!

What about the CD57 then? How can you explain people having at the same time low CD57 and being positive to arminlabs test? What you found could also comprises the CD57 count?
Thank you!
 

serg1942

Senior Member
Messages
543
Location
Spain
*** Hi @Rossy191276,

[I have edited my original post, where the ++++ are--below]

A criticism of the LTT has been:

"It is often criticized that the detected T-cell reactivity is not specific to borreliosis but simply a general T-cell reactivity of patients with other inflammatory diseases."

*** Well, I have re-read very carefully the large paper on LTT and Lyme in more than 1500 patients, as in the Spanish ME/SFC-investigation forum I run we are treating these issues quite effusively, so it’s a matter I am very interested at:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3474945/#R7

*** first we need to distinguish between the lymphocyte transformation test (LTT) and the ELISPOT Assay. The first measures the number of new T helper cells specific for the borrelia antigens added to the culture of your serum--they are the ones that get activated, so this is a measure of the acquired responsiveness towards the bacteria:

(…) The proliferative response of cultured lymphocytes is measured by quantifying the uptake of tritium-labelled thymidine (3 H- thymidine) into the DNA of antigen-activated T cells. (…):

http://www.jiaci.org/issues/vol15issue04/1.pdf

*** The ELISPOT on the other hand measures the activity of antigens-specific-T cells by quantifying the amount of IFN-gamma secreted when these specific T cells encounter the borrelia antigens:

(…)The enzyme-linked immunospot assay (ELISPOT) has emerged as a superior method for assessment of the magnitude and the quality of T cell immunity. It enumerates at the single cell level the frequency and cytokine signature of activated antigen-specific T cells (…).:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972671/

*** I have read several studies as well on the ELISPOST, and the results seem to be similar. Also, this is a test approved by the CDC for TB and recommended over other tests in certain cases. Well, for me this is a solid confirmation of the validity of this test to meassure Th responses to antigens:

http://www.cdc.gov/mmwr/pdf/rr/rr5905.pdf

*** So, in response to your question, in my humble opinion these studies make clear how both tests are highly sensitive and specific to detect the specific T responses, with little non-specific stimulation. The immunological bases are described in the first large study:

(…)Each humoral immune response to an infection requires a specific cellular immune response with clonal proliferation of various antigen-specific lymphocyte subpopulations. Of central importance here are antigen-specific T helper lymphocytes (CD4+ TH cells). In addition to effector T cells, long-lived T and B memory lymphocytes are formed. In the presence of antigen-presenting cells and protein antigens, specific CD4+ T memory cells also proliferate in vitro. The lymphocyte transformation test (LTT), also known as the lymphocyte proliferation or lymphocyte activation test, is based on this principle(…)

(…)The results of our study differ in part from some published data which show a low specificity of the Borrelia-LTT [24, 25]. This is very likely due to methodology. The addition of interferon-α to the cell culture medium inhibits nonspecific proliferation of lymphocytes and promotes the function of antigen-presenting cells. This improves the discriminatory power of positive and negative LTT results(…)

I have read widely that it seems ME/CFS patients have a very high positive rate on the LTT test...Of course it would make sense that it is higher given that Lyme could lead to ME/CFS...But is it possible that ME/CFS itself results in false positives without having a lyme infection?

*** Well, most tests (ELISA, PCR, serologies) have demonstrated to show many false negatives, but a high positive predictive value (a positive is most times a real positive). The only tests that have created controversy about the possible false positives are the LTT and the ELISPOT, and both have been improved over the years in order to reduce these non-desirable outcomes. It doesn’t matter if they are used for ME/CFS or for other conditions, they have shown high “reliability” to measure the specific T reactions to antigens in vitro, and this is what determines the sensibility of these tests, regardless of the condition. The large study on LTT noted that false positives due to inflammation, or to other chronic infections had been excluded (although they don’t publish this data). More over, the percentage of Lyme + shed by serology and by LTT in 1480 clinically suspected Lyme patients, was similar, so, given that the positive predictive value of serology is actually high, we can infer the same for the LTT.


For example- I have seen the following quotes on various forum threads:


"What's also interesting is the possibility that the false positive rate for the LTT in ME/CFS patients might be higher than it is in healthy individuals. If that's true, I think it might suggest an underlying problem in some ME/CFS patients that could be mediated by memory T-cells."

*** it could be the other way around given that the acquired Th1 and Th17 responses in ME/CFS are depressed… So I don’t see bases for this assumption. Yes, we do have less T regs and less memory T and B cells, and this means that effector T and B cells over-react to some antigens. But this does not reduce the specificity of a Th cell towards its unique (almost) antigen, it only makes it to react strongly…


Also here is comment from Dr Edwards: "I personally suspect that a subset of ME is likely to be due to the sort of non-specific T cell overreactivity you see in Reiter's syndrome."

