A comparison of Lyme disease serologic test results

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
duncan
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Re: A comparison of Lyme disease serologic test results

Post by duncan » Sat 20 Sep 2014 21:52

Just re-read the entire thread.

susank, despite my misgivings of the possible misuse of the C6 peptide test by individuals who have a vested interest in downplaying the prevalence of Late Stage Lyme or chronic Lyme, I agree with LHCTom that it is a good test to request.

I ALWAYS request it through my Lyme physician. Always. Whereas my WB bands vary over time, both in number and in specific bands, and sometimes I am CDC-positive, sometimes not, I have always been positive by C6 peptide. I would think IgeneX would have run that test, but I don't know as I've never used that lab.

But keep in mind that the primary utility of the C6 purportedly is in acute cases.

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LHCTom
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Re: A comparison of Lyme disease serologic test results

Post by LHCTom » Sun 21 Sep 2014 4:45

I was reading a paper discussing the development of another more specific epitope early Lyme test and encountered some interesting statements with regard to the C6 test.

Outer Surface Protein C Peptide Derived from Borrelia burgdorferi Sensu Stricto as a Target for Serodiagnosis of Early Lyme Disease

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3623407/
Clearly, new approaches are needed to develop better diagnostics. Peptides containing specific epitopes represent a logical alternative to whole-protein antigens as targets in diagnostics because this allows for the elimination of cross-reactive epitopes, retaining only those highly specific for Borrelia. An ELISA (IR6) using a peptide derived from the VlsE protein of Borrelia has demonstrated greater specificity in the detection of Lyme disease than whole-cell ELISAs and has been approved for use by the FDA (19, 23). However, C6, the peptide derived from VlsE, does not bind IgM particularly well, is derived from an antigen that is expressed only after infection is established (fewer than 1% of bacteria in the tick express VlsE, and transcription of the gene is suppressed prior to transmission of the bacteria), and the IR6 region of VlsE from which the peptide is derived has shown a greater degree of variability than originally thought (19, 23–26). Though the IR6 assay represents a significant improvement, in terms of specificity, compared to the whole-cell ELISA (27), these concerns have precluded the use of the IR6 assay as a stand-alone diagnostic test for early Lyme disease. These limitations could be addressed by combining multiple peptide epitopes into a single assay (28). Thus, the identification of further epitopes is of paramount importance to the advancement of Lyme disease serodiagnostics.
I haven't read the refrences (19, 23–26) yet but that's where I'm going next. But I agree with Duncan that the IR6 epitope appears very unique and so its ELISA has very good specificty if positive and has the advantage ( in my opinion) that it detects not only Bb but the European species Bg and Ba and probably others. This is because that 26 amino acid sequence found on the VlsE surface protein is highly conserved. That means evolution has not altered that amino acic sequnce "very much" even from Bb to Bg to Ba. The CDC actually counts "other" Borrelia infections against the C6 specificity. The only word I can think of is "Bonehead". I've yet to find any information one whether it catches B miyamotoi but it wouldn't be very difficult to look at the VlsE gene and see if it cosed for that amino acid sequence fairly closely. Then the next question is whether B miyamotoi expresses VlsE during an infection and how much?
19. Bacon RM, Biggerstaff BJ, Schriefer ME, Gilmore RD, Jr, Philipp MT, Steere AC, Wormser GP, Marques AR, Johnson BJ. 2003. Serodiagnosis of Lyme disease by kinetic enzyme-linked immunosorbent assay using recombinant VlsE1 or peptide antigens of Borrelia burgdorferi compared with 2-tiered testing using whole-cell lysates. J. Infect. Dis. 187:1187–1199 [PubMed]

23. Liang FT, Steere AC, Marques AR, Johnson BJ, Miller JN, Philipp MT. 1999. Sensitive and specific serodiagnosis of Lyme disease by enzyme-linked immunosorbent assay with a peptide based on an immunodominant conserved region of Borrelia burgdorferi vlsE. J. Clin. Microbiol. 37:3990–3996 [PMC free article] [PubMed]

