The Marshall Protocol Study Site > ABOUT THE MARSHALL PROTOCOL > General Information and FAQs > Post Treatment Lyme Disease Syndrome
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The Marshall Protocol Study Site > ABOUT THE MARSHALL PROTOCOL > General Information and FAQs > Post Treatment Lyme Disease Syndrome |
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Aussie Barb Research Team 
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(filelink) Post Treatment Lyme Disease Syndrome  Post Treatment Lyme Disease Syndrome (PTLDS) commonly known as chronic Lyme only occurs in a small fraction of the people who are bitten by ticks, those whose immune system cannot withstand the sudden challenge. I have no doubt that borrelia L-forms are transmitted during sexual contact, and are probably spread by immunizations and blood transfusion. These bacteria are too small to be filtered during the 'purification' processes used in pharmaceutical manufacturing procedures. Vectors are not the only method of transmission, in fact there are more cases where a vector cannot be implicated than where there is evidence of a clear bite. We have shown how the susceptibility to Th1 inflammatory diseases most probably accumulates over a lifetime, and many of the elements of susceptibility seem to occur in the pre-natal or neo-natal timeframes. It is thus misleading to focus on the tickbite as being "the cause" of the chronic disease. And treating the patients for tickbite pathogens does not return them to 'health'. Only when the underlying innate immune system overload is addressed, by the MP, does the Borrelia titre start to disappear, along with the signs of other pathogens. Susan explained this very well during her talk about her own recovery from chronic Lyme, in the "recovery" panel session at our 2006 LAX conference. It doesn't have to be Borrelia which pushes the patient over the cliff, it can be Rickettsia, Mycobacteria, and no doubt many other pathogens yet to be identified ('TBD') Dr. Andy Wright has found pleomorphic bacteria (in the blood of his patients), but they are not necessarily Borrelia Burgdorferi. It is hard to guess how much of the DNA of the pleomorphs maps to Borrelia. Indeed, one of Andy's patients had the same-looking pleomorphs, but did not flourescent-stain at all for Borrelia. Borrelia, in the intracellular coccoid form, does not have a discernible 'natural life cycle.' The host phagocytic cells do regenerate due to apoptosis (programmed cell death) but there is now abundant evidence that the bacteria actually cause the phagocytes to live longer than the average 40 days (so as to not have to move-home so often, I guess  ).The reason that we have had success with the MP is that we realized early on that there were many species involved in Sarcoidosis. Borrelia, Propionibacteria, Mycobacteria and Rickettsia have all been isolated with PCR from sarc patients. So we had to design a therapy based not on the microscopic observations, but on the way the bacteria exert their damage upon the immune system. It turned out that all Th1 diseases seem to have a similar multi-family mix of pathogens. We are almost certainly dealing with inter-species mutants. The pleomorphism is the key. There are a number of species, including Borrelia, which can change to CWD, depending upon the environment they are in. Dr Andy Wright can culture the Spirochetes (characteristic of Lyme) right at the very edge of the slides on which he films the tubule-protected, the cyst, and the coccoid forms. The spirochete seems to be the adaptation for the harshest environments, while elements of the spirochete, like the flagellin, are not expressed (manufactured) when the microbe is in the CWD state. Treponema can also form a spirochete, and, surprisingly, I have found that Benicar acts as an antibacterial for Treponema Denticola, the form of Treponema found in CWD form in the mouth and gums (in 'biofilms,' mainly). IMO, Borrelia is a better term than 'Lyme.' Borrelia is a potent pathogen. But it is not a single entity. The genome of B.Burgorferi, for example, has a chromosome, and between 17-21 plasmids (depending on the study). The plasmids contain almost as much DNA as the chromosome, and are self-replicating and capable of horizontal DNA-transfer to other other pathogenic species. So B.b is a moving target, not a single entity. Similarly Baciillus anthracis has two plasmids, one of which contains the genes by which it evades phagocytosis. Rickettsia has one plasmid. These species can share their plasmids, share their ribosomes, share their toxins, and in a chronic disease they have plenty of time to figure out how to share the very best features of each species. So from a scientific perspective, it is statistically unlikely that any one pathogen is the primary pathogen in these chronic diseases. By using the term "Lyme" one tends to think of a primary pathogen, and a vector-borne pathogen at that, and this tends to blind one to the complexity (and sophistication) of the antibiotic-resistant pathogens we are dealing with in Th1 disease. There are bacteria with bigger genomes than Borrelia, and certainly there are more dangerous species, but I haven't seen any with a greater number of plasmids. The potential for horizontal DNA transfer to other pathogens is what makes Borrelia a 'bad guy,' in my opinion. But there is no indication (at this point) that Borrelia, acting on its own, can evade phagocytosis. A strong immune system will kill it. But an immune system weakened by other chronic Th1 pathogens cannot deal with the challenge Borrelia poses. The longer one is infected the higher the intensity of mutation and the more chance it will be visible in DNA testing for the HLA haplotypes. The HLA haplotypes are more likely to be the result of an infection than the cause. Again, I continue to maintain that Borrelia burgdorferii is not the primary cause of Chronic Lyme symptomology. Chronic disease is due to a mixture of pathogens, accumulated over a lifetime. This accumulation makes one more susceptible to subsequent viral or bacterial infection, including Tuberculosis and HIV. All Chronic-Lyme is CWD Further, I am sure that Borrelia is not the primary pathogen, as it is present in not all Th1 patients. Andy (Wright) has some who are Borrelia-negative, and several Sarc studies have shown varying percentages with Borrelia PCR. The issue of testing is very complex because you are dealing with imperfect tests, and pleomorphic organisms. Another key point is that Dr Garth Nicholson's data shows several species of pathogens are common, but not universal, throughout his GWS and CFS cohorts. and: Folk commonly confuse spirochetes with Borrelia. All that they found in the PCR study you linked to was DNA. http://www.anapsid.org/lyme/bach.html In fact, it would have been RNA, since it was dicovered by PCR techniques. And that RNA would more likely have come from L-forms than spirochetes. FYI, intracellular Mycobacterium tuberculosis bacteria have also been found in semen. The basic concept the story at your link is trying to convey is correct, but their understanding of pathogenic science is minimal, to say the least Dr. Trevor Marshall, Ph. ======================== Please see: Dr Marshall's presentation at "30th Anniversary of Lyme" Download RealPlayer - Free Related FAQ: Will the Marshall Protocol treat co-infections? |
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Aussie Barb Research Team
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(filelink) Post Treatment Lyme Disease is successfully treated with the Marshall Protocol: Dody's progress: Lyme: posting current status joannem progress: Lyme CEB success with MP Teen with Lyme Anne Scott progress: Lyme, babesia joannem progress: Lyme Markt's progress: Vertigo, fatigue, skin lesions, tinnitis, brain fog Jeannine R.N.: CFS FM Lyme Morgellons: I missed me and now I am back. Slowly like a beautiful butterfly. Ceredwyn: Ph3: Lyme: greatest gains in the emotional/cognitive area Dody: Lyme: quality of the life. camping activities. MaBear: Lyme: great improvement I have made on the MP. Corey K. ph1 + ph3 update: 13yo son of Teri K: Lyme ADD w/cardiac symptoms: enjoying his new-found energy and health Izzy: on a break: noting overall improvements: pain, energy, thinking, BP, eyes. BenK: Lyme: 17 months on MP & never better. Interview with Ken L. - Post Treatment Lyme Disease Syndrome (PTLDS) Interview with Melinda Stiles – Lyme, Irritable bowel syndrome/colitis, radiculitis (inflammation of the nerve roots) Interview with Robyn Russell - Lyme, myoclonus Interview with Sue Andorn - Lyme, babesia Interview with P. Bear R.N. - chronic borreliosis, multiple chemical sensitivities, chronic spinal inflammation, peripheral neuropathy joannem: Lyme: Noting multiple improvements Jasmine: Lyme: multiple improvements Mike27: Lyme: Young man completes Law School using the MP!!! Sue A: Lyme and bartonella gone....vision improved davbrkr Dave: Lyme 40+ yrs: 1 month-17 days on Phase I afetzer: Lyme: early improvements Cold Feet: Lyme: back to work again! tadpole: Borreliosis EM: improvements: alopecia, brain fog, strength. DrVikki: Lyme co-infec: great gall bladder test results Jay4me: Lyme, FM, CFS: improvements. Staph mass gone hellohope: Rickettsia, CFS: from disabled to able. joannem: Lyme / FM noticable changes for the good TeriK: Sarc / Lyme: I am so much better just after the first year! Matt Happy New Year 2007 Lori Lyme includes tale of woe re IV Treatment Pre-MP Lori - Lyme neuro immunopathology and sensation returning: LH1953/Lori: Lori: w C LYME: MCS IC Asthma ... How grateful am I. DrVikki Lyme co-infec: Phase 3 update: social / cognitive improvements Joyce Waterhouse: CFS/FM/Lyme for 18 years: neurological improvements. Marie's Progress - Lyme Desert Marie Lyme so much better after 8 months Melinda Progress Report/Lyme 2 yrs end of Aug06 Melinda LYME: The MP has given me my life back. Aunt Diana Lyme AuntDiana: LYME: MP for 8 months. I am definitely going in the right direction. Linda Jones - Lyme- many improvements Matt 14 Lyme symptoms/record of progress Lonestartick: Late-stage Lyme patient with co-infections - MP is the only treatment that has ever handled all of my infections. Lonestartick: neuro-borreliosis (chronic, late-stage Lyme disease) turned the corner.. P.Bear R.N.: LYME: MCS: There is more than a light at the end of the tunnel... livitup/ Linda: Lyme: improvements.. DrVikki:- going out in the world DrVikki: LYME with co-infection. thrilled with the MP Debbie PCRLyme: improvements Semper Fi LYME: I feel great 100%. Jolbell The MP has been a miracle for me!! Chronic Borreliosis & Bartonella Physical & emotional improvements GeorgeinRollaMO: Borreliosis does respond to the Marshall Protocol safely!!! GeorgeinRollaMO: Libido Marianne L. walking, balance, fine motor skills, swallowing, talking, strength, weight: Improvements.... -I'm reading from your posts that you (and your doctor) are not sure your body can recover from the damage that has been done over the course of your illness and the 12 years of antibiotic treatments you have already been through. That can't be an easy place to be in and I have not faced as long a history as you, so I can't say I know how you feel from my own experience. But I also have been diagnosed with Lyme Disease and much of my symptoms relate to my CNS (neuro stuff). And I have read over and over on the lymenet.org about relapses and how the neuro stuff just snowballs with each relapse. It was very alarming to consider that my future could be that bleak. but I am not afraid anymore and I'd like to share some of why with you in hopes that you will be less concerned and more hopeful too. {Hey, take note: I'm not a medical person, but I'm a very interested patient! So, please read my following opinions with that in mind.}  It is true that many people seem to be unable to recover from damage to not only the HPA, but also lungs, joints, eyes and other parts of their bodies during chronic disease. But I am not worried about these issues on the MP for some very specific reasons. (1) there is scientific evidence, published over the last 100 years, that the stealth pathogens the MP is targeting exist in chronic disease and are even infecting our stem cells. This prevents our bodies from having the capacity to heal themselves. (2) by lowering inflammation using the Benicar, these stealth pathogens will no longer be hidden from my immune system and therefore will be dealt with by my own immune system during my treatment. (3) by inhibiting key protein synthesis by the stealth bacteria using the Minocycline and other bacteriostatic antibiotics, these stealth pathogens will be at an even greater disadvantage against my immune system and therefore will be slowly, but surely eliminated. (4) we know that the co-infections (like babesiosis and boreolosis) are not the root cause of our body's failure to heal themselves and our immune systems will only be able to truly eradicate them once the stealth pathogens are cleared from our stem cells, immune system cells, etc.. I wonder if some of the symptoms that LLMDs attribute to the TBD co-infections are actually effects on our endocrine system from the imbalances created from excessive 1,25D (caused by the stealth pathogen's activities). This extra 1,25D binds to hormone receptors and interferes with everything from adrenals to thyroid to thymus to pituitary, and so on it goes. I do not fear "irreparable damage" because I have faith in my own body's ability to heal itself ... once it is not longer crippled by these stealth infections. After spending the past 8 months of reading individual progress reports that confirm that these processes of healing are happening in real people's experiences, I am convinced that our well-meaning doctors who are fearful of unrecoverable damage do not understand the power of our own bodies to heal. Short of a miracle, they probably have never seen what a patient's body can do to heal itself ... once their body is free from these stealth infections that our doctors have no way to identify or treat using standard practices. So, while it may feel like the co-infections are getting the upper hand and just causing you a great deal of trouble right now, those on the MP have seen how persistence towards the goal of dealing with the true root cause will brings them into a place of true healing that lasts. Therefore the MP only wants to offer methods that will help with the symptoms without stopping the underlying work of getting our own immune systems restored. The MP folks have also seen how adding antimicrobials (the big guns, like high dose garlic, or even arteminisin) to a person after they have started the Benicar can cause intolerable symptoms that may put the person off from continuing the MP at all. They want to help us avoid all that pain and suffering. I think the hardest thing to get my brain around is that the MP medications are not being taken to chemically "kill" anything. They are only there to level the playing field for my immune system to take over. Antimicrobials create an environment where the pathogens shift into hiding. But, we need the bacteria to sense that the 'coast is clear' so they come out of hiding where our immune system can deal with them, therefore we avoid the antimicrobials on the protocol. I also find it difficult to be patient with allowing my own body to reset and rebalance itself. I want to be better and I want it now! No more weird skin stuff, no more hair loss, no more cognitive struggles! I'm sure you can relate to that! However, my intuition says to me that it is wiser and I will be stronger if I allow my body to rebalance on it's own without propping it up with supplements. Well, there I go again, my thoughts ran away with my fingers... Maybe something in this long note to you will be of some benefit.  Chronic Lyme is tough. Weaning steriods is tough. The MP is tough. Good thing you have what it takes (motivation), and you have people that are going through the same things (me included) who care and who will try to encourage you along the way. May your vision guide you through! ~JoyfulPatient 1 is a 14-year-old boy who has been ill with chronic Lyme Disease (with Rickettsial and Chlamydial coinfections) since June 2004. He suffered from chronic severe headaches, fatigue, a tourette-like tic occurring every few minutes, blurred/double vision, photophobia, nausea, vertigo, insomnia and visual tracking problems making him unable to read or write. He began the MP in September 2005 and has had significant improvement in all his symptoms, including disappearance of his tic and visual problems. He is now able to resume many of his previous activities and continues to improve on the protocol. Patient 2 is a 58-year-old woman who was diagnosed with Lyme disease in 1999. She had been treated with oral doxycycline in 1999 and 2001. She relapsed after having begun extra vitamin D supplements and increasing sun exposure. Many symptoms have greatly improved in the 29 months since she began the MP, including muscle pain, stiffness and weakness, fatigue, headaches, panic attacks, colitis attacks, nausea, bloating, indigestion and insomnia. She reports that on the MP, her low back pain has gone from a level 8 to a level 1 on a 10-point scale (attributed to bulging discs at L4 and L5 on MRI), despite decreasing her use of pain medication. Patient 3 is a 55-year-old female who was diagnosed with rheumatoid arthritis 10 years ago. She had previously been on high dose antibiotics (mostly oral, with some IV and IM) for 6 years prior to the MP and had minimal improvement. Her condition worsened while taking vitamin D prior to the MP (800 to 2400 IU daily over a 2 year period). She also reports reduced pain medication use, significantly greater strength and less pain in her hands and upper body and less fatigue after her 29 months on the MP. Recently, her ANA (anti nuclear antibody) tested negative, after having all 17 prior tests showing elevated levels (usually 1:640 or more). Patient 4 is a 42-year-old man diagnosed with chronic fatigue syndrome and fibromyalgia. His illness began after he became ill with infectious mononucleosis at the age of 22. Prior to beginning the MP, he could only work 2 or 3 days per week and had adverse consequences for days following exercise. He began the MP in March of 2005, and since then he has had 90-100% resolution of his headaches, light sensitivity, tinnitus, sinus congestion, sore throat, unrefreshing sleep, swelling of fingers and feet, fibromyalgia and heart palpitations. He has had 70-75% resolution of brain fog, fatigue and lymph node swelling. He still requires injections of IgG due to a deficiency of IgG3, but the injection interval has increased from an average of 14 days to more than 24 days since commencing the MP. After 22 months on the MP, he reports feeling markedly better than anytime in the last 20 years and is able to work full time and perform strenuous physical activity. Patient 5 is a 43-year-old man who had psoriasis since the age of 7, chronic insomnia beginning at the age of 26 and sarcoidosis, diagnosed at the age of 36. His wife had been diagnosed with sarcoidosis several years before. This is in accord with the familial tendency that has been observed among Th1 diseases due to spread of the bacteria among family members. The psoriasis had been treated with a variety of treatments, including PUVA, steroids and fish liver oil unsuccessfully for many years. In contrast, while on the MP, the psoriasis went from 70% coverage of the skin to 1%. The insomnia resolved completely soon after the Benicar was begun in 2003. The patient had suffered from chronic kidney stones, which ceased when he began the protocol. Two courses of prednisone left him worse afterwards. Treatment with the MP has resulted in more than 95% resolution of his symptoms of sarcoidosis (coughing, fatigue, sinusitis, memory problems, muscle aches etc…), and his chest x-ray is now normal as he continues his fourth year of the MP. Patient 6 is a 48-year-old woman who was diagnosed with sarcoidosis in 1991. In 1998, she developed seasonal affective disorder (SAD) and began taking anti-depressants every winter to treat the depression. After beginning the MP in October of 2006, she found she was not depressed and did not need her anti-depressant. The combination of 40 mg Benicar every 6 hours and avoiding vitamin D was sufficient to relieve her SAD (she wears a zinc oxide-containing sunscreen to help minimize vitamin D production and NoIR sunglasses). She has only been on the MP for a few months, but finds her fatigue has significantly lessened. Patient 7 is a 61-year-old woman with presumed sarcoidosis (based on CT scan), with unilateral tibial neuropathy presenting with altered sensation, severe foot atrophy and calf muscle cramps. So far on the MP, she has regained 95% of her muscle tone, strength and mobility in her foot and leg. Her fatigue, depression and cutaneous lesions also resolved. Two other examples of severe neurosarcoidosis showing marked improvement on the MP are described elsewhere (3). Patient 8 is a 67 year-old man who has had sarcoidosis of multiple organs, including the heart and lungs, for over 20 years. He had a pacemaker implanted in 1995 and has undergone two quadruple bypasses. He had been in atrial fibrillation over 90% of the time in the two years prior to the MP. In 2005, after 3 months of treatment with the MP, with no other changes in medication, his atrial fibrillation disappeared and has not returned in the following 20 months. His chest x-rays have improved significantly and his shortness of breath and fatigue have also improved as he continues on the MP. Patient 9 is a 51-year-old woman who has been diagnosed with numerous conditions over many years of being ill. Since beginning the Marshall Protocol, her symptoms of Lyme disease (muscle/joint pain, fatigue, cognitive problems) and her Sjogren’s syndrome and Raynaud’s symptoms have significantly improved. Her myasthenia gravis, diabetes insipidus, gastroesophageal reflux disease, Barrett's esophagus, interstitial cystitis, allergies, multiple chemical sensitivity, and migraines have greatly improved and her chronic yeast infections (vaginal and esophageal) have completely resolved. She can now read, use the computer, drive a car and walk without a cane, things she could not do before the MP. Last edited on Mon Sep 15th, 2008 15:01 by Aussie Barb |
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Aussie Barb Research Team
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(filelink) Pertinent FAQs Is pulsed minocycline alone effective? Should I treat my co-infection before I start the MP? Do the D tests rule out Babesia? Will the MP treat other co-infections? Will the MP treat paresthesia and neuropathy? Topic Could a parasite hinder effectiveness of MP on Lyme? CELL WALL DEFICIENT BACTERIA AND THE MARSHALL PROTOCOL A Simple Explanation The Marshall Protocol -- simple explanations for patients and physicians Dr Marshall's presentation at "30th Anniversary of Lyme" Download RealPlayer - Free |
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Foundation Staff . 
