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Hveragerthi Views: 2,910
Published: 10 years ago
 
This is a reply to # 1,850,060

Re: Lyme disease revisited


 So what?  That is a long stretch to claim that he had Lyme simply because he lived in a town named Lyme!!!  What about people who develop ALS in parts of the world where deer ticks are not an issue?

Lyme is very much prevalent all over the world.  Not just caused by deer ticks.  Only ignorant Americans think that way.

Again you lack any credible evidence to support your claim.  And the few links you did provide were full of assumptions and contradictions.

 

You need to read more carefully, because that is not what I said.  I said the ONLY way to confirm Lyme is to have the characteristic rash.

That's non-sense.  Blood tests can show you.  Funny how that isn't enough PROOF enough for you (because it dosn't fit your agenda)

You make up some non-sense about cross reaction.  gtfoh

LOL!!!  Great example of projection.  Apparently for someone who works with Lyme patients I would think you would know about how antibody tests work, including their shortcomings.  I guess you are determined that I continue proving how little you know about the subject to the point where you have zero credibility.  Well if that is what you want here it goes.  Information on the "cross reaction", which as I pointed out previously is a well known problem really called serological cross reactivity:

http://www.everythingbio.com/glos/definition.php?word=cross-reactivity

"Definition of cross-reactivity :

 

The ability of an antibody to react with or bind an antigen that did not stimulate its production. This is sometimes seen in western blots, where an antibody detects other proteins other than the one the antibody is specific for. "

 

http://en.wikipedia.org/wiki/Cross-reactivity

 "Cross-reactivity is the reaction between an antibody and an antigen that differs from the immunogen. It is sometimes also referred to as crossimmunity or cross-protective immunity.[1] A few examples of cross-reactivity have been confirmed in humans, one of which involves influenza virus-specific CD8+ T cell and hepatitis C virus antigens.[2]

An adaptive immune response is specific to the antigen that stimulated it (called the immunogen). However, many naturally occurring 'antigens' are a mixture of macromolecules (e.g. from pathogenstoxinsproteinspollen) comprising several epitopes. Contact with a complex antigen such as a virus will stimulate multiple immune responses to the virus' different macromolecules as well as the individual epitopes of each macromolecule. For example, the tetanus toxin is a single protein macromolecular antigen but will stimulate many immune responses due to the tertiary structure of the protein yielding many different epitopes."


And guess what, even Lyme can cross react!!!:

http://www.lymeneteurope.org/forum/viewtopic.php?f=5&t=1686

J Infect Dis. 1987 Jul;156(1):183-8.Links

"

Cross-reactivity in serological tests for Lyme disease and other spirochetal infections.
Magnarelli LA, Anderson JF, Johnson RC.

Serum specimens from 163 persons with Lyme disease, tick-borne or louse-borne relapsing fever, yaws, syphilis, leptospirosis, or Rocky Mountain spotted fever were analyzed to assess the specificity of indirect fluorescent antibody (IFA) tests, an enzyme-linked immunosorbent assay (ELISA), and microscopic agglutination (MA) procedures. 

Strong cross-reactivity occurred when sera from individuals with Lyme disease, tick-borne relapsing fever, and louse-borne relapsing fever were tested against heterologous Borrelia antigens. Antibodies to Borrelia burgdorferi bound to Treponema pallidum in immunofluorescence tests for syphilis. 

Sera from subjects with syphilis cross-reacted in IFA tests and the ELISA for Lyme disease. Immunoglobulin antibodies to Borrelia or Treponema spirochetes, however, did not react with serovars of Leptospira interrogans in MA or IFA tests, and the prevalence of false-positive results in the reciprocal analyses was negligible."

 

"B. burgdorferi cross-reactions:


kDa
18: C. pneumonia
23-25: B. Hermsi, leptospirosis (band 25), Yersina, C. pneumonia (band 25)
35: Yersina, C. pneumonia
39: B. Hermsi
41: S. pallidum, L. interrogans, Yesirna, potentially all spirochetes
60: S. pallidum, E. coli, Bartonella, Staphylococcus, M tuberculosis, E. coli
70: HGE

Proteins that could be close enough possibly to get confused, if test or interpretation is sloppy:

kDa
18: S. pallidum (17 kDa)
30: C. pneumonia (29 kDa)
31: L. interrogans (32 kDa)
34: B. Hermsi (35 kDa)
41: C. pneumonia (40 kDa)
45: T. pallidum (47 kDa),
66: M. tuberculosis, E. coli (65 kDa)"

http://www.igenex.com/labtest.htm

"

 

RESULTS AND DISCUSSION

 

 

Table 1 presents the types of tests that are most commonly available for Lyme disease. To provide adequate support for the clinical evaluation, multiple tests should be used. Not only is a correct diagnosis advantageous for the patient, but also ultimately is the most cost effective.