24. Gomes-Solecki MJ, Meirelles L, Glass J, Dattwyler RJ. 2007. Epitope length, genospecies dependency, and serum panel effect in the IR6 enzyme-linked immunosorbent assay for detection of antibodies to Borrelia burgdorferi. Clin. Vaccine Immunol. 14:875–879 [PMC free article] [PubMed]

25. Ohnishi J, Schneider B, Messer WB, Piesman J, de Silva AM. 2003. Genetic variation at the vlsE locus of Borrelia burgdorferi within ticks and mice over the course of a single transmission cycle. J. Bacteriol. 185:4432–4441 [PMC free article] [PubMed]

26. Bykowski T, Woodman ME, Cooley AE, Brissette CA, Wallich R, Brade V, Kraiczy P, Stevenson B. 2008. Borrelia burgdorferi complement regulator-acquiring surface proteins (BbCRASPs): expression patterns during the mammal-tick infection cycle. Int. J. Med. Microbiol. 298(Suppl 1):249–256 [PMC free article] [PubMed]
Because of the need to maintain a reasonable balance between specificity and sensitivity, current laboratory tests fail to serodiagnose early Lyme disease approximately 50% of the time (1, 4, 10, 20, 22). Clearly, new approaches are needed to develop better diagnostics.
Duh! Am I reading this right? It sure seems like they say a lot of contradictory things relative to public positions without explaining themselves very well. I think they finally got to the door when they were handing out confused brains.
As a target for a serological diagnostic assay, OspC1 has a number of desirable attributes: it is derived from a principal virulence factor that is required for mammalian infection, it is expressed very early in infection, increasing the likelihood of an immune response being mounted against it, it is highly conserved among different OspC genotypes, and it identified a significant majority of patients with early disease. Our data suggest that OspC1 should be considered as a viable candidate for testing in a multipeptide diagnostic assay. An assay containing 5 or more specific peptide antigens, derived from multiple B. burgdorferi proteins, would markedly improve upon currently available technologies in both specificity and sensitivity (28) and may represent a potentially viable stand-alone laboratory test for all phases of Lyme disease diagnosis, especially early disease.
The IR6 assay, based on a peptide (C6) from the 6th conserved region of the VlsE protein of B. burgdorferi, demonstrates that a peptide target can significantly improve both sensitivity and specificity compared to whole-protein/cell-based assays. A recent report by Wormser et al. (27) provides evidence suggesting that the IR6 assay has both the specificity and sensitivity to function as a stand-alone diagnostic assay for Lyme disease. In that study, the authors compared the IR6 assay to a standard two-tier assay against a large panel of Lyme disease patient and negative-control sera and found that IR6 had a much higher sensitivity than the standard two-tier assay while demonstrating a nearly similar level of specificity. However, as the authors noted, the patient population was derived from a single area of hyperendemicity; therefore, it is unclear if similar results would be obtained using sera from different geographical locations. Furthermore, the individual second-tier Western blot assay utilized in the study has been demonstrated to be less sensitive than other, comparable kits, suggesting that the use of a more sensitive second-tier assay could alter the results. The use of a single epitope increases the likelihood of generating false negatives, as there is only a single antibody binding site and a relatively small variation in the amino acid sequence at that site would decrease the ability of such an assay to detect infection. C6, which is more variable than originally recognized, places the IR6 assay at risk for this limitation (19, 23, 24). Despite the recent results, it is unlikely that the current paradigm will be changed in favor of the single-peptide IR6 assay.
Are they all over the map?
The greater the ignorance, the greater the dogmatism.

Attributed to William Osler, 1902

susank
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Re: A comparison of Lyme disease serologic test results

Post by susank » Sun 21 Sep 2014 7:05

Sheesh. Madness.

May I please revisit the Igenex epitope test?

From 2008 - IGG 31 IND - Result: negative (me)
--------
Quote:
This test determines whether the band present at position 31 kDa on the Igenex IGG Western Blot is specific for Bb. Serum from the patient is treated against a Western Blot strip with fixed Bb specific recombinant fragments.

Igenex interpretation is based on internal validation studies performed on well defined Lyme patients:
67 positive and
161 negative.
The assay sensitivity is 95% and specitivity is 98% for late Lyme.

Limitations: Positive results for the 31 kDa band may be present after vaccination in uninfected persons.
The Lyme 31 kDa Epitope Test specifically was >97% in a viral positive panel.