*** I agree, but let’s try to clarify this: more and more evidence supports that the origin of autoimmune arthritis is a cross-reaction, and some pathogens have been indentified as possible culprits. These process involves T over-reactivity (loss of tolerance, mainly of Tregs), in different forms, including polyclonal T cell proliferation, what entails many T cells attacking many antigens that shouldn’t, what subsequently causes autoimmunity. But the specificity of these T cells towards their specific antigens (let’s say, a protein of the joint tissue) does not change. This is the key idea to keep in mind.

Personally, I have tested positive to LTT tests from 2 different labs (Armin + Australian Biologics) but I am seronegative on 3 different Western Blots (with band 41 the only band ever positive once which i have now read is quite common without having lyme)...In the study of LTT testing they reported that only 2.2% of the 1500 cases was seronegative and LTT positive...

*** Well, serology test shave shown very clearly that they are just not reliable for chronic Lyme disease. For example (you can find many studies showing this):

(…)Seronegative cases with late stage Lyme borreliosis have also been recently described(…):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3474945/#R7

(…)The standard two-tier tests used to detect specific antibodies to B. burgdorferi include an enzyme-linked immunosorbent assay (ELISA) and a Western Blot assay (WB) [13]. However, the limitation of these assays is that they have low sensitivity and specificity, frequently producing false negative and false positive results (…):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972671/#B27-cells-02-00607


*** About that 2.2% of patients seronegative and LTT-positive,

++++ EDITED:

***the paper states:

(...)In 1182 out of 1480 patients (79.8%), the Borrelia serology and Borrelia-LTT showed corresponding results. 37,8% (n=560) showed a positive serology and a positive LTT whereas 42% (n=622) were LTT as well as serology negative. The combination of a positive serology with a negative Borrelia-LTT was found in 266 patients (18.0%). 32 patients (2.2%) were seronegative and LTT-positive.(...)

*** As for the seronegative and LTT-positive being so low, my explanation given in the paragraph edited (below, with ++++) I think explains these findings: because with these cohorts of patients (an average of "sub-acute" stages, where their immune systems are still quite reactive and able to form specific Igs), we should expect the serologies to be reliable, so, in agreement to this, we see a 37.8% with serology+ and LTT+ (LTT equally reliable to serology when this is +, confirming its high PPV).

*** In the same vein, and for the very same reason, when the serology is -, because of its high NPV, the LTT shows similar results conforming thus also its ability to discard the disease: a 40% of serology - and LTT-

*** But, when does concur a serology - and a LTT+?? Well, this is VERY NORMAL to be observed in late states of chronic Lyme disease, not assessed in this study (more than 3-5 years sick, and severe symptoms). This study shows the other occasion when this combination occurs: In more "sub-acute" states. As I explain below, at this early point, the reliability of serology is still high, so the discrepancies between serology and LTT at this point are almost insignificant--hence the 2.2%!!!! Alright, now this makes more sense!

++++ [paragraph complemented with the new info I've written above] out of the 1480, it makes sense, as in that study they define late stage Lyme as those who have been sick for more than a year, and early Lyme for those who have been sick for less than a year. Alright, This is a too early cut-off point. If you read studies on chronic Lyme, you can see that after a year they are still very reactive, with a Th1 dominance. These patients will for sure shed high percentage of real positive results from serological tests. The problem comes over time, after more years of disease, or when the symptoms become severe. At this time the immune response has evolved towards a Th2 dominance, and the capacity of secreting antibodies has diminished greatly (borrelia b. does attack and destroy the lymph nodes, then the B cells cannot convert into plasmatic cells, or their ability to form specific IgGs from IgMs (change of class process) has been haltered, etc.). In short, the study uses the ELISA and the Wetern Blot tests in order to asses positive or negative cases of lyme by serology. Putting together both techniques sensitivities and a mixture of patients comprising early Lyme patients and late ones (taking into account that their definition of late does not really fit what a late chronic stage lyme disease means), then it is understandable that both serology and LTT show high sensibility.


My clinical picture is classic severe ME/CFS- extreme exertion intolerance, PEM, cyclical, extreme ANS disregulation, other neural symptoms, and much more.... But from a lyme perspective this can be seen as chronic lyme...(I realise I could also have both)...I have been doing antibiotic/herb combo treatment for lyme for 3 months...


But it seems to me that if ME/CFS spikes T Cell reactivity my positive results may be due to ME/CFS...What are peoples' current thoughts on whether ME/CFS without Lyme is causing/can cause False positives on the Armin LTT?