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Lyme disease Lyme and borreliosis are both caused by the CWD bacteria called a borrelia. Lyme, by definition of the US's CDC (Center for Disease Control), is caused by the borrelia that was found around Old Lyme and Lyme, Conn. It was named borrelia burgdorferi after the man who discovered it, Dr. Willy Burgdorfi, Phd, a micro-biologist. It was further named borrelia burgdorferi sensu stricto, a sub-species of the family of borrelia, Bb sensu lato. There are at least 82 strains of Bb sensu stricto in the US. There are over 100 strains of BB sensu lato in the US alone....I understand over 300 worldwide. The medical name should have been used for the disease, borreliosis. But it sure is easier to say Lyme, and the media loved that name for the "new" disease that was "discovered" by two mothers in about 1975, but which really goes back to 1895 or so in the US, and back further in Europe. Borreliosis is the medical name for a disease in which any borrelia is involved. The world outside of the US uses borreliosis. The folks on the East Coast particularly like to use, and almost insist on using the term "Lyme" for all borrelioses. "...ses" is the plural. The CDC has within the last two years isolated and named another borreliosis, STARI, caused by the borrelia lonestari....which has the same symptoms as the earlier Lyme. More researchers and clinicians within the US are starting to use the term "Lyme borreliosis", because in their minds, I guess, they realize that the greater term "borreliosis" is the better... it can then be divided into the various strains as found. And it is sometimes said as Lyme borreliosis in the rest of the world. I think that when the term Lyme is used, they are referring to the symptoms that everyone has come to learn rather than a particular strain of disease of a particular strain of bacteria. I am a strong advocate of using borreliosis, as you may have been able to tell. Influenza is a good analogy. One can have Hong Kong A flu, Hong Kong B flu, etc. The problem would be, but does not exist for influenza, if the test were set up for only Hong Kong B flu, and denying the existance of any other flu if one did not pass the test for HK B. The test criteria as setup is designed only for the one strain of borrelia, Bb sensu stricto. The big fallback for the CDC is their saying that that is the only strain of disease that "is proven" for Lyme. And in a sense of strict terminology, they are correct. But there are many other strains of borrelia not yet isolated, cultivated, and "proven" to cause a disease. However, borrelia do not like to be grown outside of a living animal. You can have borreliosis and not have Lyme. If you have Lyme, you have borreliosis. Don't forget, that borrelia have been found in the gut of mosquitoes, fleas, sandflies and horseflies... and some others that I cannot remember. Don't get locked into thinking that borrelia will be vectored by only ticks. Again, the word "proven" is used. Borreliosis will, and does, respond to the Marshall Protocol...safely!!! Provided that one does THE Marshall Protocol, and not something else, such as, even using the same meds, but in a different way. George Rollo  LYME/BORRELIOSISlink |
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Aussie Barb Research Team
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(filelink) Fibromyalgia masks as PTLDS George wrote: Dr. Charles Ray Jones, a noted pediatric LLMD from Conn, who has treated thousands, has said in a tape he made, that fibromyalgia is really Lyme disease. My LLMD has said to me that he thinks fibro is really Lyme, also, or, as he likes to call it, borreliosis. I do not know that one needs to know if it is Lyme or fibro if one is doing the MP, but perhaps for personal satisfaction of knowing a reason for the fibro. The orthodox medical community says that fibro is of unknown cause, as you probably know already. As mentioned previously, the premier labs for testing is Igenex for the WB test, which looks for the antibodies (which have some problems with being produced, such as you may not have any spirochetes in your body for antibodies to be produced against, but have cyst and/or coccoid forms, and you will have the disease), and, the Bowen RIBb test which looks for the borrelia burgdorferi bacteria itself, spirochete and cyst form. I do not know about the coccoid form. The Bowen RIBb test also looks for two or three other pathogens at the same time. The Bowen also gives a relative quantitative measure of the number of bacteria by the dilution ratio. The last feature is handy to see an objective improvement while doing the MP, and may assist one to decide an end point in doing the MP. But endpoint is only for the borrelia CWD. You may have other CWD besides borrelia that may be causing the Th1 inflammation. When I have been feeling real lousy from herxing, and might wonder if it is all worth the trouble, I now have the objective dilution ratio for me to remember is going down… for the very first time. The AP (antibiotic protocol) did not move my dilution ratio from the highest, 128. After six and a half months of mino on the MP, my Bowen was 32. I am going to do another Bowen in August. Trevor has said that someone has gone from Positive to Negative on Bowen RIBb tests, after doing the MP. Technically, if you really want to know if you have “Lyme disease”, you need to do a next to worthless ELISA test, followed by a Western Blot… so says the CDC, and which criteria is followed by most other countries. EXCEPT, in Germany, you need only two out of nine titers on a WB for one to be reported as having “ borreliosis”. Since the Bowen RIBb looks for borrelia burgdorferi, IMO, it cannot tell you for a certainty that you have the Bb that causes Lyme disease or not. But it will find Bb if they are present. Lyme disease is caused by borrelia burgdorferi senso stricto, which is but one subspecies of the greater family, borrelia burgdorferi sensu lato. Bb senso stricto is what the CDC found to be causing the illness around Lyme and Old Lyme, Conn, and is what the CDC is calling Lyme disease. You can be feeling like pure misery with all kinds of symptoms but if you do not present with the results of an ELISA and WB tests for the Bb sensu stricto, the CDC does NOT want to know about you. They only want to know about this very select case….for surveillance purposes. This is part of the big controversy about this illness. (Oh, you can fulfill the criteria if you have the EM.) I understand that there are 82 known strains of Bb sensu stricto, and over 100 strains of Bb sensu lato in the U.S. alone. And that does not include the other known varieties of borrelia. Don’t forget the New Jersey researchers have found out that borrelia bacteria mate, and share genetic material, so that new strains are being formed quicker than tests can be devised for the new strain. I personally like the Bowen test just because it does as dsiebenh says, “and tends to report positive results for many specemins.” Those specimen are Bb if Positive, but may not be the Bb sensu stricto. I know that I failed to test for Lyme disease on a WB test per CDC criteria, but I did have some bands for borrelia. I also tested Positive for Bb on a Bowen RIBb test, at the highest dilution ratio of 128 to begin with. I have borreliosis, the better name for the illness… by far!!! It is the medical name if one has borrelia in one’s body, and has illness. This whole thing can be compared to designing the test to find Hong Kong B flu only, and, if you do not test for Hong Kong B flu, telling you, you do not have flu. Yet, one may know full well that one has flu by the symptoms. U. S. Public Law 107-116, signed as law in January 2002, told the CDC to correct this discrepancy, and the CDC has not done one iota so far in the over three years since the law went into effect, except to make disparaging remarks about “certain labs” via their bulletin system. Guess which labs those are? Forget “Lyme”. Think and say, “borreliosis” pronounced bor rel e o sis For some reason that I cannot understand, folks from the East Coast insist on the saying, Lyme disease, instead of "borreliosis". They would be better off using the medical name, IMO. It would then include all of those cases that are falling through the cracks in the CDC criteria for surveillance purposes, and in the very least, we would have much better statistics of the extent of the illness. Does it make a difference if you are sick with the flu to know whether which flu you have? George Rollo ..... I forgot to mention that there is also another illness now recognized by the CDC within the last two years...STARI Disease, which the CDC says is caused by borrelia lonestari, which is supposed to have "lyme-like" symptoms. STARI is for Southern Tick Associated Rash Illness, and is supposed to mainly in the S.E. U. S. Two researchers in Missouri, Dr. Ed Masters, M.D., a clinician specializing in tick-borne diseases, and, Dr. Greg McDonald, Phd, a microbiologist, who was affiliated with UMissouri-Columbia, both have found evidence that there is a third borrelia that is causing illness, which has not been recognized by the CDC. Curiously, a CDC website that I found in the beginning of April 2005 said that there are fifteen borrelioses. Sorry, I did not bookmark the site. I found it under borreliosis, I believe. I think that what was found around Lyme and Old Lyme, Conn is just the tip of the borreliosis iceberg. I think that many more will be found as the tests are developed and the effort is made to look for ALL of the other borrelioses. IMO, knowing is good for encouraging one doing the MP, and, for the other very good purposes that Hrts has mentioned. George ................. |
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Foundation Staff .
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LYME/BORRELIOSISlink Testing Note: Bowen Lab closed 12-22-07 when its director retired. Many Lyme disease patients have been diagnosed with Lyme using the Q-RIBb direct detection test at the Bowen Research and Training Institute in Palm Harbor, Florida. The lab closed on December 22. The director and president, Dr. JoAnne Whitaker, has retired. People are being referred to The Central Florida Research Lab, a new laboratory at 245 N. Seminole Ave., Lake Alfred, FL 33850, phone 863-956-3538. They are working on a new Lyme disease test that should be available soon. The Q-RIBb direct detection test is no longer available. Dr. Whitaker has had Lyme disease since childhood and has worked well past normal retirement age to help Lyme disease victims. Her dedication has enabled thousands of Lyme disease patients to get diagnosed and treated. We are very grateful for her dedication and accomplishments. As reported in the Greater Kansas City Lyme Disease Asso's January '07 Newsletter. =================================== The consensus within the Lyme community seems to be that the Lyme ELISA test is worthless, Western Blot tests from most labs are questionable, and the "gold standard" is the IGM and IGG Western Blot test from Igenex Labs (http://www.igenex.com). There is also a lot of interest in the Flourescent Microscopy tests done by Bowen Labs (http://www.bowen.org), but this test tends to be questioned by the medical establishment, as it is not yet approved by the FDA, not covered by insurance, and tends to report positive results for many specemins. dsiebenh  ....................................................................... GeorgeinRollaMO writes: "If you will go to http://www.bowen.org, you can read/make contact with the Bowen Research and Training Laboratory yourself. I believe that I have read that they have accepted samples from Europe. You will need to ship the sample Priority Overnight Express. It is a long flight from Melbourne, but I would think it is a do-able, if packaged correctly. Not inexpensive! But a person can throw away a lot of money on this disease if one does not get a good diagnosis. May I offer a suggestion? Stop using the term "Lyme disease". Use "borreliosis" instead. The bacteria that cause Lyme disease are borrelia, therefore, "borreliosis" is a more correct medical terminology, though it is not as easily said. The word is pronounced bor rel e o sis. Well, in my part of the world. Lyme disease does exist. However, it is so narrowly defined that too many people fall through the cracks of the definition. Too many medical doctors and insurances take the very strict definiton for surveillance purposes as the definition for diagnosis and treatment... and not give treatment, based upon the fraudulent criteria, and rather poor tests that it is based upon. Please read the excellent report by Pamela Weintraub on the CDC Dearborn Conference that set up the criteria... http://www.astralgia.com/magazine/bitterfeud.htm Our US Congress passed a law in January 2002, Public Law 107-116, that told the CDC to get their act together and correct things based upon a Senate Committee looking into the situation. It is now over three years since that Public Law went into effect, and the CDC has not done one iota to correct the fraudulent criteria... eg, titer #31 is not included in the array of titers that are allowed for the ten titers. Yet, the titer is soooo specific for the bacteria that that is the titer that the pharmaceutical vaccine companies based their vaccines upon. And in direct conflict with that Public Law, the CDC is putting out disparaging remarks via their bulletin system against those labs that have come up with a better test than what the CDC is requiring for reporting for their surveillance purposes. The Bowen test is one of those better tests!!! Though the CDC does not use the name in their disparaging remarks. After nuclear amounts of varying antibiotics over a long period of time, I tested at the highest dilution ratio of 128 on the Bowen RIBb test in June 03. I continued those abx, and was re-tested in Dec 03 at ratio of 64. I thought that I was gaining ground, so continued the abx including as much as 1,500 mg of Flagyl abx, which is tauted to cause very strong herxes. In April 04, my Bowen dilution ratio was again at the highest, 128. I was very depressed about the situation. I discovered the MP on June 9, 2004, and started the MP on September 1, 2004. I re-tested with the Bowen on April 19, 2005, and had a dilution ration of only 32. I am elated!! My herxes on the MP have been harder than any that I had on the AP (antibiotic protocol). Uncomfortable at times, but controlable, and certainly within my limitations. I do take short vacations from the minocycline every so often. I recommend the Bowen RIBb test! Whether it is the exact same strain of borrelia (borrelia burgdorferi sensu stricto) that causes Lyme disease is questionable in my mind, because that strain is so narrowly defined. I think that any borrelia burgdorferi sensu lato, the greater family (genus) might be causing the Th1 imflammation, not just the Bb sensu stricto. But who cares? What one really wants to know is whether one has borrelia in their body. The Bowen test does that!!!! Even the CDC on one of their websites says that there are "fifteen borrelioses" that cause disease. I would wager that there are many more borrelia when the test are developed to find them, and the effort is expanded to do the searching. Please think and use the word, "borreliosis". It will at least not raise the red flag with doctors and insurance that Lyme disease seems to do. If you wish to discuss this further, please send me a PM. I am on a project with my Missouri State Dept of Health to have them change their regulations to have docs report "borreliosis" as well as "Lyme disease", so that at least my State will get a better handle of how many people are suffering from borrelia caused disease. My Petition is getting "due process". The laws are already on the books requiring surveillance of "contagious disease", even by "arthropods". I am hopeful." Dark Vader (aka, George) ............................................................ When you say "titer 31", I don't know what you're referring to. Is it one of the bands on the Western Blot? ....... Yes, titer is another name for band. Titer #31 is band 31. .................................... I have noticed that I should make a few corrections to my spelling in my posting... The bacteria name is borrelia burgdorferi sensu stricto... leave the "s" off of the "burgdorferi". I wrote, "Even the CDC on one of their websites says that there are "fifteen borreliosis" that cause disease." The plural of "borreliosis" is "borrelioses", so I should have written "fifteen borrelioses", as the CDC site has done. And, I wrote, "...so that at least my State with get a better handle of how many people are suffering from borrelia caused disease." I should have written, "...my State will get a better handle..." Under what I have proposed for new regulation in this State, you would be reported under "borreliosis". I secured a copy of the number of case reports in my State going back numerous years before the CDC Dearborn criteria and after. I realized that what the doctors were seeing did not go away, but that it needed to be reported, also. And, it is a much larger number than the CDC "Lyme disease", by a factor, based on those case numbers of approximately three to one. "Borreliosis" is the answer. I suspect, like every one, that the number is much larger. But it is a start to get changes! I would like to see folks in other States push for the same change... at their State level. The CDC is too entrenched in their thinking, or whatever. We have to side-step them. And the same could apply in Australia, as well. BW! George ...... I emailed Dr. Whitaker's lab in Florida, and they sent me details regarding getting this test done by sending a sample (from Australia) to the USA. The cost is $250 U.S. The cost for the the Bowen RIBB is $250 for the lab fee, which must be paid either by money order or credit card. It is not FDA approved as yet, but they have done over three thousand, or even more since I last heard, so is not insurance paid. There is also the FedEX Priority Overnight shipping fee (to reach the lab by 10:00AM the following morning... on Mon, Tues, Wed and Thurs only). Plus whatever the doc needs to charge for his participation, which is required by the lab, per new U.S. Federal law (to protect our privacy ).I believe that Igenex's name for their test is "Western blot for Lyme". http://www.igenex.com Bowen calls theirs "Bowen q-RIBb" (Rapid Identification of Borrelia Burgdorferi) http://www.bowen.org Since you say that the medical community says that there is no Lyme in your area, they may be correct (considering the CDC criteria for Lyme disease), but there might just be a lot of "borreliosis", which they might be more willing to explore with you than "Lyme disease". All that is needed is to have two 5-ml purple stoppered vials of blood drawn by the doc/lab tech there, and packaging it to send. Saying "Lyme" seems to raise a red flag with docs and insurance!!! You might be able to talk one of them into giving you an order for the RIBb test, and work with you to do it, as though he and you were on an exploring adventure. All paper work can be handled by FAX, rather quickly. Then, if that test came back Positive, you would be on stronger ground for asking to do a "Western Blot for Lyme disease", if you still wanted to know if your illness was "Lyme disease", instead of one of the many other "borrelioses". And you do not have to "prime" the immune system into making antibodies with the Bowen RIBb test as you do with the WB test, with all of that expense (LLMD, abx, transportation, lodgeing, etc... at least not in the beginning of this exploration. The RIBb looks for the antigen itself. Borrelia are CWD, and really what you want to know for your own information, and a buttress for all of the reasons that Hrts gave you for getting financial help. George Rollo ================================================ I am pleased to announce that IGeneX, Inc. recently passed two inspections on September 7 and 8, 2005, for its biannual recertification from the State of California. A federal inspector also arrived simultaneously, indicating she was present due to the NY Times article August 23 which had made allegations against IGeneX laboratories. The inspection was intense, with a focus on the Western Blots which had been cited in the NY Times article. The lab has been fully recertified, and the inspectors clearly saw the allegations were without merit. Despite a volume of letters to the Times after the article by patients, groups, and doctors in support of IGeneX, nothing was printed by the Times. IGenex thanks all the Lyme community for your support. Perhaps the Times will relent and print another piece on this issue. Sincerely, Nick Harris CEO, IGeneX Labs Palo Alto, California ==================================================== Bowen q-RIBb test: Dr Marshall wrote: There is only one true marker of progress, the rate at which you regain your health. There are a plethora of markers used by phsyicians these days, and they go in and out of favor every few months. These include CD-57 and VEGF. But they are just markers of inflammation. Flourescent antibodies, of the type used by Bowen (borrelia) and Jardin (Rickettsia, in South Africa) have been proven for decades to be accurate markers of the actual organisms themselves. The CDC has just issued a directive that Bowen Labs is contaminated, and not to be trusted. This is because, according to the CDC, nearly every test from Bowen comes back positive. However, we don't see that. In two of the MP folks their titres have steadily dropped, every 3 to 6 months. This indicates, to me, that Bowen labs is accurately reporting the organism, but that the organism is endemic. Oct 08 You are assuming that the Igenex test is accurate. It is not accepted as accurate by the CDC. Unless you understand the specifics of how the Igenex test is conducted, of the multiple genomes it targets, there is no way you can understand the complexities of what can go wrong with the interpretation of its results. If I were you I would focus on the fact that not one patient with chronic Lyme has ever been cured by the pragma which are put forward by ILADS (or IDSA). Whereas there are many who have returned to an active life after treatment based on our disease model. ps: the Th1 pathogens had disabled your innate immune system long before you were "tikbitten" ..Trevor.. see George Rollo Personal TestsLike everybody, I would love to know exactly what microbe is causing my problem. However, I do not think that is possible in this day and age. And, it may well be more than one microbe that