posted
The test they gave me was the lyme antibody with western blot confirm.
Basic hospital test. The result mailed to me was
b.burgdorferi antibody = .401 (normal)
however, I'm wondering given the inaccuracy of basic tests that the fact that it was not zero, and that I had any result could be indicative that something is going on.
I'm reading a lot now about facial nerve problems, and they describe me to a T, along with PVC's, nausea, and a cycle that this goes through every month.
Posts: 10 | From michigan | Registered: Sep 2006
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posted
The very best way to settle this is to get a dr who is willing to draw blood and send it to Igenex Labs in CA. That is the BEST lab, in my opinion.
posted
REASONS WHY A SERONEGATIVE TEST RESULT MIGHT OCCUR 1. Recent infection before immune response 2. Antibodies are in immune complexes 3. Spirochete encapsulated by host tissue (i.e. lymphocytic cell walls) 4. Spirochetes are deep in host tissue 5. Only blebs in body fluid; no whole organisms needed for PCR 6. No spirochetes in body fluid on day of test 7. Genetic heterogeneity (300 strains in U.S.) 8. Antigenic variability 9. Surface antigens change with temperature 10.Utilization of host protease instead of microbial protease 11.Spirochete in dormancy phase 12.Recent antibiotic treatment 13.Recent anti-inflammatory treatment 14.Concomitant infection with babesia may cause immunosuppression 15.Other causes of immunosuppression 16.Lab with poor technical capability for Lyme disease 17.Lab tests not standardized for late stage disease 18.Lab tests labeled "for investigational use only" 19.CDC criteria is epidemiological, not a diagnostic criteria
-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96239 | From Texas | Registered: Feb 2001
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Found it interesting that is was not zero... figure an antibody specific to lyme should be "all or nothing"?
I'll look into igenex. Just wondering if anyone else knew much about the fact I had any antibody reaction. Thanks.
Posts: 10 | From michigan | Registered: Sep 2006
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My questions though with this being a not so hot test, should I have registered any antibodies in my system?
Posts: 10 | From michigan | Registered: Sep 2006
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Could you explain how "Antibodies are in immune complexes" affect the test results?
Except in immunocompromised situations, I thought the body's immune system normally produces antibodies when it detects "invadors."
Do the spirochetes go into deep hiding so quickly that the immune system won't have a chance to detect them?
Also, I wonder at what point of the infection the person's immune system might become weakened if it does.
Thanks for your help.
shizuko
Posts: 110 | From Northern Virginia | Registered: Nov 2005
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treepatrol
Honored Contributor (10K+ posts)
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quote:Originally posted by shizuko: Hi Lymetoo,
Could you explain how "Antibodies are in immune complexes" affect the test results?
Except in immunocompromised situations, I thought the body's immune system normally produces antibodies when it detects "invadors."
Do the spirochetes go into deep hiding so quickly that the immune system won't have a chance to detect them?
Also, I wonder at what point of the infection the person's immune system might become weakened if it does.
Thanks for your help.
shizuko
Ian not lymetutu but
Spirochetes actually attack immune system in a number of ways. One way is they directly attack lymphocytes drilling into them then emerging out the otherside wearing our dna and protiens like a cloak.
So heres what they did.
"Lyme disease is a persistent low-density spirochetosis caused by Borrelia burgdorferi sensu lato. Although spirochetes causing Lyme disease are highly immunogenic in experimental models, the onset of specific antibody responses to infection is often delayed or undetectable in some patients. The properties and mechanisms mediating such immune avoidance remain obscure.
To examine the nature and consequences of interactions between Lyme disease spirochetes and immune effector cells, we coincubated B. burgdorferi with primary and cultured human leukocytes. We found that B. burgdorferi actively attaches to, invades, and kills human B and T lymphocytes. Significant killing began within 1 hour of mixing. Cytopathic effects varied with respect to host cell lineage and the species, viability, and degree of attenuation of the spirochetes.
Both spirochetal virulence and lymphocytic susceptibility could be phenotypically selected, thus indicating that both bacterial and host cell factors contribute to such interactions. These results suggest that invasion and lysis of lymphocytes may constitute previously unrecognized factors in Lyme disease and bacterial pathogenesis."
