May 032007

or as I refer to them-Cell Wall Deficient form (CWD).

The CWD form of bacteria, and Lyme CWD, presents a very difficult form to treat (of course Lyme Cyst form is difficult to treat too) with conventional courses of antibiotics. While the specifics of the CWD form are a bit over my head, the idea is that the bacteria cell wall changes (I think into just a peptide wall) and can now move into and live within a human cell. CWD Lyme is another form that the bacteria can change into as a defensive measure to escape antibiotics, etc., and one that is difficult to treat because it typically resides within another cell. There is a treatment option that works well for this, but maybe another day.

What I find most interesting about CWD is that it offers a very compelling explanation for all autoimmune diseases. The reason for this is that when the CWD bacteria is living within a host cell the immune system treats the host’s cell as an invader. Using Multiple Sclerosis as an example the CWD bacteria living within Myelin would trigger an autoimmune response against the infected Myelin. Of course this isn’t something that your read on the National MS site (my searches yielded nothing from them); though it is something being studied. To me this seems like a very reasonable explanation as to why your body just suddenly turns against itself. Of course why would companies be interested in looking into something that can be cured with a couple of years of low-dose, cheap, oral antibiotics. If CWD bacteria is the cause of Multiple Sclerosis than it would explain the different disease courses (different strains of the mystery bacteria, and severity based on how far the disease has spread), and it would also mean that the disease modifying therapies (e.g. Rebif, Avonex, Tysabri, etc.) while suppressing the immune response are actually making the infection work. CWD bacteria as a cause would explain why people respond well to Bee Venom Therapy (BVT) and Low Dose Naltrexone (LDN). “A different bacteria, operating on similar principles, seems to be the organic cause of multiple sclerosis, says Dr. Hoekstra. It’s tentative name–not yet widely accepted by other microbiologists–is Borrelia mylophora, so named because its characteristics seem to resemble those of Borrelia burgdorferi, the bacteria believed responsible for Lyme disease.”ref.

The reason that Lyme may be called the “Great Imitator” is because it isn’t that different than the cause of many autoimmune diseases (e.g. ALS, Multiple Sclerosis, Rheumatoid Arthritis, etc.)

More information on the “Stealth Pathogens”:

  • ALS2Lyme
  • New ideas about the cause, spread and therapy of Lyme Disease
  • Book: Cell Wall Deficient Forms: Stealth Pathogens, Third Edition by Lida H. Mattman PhD. (I’m not interested in the book since it is a technical reference way too complex for me. I think the intro to the book is here) [Also, I think the author was nominated for a Nobel prize for her work on stealth pathogens]
  • New Pathways. Stealth Pathogens are mentioned, but not much said.
Apr 162007

The second doctor visit was a huge disappointment; especially since this one was supposed to be a “Lyme Specialist.” Also, he really enjoyed to hear himself talk, and it frequently involved sports (side note: I could care less about football, hockey, etc.) – I think he said 30-50 words for every word Eriksgirl+me said. He said that he tries to take a middle of the ground position in the “Lyme wars” (my phrase); but it is obvious he falls in the easily tested for and easily treated camp. Some tidbits from this visit:

