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Eve Sapi's work - a post from my lyme group - antibiotics and borrelia

Discussion in 'Lyme Disease and Co-Infections' started by sianrecovery, Apr 29, 2013.

  1. sianrecovery

    sianrecovery Senior Member

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    Hi Guys

    A member from my lyme group posted this and I thought you might find it helpful. I haven't followed it to source. Have attached as document.

    Attached Files:

  2. golden

    golden Senior Member

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    Unfortunately I cant access it..

    but just in passing can I ask...

    if there isnt a reliable test for lyme in the UK, how are people knowing they have it?

    :-/

    thanks
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  3. sianrecovery

    sianrecovery Senior Member

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    http://www.betterhealthguy.com/joomla/blog/264-physicians-round-table-2012
    Have pasted it. In terms of testing in the UK, I don't know the answer anymore - it used to be Dr Wright. Eurolyme might have some suggestions. I have not tested for lyme - I tested for protomyxzoa with a doctor in the US. Some people go to the Breakspear. There is a good lab and clinic in Germany I believe - it might be infectolab - perhaps someone could remind me?
    Dr. Eva Sapi PhD
    • 30 years after having identified Borrelia burgdorferi, we still don't have a solution.
    • Her goal is to kill Borrelia, and she continues to work on her ideas in the lab with her research.
    • For cysts, Flagyl, bismuth citrate, Plaquenil, and Tigecycline may be useful considerations.
    • A study done by Barthold showed persistence of Borrelia in mice after using Tigecycline.
    • With Doxycycline, higher doses pushed spirochetes into cyst forms.
    • When you stop Doxycycline, three weeks later, the spirochete level was back almost to the control.
    • Metronidazole (Flagyl) decreases cystic forms and has a minor impact on spirochete forms.
    • Tinidazole was shown to be good for both spirochetes and cyst forms.
    • Plaquenil has been shown in the past to be potentially helpful for cysts. However, this was not replicated by Dr. Sapi's lab.
    • Alinia may be good for both cysts and spirochetes.
    • Metronidazole and Doxycycline combined appeared to have a very good effect on both spirochetes and cyst forms.
    • Doxycycline + Tinidazole was shown to be the best combination. It appears to be effective against both the spirochetes and the cyst forms.
    • Fluconazole (Diflucan) has a modest effect on spirochetes.
    • Samento and Banderol were studied. Separately, the effect was not that strong, but together, they had an additive effect.
    • After 2 weeks, Samento + Banderol showed a significant reduction of spirochetes and cyst forms.
    • Looking at the spirochete and cyst populations relative to Doxycycline, Samento and Banderol tested better.
    • Doxycycline alone increased cyst forms while Samento + Banderol reduced them.
    • Antibiotics are 1000x less effective when an organism is protected by biofilm.
    • Tinidazole may be useful for biofilms as well.
    • Samento and Banderol both separately showed a biofilm reduction property. The combination was quite effective for the biofilm colony.
    • Biofilms from Borrelia can attach to glass, plastic, collagen, and other substances.
    • Calcium alginate may be a major component of biofilms.
    • Earlier research identified filarial nematodes in ticks. Ivermectin may be useful here.
    • They looked for XMRV in ticks, but did not find it.
    • The lower the oxygen level, the better that bacteria will grow. Borrelia is sensitive to oxygen.
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  4. golden

    golden Senior Member

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    Oh thats great thanks :)

    Its just after an alternative machine tested me positive for lyme, I wanted to get a blood test to see.

    I asked Dr. Myhill and she said a reliable blood test doesnt exist. I dont know if she is bound by NHS though.

    This swiftly brought this path of enquiry to an end. :(.
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  5. sianrecovery

    sianrecovery Senior Member

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    I tested positive on machine thing too, cant remember which variant. There now a test available in the US based on blood culture I believe, but I don't know anyone who's taken it. I think if Doc Myhill thought there was an effective test available to her she would do it, NHS or no. Clinical history is really your best insight.
  6. Sushi