Thank you in advance for your insights!

*** Well, I think I have answered to these questions above. I do hope this is helpful!

*** Best!
Sergio
 
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serg1942

Senior Member
Messages
543
Location
Spain
Hi @paolo, I just read your work, and just wanted to congratulate you. I'll study it in depth and will share my opinion, as I am very interested on this subject.

Well, I think we could find many similar antigenic epitopes between most common bacteria in the body, especially those who have been very well conserved, so that is why in order to mount a specific acquired response, many signals need to occur at once, or otherwise those Th cells become anergic.

However, of course these kind of cross reactions in tests might take place.

I just want to point out a practical deduction. The study validating the high sensitivity and specificity of LTT did find western blot's and ELISA's sensitivities and specifictities to be similar to those of LTT, especially for early phases patients. So, at least for the 1500 patients participating in this trial, there wasn't a cross reaction as the Th1 response does not involve IgAs. If there had been cross reaction in this paper, the LTT should have shed higher numbers of positives than serological tests, not being the case.

The other important thing I'd like to emphasize is that Lyme Dx is NEVER done only based on a LTT result. You need a good anamnesis, to support the Dx with other tests results (CD3-CD57+, MCP-1, PEG2...). This of course ensures a correct Dx.

Anyway, I do want to study the specific immune response to the chronic P. A. infection, and try to find a scientific explanation to these results, so we can maybe extrapolate them beyond this paper (or maybe find that your theory is really solid!)--You made me really curious about this subject! :)

Again, congrats for your fantastic work!

Sergio
 

paolo

Senior Member
Messages
198
Location
Italy
Hi @paolo, I just read your work, and just wanted to congratulate you. I'll study it in depth and will share my opinion, as I am very interested on this subject.

Thank you @serg1942 , very kind of you! I look forward to your comments.

Hi @paolo
If there had been cross reaction in this paper, the LTT should have shed higher numbers of positives than serological tests, not being the case.

In the paper you mentioned, they used a control group of 120 healthy subjects and another of 40 patients with autoimmune diseases (rheumatoid arthritis, lupus, Hshimoto's thyroiditis, diabetes mellitus type 1). As far as I know, increased gut flora translocation has not been described in any of these groups, so we should not expect false positive results due to the kind of cross reactivity that I have proposed in my blog post.

Moreover, the cross reactive T cell epitope I wrote about is peptide 111-120 from OspC of Borrelia burgdorferi strain B31, and it is not shared by OspC from the other two species of European pathogenic Borrelia, if I well remember. Thus, only one of the four antigens used for the LTT studied by von Baehr and colleagues could theoretically lead to cross reactivity with OprG of Pseudomonas aeruginosa. This antigen is lysate antigen of B.b. sensu stricto, the other three antigens being: lysate antigens of B. afzelii, lysate antigen of B. garinii, and OspC of B. afzelii. Since "a test result is considered positive if at least two of the four Borrelia antigens show SI values of 3 and higher" I guess that this particular LTT is not affected by the risk of cross rectivity with Pseudomonas aeruginosa.

In conclusion, according to my hypothesis, the risk of false positive LTT for Lyme disease is theoretically possible only for LTTs which use full lenght OspC of B.b. sensu stricto in patients with gut bacteria translocation, such as ME/CFS patients, where an increased adaptive immune response (IgM and IgA) against LPS of Pseudomona aeruginosa has been described in at least one paper (Maes, et al., 2007).
 
Last edited:

Rossy191276

Senior Member
Messages
145
Location
Brisbane, Australia
*** Hi @Rossy191276,

[I have edited my original post, where the ++++ are--below]

A criticism of the LTT has been:

"It is often criticized that the detected T-cell reactivity is not specific to borreliosis but simply a general T-cell reactivity of patients with other inflammatory diseases."

*** Well, I have re-read very carefully the large paper on LTT and Lyme in more than 1500 patients, as in the Spanish ME/SFC-investigation forum I run we are treating these issues quite effusively, so it’s a matter I am very interested at:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3474945/#R7

*** first we need to distinguish between the lymphocyte transformation test (LTT) and the ELISPOT Assay. The first measures the number of new T helper cells specific for the borrelia antigens added to the culture of your serum--they are the ones that get activated, so this is a measure of the acquired responsiveness towards the bacteria:

(…) The proliferative response of cultured lymphocytes is measured by quantifying the uptake of tritium-labelled thymidine (3 H- thymidine) into the DNA of antigen-activated T cells. (…):

http://www.jiaci.org/issues/vol15issue04/1.pdf

*** The ELISPOT on the other hand measures the activity of antigens-specific-T cells by quantifying the amount of IFN-gamma secreted when these specific T cells encounter the borrelia antigens:

(…)The enzyme-linked immunospot assay (ELISPOT) has emerged as a superior method for assessment of the magnitude and the quality of T cell immunity. It enumerates at the single cell level the frequency and cytokine signature of activated antigen-specific T cells (…).:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972671/

*** I have read several studies as well on the ELISPOST, and the results seem to be similar. Also, this is a test approved by the CDC for TB and recommended over other tests in certain cases. Well, for me this is a solid confirmation of the validity of this test to meassure Th responses to antigens:

http://www.cdc.gov/mmwr/pdf/rr/rr5905.pdf

*** So, in response to your question, in my humble opinion these studies make clear how both tests are highly sensitive and specific to detect the specific T responses, with little non-specific stimulation. The immunological bases are described in the first large study:

(…)Each humoral immune response to an infection requires a specific cellular immune response with clonal proliferation of various antigen-specific lymphocyte subpopulations. Of central importance here are antigen-specific T helper lymphocytes (CD4+ TH cells). In addition to effector T cells, long-lived T and B memory lymphocytes are formed. In the presence of antigen-presenting cells and protein antigens, specific CD4+ T memory cells also proliferate in vitro. The lymphocyte transformation test (LTT), also known as the lymphocyte proliferation or lymphocyte activation test, is based on this principle(…)

(…)The results of our study differ in part from some published data which show a low specificity of the Borrelia-LTT [24, 25]. This is very likely due to methodology. The addition of interferon-α to the cell culture medium inhibits nonspecific proliferation of lymphocytes and promotes the function of antigen-presenting cells. This improves the discriminatory power of positive and negative LTT results(…)

I have read widely that it seems ME/CFS patients have a very high positive rate on the LTT test...Of course it would make sense that it is higher given that Lyme could lead to ME/CFS...But is it possible that ME/CFS itself results in false positives without having a lyme infection?

*** Well, most tests (ELISA, PCR, serologies) have demonstrated to show many false negatives, but a high positive predictive value (a positive is most times a real positive). The only tests that have created controversy about the possible false positives are the LTT and the ELISPOT, and both have been improved over the years in order to reduce these non-desirable outcomes. It doesn’t matter if they are used for ME/CFS or for other conditions, they have shown high “reliability” to measure the specific T reactions to antigens in vitro, and this is what determines the sensibility of these tests, regardless of the condition. The large study on LTT noted that false positives due to inflammation, or to other chronic infections had been excluded (although they don’t publish this data). More over, the percentage of Lyme + shed by serology and by LTT in 1480 clinically suspected Lyme patients, was similar, so, given that the positive predictive value of serology is actually high, we can infer the same for the LTT.


For example- I have seen the following quotes on various forum threads:


"What's also interesting is the possibility that the false positive rate for the LTT in ME/CFS patients might be higher than it is in healthy individuals. If that's true, I think it might suggest an underlying problem in some ME/CFS patients that could be mediated by memory T-cells."

*** it could be the other way around given that the acquired Th1 and Th17 responses in ME/CFS are depressed… So I don’t see bases for this assumption. Yes, we do have less T regs and less memory T and B cells, and this means that effector T and B cells over-react to some antigens. But this does not reduce the specificity of a Th cell towards its unique (almost) antigen, it only makes it to react strongly…

Hi


Also here is comment from Dr Edwards: "I personally suspect that a subset of ME is likely to be due to the sort of non-specific T cell overreactivity you see in Reiter's syndrome."

*** I agree, but let’s try to clarify this: more and more evidence supports that the origin of autoimmune arthritis is a cross-reaction, and some pathogens have been indentified as possible culprits. These process involves T over-reactivity (loss of tolerance, mainly of Tregs), in different forms, including polyclonal T cell proliferation, what entails many T cells attacking many antigens that shouldn’t, what subsequently causes autoimmunity. But the specificity of these T cells towards their specific antigens (let’s say, a protein of the joint tissue) does not change. This is the key idea to keep in mind.

Personally, I have tested positive to LTT tests from 2 different labs (Armin + Australian Biologics) but I am seronegative on 3 different Western Blots (with band 41 the only band ever positive once which i have now read is quite common without having lyme)...In the study of LTT testing they reported that only 2.2% of the 1500 cases was seronegative and LTT positive...