  • The rash pictures I showed him he wrote off as just a weird rash, and that the rash is not Bartonella (WTF?!). He repeatedly said that the EM rash does not come back, even though he was repeatedly told that we thought it was Bartonella (also, I think there is a strain of Lyme that affects the skin, and the EM rash can come back). He noted on one picture that he was most interested in this one circular “rash”; since that would be more like an EM rash (ignoring the fact that I would have had Lyme for years at that point – but with no clinical history [see below] that might be a little hard). I decided to skip the detail that the “rash” he saw in that one picture was actually a compression mark from my working on the floor assembling an entertainment center.
  • He also wrote off the Bartonella rash because I tested negative for it on a blood test. He views those tests as very accurate. So Bartonella, and other co-infection, tests are accurate, but the tests for Lyme suck. Right. Furthermore, I thought I had read somewhere that the Bartonella test would be more accurate if you sent a tissue sample from the rash area; of course “more accurate” means that the test is not 100% accurate. Of course it is possible a round of antibiotics I took last year took care of the Bartonella since the rash hasn’t returned in quite a while.
  • He completely wrote off the CD-57 test. I can understand not using it as a diagnostic tool for Lyme, but he viewed it as basically worthless. His point was that until they can definitively prove nothing else lowers that value than he won’t use it for anything. I think a more balanced approach to the test would be the best policy, but what do I know.
  • He absolutely could not get over the Multiple Sclerosis diagnosis. He repeatedly commented that if you were diagnosed with MS by spinal tap and lumbar puncture (I was) than you have MS (as opposed to MRI alone). He tried explaining MS, and demylination, to me (did he really think someone treated for MS for 4 years didn’t know what the MS did to the Myelin?!); but it was clear I had a better understanding of MS than he does. Furthermore, the test run on the spinal fluid was testing for Myelin, and I do not think it would be surprising to find Myelin in the spinal fluid when there is any kind of brain infection since the infection would involve brain/spinal tissue.
  • He asked about current symptoms, but never took a clinical history. This borders on negligent. Because of this he never got the history of entering stage 2 and then stage 3/chronic Lyme. He never got an expiation of when I though I got Lyme. Lyme isn’t the flu; when treating a chronic illness I would think that clinical history is very important.
  • I can’t remember how it came up, but I asked about cell-wall-deficient form of Lyme. He said how can a cell live without a wall (true, but it is a different type of wall that exceeds my understanding of cell behavior). Eriksgirl noted about the CWD Lyme living within other cells. He completely wrote that off, and in general knew nothing about L-Form bacteria (including their existance).
  • I think he wanted to write me off completely, and he never said I had Lyme. He had to keep coming back to the C6 Peptide, but I think he wanted to write that off as a false positive too.
  • His treatment philosophy was to “let sleeping dogs lie” (He couldn’t remember the phrase, but tried several variations). I take this to mean that if there are no symptoms then there is no reason to treat. I am more of the opinion that you treat until there are no more herx reactions.
  • He listened to my chest, but never caught the Mitral Valve prolapse (I’m not sure he listened to my heart, so who knows what he was listening to). He also never checked to see if the Lyme had affected other organs (e.g. liver, spleen). Overall, it was a shoddy exam.
  • In the end I left with a 30 day prescription for 100mg Doxycycline, and if I had problems at the end of the 30 days he would give me another 30 days. I don’t know what would be done after 60 days. When talking on the phone he had said 4 months of IV antibiotics. I can only assume he thought all my problems were MS, and thus not really worth treating me.

Overall, this was like seeing the guy who graduated last in his class from medical school. Of course this doctor is the one who recommended MDLab which got my diagnosis so he isn’t all that bad. I’m sure Eriksgirl will have more to say too.


Apr 122007

I have visited with the first of the Lyme doctors. Overall it went well, and I liked him (and he came off as extremely flexible with treatment). He could feel that I have an inflamed liver and spleen. He also listened to my heart and I have a Mitral Valve prolapse (apparently there is a click after a beat that can be heard). He also looked at my eyes and noted that they looked a little inflamed, and the optic nerve looked a little fuzzy at one of the edges. No surprise since I have been having a problem with my distance vision. He also noted that I am having a reaction when pulling up on my toes that my foot quivers, but I can’t remember what he called that neurological reaction.

His treatment is to start with a month of Ceftin, and then proceed with IV Rosephin(?) if I’m not better. After looking up Ceftin and Rosephin they are both Cephalosporins. I am sure they can be effective against the spirochete, but I have concerns that they would mostly throw more of the Lyme into a cell-wall-deficient (CWD), L-Form, bacteria state (more on CWD form later). This would then be much harder to treat, and there are concerns that the CWD form of Lyme causes the most disability. Unfortunately, I did the antibiotic research after getting home so I was unable to ask this in the office. The other concern is that he is not necessarily a Lyme specialist, though he does treat a lot of Lyme. In fact he was incorrectly diagnosed with Multiple Sclerosis at one point, but, like me, has Lyme. A positive was that he immediately recognized the Bartonella rash, and suspects that I probably have other co-infections that would have to be treated. A negative was that I was left with the impression that he treats to get you symptom free (which is not necessarily Lyme free), and will treat again if/when symptoms occur.