Figure 1. Micrographs revealing attachment to and invasion of lymphocytes by Borrelia burgdorferi. Cultured SKW 6.4 cells and primary human peripheral B cells were coincubated with virulent or attenuated B. burgdorferi for 1 hour; the mixtures were then prepared for and examined by light or electron microscopy.
The micrographs are representative of each susceptible host cell population.
a: Light microscopy revealed attachment of spirochetal tips to SKW 6.4 cells; attached spirochetes remained highly motile yet anchored to host cells.
b: Scanning electron microscopy revealed that adherent spirochetes penetrated lymphocytes through endocytotic pits; penetrated lymphocytes exhibited a noticeable loss of filopodia and other surface projections.
c: Transmission electron microscopy showed that intracellular spirochetes were retained within vacuoles; no fusion of lysosomes to endocytotic vacuoles was observed.
d: Continued coincubation with virulent spirochetes resulted in numerous lymphocytes with disrupted cell membranes.
e: No such cytopathic changes were observed with uninfected control lymphocytes. No such cytopathic changes were observed with lymphocytes incubated with Borrelia hermsii or attenuated B. burgdorferi (not shown). Bars � 1 mm.
And
``...the Western blots displayed consistent differences between the protein antigens recognized in vegetative cells and cysts. ...By forming cysts, it is also conceivable that B. burgdorferi cells evade detection by the immune system.'' --Alban PS; Johnson PW; Nelson DR. 2000.
``We found that cysts which are produced by inoculating B. burgdorferi in CSF at 37�C can be PCR negative using conventional DNA extraction and OspA primers (unpublished observation). This is either because the cyst wall inhibits the entrance to the genome or because the genomes of spirochetes have been changed. ...PCR detection of B. burgdorferi spirochetes often may given false-negative results [19].'' --Brorson O; Brorson SH; Henriksen TH; Skogen PR; Schoyen R. 2001.
``Very interesting are the studies by Hoyer and King who demonstrated the loss of a portion of the chromosomal DNA in an L-form of Enterococcus.'' --Mursic VP; Wanner G; Reinhardt S; Wilske B; Busch U; Marget W. 1996.
As parasitic bacteria with obligate alternate acarid and mammalian hosts, B. burgdorferi spirochetes likely encounter lymphocytes during multiple phases of the infectious cycle.
Thus, development of physical interactions between the spirochete and lymphocytes hypothetically could influence several phases of the cycle, such as spirochetal activity within the tick during feeding, colonization and dissemination within mammalian hosts, immune recognition of and response to the infection, and eventual transmission of the spirochetes back to feeding ticks.
Use of this murine model to follow associations between spirochetes and mammalian lymphocytes in vivo may help us understand whether these or other possible factors contribute to the virulence of B. burgdorferi or elicit pathogenic consequences in Lyme disease.
And dont forget it changes its surface protien expression immediatly upon enetering a human from a to c. Also at the bite area tick injects a numbing agent and a immune suppression agent.
It also throughout the infection gains dna from every incounter it has with phagocytes&lymphocytes it grabs ndna also possibly rna acting like a virus it also enters cells and incubates babies in there incorporating our plasmids & dna at the same time as each phagocyte & lymphocyte is being created over the life of infection it is using the same or some of the same materials that phagocyte & lymphocytes use magnesium b vitamins etc slowly waring down our body ability to make healthy attack cells.
While this is going on our bodies get inflamation which intern cause it to manufacture good and bad choleterol HDLgood LDLbad thus you may get heartblock because the ldl starts lining the arteries. And guess what Bb feeds off of oh yeah cholesterol pathway. Damn intelligent disease ?
Is that enough to go on?
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
I wonder, then, how/when antibodies can be produced.
Some people do have positive antibody tests before starting any ABX, don't they?
Sorry to ask more questions!
shizuko
Posts: 110 | From Northern Virginia | Registered: Nov 2005
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treepatrol
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The scanning electron micrograph above, shows a human macrophage (gray) approaching a chain of Streptococcus pyogenes (yellow). Riding atop the macrophage is a spherical lymphocyte. Both macrophages and lymphocytes can be found near an infection, and the interaction between these cells is important in eliminating infection.
Here is an animation that illustrates the basic cell-cell interactions that lead to antibody production.