*** Well, serology test shave shown very clearly that they are just not reliable for chronic Lyme disease. For example (you can find many studies showing this):

(…)Seronegative cases with late stage Lyme borreliosis have also been recently described(…):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3474945/#R7

(…)The standard two-tier tests used to detect specific antibodies to B. burgdorferi include an enzyme-linked immunosorbent assay (ELISA) and a Western Blot assay (WB) [13]. However, the limitation of these assays is that they have low sensitivity and specificity, frequently producing false negative and false positive results (…):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3972671/#B27-cells-02-00607


*** About that 2.2% of patients seronegative and LTT-positive,

++++ EDITED:

***the paper states:

(...)In 1182 out of 1480 patients (79.8%), the Borrelia serology and Borrelia-LTT showed corresponding results. 37,8% (n=560) showed a positive serology and a positive LTT whereas 42% (n=622) were LTT as well as serology negative. The combination of a positive serology with a negative Borrelia-LTT was found in 266 patients (18.0%). 32 patients (2.2%) were seronegative and LTT-positive.(...)

*** As for the seronegative and LTT-positive being so low, my explanation given in the paragraph edited (below, with ++++) I think explains these findings: because with these cohorts of patients (an average of "sub-acute" stages, where their immune systems are still quite reactive and able to form specific Igs), we should expect the serologies to be reliable, so, in agreement to this, we see a 37.8% with serology+ and LTT+ (LTT equally reliable to serology when this is +, confirming its high PPV).

*** In the same vein, and for the very same reason, when the serology is -, because of its high NPV, the LTT shows similar results conforming thus also its ability to discard the disease: a 40% of serology - and LTT-

*** But, when does concur a serology - and a LTT+?? Well, this is VERY NORMAL to be observed in late states of chronic Lyme disease, not assessed in this study (more than 3-5 years sick, and severe symptoms). This study shows the other occasion when this combination occurs: In more "sub-acute" states. As I explain below, at this early point, the reliability of serology is still high, so the discrepancies between serology and LTT at this point are almost insignificant--hence the 2.2%!!!! Alright, now this makes more sense!

++++ [paragraph complemented with the new info I've written above] out of the 1480, it makes sense, as in that study they define late stage Lyme as those who have been sick for more than a year, and early Lyme for those who have been sick for less than a year. Alright, This is a too early cut-off point. If you read studies on chronic Lyme, you can see that after a year they are still very reactive, with a Th1 dominance. These patients will for sure shed high percentage of real positive results from serological tests. The problem comes over time, after more years of disease, or when the symptoms become severe. At this time the immune response has evolved towards a Th2 dominance, and the capacity of secreting antibodies has diminished greatly (borrelia b. does attack and destroy the lymph nodes, then the B cells cannot convert into plasmatic cells, or their ability to form specific IgGs from IgMs (change of class process) has been haltered, etc.). In short, the study uses the ELISA and the Wetern Blot tests in order to asses positive or negative cases of lyme by serology. Putting together both techniques sensitivities and a mixture of patients comprising early Lyme patients and late ones (taking into account that their definition of late does not really fit what a late chronic stage lyme disease means), then it is understandable that both serology and LTT show high sensibility.


My clinical picture is classic severe ME/CFS- extreme exertion intolerance, PEM, cyclical, extreme ANS disregulation, other neural symptoms, and much more.... But from a lyme perspective this can be seen as chronic lyme...(I realise I could also have both)...I have been doing antibiotic/herb combo treatment for lyme for 3 months...


But it seems to me that if ME/CFS spikes T Cell reactivity my positive results may be due to ME/CFS...What are peoples' current thoughts on whether ME/CFS without Lyme is causing/can cause False positives on the Armin LTT?


Thank you in advance for your insights!

*** Well, I think I have answered to these questions above. I do hope this is helpful!

*** Best!
Sergio

Hi Sergio....

Thanks again for this great reply...

I have been reading your paper again with interest.... And I was wondering your opinion on a particular issue...

You present the case in the final paragraph:

Finally, it is clear for both LD and ME/CFS, that symptoms are the direct result of the chronic inflammation and related autoimmunity. Interestingly, even though LD is an infectious condition (at least in the first stages), the bacteria does not display any virulent factor. Instead, it is the host's response toward the bacteria what directly causes the characteristic inflammation and related autoimmune processes responsible for the symptoms. In this respect, as earlier discussed, there is evidence supporting chronic LD pathogenesis to be mostly autoimmune.

Regarding the chronic inflammation, I have high Ferritin levels which my doctor interprets to mean that I have high inflammation in my body (I have read several articles with specialists asserting that high ferritin is increasingly being understood as a marker of inflammation/infection). With this in mind it would make sense to me that high ferritin may be a good marker for the processes you speak of above in LD and ME/CFS... And to my way of thinking could be a further marker to indicate the potential help of LDI...