is causing trouble....a stew or soup of troublemakers may be at work. But for the buck spent, I think doing the Bowen q-RIBb test is worth the expense. It will give one the knowledge of at least one CWD bacteria, and one that may be more widespread than authorities would like to admit. I truly believe that Borrelia bacteria are epidemic, and our trouble is really "borrelioses" (plural), not Lyme disease, which is just one "borreliosis", in many, if not most, cases. And having the Bowen dilution ratio as a relative quantitative guide should be helpful to see that the MP does work. It is reassuring for me to see my numbers get lower! If one gets a Positive on the Bowen, does the MP, and sees the dilution ratio go down, one will know that the MP should be working for all of the CWD bacteria. The test is a bit more objective than "I feel better!", during a period when one is herxing, and that feeling can change from day to day. To search for all CWD bacteria, and keep tabs on all of them, would require a research lab dedicated for the individual alone. Perhaps, Howard Hughes could have supported such a scheme of things. It would be out of the question for most people, self included. To my understanding, the Bowen test is an antigen test, meaning it looks for the bacteria itself, rather than the antibodies that our immune system produces in reaction to the antigen (bacteria). To my understanding also, the current antibody tests, such as ELISA and Western Blot tests, can not show a quantitive amount...this is what makes the Bowen test, a test for the antigen, so much more valuable. Would you clarify this for me, please? George ============================================= I agree with George. I was chatting with an ID specialist in Germany who routinely sends blood from his patients to the US to be tested for Borrelia by Bowen Labs, and down to South Africa to be tested at the Jardin lab, which has had been doing flourescent antibody testing of Rickettsia for nearly a decade. This is another of the nasty bugs, and he tells me they are almost all positive at the highest dilution. I have just identified, using bacterial genomics, another couple of possible nasty species, but there are no decent tests for them yet. However, at least in Sarcoidosis, both Borrelia and Rickettsia have been identified at high rates, so, if money is not an object, you might find antibody testing for both these species will allow you a quantitative track of your progress. ..Trevor.. ============================================ To my understanding also, the current antibody tests, such as ELISA and Western Blot tests, can not show a quantitive amount...this is what makes the Bowen test, a test for the antigen, so much more valuable. Would you clarify this for me, please? George ====================================== The Bowen test uses a Flourescent Antibody to identify the Target Bacteria. So when I talk about an 'antibody' I am not implying any are present in the patient, they are the basis of how the Bowen and Jardin testing procedures work. ..Trevor.. ============================================ http://www.bowen.org/index_018.htm George this Bowen link, which I have pasted an excerpt below, has helped me to understand their testing and maybe will others who are interested. _________________ "...Dr. Whitaker developed the titration serial dilution method for quantitating the amount of Bb antigen in the blood. This may help to differentiate the carriers from the patients with serious disease by comparing persistence of fluorescing structures. In this part of the test, whole blood is diluted and fluorescent antibody added. The solution containing the antigen is progressively diluted down until a count of the antigen in that particular blood sample remains. Findings are documented with digital photography using Darkfield microscopy. The Bowen Q-RiBb isn’t looking for antibodies; it detects the actual antigen - the L-Form (cell wall deficient form) of the bacteria in the blood. The Bowen Q-RIBb accomplishes this with the use of fluorescent staining specific for detecting Bb that attaches to the protein in the L-Form. They use green in the stain because the eye is more sensitive to green and it can easily be seen under the Darkfield microscope. The Darkfield microscope is a high magnification microscope with a special lighting feature which allows for greater observation of the blood samples. Fluorescent staining for specific bacteria has been around for over fifty years. We chose, due to having to work with other specialists to run Igenex IgG and IgM Western Blots, after "priming" with abx to stir things up....we are all CDC positive. Had this not occurred, as I am aware that false negatives do occur (especially with inferior labs and not priming) we certainly would have gone with Bowen. Our hanging point though was that other physicians and specialists with whom we must deal----are accustomed and more inclined to take a positive Western Blot at face value." hrts =================================================== I have just rec'd my B. burgdorferi test results back from IGenex. In a nutshell, they reported my IgM as positive, but my IGG as negative. What does this mean? IMO, if a person has even one titer on a WB test for borreliosis, the person has borrelia in his body. Any borrelium is a CWD bacterium from what I understand. Therefore, if one has CWD bacteria in their system, and symptoms of illness, they will have a Th1 inflammation, whether they are aware of it or not. This opinion is not shared by the orthodox medical community, and insurance, I realize. You have more than one titer on your WB test for borrelium. An "IND" on your test means that the technician saw something, or otherwise he/she would have given a "-" for that titer. The technician compares two things with his/her eyes for determining whether there is a titer to report. If the tech sees absolutely nothing, then the "-" is given. IMO, an "IND" is the very first step of reporting a titer, then comes a "+", then "++". I was first bit by a tick in the Spring of 1958. I was not aware then that anything was caused by that tick bite. I thought that it was just a nuisance. However, I NOW realize that the "sun stroke" stroke that I had just a few months later from being in the sun all day sailboating was the first of such sun intolerances when I went sailboating in later years. I did a WB test in August of 1999 to be used as a "base" of information for later use should I come down with any tick-borne disease. I felt well through all of those years. However, that "base" WB showed two titers for borrelia. I did not qualify for a diagnosis of "Lyme disease", but those CWD bacteria were at work causing me some silent symptoms, caused by a dysregulated 125D hormone, causing resorption, which caused me my osteoporosis and osteoarthritis (bone spurs that had to be removed surgically). I had another tick bite in March 2000 that caused me to "crash". Another WB done in August 2000 did show an increase in titers, but not enough to qualify for "Lyme disease". I did have titer #31 though!!! My LLMD did treat me based upon my symptoms/clinical diagnosis. I did my first Bowen RIBb test in June 2003, after three years of the AP (ILADS LLMD antibiotic protocol), and had a Positive for Bb at the highest dilution ratio, 128. My wife, who had been bitten at the end of June 1999, (nine months ahead of me in relation to my "crash"), and had her first Bowen test in August 2003, had a dilution ratio of only 16. Those two titers that I had on that first WB, and my high Bowen dilution ratio, had to be saying that my disease was in the making a very long time. I would suggest that you read the following material CAREFULLY, and make your own decision as to what your WB means: 1.) Article by Pamela Weintraub at http://www.astralgia.com/magazine/bitterfeud.htm on CDC Dearborn Conference of 1994 setting WB test criteria and Lyme vaccine 2.) Article about WB bands at http://www.geocities.com/HotSprings/Oasis/6455/western-blot.txt by Art Doherty 3.) Article ritten by Tom Grier, which can be found at http://www.canlyme.com using Search for "Tom Grier", part of which follows: Immune Responses The first antibody our body makes in response to a foreign invader is usually immunoglobulin type M, abbreviated as IgM. This large antibody takes two to four weeks to be made in quantities large enough to be consistently measured. It is at its peak of production four weeks after exposure to an antigen. The IgM antibody will only stay in circulation for about six months, and then levels are usually too low to detect. If infection persists, this antibody may also persist. In general, a Lyme patient who consistently has detectable IgM levels is usually chronically ill, but its absence is not a reliable indicator of cure. The second antibody we make after the IgM is the IgG antibody. This antibody takes four to eight weeks to form, and is gone in less than twelve months. It peaks at about six weeks. This antibody crosses the placenta, so an infected mother can pass this antibody to her child. An IgG antibody titer in a newborn does not have to mean active infection. It does mean the mother has had exposure, and the child must be carefully monitored for signs of the disease. IgM: This is the earliest of the antibodies to appear in response to an infection. It is produced in quantity. It is six times larger than the IgG antibody. Because of its size, this immunoglobulin does not cross the placenta. Since it cannot enter the fetus from the mother, any newborn that starts to make IgM antibodies against Lyme disease must be infected. However, a fetus exposed to Borrelia burgdorferi early in the pregnancy may never make an antibody response to the Lyme bacteria because the baby's immune system doesn't recognize it as foreign. IgG: This antibody remains the longest and is the foot soldier of the immune system. It attacks viruses, bacteria, yeast, toxins, and transplants. The IgG antibody can kill bacteria indirectly by tagging or marking the foreign invaders for destruction by the killer cells (T-cells, macrophage). Or, it can kill the bacteria directly by evoking compliment, a series of enzymes and proteins that will dissolve the intruder. Conspicuously absent are the most important bands, 22, 23, 25, 31, and 34, which include OSPA, OSP-B and OSP-C antigens - the three most widely accepted and recognized Bb antigens. These antigens were the antigens chosen for human vaccine trials. This abstract showed that, under the old criteria, all of 66 pediatric patients with a history of a tick bite and bull's-eye rash who were symptomatic were accepted as positive under the old Western Blot interpretation. Some of the information in these are outdated now by the knowledge of Dr. Trevor Marshall, Phd, but are useful, nevertheless. George (aka, Dark Vader) ======================================= CD-57 This is a new test done by labcorp. Lb is, reportedly, the only bacteria to lower this subset of the natural kiler cell. CD-57 cells "are down-regulated by so-called TH1 cytokines (such as IL-2, IFN gamma, TNF alpha)" - Dr. Ray Stricker - York 2004 LDA Conference. George Howell writes: "Instead, it remains low until the LB infection is controlled, and then it will jump.", and the last sentence, "If the CD-57 count is not in the normal range when a course of antibiotics is ended, then a relapse will almost certainly occur." makes me cautious about this test. I suspect that this test does not really show much about the Th1 inflammation caused L-forms (cyst and coccoid) of the bacteria as a factor. Dr. B sure seems to think that the spirochete is the only factor in Lyme borreliosis if you read his Guidelines. IMO, and experience, the spirochete is a factor. However, the Th1 inflammation caused by L-forms living in the macrophages is definitely a big factor, in my experience, for a whole set of symptoms, and the reason for relapsing. I see this test leaving one really open to NOT knowing whether one is 'cured'." Hrts writes: "Our Lyme care provider is very much on the cutting edge----we have had CD57's run. In our cases-----I am the most disabled---on disability, and yet my CD57 is not nearly as poor as other patients I have conversed with or my own family members. I would not use this as a diagnostic test, personally at this time. Perhaps in some it can be used to monitor treatment progress." Dr Marshall: I wouldn't trust the CD-57 test further than I could throw it, as I don't agree that the science underlying this test is sound. One of the Pubmed articles describing this test is here: http://tinyurl.com/o9faj and here is another: http://tinyurl.com/myp6n I would be happy to talk with your LLMD and explain why I think a test based on such limited immunological knowledge, and such a tiny cohort of patients will ill-defined disease presentation, is hardly suitable to be used as a basis for clinical decision making. You need to understand that chronic Lyme patients have gone seronegative due to MP therapy, something that was never contemplated by the authors of the two studies cited above. One of those chronic Lyme patients tells her story on the DVDs of our 2006 conference, which should be out in a few weeks. ..Trevor.. CD-57 test is irrelevant unless you are bound to prove that you are infected with borreliosis. However, if you are chronically ill, you don't need any tests. A simple therapeutic probe with the MP with demonstrate the need for MP treatment. Last edited on Sat Oct 4th, 2008 20:23 by Foundation Staff |
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LYME/BORRELIOSISlink Testing may be needed for disability For many chronic late-stage disseminated borreliosis is a very disabling disease. Many times previous diagnoses have included Fibromyalgia and Chronic Fatigue Syndrome or ME. For some who are no longer employable, it might behoove them to be tested through the two best labs, Igenex and Bowen. (Some may even become unable to work during the treatment phase, as the herxing or light exposure may increase symptomology). In that case we may be looking at an extended time, as a possibility for unemployment. Therefore, I think that testing is a very good idea for those who suffer from some of the various syndromes, and in which Borreliosis may be a factor. Many with this disease are diagnosed as having Fibromyalgia Syndrome, or Chronic Fatigue Syndrome. While this is true in and of itself (the patients meet all the criteria for diagnoses of such), many are carrying a bacteria, which can be detected and will assist them in documentation to support a disability claim if unable to work. Having comorbid diagnoses of FM, and/or CFS, documented by one's physician, along with the borreliosis diagnosis, and the disabling reports in the functional tests one's physician provide the SSA will greatly help someone being awarded a favorable claim. This will allow the unemployable to receive some income while unemployed and disabled, and Medicare health coverage, which may be very helpful. As we all know chronic illness is a huge financial setback for most. FM and CFS are often difficult to "prove" in the manner that the SSA desires, as they look for testing as a mainstay. Many times FM and CFS patients are told they they test normal in areas investigated. For that reason alone, I think one should have as much testing done to support one's case, as did my lawyer. It can be difficult (not impossible though) to receive a disability award with FM and/or CFS alone. I was one of the fortunate, but now I know at review time, that I have even more documentation, after being seropositive on an Igenex Western Blot, and seropositive for co-infection, also. Although, I do hope to be well enough to return to my vocation in the near future, SSDI and Medicare has been a necessity for myself. The Western Blot often does not come up positive in patients who have not been on abx therapy prior to testing, as their bodies do not seem to be manufacturing antibodies. This situation is very often remedied by LLMD's "priming" the patient with a short antibiotic protocol, prior to testing, thus achieving some die-off of Borrelia organisms, and an antibody response, making for seropositive test results. We had seronegative tests in the past, until we were "primed" for a few weeks with abx in 6 of our family members. Our bodies then made antibodies---and we recieved positive results for Borrelia infection, and other co-infections, such as Erlichiosis, Babesia, and Bartonella. We highly recommend Igenex, as compared to a lab one's physician regularly uses. Although, I believe that the Bowen Labs, are very accurate in their assessments, one will often find that in conventional mainstream medicine, if one waves a positive Western Blot in their face, will take it much more seriously. I have heard rumors that Bowen will be moving on, and changing from research lab designation in the future. (This would be great). We have heard many physicians disclaim their tests, unfortunatley due to this designation. This is the reason we went with Igenex, as it seemed to be a less bitter pill for mainstream docs to accept, as many do not believe that "chronic Lyme Disease" exists, and they are more convinced when they see a positive Western Blot. They are familiar with Western Blots, and hold them to be "proof positive". We also ran PCR's at the same time for further proof, avoiding the Elisa altogether, as it doesn't have a great track record. Since Borreliosis is a systemic disease one can have to deal with many areas of specialities, and will want the doctor to consider the disease in their assessments, another reason for testing. One can convince a nephrologist, endocrinologist, cardiologist, pulmonologist etc. that as the abx protocol does its job, that the manifestations of the disease will diminish, and can avoid some pretty aggressive treatments, that may be not be needed. Most of all though, none of us is sure with our level of health and subsequently our employability that it may not change at a moments notice, it would seem testing for Borreliosis, would be a wise investment to protect one's income and health benefits if the need arises. Many hesitate since they do not believe they have had tick exposure. We all now know that they are many more modes of transmission than this. I would like to stress that testing may be beneficial if the need arises to make a disability claim, or to sustain one. Hrts PS. I also wanted to add it is most beneficial to be seen and tested by an LLMD (Lyme Literate Medical Doctor), as they will know what priming may be necessary, and are very familiar with the labs that are most accurate. Many physicians are not Lyme literate, unfortunately. |
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Aussie Barb Research Team
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Will the MP clear cyst forms and coccoid forms? The MP should kill all the species of tick-borne aliens, including the cyst and coccoid L-forms. The antibiotics we use target the 70S ribosome that all forms of the bacteria use to create the proteins they need to survive. ..Trevor.. Lyme Disease (Bacterial Survival In Adverse Conditions) The Strategy of Morphological Variation in Borrrlia burgdorferi and Other Spriochetes "If it's a manipulation ((of the host by the parasite)) and you treat it, you're avoiding damage, but if it's a defense and you treat it, you sabotage the host." Paul Ewald, PhD (professor of biology at Amherst College) Last edited on Thu Jul 26th, 2007 04:10 by |
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LYME/BORRELIOSISlink What to do if you are bitten by a tick See How to remove a tick Standard treatment When you are bitten by a tick, you may or may not develop the classic bulls-eye (or other) rash that signals an acute borreliosis (Lyme disease) infection. For this reason, many doctors routinely prescribe a course of doxycycline after a tick bite. This may be as little as a one time dose of 200mg or 100mg twice daily for 21 days. Lyme disease caught in its early stages is highly favorable to treatment and this is the best course of action for those not already on the MP. "Most medical treatments are developed by consensus over a period of time. The medical profession (as a whole) thinks that doxycycline will do the job. Minocycline would work better, but it is usually a fruitless task to try and explain 'why' to a Doc who routinely uses doxycycline." ..Trevor.. If you are already on the MP and you develop a bulls-eye rash after a tick bite or you think a tick bite has put you at risk for Lyme disease, ask your doctor about taking 100mg minocycline twice daily for 30 days. If your immune system reactions do not yet allow you to take 100mg of minocycline with Benicar, your symptoms of immunopathology suggest that bacteria are already being killed and you are at low risk for developing Lyme disease. If you have already progressed to the maximun dose of antibiotics in phase 3, you may opt to continue this effective treatment for killing many bacteria. |
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LYME/BORRELIOSISlink The Marshall Protocol and borreliosis There are many patients with confirmed Borrelia who are using the MP to kill that chronic infection. Some of the pathogens, notably Borrelia, extract their energy from glucose, and I think it is not a good idea to increase the pathogens' level of well-being. ..Trevor.. ============================================ Does Elisa test and western blot drop down after or while progressing on MP? Yes ..Trevor.. ============================================ Lyme PCR (urine) test showed positive for the first time. Is there any basis for that being associated with the protocol? The bacteria causing chronic illness hide inside the phagocytes of the immune system. In sarcoidosis patients there are no antibodies, no sign of bacteria at all, until they start taking the MP antibiotics, when their antibodies and SED rates often immediately start to show the bacteria which are being killed. I would surmise you are seeing the same effect. As the bacteria die within the phagocytes, and cause apoptosis of their 'homes,' the fragments of their RNA appear in the bloodstream in sufficient quantity to be measured by PCR technology (I am assuming it is an RNA based PCR assay). That's good news indeed! ..Trevor.. ============================================ Dr. Marshall is finding a high rate of improvement in the more than 50 chronic LD patients that he is tracking on the MP. Some of these patients are at an advanced stage of recovery, despite many years of chronic illness and unsuccessful antibiotic treatment. Full recovery may take 18-36 months, though most patients experience significant improvement in the first 9-12 months. ============================================ "The spirochetes in-vivo are not classical 'ketes. In particular, they have no flagella (you know, the things that all the tests are looking for). They are coccoid forms inside some sort of transparent biofilm, I think. Anyway, all these antibiotics will kill them at the peak MP concentrations. 100mg Mino for 2-6 hours after you take it is above the MIC, for example. So the mobile bugs will be dispatched as well. But remember that when the intra-cellular form is killed there are no more blood-borne 'ketes eminating from them. It takes a long time to kill them all, While there are still some inside the cells they will eventually leave the cells and enter the bloodstream, especially as the cells die through apoptosis." ..Trevor.. Last edited on Fri Jan 27th, 2006 06:24 by Foundation Staff |