Indirect fluorescent antibody (IFA)

B. burgdorferi spirochetes are affixed to glass slides and usually a fluorescent-conjugated goat antihuman immunoglobulin of either IgM or IgG specificity is used (20). Tests for Lyme disease using IFA have received mixed reviews and some authors believe that the interpretations of IFA assays are overly subjective and that the tests are either functionally insensitive for Lyme-specific antibodies or display considerable cross-reactions with antibodies to other spirochetal organisms (21,22). Magnarelli et al (23,24) and Mitchell et al (20) supported IFA if used in conjunction with a clinical evaluation. Mitchell's study with the IgM IFA showed excellent specificity and no observed cross-reactivity with infectious mononucleosis (n = 20), rheumatoid arthritis (n = 19), systemic lupus (n = 22), syphilis (n = 13), streptococcal sequelae (n = 20) or healthy subjects. Mitchell related the success of this test to the quality of the substrate slides and the level of experience of the technologists, and concludes that IFA microscopy becomes less subjective with experience.

Enzyme-linked immunosorbant assay

ELISA for B. burgdorferi has been available since 1984 (25). Most commercial assays use a whole cell sonicate of B. burgdorferi. Complete descriptions of methods for a Lyme ELISA can be found in the publications by Craft et al (25), Magnarelli et al (23), and Russell et al (21). Standard ELISA techniques have been employed (26) in all these assays.

There are a large number of commercial ELISA tests available. A review of past proficiency events by CAP and the NYS Health Department show the relationship between the various tests. Most commercial ELISA tests have comparable sensitivity and specificity because they were made to compare to one another for the FDA 510K process. However, most are inadequate as a screening test because they were not designed by the manufacturers to be sensitive at the 95% level, which is required for screening (14). A substantial change in the 510K approval process would be required to make the ELISAs for Lyme disease diagnosis more sensitive.

The goal for a new generation of ELISAs should be sensitivity for the more unique and specific B. burgdorferi antigens that are visualized in the Western blot (Figure 1). They are Osp A (31 kDa), Osp B (34 kDa), Osp C (23-25 kDa), 39 kDa, and 93 kDa (27-32). Initially, some investigators identified 93 kDa as 94 kDa and Osp C as 22 kDa. While most ELISAs do have reactivity to these antigens, because they are prepared with a sonicate of B. burgdorferi, they also have reactivity against 41 kDa, 58 kDa, 66 kDa, and 73 kDa. While the later antigens are components of B. burgdorferi, they also have considerable cross-reactivity to other spirochetes, heat-shock proteins, and some viruses (33)."
 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC267918/

Cross-reactivity of nonspecific treponemal antibody in serologic tests for Lyme disease.

 

http://www.ncbi.nlm.nih.gov/pubmed/18844689

 

Cross-reaction between Yersinia outer membrane proteins and anti-Borrelia antibodies in sera of patients with Lyme disease.

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287758/

Evaluation of a Western Blot Method for the Detection ofYersinia Antibodies: Evidence of Serological Cross-Reactivity between Yersinia Outer Membrane Proteins andBorrelia burgdorferi

 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1287758/table/t3/

Cross-reactivity observed for the Yersinia CF assay, Western blot assays, and ELISAs with samples positive for antibodies to various organisms

So now that you have thoroughly embarrassed yourself by showing your complete lack of knowledge of the subject you still want to keep this up?

 Yes, a small number of people may not develop the rash, but without the rash it is virtually impossible to confirm infection.  Why?  Simple, because the antibody tests and PCR tests used for "diagnosis" are EXTREMELY inaccurate.  Antibody tests in particular are notorious for creating false positives.

LOL - ok

You should not have laughed so much before doing your homework since you have just been COMPLETELY discredited!!!

In addition, you totally missed my point.  The rash appears in the majority of people that actually have the Lyme bacteria.  Yet this rash does not appear in MS, ALS or the various other diseases you have tried to link to Lyme.  In other words if these people REALLY did have Lyme then they would most likely have developed the characteristic rash, which they do not.

As I referenced to in my other post.... I guess the 100s of patients I've come aross (Uncle included) who were once WRONGLY diagnosed with MS, ALS, CFS only to later test positive via Western Blot or spinal tap for Lyme Disease were just imagining things?

 And once again the lab tests for Lyme ARE NOT accurate as the evidence I have posted shows.  And again, if you were such an expert on the subject then you should have been aware of that.  So you have just shown that you are in no way an expert on the subject.

 

Good for you.  So you may be one of the many misdiagnosed based on the inaccurate antibody and PCR tests.

LOL You're a stubborn man

I am not the one making unfounded claims that keep getting disproven.

 

We are going to have to agree to disagree because I see your comments as being the very dangerous ones since they are merely speculation severely lacking any credible evidence.  Like assuming Gerhig had undiagnosed Lyme because he lived in a town named Lyme.  Using your rationale then people from Blue Ball, Delaware should go to Hooker, Oklahoma then  move to Intercourse, Pennsylvania and finally Climax, Colorado.  And I would hate to see what the people in Square Butt, Montana look like!!!

As long as you don't delete my post so others can see I'll be fine agreeing to disagree.

No, I am not going to delete the posts since they clearly show your lack of knowledge on the subject, and people need to be aware of this.  But I am putting a stop to this nonsense by blocking you from this board since you seem to only want to argue over things you clearly have no understanding of.  And I am not going to waste any more time addressing your unproven and disproven claims.  You can take this garbage over to the Lyme board.

 

 
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