BUT.... in my readings of forums it seems many people with Lyme and ME/CFS report low ferritin which doesn't make sense to me in the case that autoimmune/inflammatory responses are occurring...

What are your thoughts on this?

Thanks again---- Anthony
 
Messages
47
Hi am new to this site but have always been aware of Lyme. From a early age.

There are over 3,000 + different types of Tick. + Nymphs so most may not have seen what's bitten them? And 4 main types across Europe.
Most don't see.

Let alone known what it might be.
As there is no one in the U.K. Servaying on a professional basis.

They rely on someone in a lab. Or museum. Oxford museum knew there was a problem.

Who may have read anidoctical evidence how Tick move.
Pest controls Money makers.

This has happened over many years.
Things get retweeted from the past.
It over shadows what's really happened.
Antibiotics don't work ! I am told too day.

Only because they are not rotated and pulsed. Non experts trying to tell the expert patient.

First of all over the last 10 years where I have been bitten most days.

I have see 2 that looked like Wood Ticks in my bathroom. I took one it to the natural history museum. They mashed it up and said it turned to blood,

Far from standing still on ceromony,
They moved like any other spider.
Only they were much reder.

They had different bodies to a spider.
So called experts tell me Tick don't move. They don't climb tree's.
Of cause they do.

I did a search on the net they do not move when they are not fed.

One site said they don't move.
So many of us may well of seen a tick, but just thought it s spider

While in the main these creaters are in the nymph stage and can't easily be seen just like plankton. They can't be seen with the naked eye.

They can live high up in the tree's.
not low down the tree acts as
caterpult spreading them all over.
So wearing socks up to the neck is not going to protect you.

I've been told they might be spider mites.
Before I caught Lyme in 2005.
I had been exposed to huge amounts of
radiation from several factories I lived near and a G3 Transmitter.

Tick and other similar creatures are radiation prof. They can even be put in space without a suit or microwaved.

While their preditors are kill by such extremes and we are.

Before the electropollution levels increased there was enough preditors to eat most of the tick. Right down to the nymph or egg stage. Like Bee populations the preditors are vanishing.

One Tick producing 20,000 eggs.
Chris Packham naturalist says this on UTub.com. Along with Prof Wall dogs they are more intesting.
Than humans.,
Chris P said on ITN news 3/4 or dogs had tick. That seemed to vanish. He now says 1/3. Are the problem.
Not each tick can reproduce 20,000 times.

I have 5 open wounds right now so there must be another 100,000 baby tick in my environment. Pulse the 100'000 of scares. It's scary!
The only source I have is a Tree outside the flat. I hardly go out yes my flat is sprayed.

But not the whole building or the tree.

I have 3 positive blood tests.
EU approved and FDA approved.
All tests were meant to be made international European Union .

It's assumed the NHS test is the gold standard. By some here?
It's not..

Sir Richard Murley re -elect to UCHL chair said that NHS tests were only exceptable.
He's a solicitor so he should know?

Where in fact the CDC lab was closed for antiquated testing the manager was given early retirement in 2012.

I found this out in 2015 parliamentary meeting. All rights where transferred to Mod/DSTL porton down. It reemerge as
Public health England. (HPA)


I met the manager in 2006 at a HPA meeting. Amoung other things the manager said her test was the best

At the time it was mentioned on the net
on euro Lyme. The manager of
Pro health.nl who told me he knew the NHS lab was using a less broad spectrum test.
(Now known as C6.)

It took from 2006 to 2012 to close the CDC department.

He didn't say how he knew.
Also "what doctors don't tell you"said Lyme disease tests where 50% accurate.
In 2006.

Baring in mind the NHS and this manager( NHS) had been doing tests since 1986. So she should of be good extremely good The gold standard

It turned out she was doing manual testing using a grey scale?
◾️◽️◾️◽️◾️◽️◻️
So I read.

I used to test for colour fade in materials
and staining on to white cloth.◻️

A grey scale was a rule with a dark grey
and a light grey next to one another.
It would get lighter along the strip.

I thought chromatograph was a little more complex than this.

The comment made to me you would only use this method for experimentation, not for rueteen testing.

So what were they up to only half heartedly doing a test at all?
The manager had tested samples from other labs that found positive she found negative.
Because of cross contamination.
She was saying these were dirty samples. Not Lyme.

Then in 2012 the lab was closed.
Various within Public Health England and government made comments like we only have low numbers of Lyme Disesse in the UK. Because we are an island birds don't fly over here with Lyme disease.
don't fly.

You can see the level of intellect.
As if being an island made any difference. Yet no one questioned.
Europe is swarming with Tick and the ones that are carried on birds to the UK
are magically transferred into Lyme Free Tick..Hocus pocus now you see it now you don't.