    Sushi Moderator and Senior Member Albuquerque

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  7. Lotus97

    Lotus97 Senior Member

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    Luckily, I've had a recurring rash where I was bitten by a tick so I'm not sure I need to get tested except maybe for coinfections. I'm planning on trying Buhner's protocol which uses herbs rather than prescription antibiotics. I realize Buhner might be biased, but he seems to think herbs are more effective overall. Based on what sianrecovery posted it seems maybe the problem isn't necessarily prescription antibiotics, but rather that the right kinds and/or right combinations aren't always used. Since I can't afford to see a Lyme specialist right now my only option is to take supplements. Has there been any advances in Lyme antibiotic drugs in the past few years or are the same ones used now the ones that were used a decade ago?
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  8. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    so if one did doxy and flagyl what is the dosage and length of treatment. Is it a few weeks or we talking months??
    Whats recommeded for biolfilms? serepatase is what im using now.
  9. Lotus97

    Lotus97 Senior Member

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    Do people experience herx when they break down the biofilm?
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  10. sianrecovery

    sianrecovery Senior Member

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    Sometimes, tho what is herx and what is illness is hard to tell for me. I haven't yet had the extreme put you in the emergency room type reactions I've read others have had, but some for sure - just done my first four days on tindamax, and the herx was like a virus, and is now receding a little. It really varies.
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  11. sianrecovery

    sianrecovery Senior Member

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    ps ultimately, I think herbals are the answer. I don't think these bugs with their protean effects and robust longevity are going to be controlled by a pharma drug with a narrower range of action
  12. jenbooks

    jenbooks Guest

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    Anyone know how she tested? In vitro? Because that often doesn't translate. I'm a bit skeptical of the above results.
  13. sianrecovery

    sianrecovery Senior Member

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    Yeah me too. In vitro I assume. Think there's more description under the notes at betterhealthguy
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  14. baccarat

    baccarat Senior Member

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    Thanks Sian, interesting thread.

    I've just read Buhner's book and he actually says that antibiotics plus herbals are better than antibiotics alone, he writes that he's anti antibiotics but not in the case of Lyme. according to him herbals can make antibiotics more effective but also help with other issues like immune strengthening, repairing tissue damage, etc.

    At the end of the day you can't eradicate Borrelia and the best antiborrelia treatment is a fully functioning immune system that can fight it because the illness is very immunosuppressive.
    In this respect, checking nagalase can be helpful. And then I think it's a bit artificial consider Borrelia as the only problem.
    When you get bitten you are usually injected with several microbes together with borrelia, particularly parasites, which most doctor don't seem to consider or treat as antibiotics are ineffective against those.

    But if you noticed, the antibiotics that appear to work best against Lyme are those few that also have an effect against certain parasites. Sapi in more recent research also mentioned the use of Ivermectin. In my case, I have never been completely sure of whether I have Lyme or not but coincidence or not Flagyl and Ivermectin have been very effective.


    Introduction


    Lyme disease is caused by the species of bacteria, Borrelia burgdorferi, and is transmitted to humans by a vector ticks, Ixodus scapularis. (1-2) Many investigators, including the University of New Haven Lyme disease research group, focused on identifying novel tick-borne bacteria, viruses and fungal co-infections in ticks or in patients with a tick bite history. (1-2) Despite these efforts and the introduction of novel treatment protocols, there are little improvements in the outcome of some of the Lyme patients.
    Can species other than bacteria, virus or fungus be responsible for these chronic problems found in Lyme patients? It has been proposed that certain parasites could also be a factor in Lyme disease. European doctors have already incorporated Ivermectin, an antihelminth drug, into their Lyme disease protocol with surprising success. Ivermectin is well known for its effectiveness against filarial nematode infections and is often used by veterinarians to eradicate parasitic infections. (3)
    Can Lyme disease patients have filarial nematode co-infection and can they acquire this infection from ticks? The only evidence reported of filarial worm presence in ticks was from a study by Burgdorferi’ in 1984 where thirty microfilarial worms (species not identified) were found in one adult Ixodis dammini tick in Shelter Island, NY. (4) Black flies have already been identified as vectors of filarial nematodes. (5)Interestingly, ticks can also be used as an in vitro experimental vector system to study the transmission of filarial nematodes and it was shown that the infected nymphal stage could transmit the filarial worms. (6) If filarial nematodes could be a tick-borne co-infection of Lyme disease patients, their eradication would require additional treatments using specific filaricidal drugs, which could explain why standard antibiotic based protocols often fail in some chronic Lyme disease cases. (7)
    Preliminary research data on the potential presence of filarial nematodes in ticks from the University of New Haven research group, suggested that Ixodes tick could harbor filarial nematode DNA sequence and these sequences have high similarity to one of the filarial nematode species called Onchocerca (Presented at ILADS conference on October 29th, 2009 and at the University of New Haven Lyme Disease Conference on May 8th 2010.)
    Filariasis infects more than one hundred and twenty million men, women, and children throughout the world (8). There are a number of nematode species that use mosquitoes as their vectors, causing different lymphatic filariasis infections. Onchocerca volvulus, for example, is responsible for river blindness.(9) However, it is very possible that the species we have found in deer tick is a novel Onchocerca species due to that there are only being partial similar to known Onchocerca species. A phylogenetic approach is being used now to determine the exact filarial genus and species similarity.
    Identification of this potential novel tick-borne pathogen could help to design more specific tests and treatment for patients with a tick bite history and could provide a novel therapeutic target for physicians to explore for those chronically ill Lyme disease patients.
    This study is supported by the Turn the Corner Foundation to E.S.