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LYME/BORRELIOSISlink http://tinyurl.com/55cf7 Study finds changes in Lyme bacteria - Lyme Bacteria mate! Discovery expected to improve treatment Tuesday, September 28, 2004 BY ANGELA STEWART Star-Ledger Staff New Jersey researchers have discovered unique genetic elements associated with different strains of Lyme disease, which could aid vaccine development and improve diagnosis, according to a study released today. Led by scientists at the UMDNJ-New Jersey Medical School in Newark, the study focused on the genetic makeup of the bacteria that causes Lyme, including the proteins. The findings may help explain why some people get a mild form of the disease while others experience major complications, such as neurological problems, said Steven E. Schutzer, an immunologist at the UMDNJ-New Jersey Medical School who served as principal investigator of the study. To the scientists' surprise, said Schutzer, they discovered that the bacteria that cause Lyme disease (Borrelia burgdorferi) do indeed mate and exchange genetic material, a process that may lead to infection. "Before this, scientists were unaware that the Lyme disease bacteria could modify themselves so rapidly," he said. "The implication is that the bacteria may produce a more disseminated infection in the patient that results in infection involving multiple parts of the body." The study appears in the journal, Proceedings of the National Academy of Sciences. It was funded by the Jackson-based Lyme Disease Association Inc., the National Institutes of Health and the Howard Hughes Medical Institute. Pat Smith, association president, said the study "opens up a whole new world of possibilities" for Lyme patients in the areas of diagnosis and treatment. "If scientists could figure out how they could possibly disrupt the ability of the organism to exchange this genetic material, maybe the disease would be a lot less virulent than it is," she said. Lyme is a tick-borne illness that peaks in the spring and summer months. It is sometimes characterized by a red bull's-eye rash surrounding the tick bite. But diagnosis is a problem, since Lyme can mimic other diseases and not everyone gets the classic rash. To conduct their study, Schutzer and his team identified and studied strains associated with Lyme disease in the United States. They then performed sequencing to determine the genetic compositions of each Lyme strain. "This study really lays out all the different proteins of Borrelia, and as a result of that, we know we have a much larger group of substances to use for both a vaccine and (as targets) in helping diagnose the disease," said Benjamin J. Luft, chair of the Department of Medicine at the State University of New York at Stony Brook and a senior author on the study. New Jersey ranks third in the nation in Lyme cases, with 2,887 reported last year to the Centers for Disease Control and Prevention. However, the actual number is believed to be much higher because many cases go unreported. Angela Stewart writes about health care. She can be reached by e-mail at astewart@starledger.com or at 973 392-4178 Copyright 2004 NJ.com. All Rights Reserved. |
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LYME/BORRELIOSISlink Tick-Borne and Other Emerging Infectious Diseases |
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LYME/BORRELIOSISlink Dr Garth Nicholson's presentation at "30th Anniversary of Lyme" Conference http://autoimmunityresearch.org/garth-30th.ram and from the Hartford group's website at URL http://www.ctlymedisease.org/video/nicholson.ram You need a 100KBps broadband connection. Dial-up will not work, and no, there is no transcript. If you have a dial-up connection you can download the video to your disk and play it from the disk by clicking on http://autoimmunityresearch.org/garth-30th.rm |
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LYME/BORRELIOSISlink Plasmids and resistance http://tinyurl.com/8lf88 Borrelia has 17 of these ..Trevor.. |
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LYME/BORRELIOSISlink gbppez wrote, "The nurse told me that it was positive, but that it was at the "lowest possible dilution". This is getting off the original topic, but does anyone have an explanation for that? Is it possible to have what appear to be classic Lyme symptoms over a long period of time, and then get test results that are at the lowest possible dilution?" Yes, I do have an explanation for that. Your nephew's blood was the source of the sample for the Bowen testing. The results that you received show the amount of bacteria (Borreliosis) in the blood stream. Borreliosis, the bacteria that causes chronic late stage disseminated lyme disease doesnt just remain in the circulatory system, but perfuses throughout tissues and organs of the body. It resides within the bodies own cells, using them as host cells. It has even been found inside cells of the immune system. So what you are being told in the dilution is simply the amount of the bacteria in the blood stream, not in the body in its entirety. From a sampling of those with Bowen testing, in a Lyme group I am involved with, dilution does not always indicate the severity of the disease, quite often. In other words, those most debilitated often have lower dilutions than those who are more mildly affected. (The same can be said of the number of positive bands in Western Blot testing). As an aside, the reason that many/most receive negative results on Western Blots is due to borreliosis ability to hide, evading detection from the immune system. The patient produces no antibodies---thus a seronegative test. Patients who most often receive positives on Western Blot testing, have been "primed" by a short course of antibiotics. THEN there is die off of the bacteria, and the body begins producing antibodies, and a seropositive test result occurs. There are also co-infections that take up residence in a sick body, not to mention that at the time of transmission of the borreliosis bacteria, many are infected with other pathogens. Your nephews symptoms are very common borreliosis (lyme) symptoms. You can see by his symptom list that this is a bodywide infection. So, now you know that the borreliosis bacteria is present through the Bowen testing, this is the crucial revelation, not the amount detected in his blood stream. You asked about antibiotic therapy. The MP antibiotics are designed to attack all forms of the borreliosis bacteria. Choice in antibiotics is of great importance as all forms of the bacteria must be attacked to eradicate the infection. Best wishes to your nephew, he has a wonderful advocate in you. hrts ============== Hrts, The logical extension of your arguments is that Borrelia itself may not be the primary pathogen. We already know that many of the co-infections (EBV, etc) are relatively harmless, so why are we elevating Borrelia to status as the primary pathogen? In Sarcoidosis it has been thought that Mycobacteria are the root pathogen, and recent studies out of Japan have fingered Propionibacteria. The "jury is still out," IMO. Here is another curved ball, too. In my opinion it is likely that Borrelia burgdorferi sensu stricto is not a homogenous organism, is not a homogenous genome. If you look at my talk at the "30th Anniversary of Lyme" conference last May you will see that I describe the Borrelia genome as having a huge proportion of its genome on its linear and circular plasmids. Plasmids which are self-replicating, and which are the primary communicators of antibiotic resistance and other genetic mutations/adaptations. I have this nagging feeling in the back of my mind that the Borrelia spirochete that eveybody is focusing upon is not an homogenous organism, but a colony of organisms. Look at Lida Mattman's electron micrograph of a spirochete cross-section which she showed at the Chicago conference. Is that best described as an organism, or a colony? ..Trevor.. ps: link to simple info on plasmids: http://tinyurl.com/8lf88 |
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LYME/BORRELIOSISlink From George Howell: Trevor asked, ".so why are we elevating Borrelia to status as the primary pathogen?" This may be an imperfect explanation, but one that is a beginning. Synergism may help make it perfect. The answer as I see the picture is that: 1.) The CDC has given us a starting point by saying that the PROVEN causative agent of so-called Lyme disease is borrelia burgdorferi sensu stricto. They have also given us another PROVEN borrelia disease, STARI (Southern Tick Associated Rash Infection), in the U. S., and there are other borrelia, worldwide, acknowledged as being PROVEN to be pathogenic. There aren't many other CWD bacteria caused diseases acknowledged as PROVEN, and well known. 2.) To slide from these borrelia primary pathogens to the real cause of symtoms, Th1 inflammation, is easier to do, then going from some unknown, undetected cause. 3.) Marketing! The brand has been established already. borrelia are the bad guys!!! Acknowledged borrelia primary pathogens are here and now! Use it to help sufferers and to promote the concept of "Th1 information". There may also be other borrelia that are primary pathogens, that need to be found yet, and will, one day, be found, when the tests are developed and effort put into the project to find them. If the one strain is found that measures up to the criteria, then it is the CDC's "Lyme disease". But if it is any borrelia, the disease should be given the family name of "borreliosis".bor rel e o sis.a more inclusive primary pathogen disease that is wide spread. Trevor also stated, "In my opinion it is likely that Borrelia burgdorferi sensu stricto is not a homogenous organism, is not a homogenous genome." This is a most true statement from all of what I have read!!! There are at least the eight-two known strains of the Bb sensu stricto alone, plus all of the other 100 U.S. strains of borrelia, with over 300 worldwide, Bb sensu lacto members, plus other borrelia. Borrelia are probably changing as fast as one reads this post. This writer may have been infected from a known tick bite in Southern Louisiana, one in Northern Wisconsin, and one in Central Missouri, over many years. And mosquitoes from all over the globe! What with researchers at the New Jersey Medical School having found that bacteria "mate" and share DNA material, I cannot phantom my Body Snatchers being homogenous organisms. What a polyglot of languages must be being spoken within my body by borrelia! If three members of the 53 known CWD bacteria have angiotensin receptors, and it is assumed that the others do also, is it not reasonable and prudent to consider that all borrelia are capable of causing illness, since all borrelia are all CWD bacteria, with angiotensin receptors? Is it not this receptor's ability that enables the bacteria to not be discerned by the immune system, and be able to hide out in the macrophages? This process is the beginning of the Th1 inflammation!!! The way I see that things ought to be done for maximum protection for people, until we develop the necessary tests to determine which borrelia are pathogenic or not, is to assume that all borrelia are pathogenic, and develop a test to look for borrelia within a sick person's body. Once the presence of borrelia has been established, then one knows that the necessary treatment is of a Th1 inflammation since borrelia are CWD bacteria, and the treatment of choice for TH1 inflammation is the Marshall Protocol. Whether it is the only CWD bacteria in the person's body is inconsequential. It may well be a stew.of borrelia, and/or other microbes. There are borrelia burgdorferi, borelia lonestari, borrelia recurrentis, borrelia garninii, borrelia afzelii, borrelia valaisiana, borrelia lusitaniae, borrelia Japonica, and borrolia miyamoto to start a short list of PROVEN borrelia troublemakers. While these borrelia are thought of as being indigenous to certain areas, I would suggest that our testing abilities have not caught up to the job of finding, or disproving, that these borrelia are more universal than normally thought of. We have had ships that transported people across oceans with all of their baggage, some of which could have been concealed within the peoples bodies. We now have airplanes that make the transportation of that concealed baggage that much quicker. Then, too, do not forget those millions, perhaps, billions of intercontinental travelers, the ground feeding birds that do their thing twice a year. And, of course, with some interplay by the zillions of zillions of arthropods to further mix the concealed baggage. What we think of as one "brand" of borrelia this year, may change to another "brand" next year. But borrelia are borrelia, no matter what name one might want to call the Body Snatchers, and troublemakers. This simple process of looking for the widespread borrelia and treating the ensuing Th1 inflammation could save people and the nation tremendous amounts of money. I know of one family that has spent $50,000 of their own money in addition to what their insurance paid for all kinds of tests, and non-successful treatment of just one member. I am gung-ho for the Bowen RIBb test at this time, until a more universal test for all borrelia is developed. The current Bowen can find Borrelia burgdorferi in at least two of its three forms to my knowledge, maybe, the third as well; I just do not know about the third form. But this leaves the question of the other "brands" open, which slack needs to be taken up. I do think it reasonable and prudent to consider borrelia as a primary pathogen. One man's thoughts on the question. And with THANKS! to Trevor for deducing the remedy to getting rid of them! J Dark Vader (aka, George) ======================================= Munchausen’s syndrome by proxy and Lyme disease:medical misogyny or diagnostic mystery? Virginia T. Sherr, M.D Medical Hypotheses. 2005;65(5):440–447 May 27, 2005 Last edited on Tue Mar 7th, 2006 03:54 by Foundation Staff |
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LYME/BORRELIOSISlink The use of antifungals for chronic Lyme ALL THE ANTIFUNGALS PROFOUNDLY AFFECT THE HOST IMMUNE SYSTEM. Do not use any of the antifungals unless it is absolutely 100% necessary. Generally, you must have a positive culture (even though sensitivity testing on isolates tells you virtually nothing about how to treat the infection in the human host). " fluconazole (Diflucan) is sometimes prescribed to treat fungal (candida) infections. It directly inhibits the enzyme CYP27B1, which is needed for the mitichondria in the macrophages to convert 25-D to 1,25-D. With a lower generation of 1,25-D in the inflammation folks will feel better - for a while - and then relapse worse than ever. This is also the action of ketaconazole applied the skin. The keratinocytes in the skin still convert 7-dehydro-cholesterol to 25-D but ketaconazole tends to block the conversion of the 25-D to 1,25-D. We typically deprecate the use of fluconazole because its safety profile is not as good as the other MP medications, especially in the high doses which are typically used by the LLMD and CFS Docs. Azoles affect the operation of the D-metabolites, and/or the VDR but they do it in a manner which is not dose-controllable, as Benicar does. ..Trevor.. "It is interesting that LLMD's stumbled into using at least two drugs that effect vit D, fluconazole and cholestyramine (CSM). I suspect the CSM may bind 25-D from foods while in the gut. It caused what they called an intensification reaction in me with a mild skin rash, but was it hormonal shift?" P.Bear, R.N. Clinical effects of fluconazole in patients with neuroborreliosis "The 'cure' (cited in this study) was obviously assessed based on a pretty optimistic definition of the word. I do know exactly why the azoles make patients feel good, but the complexity of the biochemistry is such that the LLMDs just look blank when I try to explain it, so I have given up doing that some months ago. I am working on a paper which will explain exactly what the azoles do in chronic disease, and maybe putting together a complete 'flow chart' will help folks understand why the azoles are solely palliative, never curative, in chronic Lyme." ..Trevor.. =========================== You attributed the following statement to 'Lyme MDs:' The only medication which can attack the cyst being Flagyl or Tinidazole. This statement is totally incorrect. I am happy to discuss the precise Molecular actions of each antibiotic, including the Azoles. Indeed, my presentation at "30th Anniversary of Lyme" dealt with precisely this topic. I would recommend you take a closer look at that presentation. ..Trevor.. See also: Candidiasis (yeast infection) I have a yeast infection. What should I do? |
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LYME/BORRELIOSISlink NEUROLOGICAL MANIFESTATIONS "When borreliosis infects the CNS many have neurological manifestations that you mention, and as the pathogens are eradicated from this area, you will see a worsening of symptoms due to the toxins produced in die-off. The good news is, that as the infection(s) clear that these areas of symptomology will resolve. With a trickle down effect the ANS is involved and many have dysautonomia, orthostatic intolerance, difficulties controlling pulse, blood pressure, respiration, temperature regulation and may have vagal nerve responses/involvement. Cardiac manifestations may also occur, in that there can be conduction problems and others associated with late stage chronic neuro-borreliosis. Neuroborreliosis commonly causes insomnia, psychiatric manifestations, seizure disorders, memory and cognitive difficulties, neuropathies, swallowing impairment, nausea and malaise, the list goes on extensively, as the systems that are controlled by the CNS and ANS, such as cardiovascular, pulmonary, endocrine, GI, etc. are all going to be affected. Borreliosis is truly a system wide infection, in that the brain, other organs, joints, tissues, all can be infected. It is no wonder why the list of symptoms are so great. I understand your concern with neuro symptoms, they can be very debilitating, and concerning. You know, you can be assured that die off is taking place, and the infectious disease is being diminished when you see herxing in this area as a result of the antibiotic's effectiveness in the protocol. If one were not to see an increase of symptomology in this area, one would doubt that the antibiotic(s) were effective; thankfully, this is not the case." hrts4me  ======================================================= http://msnbc.msn.com/id/3540627/ Diseases of the Mind Bacteria, viruses and parasites may cause mental illnesses like depression and perhaps even autism and anorexia By Janet Ginsburg Newsweek International Dec. 1 issue - Olga Skipko has had the good fortune to live most of her adult life in the Polish village of Gruszki, in the heart of the Puszcza Bialowieska, one of Europe's most beautiful forests and home to wolves, lynxes and the endangered European bison. Unfortunately, the forest is also a breeding ground for disease-carrying ticks. Skipko, 49, thinks she was bitten about 10 years ago, when she began having the classic symptoms of Lyme borreliosis, a tickborne nervous-system disease: headaches and aching joints. She didn't get treatment until 1998. "I was treated with antibiotics and felt a bit better," she says. That was only the beginning of her troubles. A few years later, she began to forget things and her speaking grew labored. It got so bad that she had to quit her job in a nursery forest and check herself in to a psychiatric clinic. "I hope they will help me," she says. "I promised my children that when I come back home, I will be able to do my favorite crosswords again." Doctors ran a battery of tests and concluded that her mental problems were the advanced stage of the Lyme disease she had contracted years ago. Scientists have long known that some diseases can cause behavioral problems. When penicillin was first used to treat syphilis, thousands of cured schizophrenics were released from mental asylums. Now, however, scientists have evidence that infections may play a far bigger role in mental illness than previously thought. They've linked cases of obsessive-compulsive disorder, bipolar disorder and schizophrenia to a variety of infectious agents, and they're investigating autism, Tourette's and anorexia as well. They're beginning to suspect that bad bugs may cause a great many other mental disorders, too. "The irony is that people talked about syphilis as the 'great imitator'," says University of Louisville biologist Paul Ewald, "but it may be the 'great illustrator'-a model for understanding the causes of chronic diseases." Mental illnesses constitute a large and growing portion of the world's health problems. According to the World Health Organization, depression is one of the most debilitating of diseases, on a par with paraplegia. Psychiatric illnesses make up more than 10 percent of the world's "disease burden" (a measure of how debilitating a disease is), and are expected to increase to 15 percent by 2020. Much of this may be the work of viruses, bacteria and parasites. Psychiatrist E. Fuller Torrey, of the Stanley Medical Research Institute in Maryland, has found from studying historical asylum records that hot spots-higher-than-normal incidences-of mental illness can shift, much like infectious-disease outbreaks, which lends credence to the notion that infectious agents play a big role. "Mental disorders are the major chronic recurrent disorders of youth in all developed countries," says Harvard policy expert Ronald Kessler, who directs the WHO's mental-health surveys. Perhaps the most well known disease that's been linked to mental disorders is Lyme disease, which is caused