1. Antigen Processing. When the macrophage eats bacteria, proteins (antigens) from the bacteria are broken down into short peptide chains and those peptides are then "displayed" on the macrophage surface attached to special molecules called MHC II (for Major Histocompatibility Complex Class II). Bacterial peptides are similarly processed and displayed on MHC II molecules on the surface of B lymphocytes.
2. Helper T Cell Stimulating B Cell. When a T lymphocyte "sees" the same peptide on the macrophage and on the B cell, the T cell stimulates the B cell to turn on antibody production.
3. Antibody Production. The stimulated B cell undergoes repeated cell divisions, enlargement and differentiation to form a clone of antibody secreting plasma cells. Hence. through specific antigen recognition of the invader, clonal expansion and B cell differentiation you acquire an effective number of plasma cells all secreting the same needed antibody.
That antibody then binds to the bacteria making them easier to ingest by white cells. Antibody combined with a plasma component called "complement" may also kill the bacteria directly.
And
Mechanisms of persistence While B. burgdorferi is susceptible to a number of antibiotics in vitro, there are contradictory reports as to the efficacy of antibiotics in vivo. B. burgdorferi may persist in humans and animals for months or years despite a robust immune response and standard antibiotic treatment, particularly when treatment is delayed and dissemination widespread. Numerous studies have demonstrated persistence of infection despite antibiotic therapy.[28][29][30][31][32][33][34][35][36]
Various survival strategies of B. burgdorferi have been posited to explain this phenomenon,[37] including the following:
Physical sequestration of B. burgdorferi in sites that are inaccessible to the immune system and antibiotics, such as the brain[38] and central nervous system. New evidence suggests that B. burgdorferi may use the host's fibrinolytic system to penetrate the blood-brain barrier.[39] Intracellular invasion. B. burgdorferi has been shown to invade a variety of cells, including endothelium,[40] fibroblasts,[41] lymphocytes,[42] macrophages,[43] keratinocytes,[44] and synovium.[45][46]By 'hiding' inside these cells, B. burgdorferi is able to evade the immune system and is protected to varying degrees against antibiotics,[47][48] allowing the infection to persist in a chronic state. Paradoxically, many of these scientific studies were performed and published by critics of persistent Borrelia infection. Altered morphological forms, i.e. spheroplasts (cysts, granules). The existence of B. burgdorferi spheroplasts, which lack a cell wall, has been well documented in vitro,[49][50][51][52][53][54][55] in vivo,[46][51][56][57] and in an ex vivo model.[58]The fact that energy is required for the spiral bacterium to convert to the cystic form[49] suggests that these altered forms have a survival function, and are not merely end stage degeneration products. The spheroplasts are indeed virulent and infectious, able to survive under adverse environmental conditions, and have been shown to revert back to the spiral form in vitro, once conditions are more favorable.[51][59][60][61][62] A number of other factors make B. burgdorferi spheroplasts a key factor in the relapsing, chronic nature of Lyme disease. Compared to the spiral form, spheroplasts have dramatically reduced surface area for immune surveillance. They also express different surface proteins - another reason for seronegative disease (i.e. false-negative antibody tests), as current tests only look for antibodies to surface proteins of the spiral form. In addition, B. burgdorferi spheroplasts are generally not susceptible to the antibiotics traditionally used for Lyme disease. They have instead shown sensitivity in vitro to antiparasitic drugs such as metronidazole,[63] tinidazole,[64] and hydroxychloroquine,[65] to which the spiral form of B. burgdorferi is not sensitive. Antigenic variation. Like the Borrelia that cause relapsing fever, B. burgdorferi has the ability to vary its surface proteins in response to immune attack.[37][66] This ability is related to the genomic complexity of B. burgdorferi, and is another way B. burgdorferi evades the immune system to establish a chronic infection. Immune system suppression. Complement inhibition, induction of anti-inflammatory cytokines such as IL-10, and the formation of immune complexes have all been documented in B. burgdorferi infection.[37] Furthermore, the existence of immune complexes provides another explanation for seronegative disease (i.e. false-negative antibody tests of blood and cerebrospinal fluid), as studies have shown that substantial numbers of seronegative Lyme patients have antibodies bound up in these complexes.[67][68][69]
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
FIG. 1. Attachment of B. burgdorferi to primary murine lymphocytes. Scanning electron microscopy of coincubation mixtures containing B. burgdorferi and immunomagnetic bead-purified lymphocytes (L) showed that spirochetes (S) adhere to immobilized cells but not to the antibody-coated beads (B).