Band Intensity:
Negative: No visible bands present
Positive: If intensity of band is equivalent to or stronger than the weak positive control.

Unquote
------------
FWIW my IGM band 30+ epitope test from 2011 was also negative.

I don't think I could understand the E. test interpretation even if my brain was normal.

All this stuff reads like it is purposely ambiguous. PYA? English not the writers's first language?

On the most basic level - WTH are they saying? Particularly if the E. test is negative?

Out of 228 patient studies 161 had negative E. test results?

susank
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Re: A comparison of Lyme disease serologic test results

Post by susank » Sun 21 Sep 2014 8:17

I think I was overthinking the E. test. Pardon.

So Lyme positive folks can have negative epitope tests. One can have Lyme and viruses. Duh.

I guess my rancor is in the reporting.

I would have preferred a footnote at the bottom of the report saying that the lab had seen something on bands 30 and 31 and had already re-tested them - and found nothing.

Desperate patients strugglng for a Dx - although hoping it's not Lyme - still know that certain bands - every band for that matter - might mean they are closer to getting an answer.

So I had two bands "given and taken away".

Igenex at least states what band 31 could be if not Bb - from the vaccine or from a virus.

Would be nice if a footnote could also be included suggesting what the crossreacting bands are picking up on.
Per band.
By now don't most in the lab/field know?

----------
O/W one reads band 18 is unknown. Or is Cpn. Or is Bb specific.

Very tired......sorry. So sick and so sick of all this.

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LHCTom
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Re: A comparison of Lyme disease serologic test results

Post by LHCTom » Sun 21 Sep 2014 20:21

I understand that when you are ill, all this confusion is frustrating and just plain wrong.

There are a couple of fundamental problems with antibody based tests that cannot be overcome and its clearly evident when you read the paper I just quoted in this thread. But there are some techniques that can be used to minimize both false negatives and false positive. But it will never be perfect and that means they must be supported by clinical knowledge. So the only way to approach testing that is close to 100% correct is to use multiple reliable tests in concert plus clinical information. There will never be an antibody based test that in one shot will deliver 100% sensitivity and 100% specificity. Its not possible but mainstream medicine looks at this from a statistical point of view while us patients care about what it means to our treatment path.

The CDC/IDSA and mainstream medicine would like a test that is "good enough" to get it right most of the time to control costs and broad quality control. But if you are one of the patients who falls into the "failed" category, the mainstream approach can ruin your life and most doctors just don't "get it". The "get it right" most of the time approach also makes controversies like "does chronic Lyme exist" go on and on. So as a patient, what can you do to compensate when the testing says you are negative but you know you are ill and frustrated.

First, antibody tests will NEVER be 100%. You need to understand and accept it. Why? Its a bit like predicting the weather next month. When there are MANY interacting factors, a system becomes chaotic. A chaotic system is fundamentally unpredictable. In the weather analogy, how do the hurricane predictors do it. They run about 20 mathematical models that all make differing but reasonable assumptions and look for convergence on one prediction. NOAA has 100's of people and computer models developed by universities all over the world to compare/contrast to estimate convergence and they still get it wrong and at best have best guesses. Antibody testing has similar problems but nobody admits it because developers wants theirs to be standardized so are optimistic and make "helpful" assumptions while the CDC doesn't want to openly admit they have a problem like weather prediction. So what are all these interacting factors that are so difficult to get convergence on a true positive 100% of the time.

This is just a brain dump so don't hold me to English or comprehension of everything - the point is there are so many factors to consider in designing a test - its impossible to make one test that is 100% all the time because of many of these issues:

+The human immune system are all different genetically and developed differently from birth
+ The Human immune system fluctuates in antibody production over time
+ The levels of antibodies fluctuate over time along with pathogen gene expression variation over time
+ The surface antigen expression and amount and expression time vary by genotype
+ B cells create antibodies on trial and error basis until they get a hit on an epitope the proliferate for this one
+ Not every immune system creates the same set of antibodies matched to the same antigen epitopes
+ The pathogen fluctuates its surface antigens expression over time and variable immune response stress factors
+The immune system produces different antibodies to the same antigen
+ One 41kDa antigen can be as many as hundreds of amino acids with many amino acid epitipe targets
+ Antigens have many epitopes for antibody binding that are all effective for the immune function
+ A typical spirochete might have as many as 20 or more target antigens
+ These epitopes can be anywhere from 3 to dozens of amino acids long and overlap
+ These epitopes can be linear or cross a protein fold
+ The many epitopes per antigen amino acid sequences vary from strain to strain to species in unpredictable ways
+ Genotype variations is a major factor, the slow rate of discovery and admission is a continuing problem
+ All the genotype antigen and their epitope variants is not known
+ Test developers tend to blind themselves and make simplifying assumptions about the above or fail
+ There is lack of competence and leadership on how to handle these variables by suites at the CDC/FDA
+ Anybody brave enough to push for acknowledgement of these issues and coordination is pushed out
+ Test developers only care about special cases like "early testing" to avoid and simplify assumptions
+ Simplifying assumptions lead to test good at one case but used for all cases which doesn't work
+ Success by developers is not measured by how well it performs in the "failed" cases
+ Developer success is measured by old FDA rules and cost/statistical performance
+ Sine a 100% perfect test is impossible, everyone agrees to agree and ignore the "failed" cases as its easier
+ Even the best tests require consistency of implementation at labs which is impossible due to complexity
+ Nobody can afford redundancy which is one way of getting closer to 100%
+Redundancy means multiple optimized tests that together cover as many issues and assumption problems
+ and on and on

So as a patient knowing this mess, its important to understand the strengths and weaknesses of the various tests and get multiple tests per lab and multiple types of tests and combine that with important clinical information like:

+ Did you get a tick bite, when and where?
+ Did you have an EM?
+ Do you have the most common Lyme symptoms?
+ Have you eliminated all other reasonable differential diagnosis possibilities as carefully as Lyme?

Once you are clinically confident its Lyme, arrange for a set of tests at good labs over time and use multiple test types to maximize the odds and lean toward high specificity tests. A positive on 2 different high specificity tests at 2 very good labs means more than a positive on a high sensitivity test that lacks specificity. When you are trying to sort out cross reactions, a high specificity tests like the C6 and this Ospc1 are very meaningful. If they would only focus on a usable culture, all this BS would go away.

Sorry to add further frustration but its complicated. Its further complicated because even if its chronic Lyme, there is no treatment that is 100% effective. Its one big mess. Its sad.
The greater the ignorance, the greater the dogmatism.

Attributed to William Osler, 1902

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ChronicLyme19
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Re: A comparison of Lyme disease serologic test results

Post by ChronicLyme19 » Mon 22 Sep 2014 1:34

Right, I mean isn't that what the UPenn study showed, that the VIsE surface antigen of lyme had a whole chunk of DNA devoted to changing it? So how could the C6 test possible capture all of those variations?

OK, dumb question here, is the C6 peptide something the immune system produces in response to the Lyme, the immune system just has normally, or is it a chunk of the surface protein on Lyme itself?

And yes, it would be really nice if the test would report what bands can cross react with other things right on the test results, so the doctor could say, you had x band positive and it can cross react, but your symptoms don't match that other disease so it's more likely lyme. Or maybe we should test you for that other disease that cross reacts as well.
Half of what you are taught is incorrect, but which half? What if there's another half missing?

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LHCTom
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Re: A comparison of Lyme disease serologic test results

Post by LHCTom » Mon 22 Sep 2014 2:17

The C6 peptide test is a standard ELISA that uses the antibody<->epitope binding properties to detect the sixth invariant peptide on the VlsE surface antigen. VlsE is one of the 20 or so surface proteins that make up the spirochete. Its like OspA, OspB, OspC etc... A protein is a long string of amino acids. VlsE is roughly 500 amino acids strung in a series. Smaller sections of proteins are called peptides that of course are also made up of amino acids. They found that the 6th peptide on the VlsE protein was a 26 amino section that appeared not to change across genotypes ( strains/some species). It was later learned there were some strains and species where the 26 amino acids differed. An antibody binds to an epitope which is a string of amino acids for about 4-n.