    1. Krause, P.J. et al. 1996. Concurrent Lyme disease and Babesiosis: Evidence for increased severity and duration of illness. JAMA; 275: 1657-1660.
    2. Adelson, M.E. et al. 2004. Prevalence of Borrelia burgdorferi, Bartonella spp., Babesia microti, and Anaplasma phagocytophila in Ixodes scapularis Ticks Collected in Northern New Jersey. J. Clin. Microbiol; June 1, 2004. 42(6): 2799 - 2801.
    3. Mullen, G. & Durden L. 2009. Veterinary Importance. Med. Vet. Entomol; Academic Press. 2nd Ed. 263.
    4. Beaver, P.C. and Burgdorferi W. 1984. A microfilaria of exceptional size from the Ixodid tick, Ixodes dammini from Shelter Island New York. J. Parasitol; 70: 963-966.
    5. Walsh E. 1983. Sampling simuliid black flies. Pest and Vector Management in the Tropics: 93-99.
    6. Olmeda-Garcia A.S. & Rodriguez J.A. 1994. Stage specific development of filarial nematodes in vector ticks, J. Helminthol; 68, 231-235.
    7. Stricker, R.B. 2007. Counterpoint: long-term antibiotic therapy improves persistent symptoms associated with Lyme disease. Clin Infect. Dis; 45(2):149-157.
    8. Rajan, T.V. 1990. Molecular biology of human lymphatic filariasis. Exp. Parasitol; 70: 500-503.
    9.Morales-Hojas, R., Cheke, R.A. & R.J. Post. 2007. A preliminary analysis of the population genetics and molecular phylogenetics of Onchocerca volvulus (Nematoda: Filarioidea) using nuclear ribosomal second internal transcribed spacer sequences. Mem Inst Oswaldo Cruz. Nov; 102(7): 879-882.

    http://www.lyme.no/index.php/gjesteskribenter/335-eva-sapi-phd
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  15. sianrecovery

    sianrecovery Senior Member

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    Yeah, totally agree - there are no certainties - and we left with our own bodies as a guide. How I yearn for an easy answer sometimes....
  16. baccarat

    baccarat Senior Member

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    In case of Lyme I think it depends on symptoms. People with severe neurological symptoms usually require long term treatment. In my case I never had neurological symptoms, mostly arthritic, skin problems, fatigue etc. and I found short courses repeated over time most effective.
    In my case the effects of flagyl tended to plateau after week or so but taken again after a four to six week break it would still work well and so on. It's probably a matter of trial and error finding out which combination of antibiotics and patterns work best. Pls also consider that with flagyl and tinidazole the likelihood of serious side effects tends to increase with length of use.

    Regarding biofilm I'm not sure any of the remedies usually suggested or read about really work. Enzymes may work a bit but one (me for e.g.) may need every high dosages and are they expensive. Vitamin K2 may have some effect by disrupting the calcium in the biofilm matrix (k2 draws calcium deposits out of soft tissues where biofilm can be) or so i read. I also read some doctors use heavy metal chelators against biofilm but I'm not sure sure which. Certain plants seem to have an anti biofilm effect but I'm not convinced samento and banderol work as well in-vivo. More question marks than answers really.
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  17. Lotus97

    Lotus97 Senior Member

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    That's easier said than done. It seems the herbs Buhner recommends for the immune system are a targeted approach, but just taking supplements to stimulate the immune system could lead to an overactive Th1 response and excessive inflammation. That's why astragalaus is contraindicated for late stage Lyme.