Examination of paired stereomicrographs showed that attachment occurred at variable locations along the axis of the spirochete. However, adherence was observed most frequently in association with the terminal ends of filopodia extending from the surface of immobilized lymphocytes. Scale bar, 0.5 �m.
15. Persistence of spirochetes within macrophages Of course mice aren't human, but they are part of the chain of evidence from tick to mouse to tick to human- so we are allowed to apply logic in "Demonstration". Malawista et al. in J Immunol 1993 Feb 150:909-15 clearly demonstrate the Bb spirochetes living within macrophages by scanning confocal microscopoy at multiple times after infection. "Persistence of spirochetes within macrophages provides a possible pathogenetic mechanism for chronic or recurrent Lyme disease in man".
16. The challenge of intracellular pathogens Although a little out of date- Kathleen Seiler and Weis in Current Opinion in Immunology 1996 8:503-509 summarize "Immunity to Lyme diseaes: protection pathology and persistence". The authors make reference to intracellular location but one of the best summaries of intracellular concern is The Challenge of Intracellular Pathogens by Mahmoud in New England Journal of Medicine March 1992 Vol 326 No 11 pages 761-2 which outlines the dangers of intracellular replication.
Summary In summary, there is ample evidence demonstrating intracellular pathology involving humans and Borrelia burgdorferi. Science is only as good as its hypotheses- and it is time to hypothesize that a cure for Borreliosis in humans must involve intracellular eradication. The autoimmunity of chronic borreliosis ( molecular mimicry) is itself evidence of intracellular location- when the organism is coated with the hosts own cell structures ( thyroglobulin, myelin, nuclear debris, cardiolipin, etc) and then recognized as partly microbe and partly self structure, the basis is set for persistent immune attack- due to intracellular location. Thus all the elevated antimyelin antibodies, anti thyroglobulin, anti DNA, anti cardiolipin etc
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
quote:Originally posted by shizuko: Wow, thanks!
I wonder, then, how/when antibodies can be produced.
Some people do have positive antibody tests before starting any ABX, don't they? YES
Sorry to ask more questions!
shizuko
Because if your body has made antibodies to Bb and you kill Bb in great numbers with abx's.
Then where do the antibodies go after they are not needed?
Ill tell you they are set free and when you dont need them because the spirochetes are either dead or in cyst or coccoid form the body starts to exspell or break them down. Guess how it gets rid of them ? Well they start floating around in your blood and then start to leave body by urine.
So you now have a lot more than before of antibodie roamming around thus they show up in blood Western Blot test and # day urine tests.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
treepatrol
Honored Contributor (10K+ posts)
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posted
Ps all this info is stored in the Newbie Help Links.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
This is indeed very interesting stuff you put up here. Thanks.
I'm going to follow the link you put in and maybe will answer my own question to you here.
I'd be very much interested in know where you got these photos from, and whether there is a possibility of finding out how the samples were obtained and prepared.
As I've posted before, my husband is a forensic microscopist (along with being a nuclear physicist and rocket scientsit), and since we've had no luck with standard medical testing, is preparing to do his own studies. He has access to all kinds of microscopes, including a scanning electron microscope. We also plan to find someone to do a draw for us for his studies along with obtaining a kit from IGenex.
I was particularly interested in learning more about the cholesterol connection. In the last three years, I've had that get out of control, not super high levels, but high, and about all I eat is bird food.
I went from having a cholesterol level of 145 to now a 257, triglicerides of about 45 to over 400, and my fasting glucose has moved into the "impaired" or prediabetes range. There is no explanation for these things based on my diet or my exercise.
Anyway, I'd like to see the full article on the HDL/LDL stuff you posted here and again, may find it in your link. If not, I'd really like to know where you found these things, how you found these things. Thanks, Moosie
-------------------- Trying to figure it all out. Posts: 38 | From Spanaway, WA | Registered: Sep 2006
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