The exact amino acid pattern is like a lock called the epitope and the antibody is like the key that binds to that exact 26 amino acid sequence. It was later found shorter sequences were actually better. But the C6 peptide test is an ELISA with a recombinant version of the 26 amino acid antigen. When you put human blood on it, any C6 antibodies that match the pattern bind and turn a color based on the amount. So when its washed off, the color darkness is a measure of how many C6 antibodies in your blood bound to the recombinant antigen 26 amino acid look-alike of the 6th peptide on the VlsE Borrelia surface antigen.

When the Borrelia in your body expresses VlsE antigens, your B cells create the antibody that binds to it at the C6 region. So if you have any of those antibodies in your blood that are tested on the ELISA, they will bind and show up as a color which cooresponds to a value like 1.5 which would be positive. So it only look for exactly one antibody that only binds to only one amino acid sequence on one surface antigen. If the spirochete in you expressed enough VlsE and your B cells made antibodies to the C6 region, you will test positive on the C6 test. Not all strains have the eact same 26 amino acid pattern and not all express VlsE in sufficient quantity to test positive. But at least its quite simple and easy to understand and has a very high specificity since they have found very few cross reactions - specificity for Borrelia ( not Bb) is in the 98-99% range. So a psoitive means you have a 1% chance of a false positive. A negative means you didn't have the right strain or enough C6 antibody or don't have Lyme.

But you can combine the C6, PEPC10 and OspC1 and all similarly have high specificity. So a positive on any one or 2 better or 3 is a home run. And you know what it found. Unlike the B31 Western Blot or sonicated ELISA antigen blend.
The greater the ignorance, the greater the dogmatism.

Attributed to William Osler, 1902

susank
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Re: A comparison of Lyme disease serologic test results

Post by susank » Mon 22 Sep 2014 5:24

More thoughts;

I know that folks can have Lyme and show very few bands.

For me - when started thinking/testing Lyme - is when was found I have an immune deficiency. Hypogammaglobulinemia then CVID.

Total IGG 570 (700-1600)
Total IGM 120 (40-230)

I think a normal person would average IGG 1100.

Somehow I managed to show reactions to many Lyme bands. Perhaps too many. Shouting that I definitely have something going on - but is it Lyme?

Me (HypoG) reacting to a good number of bands vs folks with an intact immune system showing few bands?
On a test that can be harder to detect the pathogen/antibody/whatever?

-------
Outside of that - more than one pathogen could contribute to a band being positive. ??

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I will ask to do the C6 test. That will be tricky since I am on Gamma replacement ie IVIG/SCIG - Gamunex.
I assume the donated antibodies could cause test interference? The C6 test is a kind of antibody test?

If I am to do a WB test with Stonybrook I'll need to be off Gamma replacement anyway.

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LHCTom
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Re: A comparison of Lyme disease serologic test results

Post by LHCTom » Mon 22 Sep 2014 7:13

I know that folks can have Lyme and show very few bands.
Yes
For me - when started thinking/testing Lyme - is when was found I have an immune deficiency. Hypogammaglobulinemia then CVID.

Total IGG 570 (700-1600)
Total IGM 120 (40-230)
Who diagnosed this as a problem? Were subclasses tested? Was test done more than once?

570 is fairly mild. Are you sure that requires replacement? Was it just the test or were you experiencing infections and other odd things indicating it was causing a real issue like lung infections. There are 4 diferent IgG subclasses: IgG1, IgG2, IgG3 and IgG4. I was low on IgG1 388 (range 422-1292)-Labcorp. and IgG2 it at 30 (range 41-129) Labcorp and IgG1 and IgG3 have been associated with Lyme surface antigens.

http://www.ncbi.nlm.nih.gov/pubmed/9652826

This number also varies over time so only one measurement might not mean you have a deficiency. Repeating low numbers suggest you don't have enough raw material IgG subclasses to be used as pathogen specific

My IgM was 95 (40-230)
My IgA was 201 (70-400)

Given you have gone this far, check if you have a subclass deficiency since that is more meaningful since each class performs different roles. Who made the decison to do replacement based on a 570 as its not that bad. Just curious. Its a blood product so can carry HIV and other pathogens if they are not caught. Its not riskier than donated blood but it is derivd from many people and does carry their antibodies to whatever they were exposed to. It certainly could add another dimension to antibody testing since you now have many other peoples IgG antibodies with some unique to pathogen epitopes they encountered. Its a liitle like a vaccine without any controls.