by the Borrelia burgdorferi germ. First identified in the mid-1970s among children near Lyme, Connecticut, the disease has long been known to cause nervous-system problems and achy joints if left untreated. Now scientists are finding that Lyme disease can also trigger a whole smorgasbord of psychiatric symptoms, including depression. One New York man (we'll call him Joe) found out firsthand how debilitating the disease can be. When he began having bouts of major depression back in 1992, he had forgotten all about the tick bite he had gotten four years earlier. He spent two years in a blur of antipsychotic drugs, mental institutions, jails and suicide attempts. On a hunch, a doctor at a psychiatric hospital in New Jersey had Joe tested for Lyme disease. After an intensive course of antibiotics, Joe's improvement was dramatic and immediate. "I started to have this fog lift," he recalls. Still, he will probably have to be on psychotropic drugs for the rest of his life. Some psychiatrists fret that there may be thousands of people suffering from Lyme-induced depression without knowing why. Not only is Lyme disease tricky to diagnose-not everybody gets the circular rash, and lab tests still aren't wholly reliable-it can take a decade or more for mental disorders to set in. The U.S. Centers for Disease Control says that nine out of 10 cases of Lyme diseases remain unreported. There are 15 species of borellias-making them the most common tickborne disease-producing bacteria in the world. For its part, the parasite Toxoplasma gondii, which can be found in undercooked meat and cat feces, can lead to full-blown psychotic episodes. Some studies suggest that the parasite stimulates the production of a chemical similar to LSD, producing hallucinations and psychosis. Even when the parasite lies dormant in muscle and brain tissue, it can affect attention span and reaction time in otherwise healthy people. Researchers at Charles University in Prague have discovered that people who test positive have slightly slower-than-average reaction times and-possibly as a result-are almost three times as likely to have car accidents. That's a disturbing prospect, considering that the disease is so widespread: billions of people are thought to be infected. Even a simple sore throat can lead to psychiatric problems. Few children avoid coming down with a streptococcus infection, also known as strep. Scientists now think that one in 1,000 strep sufferers also develops abrupt-onset obsessive-compulsive disorder (OCD) in a matter of weeks. Strep bacteria trigger OCD by igniting an overzealous response from the immune system, which attacks certain types of brain cells, causing inflammation. Symptoms generally die down after a few months but can flare up again, especially if there's another bout of strep, says Susan Swedo, a childhood-disease expert at the National Institutes of Health. The most effective treatment, still experimental, is to filter out the misbehaving antibodies from the blood. Best is to treat strep early on. The specter of a depression germ or contagious obsessive-compulsive disorder is unnerving, but it also opens up many more treatment options-antibiotics, vaccines, checking for ticks. Geneticists believe that diseases may trigger the onset of inherited mental illnesses by activating key genes. Avoiding and treating infection may be just as important as the genes you inherit, and a whole lot easier to do something about. With Joanna Kowalska In Warsaw © 2005 Newsweek, Inc. © 2005 MSNBC.com ========================================================= J Alzheimers Dis. 2004 Dec;6(6):639-49; discussion 673-81. Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease. Miklossy J, Khalili K, Gern L, Ericson RL, Darekar P, Bolle L, Hurlimann J, Paster BJ. University Institute of Pathology, Division of Neuropathology, University Medical School (CHUV), 1011, Lausanne, Switzerland. judmik@telus.net The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown. A number of contributing factors have been postulated, including infection. It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition. Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls. In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made. Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases. The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition. Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD. ====================================== Neurobiol Aging. 2005 May 12; [Epub ahead of print] Related Articles, Links Beta-amyloid deposition and Alzheimer's type changes induced by Borrelia spirochetes. Miklossy J, Kis A, Radenovic A, Miller L, Forro L, Martins R, Reiss K, Darbinian N, Darekar P, Mihaly L, Khalili K. Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3; University Institute of Pathology, Division of Neuropathology, University Medical School (CHUV), 1011 Lausanne, Switzerland. The pathological hallmarks of Alzheimer's disease (AD) consist of beta-amyloid plaques and neurofibrillary tangles in affected brain areas. The processes, which drive this host reaction are unknown. To determine whether an analogous host reaction to that occurring in AD could be induced by infectious agents, we exposed mammalian glial and neuronal cells in vitro to Borrelia burgdorferi spirochetes and to the inflammatory bacterial lipopolysaccharide (LPS). Morphological changes analogous to the amyloid deposits of AD brain were observed following 2-8 weeks of exposure to the spirochetes. Increased levels of beta-amyloid presursor protein (AbetaPP) and hyperphosphorylated tau were also detected by Western blots of extracts of cultured cells that had been treated with spirochetes or LPS. These observations indicate that, by exposure to bacteria or to their toxic products, host responses similar in nature to those observed in AD may be induced. PMID: 15894409 [PubMed - as supplied by publisher] Last edited on Fri Jan 27th, 2006 06:03 by Foundation Staff |
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LYME/BORRELIOSISlink Why the Borrelia Genome can reveal how the bacterium works Ginny asked how a scientist might be able to deduce how a microscopic bacterium worked, just by analysing its genome. It is not complex, but I will use a lot of words to make sure I convey the concepts as succinctly as possible. Please bear with me I will discuss 2 examples of this, first our own paper "Putative Antibacterial Actions of Angiotensin Receptor Blockers" at URL http://tinyurl.com/249ks and secondly, "A study of the Protein Structures, Functions and Metabolic Pathways in Treponema pallidum and Borrelia burgdorferi" by a group at Yale led by Mark Gerstein. An abstract of their paper is at PubMed http://tinyurl.com/cbusy and a fulltext preprint at URL http://papers.gersteinlab.org/e-print/spirochete-jmmb/preprint.pdf Let me first take a different example first, a simple illustration of how we can use genomics to try and find what species of bacteria might be generating a particular toxin. The first job is to sequence the particular toxin, and determine its structure, particularly those sections of it which are pure protein, composed of amino acid sequences. The National Library of Medicine maintains an online BLAST search containing the 387 bacterial genomes which have already been sequenced at URL http://www.ncbi.nlm.nih.gov/sutils/genom_table.cgi A diagram showing the inter-relationships and subspecies of sequenced bacterial genomes is at URL http://www.ncbi.nlm.nih.gov/sutils/genom_tree.cgi So, given our example of researching this toxin, we would take a small segment of its protein, maybe with 15-20 amino acids, and use BLAST (either online or downloaded to our workstations) to find candidate DNA in the 387 bacterial genomes which might be able to produce this toxin. Then, once we have a handful of prime candidates, we further narrow down the possibilities by using more and more knowledge of the decoded toxin structure. Finally, we have to use our biochemistry to examine each of the structural anomalies, and try to identify enzymatic reactions which might be altering the toxin between its transcription from the organism's mRNA, and its final form in the bloodstream. In this step one has to model the molecular structure of the proteins, and use a lot of computer power to figure out instabilities in that structure where folds might occur, or where enzymes might interact to change its shape or structure. Folds are very important in molecular biology, especially the transmembrane receptor proteins, where the folds are used to cleave and transport peptides and proteins from one side of the membrane to the other. Broadly this is what Gerstein, et al, did. After matching up all the candidate proteins that they thought might be involved in the bacterial energy metabolism, they then identified folds and computer-generated the resulting final proteins. At this point another set of computer programs are used to identify which molecules are likely to react with each other, and in particular, whether such reactions are likely to be involved in the energy metabolism. Not easy work, and usually one involving many, many students (doing the grunt work). In our own paper ("Putative..") we identified the section of the transmembrane G-protein called the "Angiotensin AT1 Receptor" when the ARB Benicar bound to the receptor, and looked for similar structures in the bacterial genomes, structures which might indicate how the bacteria were using the angiotensin they scrounge from the (human) host. We found no structures which correspond to that of the human, indicating that the angiotensin receptors in bacteria almost certainly have a different function from the angiotensin receptors in man. This conclusion is reinforced by Gerstein's work. Clearly, the job of identifying single proteins which can be produced by a bacterial genome is very much easier than the Gerstein group work of identifying and mapping out an entire metabolic pathway. But I hope I have given you an overview of how Genomics can produce answers to dilemmas that are not readily solved by clinical medicine alone. Dr. Trevor Marshall, PhD ================================== The genome of Borrelia has about 40% of its genes on mobile plasmids, and not on the primary chromosome. So (arguably) there could be hundreds of different versions of B.burgdorferi out there. If you look at the master Genome list at URL http://www.ncbi.nlm.nih.gov/genomes/lproks.cgi you will find only two Borrelia species fully sequenced. One was sequenced by TIGR and one from Germany. Look at the sizes - 1.52 vs 0.99 This is because the Germans are only reporting the Chromosome and 2 plasmids, while TIGR is reporting chromosome and 21 plasmids. Unfortunately the Borrelia genome has proven too complex for many of our institutions to fully assimilate, and this is an excellent example. Both groups are correct, but they are looking at the species in different ways. A similar situation exists within the Mycoplasma species. Look for example, at this species comparison: http://www.zmbh.uni-heidelberg.de/M_pneumoniae/genome/MP_MG_Comp.GIF The rapid pace of advance in science's knowledge of the genome has left 99.9% of our Infectius Diseases specialists behind. It will take a new generation to come along who can understand the new genomic tools ..Trevor.. |
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(filelink) Q: Can MP effectiveness against Lyme spirochete be shown in-vitro? A: Dr Marshall wrote: "The whole reason the MP is successful is that I figured out conceptually why in-vitro experiments can never replicate the in-vivo chronic-disease environment, and further, that the Th1 pathogens have exploited a facet of the in-vivo environment which can never be replicated in-vitro. The Lyme spirochete is not active on-vivo. It is the form the organisms take in-vitro, but the pathogenic form is not the spirochete. Please take a good look at either Lida Mattman's or Andy Wright's presentations from our Chicago conference DVDs, as they both made this point quite clearly."<< |
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LYME/BORRELIOSISlink Bacteria change to L-forms whenever their environment gets very harsh. The Brorson's found that the immune system environment in spinal fluid, which is very hard on bacteria, causes them to change to L-forms. Brorson O, Brorson SH: In vitro conversion of Borrelia burgdorferi to cystic forms in spinal fluid, and transformation to mobile spirochetes by incubation in BSK-H medium. Infection. 1998 May-Jun;26(3)144-50 http://tinyurl.com/7ccdw ..Trevor.. |
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LYME/BORRELIOSISlink Lyme Inc. David Whelan 03.12.07 Health Ticks aren't the only parasites living off patients in borreliosis-prone areas. Three years ago Heather Jenkins, a 30-year-old mom in Huntersville, N.C., was constantly fatigued and prone to colds. Her internist referred her to Dr. Joseph Jemsek, a self-described "Lyme Literate" doctor. During the initial consultation he asked if she had been bitten by a tick or gotten a rash. No, she replied, but she had gone camping once in Tennessee. He suggested she may have picked up Lyme disease there and sent her blood to a California lab that specializes in tests for tick diseases. A week later the test results came back: She had been infected by Borrelia burgdorferi, the spirochete that causes Lyme disease. Jemsek installed a tube in Jenkins' arm and every two weeks for a year and a half sold Jenkins a $3,000 course of Rocephin, a powerful antibiotic, to infuse on her own at home. When she developed infections around the catheter in her arm the nurse would switch it. When her arms wore out she got a port implanted in her chest. As she waited for Jemsek to treat her latest infection, she collapsed on the floor, vomiting. Drug-resistant bacteria had overtaken her entire body. Jenkins landed in a hospital intensive care unit for four weeks, barely surviving. A doctor at Carolina Medical Center, where she recovered, told her that their labs could find no evidence in her blood that she'd ever had Lyme. "I was outraged," she says, and is now suing Jemsek. The near-death odyssey cost her insurance company $400,000. The action is pending, and Jemsek has made no comment. Lyme disease, with 20,000 cases reported annually, ranks low on the list of the most prevalent infectious diseases. But it ranks first in rancor generated in the medical community. The disease is caused by bacteria related to syphilis that enter the body through a tick bite. The typical Lyme infection responds to simple antibiotics, although symptoms like arthritis and fatigue may linger in a subset of patients. Researchers at academic medical centers who study the disease say that so-called chronic Lyme, or post-Lyme, is very rare, hard to detect and not treatable with any further doses of antibiotics. The mainstream doctors warn about an epidemic of bunk diagnoses and dangerous treatments. Insurers often refuse to cover the cost of treating chronic Lyme. Arrayed against the establishment is a fraternity of Lyme specialists, many of whom have built large practices treating ostensible Lyme patients with expensive courses of antibiotics. Last year the North Carolina state medical board brought Jemsek in for a disciplinary hearing. Ten patients testified to nightmarish experiences. A widower said his wife had died from a morphine overdose related to Jemsek's Lyme treatments. Jemsek disputed all the charges vigorously. He also had 200 supporters show up, many of whom believe he cured them of a terrible disease. The Lyme Disease Association, a group that supports Jemsek, says that 30 chronic Lyme doctors have been similarly targeted by medical boards. Jemsek ultimately received a "suspension with stay" that allows him to keep practicing. The light penalty may reflect the power of Lyme support groups, which blast politicians with mail and phone calls to ensure their access to expensive care. Standing with them now is Connecticut Attorney General Richard Blumenthal, who has received awards from Lyme groups and late last year announced that he was investigating the Infectious Diseases Society of America, an 8,000-member organization of doctors trained to understand diseases like AIDS, malaria and tuberculosis. Their crime? Issuing Lyme treatment guidelines to doctors that warned against using long-term infused or oral antibiotics. Blumenthal, who hasn't yet issued any lawsuits in the case, says that the IDSA's guidelines may be in violation of antitrust laws. "Lyme disease is an extraordinarily insidious and widespread problem in Connecticut. We want to make sure that patients and physicians have unfettered choices," he declares. Insurance companies, he goes on, may be colluding with the IDSA to deny care. It's an odd charge, since a 1996 policy statement from the Federal Trade Commission and the Department of Justice says that treatment guidelines issued by medical societies do not limit competition. "You want medicine to advance by debate, not hampered by lawsuits," says Robert Buchanan, a medical-antitrust attorney in Boston. Despite intimidation from elected officials like Blumenthal, the establishment has scored some hits against Lyme specialists. In 1993 Vithaldis Shah, a New Jersey doctor, had his license yanked for five years for sickening Lyme patients with long-term antibiotic treatments and receiving a payment from the infusion company. In 1996 a doctor in Michigan was suspended after conspiring with a home infusion company and misdiagnosing Lyme patients. In 2000 a study described the death of an anonymous woman from complications arising from treating unsubstantiated Lyme with antibiotics. In Connecticut Dr. Charles Jones, a pediatrician, is under investigation by the state medical board for prescribing, over the phone, antibiotics for chronic Lyme to two children in Nevada, a desert state with few ticks. Jones, who pulled up to a June hearing in a stretch limo to the cheers of fans, has testified that he did not finalize a Lyme diagnosis until he saw the children in person. Since the hearings began, more upset patients have joined the action against Jones. Blumenthal, however, has criticized the medical board for its investigation. Mainstream doctors say their guidelines are based on scientific evidence. An early study identified 25 patients with gallstones or bile blockage resulting from antibiotic treatment of unsubstantiated chronic Lyme. A more recent study of infused antibiotics published in the New England Journal of Medicine was cut short after Lyme sufferers with persistent symptoms did not respond to a course of antibiotics any better than they did to a placebo. One patient getting antibiotics had a pulmonary embolism; another had gastrointestinal bleeding. Another paper in the Annals of Internal Medicine calls chronic Lyme a "functional somatic syndrome," similar to other nebulous ailments like Gulf War Syndrome, chronic fatigue and fibromyalgia. Another study in the same journal found that 60% of Lyme disease patients lacked any evidence of previous or active Lyme infections. Some of these patients suffered from depression, arthritis or other diseases. "There are lot of people who have fatigue or musculoskeletal pain. We want to help them but not with long-term antibiotics," says Dr. Gary Wormser, an infectious disease expert at New York Medical College who helped write the guidelines that prompted Blumenthal's attack. After the latest idsa guidelines came out in November, Wormser and his Valhalla, N.Y. lab were the target of a protest attended by hundreds of chronic Lyme patients and supporters; one sign said "Wormser Lies … Patients Die." Many of the chronic Lyme patients are upset that their insurance companies won't cover unlimited treatments. WellPoint (nyse: WLP - news - people ) will pay for only four weeks of IV antibiotics, citing published peer-reviewed studies. But science is no match for the Internet, where Lyme patients swarm chat boards to bemoan the persecution of their doctors and egg on politicians. Some celebrities have joined in the fray, such as novelist Amy Tan and Daryl Hall of rock duo Hall and Oates, both of whom say they suffer from chronic Lyme. Tan's doctor is Raphael Stricker, president of the International Lyme & Associated Diseases Society, which represents chronic Lyme doctors and patients. Stricker's San Francisco clinic also advertises its ability to treat obesity, infertility, erectile dysfunction and AIDS. In 1990 Stricker was forced out of UC, San Francisco after the school claimed he falsified data in what had been a seminal AIDS study. Before he discovered Lyme he spent two years as associate medical director at a penis enlargement clinic. Stricker and many of his chronic Lyme allies send their blood tests to a California lab called Igenex, which was once investigated by Medicare and the state of California for pumping out too many positive tests. Nick S. Harris, chief executive of Igenex, says he passed both investigations easily, but in 2001 the federal Office of the Inspector General put Igenex on a list of noncompliant labs. It paid fines totaling $48,000. Harris says his firm has had no recent brushes with regulators. Harris says that his tests are more sensitive than ones given by lab giants Quest Diagnostics (nyse: DGX - news - people ) and LabCorp, yielding positive results 25% of the time. The big national labs typically return positive results 8% of the time. He acknowledges that his results are more open to interpretation, which could facilitate more positive diagnoses. "Patients, because of the Internet, have become my best salesmen," Harris says. Jemsek, who in 2005 collected $6 million from Blue Cross Blue Shield of North Carolina, is still practicing, having declared his earlier practice bankrupt. He opened a new cash-only practice, spending $8 million on a building with a waterfall and grand piano. On the Internet patients exchange tips about how to keep seeing him. In his statement to the medical board after the stayed suspension of his license, Jemsek, who declines to be interviewed, said: "I've got 400 letters of support here, many single-spaced and several pages long." David Whelan is with the Silicon Valley Bureau, Forbes. ============================================================= Why are conventional antibiotics effective for some Lyme patients but not others? We Lyme sufferers hear all the time about other people who had Lyme as bad as we do that recovered from conventional antibiotic regimens. How come some of us recover from, say, Rocephin, while others don't? Is it because those who recover are not genetically predispositioned to having their vitamin D metabolisms de-regulated by the infections? (I'm currently trying to get my doctor to do vitamin D tests for all her Lyme patients. If only some of us have de-regulated vitamin D ratios, then it would explain why some of us recover from conventional antibiotics and some of us don't and hence require the MP.) Mike .............................. Mike, No, it is because your definition of 'recovery,' and the definitions of others, are probably very different. At the Chicago Conference Belinda defined recovery as basically getting to feel 20 years younger - as getting your life back. There has never been any recovery to this point before the MP. In the past patients were happy if they could just get to see it through another day... Rocephin is palliative in Th1 disease. It suppresses the Th1 symptoms, but they come back when you stop, as the bacterial load is multiplying while Rocephin inhibits your immune system from killing the Th1 pathogens. Lab workers have used Beta-lactam antibiotics for decades to induce bacteria to turn into the L-forms which cause the Th1 diseases. The beta-lactams (penicillins and cephalosporins) actually protect the L-forms as they are being created from the dying blood-borne infection. The overuse of beta-lactams may well be responsible for much of the proliferation of autoimmune disease over the last 20 years, IMO. ..Trevor.. Why doesn't the MP use some of the other antibiotics? What degree of healing is possible with the MP? Last edited on Mon Feb 26th, 2007 23:22 by Foundation Staff |