    Another issue that Rich raised is that glutathione depletion could hamper the effectiveness of natural killer cells and CD8 cytotoxic T cells. I've heard from people that Rich thought methylation might be good to do before treating Lyme.
    http://forums.phoenixrising.me/inde...lls-perforin-and-glutathione-depletion.17603/
    Natural killer cells normally kill cells that are infected with viruses. They do this by secreting a substance called perforin, which makes a hole in the cell membrane, and then injecting granzymes, which induce the cell to undergo apoptosis (programmed cell death). The CD8 cytotoxic T cells operate in the same way in terms of their killing mechanism.

    Some years ago, Dr. Kevin Maher, who was in Dr. Nancy Klimas's group, reported that the natural killer cells in PWMEs are low in perforin. It was also found that the CD8 cytoxic T lymphocytes were also low in perforin. This would, of course, inhibit their cytotoxic activity.

    I suggest that this new result is consistent with the mechanism I have proposed for low perforin in ME/CFS. It indicates that the NK cells and CD8 cells are "trying hard" to produce perforin by boosting the transcription of the PRF1 gene to messenger RNA, but the protein synthesis process is at least partially blocked and cannot respond. If glutathione is somewhat depleted in the NK cells and CD8 cells, the protein synthesis process would indeed be partially blocked.

    I continue to propose, as I did in 2007, that other features of the observed immune dysfunction in ME/CFS can also be explained by the GD-MCB hypothesis. These include the shift to Th2 immune response, the elevated RNase-L and formation of the low-molecular-weight RNase-L, the elevated inflammation, the failure of lymphocytes to proliferate when stimulated with mitogens, the reactivation of viruses and intracellular bacteria, and the accumulation of pathogens over time.

    So first, how does the immune system normally respond to viral infections? There are basically four types of responses, listed here in roughly the chronological order in which they normally occur:

    1. Type I interferon (interferons alpha and beta) responses
    2. Natural killer cell response
    3. Virus-specific cytotoxic T lymphocyte (CD-8 "killer" T cell) response.
    4. Antibody response

    Type I interferons are secreted by infected cells, to alert nearby cells, and hopefully prevent them from becoming infected. The Interferon responses include the PKR, the 2,5-OAS RNase-L, and the Mx responses, among others. The PKR response inhibits the synthesis of viral proteins inside host cells. The 2,5-OAS RNase-L response degrades viral RNA inside host cells. The Mx response inhibits viral gene expression and assembly of the virions inside host cells.

    The natural killer cells recognize virally infected cells in which the viruses are attempting to hide from the immune system by shutting off the Class I HLA mechanism that the CD-8 cells use to recognize virally infected cells. If the Class I HLA molecules are not displayed on the cell surface, the NK cell kills the cell.

    The CD-8 killer T cells kill cells that are displaying viral antigens by means of the Class I HLA molecules.

    Antibodies against viral antigens are made by B lymphocytes and plasma cells, and they bind to viruses that are outside the host cells, as when an infection is beginning or when viruses are spreading from one host cell to another.
    This neutralizes the viruses, so that they cannot enter new host cells, and it can also "mark" them for attack by other cells of the immune system, such as macrophages.


    O.K., now what happens to these responses in ME/CFS?

    Well, the Type I interferon responses continue to work, and even though they are intended to be short term responses to hold back the viral infection until the "cavalry" in the form of the CD-8 killer cells arrives, and the CD-8 cells, together with the NK cells, knock out the viral infection, in ME/CFS the interferon responses continue to work overtime (and even become dysregulated in the case of the RNase-L) because the CD-8 killer cells are not able to take over. Sadly, the "cavalry" never arrives, leaving the "civilians" to battle the "Indians" in an ongoing guerrilla war.
    What causes the formation of the dysregulated low-molecular-weight RNase-L molecules? I propose that glutathione depletion is responsible. It activates calpain, and calpain cleaves the normal RNase-L molecules. The cleaved parts join together, forming the unregulated LMW RNase-L.

    Both the NK cells and the CD-8 killer T cells are rendered impotent by their inability to make perforin and granzymes in normal amounts. Furthermore, the CD-8 killer T cells are not able to multiply to outnumber the "bad guys" as they should. Why does this happen? I propose that it is a result of glutathione depletion and depletion of folates, respectively, which are part of the GD-MCB vicious circle mechanism that I believe is at the basis of the pathogenesis of ME/CFS.