Did you see a university immunologist or what kind of doctor felt you needed replacement?

see:

http://primaryimmune.org/about-primary- ... eficiency/

http://primaryimmune.org/wp-content/upl ... encies.pdf
I think a normal person would average IGG 1100.
The normal range is 700-1600 for adults and many are lower without problems. The ranges are set by labs such that many normal people are below the lower limit. I'm not an expert but I believe they typically replace when you are low and are clearly having problems with infections or vaccine inefectiveness etc.. as opposed to just being a little low.

Somehow I managed to show reactions to many Lyme bands. Perhaps too many. Shouting that I definitely have something going on - but is it Lyme?
Where were you tested and what bands showed up and how many times were you tested. What do you mean to many. I think they get IgG replacement from many people so any one pathogen IgG is highly diluted in you. So it wouldn't likley cause a false positive. But being too low could cause falling just under the threshold for a false negative becuase you don't make enough.

Or maybe you are low on that one test because of a recent heavy demand that lowered the level but came back later. So i would check and see if its repeatable and really due to your ability to produce. Plus check the subclasses while you are at it.

I've had at least 20 WB and not one was the same band pattern - all labs seemed to favor bands but were not repeatable. C6 was repeatable at Stony Brook, Quest and IGeneX using Immunetics kit based on B31 C6. So whatever strain I have is not terribly close to B31 causing problems except with C6 since it works over a wider range of strains. My subclass deficiency could also cause me to be borderline giving erratic WB problems but the single epitope single IgG molecule C6 is just simpler.

Me (HypoG) reacting to a good number of bands vs folks with an intact immune system showing few bands?
On a test that can be harder to detect the pathogen/antibody/whatever?

-------
Outside of that - more than one pathogen could contribute to a band being positive. ??
Some bands are more likley to cross react becuase they have antigens with epitopes that match other pathogens. Some are more unique but different strains and or even species can enter the picture since not every strain has the same amino acid sequence created by its gene so some epitopes begin not working...
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I will ask to do the C6 test. That will be tricky since I am on Gamma replacement ie IVIG/SCIG - Gamunex.
I assume the donated antibodies could cause test interference? The C6 test is a kind of antibody test?

If I am to do a WB test with Stonybrook I'll need to be off Gamma replacement anyway.
Stony Brook does the Immunetics C6 which has been well tested including me and is based on the B31 C6 rather than the European C6 which is based on B garinii..

I doubt the donated antibodies will be sufficient to meet the C6 detection threshold since they come from many people and you get 4 subtypes. But its a bit like a lottery - maybe if they all lived in the Hudson Valley and had Lyme...Where do the donated products come from? Probably all over..... I've always wondered what IgG replacement therapy would do to antibody testing... something to look into.
The greater the ignorance, the greater the dogmatism.

Attributed to William Osler, 1902

susank
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Re: A comparison of Lyme disease serologic test results

Post by susank » Mon 22 Sep 2014 8:28

Quick reply - very tired.
Tested total IGG numerous times. Also subclasses. (Pre IVIG and when months off of it).
My lowest IGG was 509. I am low out of range in three IGG subclassses.
IGA and a subclass low out of range.

IVIG made me feel better initially. Doctor said "would take care of viruses". I think it does/did.
A good thing I think to take strain off immune system to work on bacteria?

FWIW I am not tolerating any meds this past year like I was able to before.

I think I get a serum sickness-like reaction.

I probably need to go off Gamma replacement and antibiotics.

Pretty bleak to have an immune deficiency, have respiratory infections and maybe Lyme and Co and not be able to take the meds for it.

I think I have SSLR right now.

I sooooooo wish I could be told that I don't have any tick diseases.

W/O Gamma and antibiotics I am toast.

I will be angry at myself for taking Abx to treat Lyme - perhaps needlessly - perhaps setting me up for SSLR - making it difficult to treat resp. infections in the future. I trusted the culture test - that I was positive - and needed to treat.

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