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(filename) Why the MP cures chronic borreliosis when other treatments fail Taken from an article written by J.C. Waterhouse, Ph.D., in her Issue 8, 2005 Update, found in CISRA's Synergy Health Newsletter which may be obtained for free from http://SynergyHN.com. "I have learned a number of additional things since I wrote it (Ed.-an earlier article) that may prove useful to others. Although many patients do report improvement with extended use of antibiotics for chronic Lyme Disease, for many, the improvement is inadequate, or relapse occurs, even with long term intravenous antibiotics. In my own case, I used various oral antibiotics in several combinations at high doses for 2 years and did not improve significantly. I also used Mepron for 3 weeks for Babesia and did not improve (in fact, the Mepron had a negative impact, in that I developed a sensitivity to it and it took a very long time to excrete the Mepron after I finished taking it). "However, the good news is that there is a newer treatment approach that is showing great promise in Lyme Disease. I have used this approach, called the Marshall Protocol, for the last 8 months and have been having much greater success than previously. The approach uses a specific type of immune modulation, together with low doses of certain antibiotics, to more effectively kill the cyst forms of bacteria hiding inside cells. Some believe the cyst or cell wall deficient (CWD) forms of the bacteria are the true source of the chronic symptoms of Lyme Disease, as well as a variety of autoimmune and other unexplained inflammatory syndromes. The Marshall Protocol (MP) was developed by Trevor Marshall, Ph.D., for sarcoidosis, but has recently been showing promise in other diseases thought to be caused by these CWD forms of bacteria (for more details and references on this approach, see Issue 7 on web site). "In this update, I also want to provide my current perspective on some other topics mentioned in the 2002 article. With regard to testing methods, although Igenex Laboratory probably still provides the most sensitive tests for Lyme Disease likely to be covered by insurance, I think the Bowen test is probably actually more sensitive in detecting Borrelia infection (http://www.bowen.org). It may be true that some people who consider themselves fairly healthy may still test positive on the Bowen test, however they will typically have low titers (and it is possible they may have some mild symptoms, or develop symptoms later). It appears that you can use the titers (or concentrations of bacteria) found with the Bowen test to monitor the level of bacteria in your body. "However, if you want to use your financial resources most efficiently, another strategy might be to skip individual tests for bacteria and instead test for vitamin D metabolites. The two vitamin D metabolites that need to be measured are 1,25D and 25D, and for the most accurate results for 1,25D, you must use a lab that freezes the samples for transport (for more information, see Issue 7 or http://www.marshallprotocol.com). The ratio of 1,25D to 25D are used in the Marshall Protocol (MP) to indicate the level of inflammation occurring due to infection by CWD bacteria, which include Borrelia burgdorferi, as well as many other species of bacteria. "Unfortunately, many studies are reporting low vitamin D levels and recommending vitamin D supplements, as a result of measuring only the inactive precursor form of vitamin D (25D). As occurred in my own case, this practice of measuring the wrong type of vitamin D can lead to problems in people with certain inflammatory conditions. My level of inactive precursor 25D was low, while my active, 1,25 vitamin D hormone was elevated, and contributing to my symptoms. The 1,25 vitamin D hormone may be elevated in patients with low 25D because infected macrophages are causing an excessive, unregulated conversion of 25D to 1,25D. The high 1,25D can directly cause many symptoms, as well as help the bacteria to increase and can actually lead to bone loss. "As for testing for other coinfections, Dr. Marshall believes that early evidence suggests that various coinfections will be eliminated by the immune system as you recover using the MP. Thus, if you do the MP, you may also choose to forego individual tests and treatments for tick-borne coinfections." |
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(filelink) Why might a person have many serious symptoms yet have a low Bowen RIBb test dilution ratio? The Bowen test looks for borrelia burgdorferi bacteria. I have read somewhere that they use commercially available borrelia burgdorferi antibodies produced from animals for their q-RIBb test. The Bb part of the name stands for borrelia burgdorferi. There is also STARI Disease now recognized by the CDC, which stands for Southern Tick-Associated Rash Illness. The CDC says that the illness has Lyme-like symptoms, but cannot be detected with the current Lyme-borreliosis lab tests, and is caused by the borrelia lonestari bacteria, and distributed by the Lone Star tick. This disease is recognized by CDC for less than two years, or, about that length of time. The CDC says that STARI is found in the Southeast section of the U.S. There may be other borrelia that are loose in the U.S. and not even thought of, much less found and proven by the CDC. Perhaps, a person had contracted STARI (borrelia lonestari bacteria) first, which may have given them time to multiply to be the greater in numbers. Then, contracted an infection of borrelia burgdorferi bacteria at a later time, which gave one the low dilution ratio on the Bowen test, since their numbers have not yet increased tremendously. Or, even some other borrelia is involved other than borrelia lonestari? Or, some other CWD bacteria other than borrelia? The symptoms of both infections are supposed to be the same. And since both are CWD (cell wall deficient) bacteria, they are combining their efforts on your immune system in a Th1 inflammatory response, to make one's symptoms so severe, yet give one the low dilution ratio on a Bowen RIBb test. Perhaps, what is needed is a rapid indentification test that will incorporate both borrelia lonestari antibodies as well as borrelia borrelia antibodies, which will then give one a dilution ratio for each bacteria. And solve this mystery! Perhaps, even a more complete gnenome study of all borrelia bacteria is needed, but with the ability to "mate", and share genetic material to the new "offspring" as proven by researchers at the NJ Medical School, this could lead to a very interesting piece of work. This is another good reason why I believe that the Dept.of Healths should require doctors to report any case that show borrelia bacteria in symptomatic peoples' bodies even if it does not pass the CDC criteria for Lyme disease. The data is needed! Thankfully, the Marshall Protocol should be able to "cure" all brands of borrelia infection, without knowing which one it is fighting. George Howell |
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Why do some Lymies say the MP doesn't work? (filelink) Q: I have received messages that some lymies don't think that the protocol works for them... any evidence of lymies getting full recovery from this??? I am reading a lot about lymies having difficulty with the MP (me included).. Does that mean that we are completely different then the sarcies and thus don't get the same good results? Or are they all similar stealth pathogens that get wiped out by this protocol? ~Flyer Reply: What it means, I think, is that there are some people out there who seem to be happy if Lymies remain sick. Every Lymie who has reported their progress to me has moved forward to recovery while on the MP. Their titres drop month by month. For example, Susan, one of the delegation that was with us in Bethesda, now has a zero Borrelia titre, and is starting to put her life back together. Yet some of the Lyme 'experts,' and some of their sycophants, seem intent on slowing our inertia. As a member of that community you need to ask yourself - why? We had a similar phenomenon in sarcoidosis, but over the last year the voices raised against truth and reason gradually fell silent. I suspect it will be the same in the CFS and Lyme communities, once folks stop trying to convince themselves that the MP doesn't work - and realize that it is their only hope Flyer, thanks for being one of the 'pioneers.' It isn't easy to pluck those arrows from your back... ..Trevor.. |
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(filelink) Can borrelia change from spirochete to coccoid to L-forms? The problem is actually a lot more complex than it seems. The genome of Borrelia has about 40% of its genes on mobile plasmids, and not on the primary chromosome. So (arguably) there could be hundreds of different versions of B.burgdorferi out there. If you look at the master Genome list at URL http://www.ncbi.nlm.nih.gov/genomes/lproks.cgi you will find only two Borrelia species fully sequenced. One was sequenced by TIGR and one from Germany. Look at the sizes - 1.52 vs 0.99 This is because the Germans are only reporting the Chromosome and 2 plasmids, while TIGR is reporting chromosome and 21 plasmids. Unfortunately the Borrelia genome has proven too complex for many of our institutions to fully assimilate, and this is an excellent example. Both groups are correct, but they are looking at the species in different ways. A similar situation exists within the Mycoplasma species. Look for example, at this species comparison: http://www.zmbh.uni-heidelberg.de/M_pneumoniae/genome/MP_MG_Comp.GIF The rapid pace of advance in science's knowledge of the genome has left 99.9% of our Infectius Diseases specialists behind. It will take a new generation to come along who can understand the new genomic tools. ..Trevor.. |
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(filelink) Why does the MP appear to be taking longer to resolve Lyme/borreliosis and CFS than sarcoidosis? I think that, in general, CFS and Lyme patients have had more long-term intervention from supplements and pharmaceuticals than many of the sarcies. Additionally, their disease is not as apparent as, for example, lupus or sarcoidosis, and this means that they generally are more ill before they get help. A sarcoidosis patient, for example, may die of pulmonary insufficiency or cardiac arrest before their overall systemic organ status degenerates to that of some of the CFS and Lyme patients. I don't think there is any fundamental difference in the species, however. I myself suffered from debilitating fatigue for almost a decade, and had to work my life around my unusual sleep and rest patterns. It was seeing that fatigue in the diabetes patients (whom I was researching) that first made me realize the common threads through all the Th1 diseases. It takes time to kill the intracellular bacteria and neurological inflammation is especially resistant because nervous tissue is poorly perfused by blood. The folks who are the sickest will need to be very patient because their inflammation is so extensive and it isn't possible to kill the bacteria rapidly without intolerable immunopathology. I do think it is important that CFS and Lyme patients do face up to the extent of their illness, however. Think about this - it takes 2 years or more for the bacteria to be killed, at the fastest rate your body can kill them. It is absolutely amazing what that quantity of bacteria must have been doing while they were living in your tissues  ..Trevor.. |
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(filelink) Info published about Lyme disease is not up-to-date This article discusses variations of Bb-spirochetes and how researchers react to it: http://tinyurl.com/77npx ===================== While I understand that the material in this release may sound earth-shattering to folks who have come in contact with only the traditional view of Lyme disease, the material here is still not up-to-date, and is very limited in its outlook. I do understand pretty well what the issues are here, and I have tried several times to communicate them to the MP membership. The problem is that the Lyme genome is not homogenous, despite what the 'experts' would have you believe. There is a chromosome with about 500,000 bp and 21 linear and circular plasmids with nearly as many genes on them as are on the chromosome. Each plasmid is mobile and self-replicating. So it is in fact stupid (IMO) to keep talking about Borrelia as one species. It is not one species. It is not even close to being one species. It is not even clear how much of the genome is necessary to create a viable spirochete, let alone viable L-forms. So to talk about variations in sub-species is missing the point. Please, first define the species itself, then talk about sub-species variation. The same goes (to a lesser degree) for Treponema and Rickettsia. Some sarcoidosis and CFS patients have no borrelia-specific markers. Clearly, borrelia is not the only organism involved in Th1 disease. But those who understand these pathogens (at the detailed level of their genome) cannot yet communicate with the clinicians who are out in the field, and who get to speak to the press. We speak a different language. How many of the sources quoted in this article would even know what a plasmid is? That is the problem that patients face. The genome has brought a revolution in knowledge about pathogenic species that only a fraction of the medical community (less than 1%) are equipped to understand. In general, patients will have to wait at least a decade for any of the concepts about these diseases to change - wait until either 'Continuing Medical Education' gets given teeth, or a new generation of clinicians comes into the workforce. Thanks for posting this article anyway, I guess it gives us the chance to discuss the real issues. .Trevor.. ps: maybe we need a conference just on this one issue. The next problem is how we get the agenda CME certified (by folks who don't have a clue) |
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(filelink) HLA tests for Lyme disease The HLA axis haplotype is almost certainly caused by the bacteria which have infected the patient, rather than by any genetic defect in the patient. You will find HLA haplotypes showing up in all the Th1 diseases. They are of no prognostic or diagnostic value at this point in time. For example, one of the strongest in Lyme, HLA-DRB1*1501, is also aberrent in Sarcoidosis, MS and Lupus (SLE). The paragraph reflecting the commonality of HLA axis haplotypes throughout the Th1 diseases can be found at http://yarcrip.com/sarcoidosissuccumbs-preprint.htm ..Trevor.. ================================= A case-control study to examine HLA haplotype associations in patients with posttreatment chronic Lyme disease. Source: Journal of Infectious Diseases, Sept 15, 2005 v192 i6 p1010(4) Author: Mark S. Klempner, Gary H. Wormser, Karen Wade, Richard P. Trevino, Jianming Tang, Richard A. Kaslow and Christopher Schmid Full Text COPYRIGHT 2005 Published by University of Chicago Press. Abstract: In a comparison of 95 patients with systemic symptoms that persisted after antibiotic treatment for acute Lyme disease (posttreatment chronic Lyme disease) and 104 control subjects without such symptoms after antibiotic treatment, we sought associations between human leukocyte antigen class II (DRB1 and DQB1) markers and posttreatment chronic Lyme disease. No strong association between posttreatment chronic Lyme disease and any class II allele or genotype was found. ............................................................... The key to understanding the results of this study are contained in the following words "Control subjects consisted of a convenience sample of patients who had been treated for early Lyme disease associated with erythema migrans during the 12 months before entry into this study." I honed in on HLA-DRB1 allele *1501, which is commonly abberent in the Th1 diseases. It has been noted to be deviant in Sarcoidosis, Multiple Sclerosis and Lupus (SLE). Sure enough, there is the allele indicated strongly as being present in both symptomatic and asymptomatic Lyme. However, because the 'control' sample were not really controls at all, but people who were already known to have been infected, the statistics used by the authors to analyse their data did not flag this *1501 allele (or indeed, any of the others). But maybe that is what the authors wanted? Useless results? Or maybe they just didn't realize just how stupid it is to select an infected 'control' group? I read this study as showing that patients with Chronic Lyme, Lupus, Sarcoidosis and Multiple Sclerosis all have aberrent alleles at HLA-DRB1*1501. Further that this study provides strong evidence that, once infected, the Lyme bacteria continue to live on in nearly all the Lyme victims, even those who are asymptomatic, and the alleles of the HLA axis provide persuasive evidence for the existence and persistence of Chronic Lyme. ..Trevor.. ============================================ I don't believe that the HLA axis genetic changes are necessarily handed down in an individual's DNA, I believe that the HLA axis (HLA-DRA, HLA-DRB and HLA-DQ) are all mutations caused by the pathogens responsible for Th1 infection. Only that hypothesis explains why so many different diagnoses end up with common HLA haplotypes, yet there is not determinate diagnostic value to be obtained by measuring them. Yes, I know, some of the HLA haplotypes are 50% greater in this, that, or the other diagnosis, but genetics should result in 100% and 0% and anything else is just statistical noise, and should be discarded, IMO. ..Trevor.. How does Th1 inflammation develop? What is successive infection? |
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(filelink) Do not donate blood if you have Lyme/borreliosis "Ms. Nguyen emphasized that "anybody who has had B microti is permanently prohibited from donating blood" and is registered in the blood bank system of the Red Cross nationwide. **However, it is important to identify those people infected with B microti prior to blood donation.** According to Ms. Nguyen, most of the transfusion-related transmission occurs through people who are infected with the tick-borne disease but who are asymptomatic". Tick-Borne Disease Transmission by Blood Donation Prevalent in Endemic Areas Mary Beth Nierengarten Medscape Medical News 2005. © 2005 Medscape Oct. 11, 2005 (San Francisco) The need to develop strategies to prevent transmission of tick-borne disease via blood transfusion is increasing as new reports continue to surface. Although not as much in the popular press as Lyme disease, Babesia microti is creating its own quieter havoc. In a study presented here at the Infectious Diseases Society of America 43rd annual meeting, Megan Nguyen, BS, from the American Red Cross in Rockville, Maryland, presented data from a six-year study that showed the prevalence of B microti transmission via blood transfusion in areas where the tick is commonly found. Examination of 13,573 samples from blood donors from 1999 to 2004 in endemic regions of Connecticut showed that 175 samples (1.3%) tested positive for B microti infection based on indirect fluorescent antibody testing. Of these 175, 129 donors consented to participate in a three-year follow-up study in which they were tested by IFA for the presence of antibodies to B microti as well as receiving nested polymerase chain reaction (PCR) testing for parasitemia on a regular basis. Overall, 27 donors (21%) were found to have parasitemia as indicated by a positive PCR test, suggesting that some patients have persistent, ongoing infection. In addition, parasitemia rates decreased from 55% in the first two years of the follow-up study to 3% in the third and final year. Ms. Nguyen said the study did not show a clear reason for this, adding that many factors could account for it. Ms. Nguyen emphasized that "anybody who has had B microti is permanently prohibited from donating blood" and is registered in the blood bank system of the Red Cross nationwide. However, it is important to identify those people infected with B microti prior to blood donation. According to Ms. Nguyen, most of the transfusion-related transmission occurs through people who are infected with the tick-borne disease but who are asymptomatic. Identifying infected people before they donate blood is therefore an important goal in reducing the risk of transfusion-related B microti transmission, but the best way to do this is not yet clear, she said. Richard Whitley, MD, a professor of pediatrics at the University of Alabama in Birmingham who moderated the session, told Medscape that prospective blood donors are not currently screened routinely for tick-borne diseases, an issue that needs to be addressed by local blood banks. However, Ms. Nguyen told Medscape she is hopeful "that there will be screening" or a U.S. Food and Drug Administration (FDA) approval for testing before donation. Unfortunately, she added, she does not know of any test under investigation for FDA approval. IDSA 43rd Annual Meeting: Abstract LB-3. Presented Oct. 7, 2005. http://www.medscape.com/viewarticle/514364?src=mp Reviewed by Gary D. Vogin, MD ================================== Can I donate blood, organs, tissue or bone marrow if I have a Th1 inflammatory disease? |