    Antibody production continues, and in fact may be increased, because of the shift toward the Th2 immune response in ME/CFS, which favors humoral immunity, i.e. the production of antibodies by B lymphocytes and plasma cells. What causes this shift? Again, I have proposed that glutathione depletion is responsible, in this case in the "naive" T cells.

    So what we have are heightened interferon and antibody responses, but failure of the main "kill" mechanisms. The result is that latent viruses in the body (such as EBV, CMV and HHV6) are able to reactivate, and the immune system continues to fight with the weapons it has left, confining the viruses and keeping the host alive, but not winning the war against the viruses by completely knocking them out or putting them back into latency.

    Now, what about your questions?

    Would interferon treatment work? Well, to some degree, but without the other dysfunctional immune responses to help them, they cannot completely knock out the viruses.

    Why don't PWMEs get colds and flus? I think it's because of the constantly elevated interferon responses. This produces what has been called the "antiviral state." With this going on, it's difficult for a newly introduced virus to get a foothold.

    Does this have anything to do with the elevated cytokines in ME/CFS? Yes. The immune system is well aware that there are enemies inside the perimeter, and it is sounding the alarm, trying to organize the defense. The cells of the immune system are sending chemical messages back and forth to each other in the form of cytokines. However, because the NK cells and the CD-8 cells are impotent, even though the trumpet sounds, they don't respond, because they are not able to, so the messages just keep flying back and forth, unheeded.

    So what's the solution to this problem? How do we win the war? Well, I'm still working on that, but I think that a big part of it will be to restore glutathione, folates and methylation, and that will probably require a methylation protocol.
    Beyond that, because viruses that are well-entrenched have various ways of foiling the immune system, even though the immune system is restored, other measures will likely also be needed. One interesting one is GcMAF, which overcomes one of the strategies used by viruses to foil the immune system, i.e. nagalase. Antivirals are another possibility, especially in view of some success using them, as in Dr. Lerner's experience.

    I hope this is helpful.

    Best regards,

    Rich
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  18. marple

    marple

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    I hear that some people use Boluoke lumbrokinase. The brand name is Boluoke and is supposed to be the best one:

    http://www.canadarna.com/b_buluoke_faq.htm

    As well as working on biofilms I understand that these enzymes are blood thinners. I've heard of people herxing on this, so may need some detox when taking.

    Regards
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  19. sianrecovery

    sianrecovery Senior Member

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    Hey Lotus, that's a great post - I cant make out which bit is you, and which is Rich, but thank you so much for posting it. It is very true to my experience - I did a year on interferon alpha for Hep C - and was much better for years afterwards. Now I don't know if the interferon predicated me to ME, or cured me of it for a few years - I was really was poorly when I started it. I am going to read the whole post until it sinks in.
    I use serepatase. I don't know if it works or not, really. There is a good section on biofilm on the pftu parasite forum, sorry, don't have link to hand. I have just bought an expensive text book on pharmaceutical microbiology with a chapter on biofilm, which while it doesn't have loads of solutions, (or any, to be fair) is good on mechanisms for their formation. If I can get it to scan, will post.
  20. Lotus97

    Lotus97 Senior Member

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    Everything below the link is from Rich, so it's mostly just Rich. I used different fonts to make the distinction. Part of the reason I didn't put his quote in quotes is because the post is more narrow horizontally and so it takes up a lot more space that way. Also, if someone wanted to quote part of my post including what Rich said it would be easier than if it was in quotes. There's actually a lot more information in that thread I linked to. I haven't really read through it myself. I have a lot of links threads and articles saved in a text document which I plan to read at some point. There's just so many aspects to health that I'm not sure what to concentrate on. I started experiencing an abrupt depression about 4 months ago. After a lot of research I seem to have traced it down to inflammatory cytokines as the cause of my depression. It's possible that Lyme is also directly causing my depression by affecting my CNS, but it seems that anything that causes a herx (including probiotics) causes the depression. I supposed I should be thankful since I knew absolutely nothing about cytokines or Th1/Th2 immune responses before this happened. Depression can be a huge motivating factor. I still don't really know what cytokines are. Not even close. But at least I know more than I did a few months ago. I've stopped a lot of my immune system supplements because it seems stimulating the immune system might be counterproductive for me at this point.
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