The manager of Southampton CDC unit said her test was the best in 2006.
You might say a gold standard✨.

The manager gave a number of doctors in the audience ammunition so they could tell their patients you have no longer got Lyme Disease. "guess what a mental health condition".☃️ Breaches human rights. For someone to call Lyme
Disease a mental health condition.

Your imagining things crawling on you.
I have photos. Well it's mental health.

Since 1986 the CDC unit had been misdiagnosing how many per year being then being given a diagnosis that they were mad their body racked with pain.⛑ call an ambulance you could end up on a psychiatric hospital with a high temperature blood pressure.
And your antibiotics taken from you take this pill We will put you in one of these and screw the lid down ⚰️

I reported the CDC unit to NHS Freud this and last year. But nothing.
They don't tell you anything.

I also reported them to MRSH and all NHS departments and nothing.
I think I tried EU bodies still no reply.

There is nowhere for wasteing lives and money on false so called gold standard.
now you see it; now you don't.

There were 3 different companies used.
The first was in Ireland then it went to the UK and Now to Germany
the German company do have various antigens like A, B and C6 OSP.
But they sell the NHS C6 OSP and will not comment.
Why the NHS /CDC/DSTL/Mod still only use C6 OSPPerhaps.

Sir Richard Murley UCHL said only NHS tests are recognised.
But it's a German test?
While these other companies who were trying to make all this profit out of us poor suffers. Used 3 or more antigens.Must be the money. Has to be??
that's what the NHS says it is they could not be trying to hide something?

They were also cross contaminating samples unlike the NHS.. and its
Who are so in the right.

Remember this you will not get IV antibiotics and you will get given these
if you think you have not got Lyme Disease. They will kill you eventually.

This has gone on for at least 30 years.

Yale university who made the vaccine also went down this path of using one antigen. A OSP..

They chosen to do this to reduce the number of false positives.
hochs pochus.

Once they vaccinated they couldn't tell who was positive and who had caught the disease.. when the vaccine started to cause more problems worse than the infection and a combination of no one trusting it the FDA stopped, it band it.

hoch pochus using A OSP on its own
illiminated false positives.
While iliminating more than 50% positive patients.

Even more
They then came up with this idea
To give a garenteed postive answer while removing 50% of the positive answers. So they then could remove 3%
False negative. Rather disproportionate.

A, B and C6 OSP. If they reacted to all three antigens together. There was this 3% false postive answer. What a gold standard? Whose money would they be wasting The NHS.
a gold standards is what?
Removing 50% of the patients in order to stop 3% who might be a false postive.

I found that if I reacted to all 3 of the antigens A B and C6 then my
tests was then 90% or as near as dame it.

You can work the - 3% into that it pains into insignificance.

For those who do not react it's still 50%
Either way.

Or less FOI 2013 the manufactures was saying with regard the NHS test was 41% accurate.

Whether that was per or post automation?after shut down. It's still poor. ⚗️it means the likes of me and you will not get treatment.

The government said the test was 90%.

What they were refurring to?
Yes if you reacting to C6 OSP without the other antigens it was 90%.

Even though they are still not treating people if they are positive on the NHS test. You can't win.

The basis may be the bloods are too normal? The white cells don't rise till IV antibiotics are given. It's like a latent effect. The spirochetes go inside the cells so the immune system can't see them. Antibiotics will make them do this so it has to be balanced.

I am covered in bites that don't heal for weeks the skin rots around the bite mark once I pull the tick out. I have put the nymph in a container and given it to my consultant.

The NHS are trying to say it's mental health.
I have photos still not believedI diserve one of these. For what I have found out and what the establishment
have been trying to hide.

When AIDS appeared in the 1980's the governments knew Lyme was an epidemic. It could not afford Lyme Disease.

45,000 are catching Lyme disease it's an epidemic. I think more like a pandemic.
Still they play tricks.

Doctors within the NHS are quite happy not to be able to ID Lyme Patients.
My GP said he didn't want to know.
He's told me he does not want to be a Lyme expert.

So all I hear is conspiracy yet more conspiracy.

The government and the media have worked so hard to cover this up over the last 30 years.
Not only in the U.K.
Insurance companies say tell doctors they are struck off if they treat patients more than 3 months.

My bank balance is going I should be in hospital on IV antibiotics.
Rather than pay carries to make me a meal and wash me still the NHS doctors no matter whole ill I get refuse to help.
It's cost me £800. And another £2000 to the court cause I could not say in my own home. I was homeless.
I came out of it with a high temperature and blood pressure.
Still I imaged it. 3 paramedics took readings. Then the doctors ignore them.
Doctors lose notes ignore notes.

If any of them get Lyme and they want to raise the concern and help others the GMC closes them down.

The paramedics on Saturday said what about the neighbors what about the community at large? I say.

As long as they don't know they have it Then were all right.
a bit more magic a few more lies.

It's perfectly safe to roll the

There is no council policy for Tick control so Watch out for

Oh and of cause doctors who don't believe you cause they will kill you to prove a point. Put you in the magic box
and tell your just mad and you will be better in the morning.
after all Tick do not exsists it's only others trying to tell you they do.

This is what an out of hours GP said.
So I must imagine my hubby died he had bites too chest pain. cats of mine where also ill they had imaging postive tests both of them. Still these people are making money out of me?. That's the NHS.

Who the NHS and the government by not doing the tests correctly.
There is nowhere to report them too☢️ Like typical socurity services ask no questions tell no lies.
Yes of course it's a conspiracy the XFILES ALL OVER:
Beam me up Scotti

By the way you must be
We can spend as much money as we like doing the wrong tests.✔️✔️✔️
Then as if by magic abracadabra
You don't have Lyme.
It's those other Buggers out there.



⚰️✔️


I should be in hospital not waiting to die!
 

Fogbuster

Senior Member
Messages
269
So is armin labs legit or would it be best going to another lab? If so, what are the best alternatives? Thanks
 

Fogbuster

Senior Member
Messages
269
I think the other main problem with Lyme testing is not the reliability of the tests themselves, but the fact that Lyme can evade the immune system and go into cyst form, where it can lay undetected. That is why a clinical dx is so important. My Armin LTT Ellispot was negative (yes it does happen!), but I have a clinical dx based on other immune markers, presence of tick born co infections and symptoms.

Hi Justy, were those immune markers which lead to a clinical diagnosis for you found through standard NHS testing? I'm one of those who slipped through the net with virtually zero abnormalities coming up in my tests via nhs so very little to work with. I did get positive for SIBO and leaky gut via Genova diagnostics and my IGA levels are extremely high, found through an endocrinologist. But unfortunately treating sibo via diet etc has proven to be extremely difficult to get any sort of symptomatic relief. I have constant 24/7 365 varying internal tremors and a hand tremor, and, definitely have a large symptom list to suggest I possibly have some form of infection. I have had some success with TH2 reducers but the latter again only relaxes me without addressing brain fog. All my constant symptoms seem to very closely match the symptom list found on the wiki page for Hyperinsulinemia, with the addition of sinusitis, clogged ears and intracranial pressure in forehead. I've had a glucose tolerance test but apparently too high insulin levels can lead to normal readings when you're levels are actually high...
 

bertiedog

Senior Member
Messages
1,738
Location
South East England, UK
Hi Justy, were those immune markers which lead to a clinical diagnosis for you found through standard NHS testing? I'm one of those who slipped through the net with virtually zero abnormalities coming up in my tests via nhs so very little to work with. I did get positive for SIBO and leaky gut via Genova diagnostics and my IGA levels are extremely high, found through an endocrinologist. But unfortunately treating sibo via diet etc has proven to be extremely difficult to get any sort of symptomatic relief. I have constant 24/7 365 varying internal tremors and a hand tremor, and, definitely have a large symptom list to suggest I possibly have some form of infection. I have had some success with TH2 reducers but the latter again only relaxes me without addressing brain fog. All my constant symptoms seem to very closely match the symptom list found on the wiki page for Hyperinsulinemia, with the addition of sinusitis, clogged ears and intracranial pressure in forehead. I've had a glucose tolerance test but apparently too high insulin levels can lead to normal readings when you're levels are actually high...
Unfortunately @justy got very unwell and I believe she doesn't read or post on PR anymore.

Pam
 
Messages
180
Regarding the above, which admittedly I only skim-read, I think it's perhaps interesting to note that personally I had a negative response on Armin's LTT, and then retested after a couple of weeks of Doxycycline and was positive. I recall others detailing similar experiences to the point of it seeming like a fairly common occurrence, and so I wonder if it is not possible that the antibiotics were a driving factor towards increased probability of cross-reactivity and hence the false-positives. Either way I'm quite sure I never had Lyme.
 

JES

Senior Member
Messages
1,322
I don't think antibiotics themselves can drive cross-reactivity to bacteria like Lyme. I think what is more likely to happen is that after taking antibiotics for some time, the bacteria gets weakened and the immune system starts to recognize and kill it again, hence the higher titers. This is what happened to my Mycoplasma antibody titers after attempting to treat it.