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(filelink) Last edited on Wed Jan 17th, 2007 04:36 by Foundation Staff |
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When To Suspect Lyme Disease (filelink) This essay, written by John D. Bleiweiss, M.D. in April, 1994 is very long, but also very comprehensive. The reader suspecting Lyme symptoms should either identify with a number of sections of this article, or, in this absence, be fairly certain of excluding the possibility of Lyme. (Any Doctor investigating prudent treatment for Lyme Disease would do well by reading this essay.) When to Suspect Lyme ..John D. Bleiweiss, M.D. Traditionally, the public has been advised to suspect Lyme (LD) if a round or oval, expanding, red rash develops 3-32 days after a deer tick bite associated with or followed by a flu-like illness. This limited description will apply to only some cases. About 50% of patients do not recall one or more of tick bite, rash or flu-like illness. The rashes associated with LD can assume a variety of morphologies including vesicular, urticarial, eczematoid or atrophic (Acrodermatitis Chronicum Atrophicans). For many patients, neurologic, cardiac, arthritic, cognitive and/or psychological complications predominate. While deer ticks and LD have a well known affiliation, other potential vectors can carry the spirochete that causes LD (Borrelia burgdorferi; Bb). These include, the lone star tick, fleas, the biting flies (e.g. green-headed fly) (and mosquitoes?). A case of suspected transmission via blood transfusion has been reported by Dr. Burrascano. The demonstration of Bb by PCR in two museum mouse specimens dating from 1894 (Massachusetts) and in ticks collected during WW II, provides a mechanism for potential life long exposure and disease which predates the formal 1975 discovery of LD. An occasional patient will date their symptoms which resolved on antibiotic therapy for LD to early childhood. Before the diagnosis was made, patients would dismiss those symptoms with the statement: "I've always had those problems". That resigned characterization implies that the longevity of the symptoms rules out a reversible cause. Subsequent resolution of the long standing symptoms on antibiotic therapy for LD belies that notion. Symptoms of LD can begin within days of inoculation with Bb or appear belatedly, but usually in the first to fourth month. Mice inoculated intraperitoneally had Bb demonstrated in the brain on biopsy 12 hours later with a peak at 48 hours (Stockholm Conference, 1990). Dr. Luft has published the detection of Bb by PCR (Polymerase Chain Reaction) in the CSF (Cerebrospinal fluid) of humans 2 weeks after the appearance of non-CNS related symptoms! If dissemination can occur early, then staging the disease according to the temporal appearance of symptoms may be irrelevant. The absence of symptoms related to a particular organ system doesn't necessarily exclude the presence of Bb from that organ. Conversely, due to the possibility of symptoms being engendered by chemical mediators and autoimmune reactions by the host (against non-viable but immunoreactive DNA blebs), organ dysfunction and attendant symptoms can appear at sites removed from the actual spirochetes. The diagnostic and therapeutic problems that these phenomenon entail should be obvious. Rapid dispersion of Bb could lead to the prompt appearance of complications; e.g., meningitis. There is no absolutely predictable clinical sequence for LD. The flu-like syndrome may be absent from the initial presentation and may endure once established without treatment. Cardiac and neurologic complications can be observed sometime within the first 3 months after microbiologically contracting the disease. Arthritis (i.e., joint inflammation; distinct from arthralgias; i.e., joint pain) can also accompany the initial clinical course, but more often develops later on between the second and sixth month from inoculation. The onset of complaints can not only be subtle and desultory, but delayed for a year or more. One of my patients denied all LD related symptoms until her husband died, whereupon, a plethora of complaints cascaded into her life beginning that very day. Another had an annual flare of LD as part of an anniversary reaction centered on the date of his mother's death. Moreover, the early constellation of symptoms can have a paucity of findings with unidimensional presentations: the onset of solitary problems such as vertigo, or recurrent upper respiratory tract infections. Over time, as the untreated LD percolates, symptoms accrue to the burgeoning clinical picture until a multisystem presentation is created. Other patients can have their manifold symptoms complex develop in the manner of an avalanche. These patterns represent the extremes of a clinical continuum between which there are many variations on the theme ranging from mild to severe disease. Thus, The failure of a pathognomonic (unique and specific) presentation to consistently unfold causes sufficient clinical confusion, that a punctual diagnosis is problematic. Therefore, a high index of suspicion is placed at a premium. If a clinician can't reconcile preconceived notions about how LD should announce itself with a patient's history and physical findings, it is a disservice to the patient and an abdication of professional imperatives to presumptuously conclude that the symptoms are psychosomatic or that the patient is faking! Antecedent or concomitant factors which can cause symptoms and physical changes de novo or aggravate contemporary problems are reliably solicited on close questioning of LD patients. Females experience an exacerbation of their LD symptoms before or during their menses, while pregnant and with oral contraceptive hormones. Many patients have symptoms intensify or reappear with physical and emotional stress, if sleep deprived, after exercise, in a hot bath, after alcohol consumption, with fasting (hypoglycemia) or dehydration. Humidity, low barometric pressure, cold or rainy weather can elicit arthralgias, fatigue, encephalopathy or headache. A cold draft of air can precipitate the appearance of pain in exposed skin and the underlying bone, or even VII cranial nerve (Bell's) palsy. Patients with poor control of symptoms abhor the extremes of ambient temperature. Typically, heat intolerance is revealed as irritability, headache, excessive perspiration or sleepiness. Photophobia can enhance the somnolent propensity that can occur while driving a car. Significant head trauma has incited severe symptoms that later resolved with antibiotic therapy for LD. A sudden acceleration of encephalopathy (see below), headache and dizziness, thought of as putative post-concussion syndrome, can be evoked by head trauma. Diagnostic inaccuracy will be minimized by not indolently attributing all problems following head trauma to the most obvious cause. I routinely advise my patients with LD to abstain from cigarettes, alcohol and steroids because therapeutic inadequacy or an avoidably prolonged convalescence is frequent (Dattwyler, RJ, Lancet 1:687, 1987 - on steroid use). Patients have described clinical deterioration when steroids were used fortuitously or intentionally when hypoadrenalism was absent. Another hazard attending palliative steroid use is that some symptoms will be concealed, rendering the clinical picture less interpretable. In a private communication, a physician related that one of his LD patients succumbed to fatal cardiomyopathy after receiving steroids. One helpful caveat is to avoid the use of electric blankets or sleeping in water beds with the electric current activated, otherwise you might wake up with one or more LD symptoms. Allergic and chemical hypersensitivities can enhance or cause symptoms to emerge temporarily. Symptoms vary stereotypically during the day. Joint stiffness and "brain fog" are often reported on rising in the AM (but not solely in the AM). Fatigue can be unrelieved by sleep, or develop between noon and 4 PM, whereupon a short nap provides refreshment. "Madman Syndrome" (explosive irritability) may appear toward the end of stressful work period or late in the evening. A "mad face" can herald imminent detonation. Prior to proper diagnosis, patients habitually report that they were assigned the following diagnoses most often: Chronic Fatigue Syndrome, Multiple Sclerosis, Fibromyalgia, Lupus, Candidiasis, Chronic mononucleosis, Hypoglycemia, and Stress-related illness. If these appear in a differential diagnosis, then LD should be considered. On cursory inspection, many patients with LD appear deceptively well but in fact feel awful Don't be fooled! The mien of a Lyme patient ranges from phlegmatic, sullen, staring off into space, to one of agitated anxiety and hyperkineticism. Their oral and written recitations similarly vary from cryptic to being overinclusive and circumstantial. Geschwind's Syndrome embraces some varieties of LD encephalopathy precisely (Textbook of Internal Medicine, Ed: Kelly, 1989, p. 2509). Stuttering was reported by several patients to coincide with the onset of their LD and often proved reversible. Patients most frequently report fatigue that varies from mild to debilitating. Usually there is a loss of interest and initiative so that lounging around becomes habitual. This derives not from laziness, but results from lassitude. Attempts to indulge avocational or vocational pursuits is frequently interdicted by either the languor of Lyme or by encephalopathy. There is a tendency to nap, sleep that is not rejuvenating, and hypersomnolence at inopportune moments; e.g., in the classroom or during a favorite pastime. Sleeping away entire days is not unknown. Paradoxically, at usual bedtimes, patients often experience insomnia or frequent awakenings. Sleep does not always provide respite as ferocious or vivid nightmares can occur. Childhood night terrors can be due to LD or more mundane causes. Intermittent fevers range from low grade to 104.5 degrees F. The typical context for high fevers is in the first week of antibiotic therapy especially if multiple agents and/or IV drugs are used. While fever is the hallmark of the classic Jarisch-Herxheimer (J-H) reaction, its appearance is inconstant. Compared with most causes of high fever, the patient can look and feel their best during or shortly after the fever with a relatively non-toxic demeanor. This can sometimes be diagnostically helpful. The differential diagnosis of febrile seizures in infants should include LD. Many LD patients have routinely subnormal body temperatures so that the appearance of a temperature of 98.6 degrees F may be compatible with a low grade fever analogous to diabetics. Very often, the pinna and ear lobes are varying shades of red. Less commonly, a similar erythema can be observed on the hands or malar (upper cheeks) areas. A malar rash is not pathognomonic of Lupus, if in fact SLE is distinct from LD (Abstract 55A, V LD Symposium). Fifth Disease (slapped face) is suspected of being due to LD. Lymphocytoma of the ear lobes has been encountered more often in Europe. Cold hands and feet even in warm environments occurs and some patients have Raynaud's phenomenon. Potentially contributing to this vasoconstriction are excessive levels of vasoconstricting hormones, magnesium and potassium deficiency, limbic or hypothalamic dysfunction due to CNS infection, local inflammation of capillary sphincter or hypothyroidism. Eczema and psoriasis can appear in conjunction with LD. A female LD patient had generalized psoriasis covering 40% of her body. Antibiotics for LD gave total relief. Alterations of cutaneous sensation are very common. Most often there is numbness and tingling (paraesthesias)of the central face, fingertips, scalp and in the extremities. Muscle twitching usually occurs in the eyelids and extremities. Tremors, myoclonic jerking of entire extremities or truncal shudders can suggest pseudoseizures but is attributed to neuritis. Patients also report electric shocks, dysesthesias (abnormal sensory responses to stimuli), painful or itchy skin and flushing. An inordinate amount of exertional or non-exertional sweating may be described in the absence of hyperthyroidism. One of my patients experience anhydrosis (inability to sweat) for 27 years until antibiotics were given for LD. Dizziness, imbalance and clumsiness can become very frustrating as patients drop objects or knock them over, trip a lot, turn into the wall when rounding corners, and develop sloppy and slower handwriting. Many use the phrase "a vibration in my head". Others remark that they feel "toxic". Along with the "brain fog", these colloquialisms connote LD until proven otherwise. Eventually the majority, but not all, complain of one or more of "foggy brain", forgetfulness, anxiety, mood swings, loss of initiative, depression, impairment of concentration, inattention, easy confusion or disorientation when attempting intellectual tasks. Paper shuffling can be the end result when patients attempt to organize or assimilate even limited amounts of information. These problems, and the others described below, constitute the salient features of Lyme encephalopathy. Short term memory impairment causes patients to forget what they were going to say, why they entered a room, where objects were placed, the previous sentence or plot content, calendar dates, their schedules, names and faces of familiar people, even family members. Cognitive neglect caused one patient to wander around the room looking for the room looking for the pencil clenched between his teeth. A mother left her infant and baby carriage in my office parking lot and went home. Others forgot how to spell even simple words, how to read or must re-read with varying degrees of comprehension. One patient drove to Philadelphia instead of the desired Princeton destination because the initial letters were identical and confused him. After shopping for groceries, another patient placed her shoes in the refrigerator and stored the food in the clothes closet. Lyme patients can lose their way home or on the way to work, bypassing otherwise familiar exits or plain forgetting where they are in time and space or how they got there. This is known as topographical disorientation or environmental agnosia. Elementary math problems may prove insurmountable. Numerical errors are common. Sequential task performance is compromised in Lyme. Lyme patients have a penchant for saying, "Wait a minute", 2-3 times rapidly when the only demand on them is to record a phone number, which also speaks of perseveration. Inattention frequently characterizes the way patients relate to the world. Some patients participate passively, unable to initiate or engage in the usual forms of social and intellectual exchange. Verbal and written forms of expression have a typical Lyme flavor. The content demonstrates disorganization, an inability to follow a train of thought and there is a proclivity to ramble on and on in great detail which propels further confusion amongst the forest of details. Ubiquitous among the myriad cognitive flaws are the frequent errors of word selection or pronunciation and the consistent word and number reversals. Concentration on a task can be problematic because attention span is abbreviated. As increasing amounts of information have to be processed, the Lyme patient becomes proportionally lost, disoriented, frustrated, fatigued and finally must desist from further intellectual activity. The desire to initiate projects and social interaction is often blunted if not absent altogether. Thus a deterioration in academic and vocational performance is a frequent manifestation of LD in children and adults.. Miklossy (NeuroReport 4:841-848, 1993) reported the detection of Bb spirochetes on dark-field microscopic examination of post-mortem brain biopsy specimens FROM PATIENTS WITH ALZHEIMER'S DISEASE! CSF and blood cultures grew out Bb from those cases. In my view, a child assigned a diagnosis of Attention Deficit Hyperactivity Syndrome (ADH) or PNI (Perceptual Neurologic Impairment) should be evaluated for LD. A 16 year old boy whose Tourette's Syndrome began at age 5, had Osp A antigen detected in his CSF. LD treatment resolved the Tourette manifestations. Another patient of mine with ADH had a positive IgM Lyme antibody in the serum. The manifestations of ADH were eradicated while on antibiotics. Distinguishing causality from mere exacerbation of ADH or Tourette by Lyme is moot, and therefore, I suggest an evaluation LD for these patients. Parenthetically, the boy with Tourette also had cognitive impairment, familial nephritis with early renal insufficiency and OCD (Obsessive Compulsive Disorder). These clinical features all remitted with antibiotics! A real estate agent's prominent encephalopathy resolved with LD treatment whereupon his commercial output jumped to a record zenith and became the recipient of numerous corporate awards. The benefits of arresting LD are self evident to him. Personality changes are nearly universal in Lyme encephalopathy with emotional and expressive incontinence being typical. Usually there is a baseline irritability which fluctuates. Patients with LD encephalopathy react to even mild degrees of stress with frustration, anger or crying spells out of proportion to the situation. Emotions can reach escape velocity and rages can become volcanic with a momentum beyond volitional control. Unpleasantness is inevitable due to volatile tempers, super critical dispositions, and impatience with themselves or others. Lyme patients can be easily irritated by anyone just walking into the same room even though eye contact is never made or words exchanged. Low threshold exasperation in unexpected circumstances is not uncommon. Thus a parent responds to an infant's needs with anger and frustration. Perpetrators of "shaken baby syndrome" recapitulate an emotional response indistinguishable from that of a Lyme patient whose encephalopathy is out of control. Many express morbid fears of occult illness, impending death and can be generally pessimistic or maudlin. Some develop intricate paranoid theories regarding imagined conspiracies against them. Lyme patients often evince a tendency for being overly sentimental. Hyperbolic thought finds expression in obstinacy, self-righteousness, being contentious, speaking in categoricals, and inappropriate and atypical vulgarity. Internalized anxiety results in the perception of being hurried even without a deadline or the inability to remain calm when there is no reason for not feeling calm. Panic attacks are the extreme of this anxious state and should arouse a suspicion of LD. I suspect that in addition to CNS infection of the limbic system, these phenomenon could also be the result of elevated adrenaline levels, Mg++ deficiency or hypoglycemia. A rare LD patient will admit to agoraphobia or claustrophobia. Depression alternating with anxiety is very common in LD. Psychiatrists should routinely evaluate a depressed patient for LD before/when initiating psychotropic medication. A patient with LD may have a plausible reason to be depressed, but their emotional response can not only be incongruous with their usual coping style but also the depression can be ablated or ameliorated with control of the LD infection. Lyme encephalopathy typically vitiates an otherwise mature and functional emotional repertoire. With a loss of voluntary and subconscious editorial control of emotions and expression in word or behavior, a patient with encephalopathy gives the general impression of being erratic, inappropriate, if not dysfunctional. Less frequently, mania, obsessive-compulsiveness, schizoaffective disorders and homicidal/suicidal ideation is encountered and has been reported. Fatal attractions are consistent with the LD style. Adolescent hormonal surges and the emotional turmoil wrought by LD at once camouflage and exacerbate each other mutually. Thus, children tend to be unruly, hard to please and prone to atypical emotional reactions. A child who is misbehaving in class should not be dismissed as a "bad kid". Lyme can catalyze inappropriate behavior and commentary. Many patients retrospectively realize that they were out of control but in the event were unable to intercept their behavior. Misattribution as to the origin of behavioral perturbations is the rule. The development of aberrant personality traits can be gradual or even situational, further obscuring the medical etiology. An acute break from normal behavior can serve to highlight the abnormalities and suggest the need for evaluation. thus, dysfunctional behavior and intellectual incapacitation are bitterly recalled by LD patients when they finally realize how their interpersonal relationships, school and vocational conduct were negatively impacted. Clinically, there is considerable overlap between LD and Chronic Fatigue Syndrome (CFS). In their masterful review of the pathophysiology of CFS, Drs. Rosenbaum and Susser (Solving the Puzzle of CFS, 1992) describe SPECT scan findings of brain perfusion (blood) in CFS patients. Hypoperfusion of the left temporal, right parietal and left frontal lobes were consistently seen. These regions control the very areas of functioning which are abnormal in both LD and CFS, namely verbal capacity, memory, emotions and higher order information processing. Dr. Jay Goldstein has proposed the term "limbic encephalopathy" to describe the disorders of memory, appetite, temperature and appetite regulation, libido and hormonal homeostasis seen in CFS. He advances the concept of an "agent X" which incites CFS and causes dysregulation of the immune system and the limbic components of the CNS. I feel "agent X" is Bb. I am encouraged in this view by anecdotal experience whereby CFS responded to antibiotics given either fortuitously or by way of Lyme treatment, due to positive serologies (antibody tests) for LD in some CFS patients and the development of a J-H reaction in CFS patients who take antibiotics. Crimson crescents, portrayed as diagnostic for CFS, I have detected in LD where the diagnosis was secure. Limbic encephalopathy elegantly embraces the preceding observations in Lyme encephalopathy. It is a potential mechanism to explain my suggestion that LD can be responsible for anorexia nervosa/bulimia. Anorexia was documented in earlier studies on LD. Uncinate fits and are characterized by hypersexuality, rage states and vulgarity, are compatible with LD. Indeed, disinhibition, the release of the usual brakes on behavior, would be part of limbic dysfunction. LD could cause reversible disturbances in brain physiology through cytokine mediators, direct infection; e.g., encephalitis and perivasculitis, demyelination, metabolic aberrations within the CNS such as regional hypoperfusion, altered rheologic (flow) characteristics of blood, intracellular acidosis and the depletion of ATP. Permanent changes may include demyelination or loss of neurons leading to atrophy. Neurologic complications in earlier reports were said to occur in 20% of LD cases. In my experience, and as published by Dr. Logigian, 90% of patients have one or more of encephalopathy, cranial neuritis or psychiatric changes. Early in the course of LD, these problems may be absent or muted, but eventually intrude and can become dominant aspects of LD. Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS and LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination. In Miklossy's study above, senile plaques stained avidly for Bb spirochetes. Vincent Marshall reviewed the MD literature in Medical Hypothesis (Vol 25: 89-92, 1988) and advances the notion that LD is causing MS! His survey revealed that multiple studies prior to 1951 were able to demonstrate spirochetes in the spinal fluid of MS patients (by inoculation into animals and on silver stain of CNS tissues). Dr. Coyle has documented the presence of antibodies to Bb in MS patients (Neurology Vol. 39:760-763, 1989). The encephalopathy attributed to MS is very reminiscent of LD. Both MS and LD are associated with sinusitis (Lancet, 1986). Dr. Leigner has reported a case of LD which fulfilled all criteria for MS. The epidemiology of MS and the geographic distribution parallels that of LD. The symptoms of both LD and MS can be aggravated if the patient takes a hot bath. Anecdotally, patients with LD, who previously had been identified as MS, responded to antibiotic therapy. LD has been documented to cause strokes, paralysis, a variety of seizures, transient or permanent blindness, Parkinsonian-like movement disorders, motor and/or sensory neuropathies, mononeuritis multiplex, radiculoneuritic pains, meningitis and encephalitis. It has been affiliated with Lou Gehrig's disease and the Guillain-Barre Syndrome. Recent reports suggest that the spectrum of neurologic LD is actually similar in both Europe and the USA (Jacqueline, MS; Surv Opthalmol 35:191-204, 1990) and belies the assertion that European LD research holds no relevance for LD in the USA. The more commonly noticed neurologic deficits involve one or more cranial nerves (I thru XII), most often the sensory divisions of the trigeminal (V) and the motor components of the facial (VII) nerves in my patients. In declining order, deficits to pain sense are detected in V2, V3, and V1. V2 neuritis appears as paraesthesias or dullness in the central face and cheeks. Gum and tooth pain can be another manifestation of trigeminal neuritis. Rule out dental abscess or sinusitis which can present with similar tooth pain. The most common cranial neuritis I see is that of the VII nerve. Abnormalities of the VII nerve can be varied. Usually there is symmetry of the central facial creases, the lips at rest or in motion, or overt deviation of the mouth or smile to one side. Colleagues have dismissed these asymmetries as normal findings, saying "well, everyone has those". I feel there is significance when antibiotics cause these so-called innate or normal findings to resolve. When Bell's palsy is present, there are the facial defects described above for VII neuritis plus a wider eye on the same side as an elevated eyebrow, often attended by complaints of tearing and drooling (usually at night) on the affected side. 10.6% of 951 LD cases were found with Bell's palsy and 25% of those have had bilateral Bell's palsy (Clark, JR et al. Laryngoscope 1985: 95: 1341-45). Bilateral Bell's promulgated as pathognomonic for LD, actually can be associated with intrapontine lesions, diabetes mellitus, syphilis, sarcoid, leukemia, Guillain-Barre, viruses or diphtheria. Considering the incidence of Bell's palsy in LD, it is improper to treat it as viral in origin without a work-up for LD. Incidentally, hyperaccusis (sound sensitivity) can be a feature of VII neuritis. Olfactory neuritis (I) is attended by dysosmia (unusual smells). Neuritis of the III, IV and VI cranial nerves will show up as double vision. When the VIII nerve is involved, vertigo and impaired hearing can result. I have had at least two cases of Meniere's Disease respond to treatment for LD. Dysphagia (difficulty swallowing) can be associated with X neuritis but not invariably. More often in my experience, a deviated uvula or soft palate is perceived. Dysphonia (altered voice) can occur with X neuritis when the branches that serve the larynx are affected. Recurrent laryngeal nerve paralysis has been seen with LD (Schroeter, V. et al. Lancet 2:1245, 1988). IX neuritis (glossopharyngeal) can cause a unilateral sore throat which was reported by 3 of my patients. XI neuritis (spinal accessory) presents as trapezial or sternocleidomastoid muscle weakness resulting in a drooped shoulder or weakness on resisted head rotation respectively. Do not confuse this with a unilateral dystonia where the affected shoulder girdle will be elevated with preserved motor strength on both sides. Hypoglossal (XII) neuritis can be associated with a heaped up tongue on the unaffected side or deviation of the tongue on protrusion toward the abnormal side. LD related headaches can have a wide variety of patterns and can broadcast the early onset of LD or a flare of LD. The headaches incorporate the characteristics of migraines, muscle tension or cervical/radicular headaches. Pseudotumor cerebri (elevated CSF pressure with normal CSF analysis in the absence of intracranial masses) can complicate the course of LD and cause headaches. Papilledema (swelling) of the optic disc is usually present when CSF pressures are elevated, but not invariable. A spinal tap will have high opening pressures and be therapeutic as well. Depending on the characteristics of the headaches, sinusitis and brain tumors may have to be ruled out. Cluster headaches have characteristics compatible with some LD headaches including responsiveness to 100% oxygen. Immunosuppression due to LD has been reported. Therefore, it is not surprising that recurrent or intractable upper respiratory tract infections (URI's) have been noted. LD can cause or worsen pre-existing sinusitis, asthma, bronchitis, otitis, mastoiditis. Frequently, the pediatric history of LD contains a pattern of repetitive URI's. Mastoiditis can also be associated with a Bell's Palsy. LD can be affiliated with the appearance of new onset allergies for the first time in a patient's life or magnify an atopic predisposition. The usual medications for sinusitis and allergies will have a predictably diminished effect, when LD is operant. Another concomitant reported by an incidental patient is the occurrence of motion sickness which can be reversed with LD treatment. Eye related problems in LD are commonplace and can include conjunctivitis, ocular myalgias, keratitis, episcleritis, optic neuritis, pars planitis, uveitis, iritis, transient or permanent blindness, temporal arteritis, vitritis and periorbital edema (Jacqueline MS; Ibid). Horner's syndrome, ocular myasthenia gravis, and an Argyll-Robertson pupil are also reported. Optic neuritis has been observed to become recurrent or intractable after treatment with steroids. Given the earlier remarks about the detrimental effects of steroids on LD, recidivous optic neuritis may be due to occult LD. Lyme hepatitis occurs in approximately 15-20% of patients. Liver tenderness is inconstant and the elevated liver enzymes respond to antibiotics. Sometimes, the hepatitis appears temporarily in the early phases of treatment with subsequent resolution. In many of my patients, cysts are found not uncommonly in various locations: thyroid, breast, liver, bone, ovary, skin, pineal gland, and kidney. Some forms of Polycystic Kidney and Fibrocystic Breast Disease may be LD manifestations. LD can cause an interstitial cystis leading to bladder pain relieved by urination. A neurogenic bladder can develop with either hesitancy, frequency, loss of bladder awareness, urinary retention, incontinence or the symptoms of UTI (urinary tract infection). I suspect that some cases of chronic pyelonephritis are actually LD. Pediatricians may want to consider that nocturnal enuresis (bedwetting) is secondary to LD. Constipation severe enough to cause fecal impaction can occur. Many LD patients will experience a spastic (irritable) colon and that diagnosis should spark a search for LD. I have treated LD attended by ulcerative colitis with substantial remission of the colitis when antibiotics were inaugurated. Fecal incontinence due to impaired rectal sphincter tone can occur. Dr. Martin Fried has demonstrated Bb spirochete in the gastric and duodenal mucosa of children with LD who complained of abdominal pain and who were documented to have gastritis and/or duodenitis. It is appropriate to work up LD when confronted by these clinical entities. Among untreated patients with LD, arthritis can ultimately develop in up to 60%. The joint swelling, which may or may not be painful, frequently is episodic, recurrent and migratory if multiple joints are involved. Any joint can be affected including the TMJ (temporomandibular) and small joints of the fingers (contrary to earlier reports). Up to 10% of untreated LD arthritis can develop into destructive/deforming synovitis almost identical to Rheumatoid Arthritis (RA). Dr. Lavoie has published the coincident findings of LD with RA, and SLE (lupus) with LD. The SLE was associated with positive DS-DNA (double stranded DNA) which is considered diagnostic for lupus. The tabulation of rheumatologic syndromes, either caused by LD or affiliated with it, is growing. Drs. Weber and Schwartzberg have reported Polymyalgia Rheumatica apparently caused by LD. Sjogren's Syndrome with LD has been published. Antibodies to Bb in the context of Psoriatic arthritis, systemic sclerosis and Reiter's Syndrome have been documented. An expanding cohort of patients in my practice appear to have long-standing LD that dates to their "growth spurt" years and their past medical history contains the previous development of Osgood-Schlatter's Syndrome (water on the knee) in their teens. A relationship to LD can't be excluded. Arthralgias and bone pain in LD can be excruciating. It is the imprudent clinician or parent who lackadaisically attributes these symptoms to "growing pains" or aging. =============== Another patient of mine recalled recurrent and migratory polyarthritis since he was 18 (1966). Monthly Medrol Dose Packs (steroids) failed to alter the clinical picture. In 1987, he was hospitalized with an acute exudative synovitis of the knee, whereupon ear lobe biopsy demonstrated the classic histologic feature of Relapsing Polychondritis, a very rare disorder with a peak onset in the 5th decade of life. In spite of continual high dose steroid treatment, (and later methotrexate with non-steroidal anti-inflammatory agents), he eventually developed a deforming arthropathy in his hands which progressed slowly between 6/90 to 12/92. Earlier physicians had discounted the significance of a positive Lyme Elisa = 1.09 in 4/91 as "low titer". An unsuspected encephalopathy betrayed its existence as memory and concentration impairment beginning 1/91. The patient presented for LD evaluation 1/93. Laboratory values include: an IgG by Elisa = 14.7, IgM by IFA = 80 and the Western Blot had bands at 31 and 41 KDA. the polysynovitis and encephalopathy proved rapidly responsive to antibiotics for LD. The patient was quickly emancipated from the other medications although steroids had to be slowly tapered and are now down to an inconsequential dose without recurrence of rheumatologic complications. The patient, although symptom free while on antibiotics, has permanent crippling deformities of the hands. ==================== Cardiac complications arise in 8-12% of LD cases. Conduction defects and heart block, of which first-degree is the most common, can be discovered on EKG. A long rhythm strip should be employed to detect intermittent blocks. Higher degrees of heart block can result in fainting or death and may require cardiac pacemaker. Sudden death can also result from arrhythmias. Fast and slow heart rates occur, usually at the time of symptom flares, and sometimes in the manner of Sick Sinus Syndrome (tachy/brady). Ventricular tachycardia has been documented to attend LD infection in the heart, confirmed on cardiac biopsy. The cardiomyopathy may be complicated by congestive heart failure (CHF) as the following case might illustrate. Mitral valve prolapse is not uncommonly found in LD. MVP can be associated with confounding chest pain and ventricular arrythmias. It is often accompanied by Mg++ deficiency and LD can cause Mg++ levels to be low. In a few of my patients, MVP developed only after the onset of LD and resolved with LD treatment. Chest pain due to LD may arise from numerous causes: myocarditis, pericarditis, angina, asthma, bronchitis, periostitis of the ribs, pectoral myositis and tendinitis, sternoclavicular and costochondral arthritis, esophagitis and esophageal spasm, stomach acid reflux, and gastritis. Elevated ACE (angiotensin converting enzyme) levels have been detected in LD (Leigner, 1990). The relationship between high ACE levels and heart disease may provide a mechanism to explain LD's anecdotally suspected tendency to accelerate Coronary Heart Disease and incite hypertension. Possibly, Syndrome X (angina with normal coronary arteries at catheterization) is due to LD induced arterial spasm, an event that might be enhanced by direct perivasculitis and/or Mg++ deficiency (see Grisold, M abstract No. 55F, V Int'l Lyme Symposium). Potassium deficiency without an obvious origin irregularly evolves in LD. Rarely, the K+ losses are profound. This could be due to Mg++ deficiency. New onset or difficult to control hypertension is more likely to be seen. LD should be part of the evaluation of hypertension. LD treatment has permitted easy BP control in several patients, some of whom were able to forego using their traditional hypertension medications. Increasingly, I am encountering thyroid disease in LD. A local endocrinologist has remarked to me privately that the incidence of thyroid involvement in LD may be greater than expected from the normal population. A final judgement awaits formal statistical analysis. In many of these patients, the thyroid dysfunction was seen to originate in the pituitary or hypothalmus. Remaining alert to the possibility of thyroid disease is essential because there can be considerable clinical overlap with LD. Subacute thyroiditis is the most prevalent thyroid phenomenon I see in LD. Hypoadrenalism can uncommonly develop. Uncorrected hormonal aberrations can vitiate otherwise effective LD therapy. Like any infection, LD can provoke the onset of hyperglycemia and alter the facility with which diabetes is managed. Impaired fertility and a loss of libido is not infrequent in LD. A reversible cause of infertility should be sought and ought to include LD. Reduced sexual interest without an ostensible justification is usually misinterpreted by the partner with predictable social and psychological turmoil. LD infection in the CNS or in the sex glands may be causal. In a few female LD patients, disturbed estrogen and progesterone levels were found. Early "menopause", skipped menses, and heavy menstrual flow represent a few of the perturbations in LD. Women with symptomatic LD can experience new onset or heightened PMS (ballistic mood swings and irritability), or perimenstrual headache or cramps. The last of these theoretically could also be due to Pelvic LD infection (ooperitis or salpingitis) and/or elevated PGE-2 (prostaglandin E-2) levels, the latter having been reported in LD. A surfeit of PGE-2, free radicals, altered fat metabolism and general immunosuppression by LD may contribute to a predilection (stimulate or predispose) for oncogenesis (forming cancer). Carcinomas are not unknown in LD: melanoma, thyroid cancer, and lymphoma have been published. Free radicals, by engendering connective tissue cross-linking, could be responsible for intra-abdominal adhesions to form, and for some LD patients to appear older than their stated age, or have a haggard facial appearance. Breast pain due to mastitis and testicular pain from orchitis have been described by some of my patients. So far, there are 3 men in our files whose chief complaint with LD was pelvic pain due to chronic prostatitis. Flawed studies have created the impression that pregnancy outcomes are not influenced by LD. There is substantial documentation to suggest a causal relationship between LD and stillbirths, congenital abnormalities, spontaneous abortion, low birth weight babies, prematurity and intrauterine fetal infection acquired from the mother. An outcome of untreated LD arising from Mg++ deficiency could be pre-eclampsia (hypertension) or eclampsia (hypertension with seizures). Magnesium is often relied on to treat these problems. Women with LD in pregnancy can experience severe morning sickness, gestational diabetes mellitus and prominent flares of Lyme related symptoms. As both LD and Sudden Infant Death Syndrome are attended by sleep apnea, this should impel further research to determine if some babies with SIDS are actually suffering from LD. Bb can appear in the breast milk. Lyme patients very often complain of heel pain. This may be due to an underlying plantar fasciitis, with or without a heel spur, or periostitis of the heel. Epicondylitis (tennis elbow) is another complication. Carpal Tunnel Syndrome can also develop in untreated LD. Lyme patients tend to heal slowly and are prone to musculoskeletal injuries, sometimes without the usual antecedents. One patient sustained a vertebral facet dislocation while shaving ( the usual context is athletic). Even in the well conditioned athlete, there can be an unexpected spate of muscle cramps, sprains, tendinitis and bone or joint pains at the sites of load bearing. Muscle weakness occurs in some LD patients, More commonly, exertional performance is limited by shortness of breath, poor coordination, musculoskeletal discomfort, or fatigue. Exercise without or early in treatment can precipitate a flare of fatigue, especially the following day. Low back ache can arise from sacroilitis, paravertebral lumbosacral muscle strain/spasm, and herniated vertebral discs. In a few patients, spinal stenosis is encountered. Inflammation of the abdominal wall muscles, in particular the rectus abdominus is not an infrequent problem. Usually the tender sites are focal, involving more often than not, the lateral borders of the rectus abdominus muscle. Nausea is often present as well. The sites are best located when the patient is performing a Valsalva maneuver or doing a partial sit up. Failure to appreciate the abdominal myositis may lead to avoidable extensive GI workup. A very helpful diagnostic maneuver is palpatory tenderness of the medial tibia shaft due to periostitis (inflammation of the tissue around the bone if not the bone itself). Periostitis is also common in another spirochetal disease, syphilis (Textbook of Medicine, Ed: Kelley, 1989, p. 1587) and is responsible for the bone pain that both syphlitic and Lyme patients experience. Tenderness is easily elicited in 95% or more of LD patients simply by pressing the bony aspect of the thumb joint against the medial aspect of the tibia about 3-6 inches above the ankle. The intensity of the pain experienced by the patient can vary, but is often exquisite and will cause the leg to recoil abruptly. The pain often lingers after this procedure. In a minority of LD cases, periostitis is generalized and I have appreciated skull involvement in a few instances. A small proportion of LD patients have periostitis. As a result of fibrositis, myositis, periostitis, is it any wonder that the ill LD patient view hugs as potential torment? The chagrin of mystified family members is understandable. Self-examination for periostitis can be unreliable. Periostitis pubis (of the pubic bone) can mimic bladder pain or be the origin of lower midline abdominal pain, especially in children. Lyme (and Brucella) should be included in the differential diagnosis of Desert Storm Syndrome, with which LD shares many features. The abundant research opportunities should be clear to all. It is unnecessary to give Lyme Disease the "Galileo" treatment. |
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IV Rocephin treatment for chronic Lyme/borreliosis (filelink) Rocephin is a Beta-Lactam antibiotic. It is totally the wrong antibiotic for Chronic Lyme. Note what this study (below) found about Beta-Lactams "these forms without cell walls can be a possible reason why Borrelia survive in the organism for a long time (probably with all beta-lactam antibiotics) and the cell-wall-dependent antibody titers disappear and emerge after reversion." That is why Rocephin does not reduce the chronic bacterial load, why it does not reduce the Bowen titre. There is nothing fundamentally wrong with the Bowen test, patients on the MP have experienced a dropping titre. Lida Mattman used Beta-Lactams and Vancomycin in her lab to make active-phase bacteria turn into the persistent L-form chronic variants. Trevor Marshall, PhD =============================================== EICS of Kansas City, MO, hosted the 2004 "Emerging Infectious Diseases" conference in Kansas City MO on November 19,2004. At ILADS Dr Fallon was unable to talk about the results from the $5 million, 4-year, NIH study he had conducted into Chronic Lyme therapy with IV Rocephin, but at this conference he gave us the detailed results, together with a request that we not publish the details until they appear in print next September. So here is my summary of only the key points: 1. Chronic Lyme is real, and is measurable with objective neurological and physical indicators 2. 10weeks of IV Rocephin makes the patients feel better, and returned their objectively measurable deficiencies towards 'health,' but the neural indicators relapsed within 3 months. Some of the skeletal and physical indicators retained some improvement. 3. MRI scans are no use whatsoever in diagnosing or tracking the disease. The Fallon study found that the MRI scans showed "MRI hyperintensity burden does not change between time 1 and time 2. Hyperintensities appear to represent fixed damage." IMO, the corollary is that, at least based on the MRI data shown by Dr Fallon at this conference, IV Rocephin does not change any irreversible brain damage. "Fixed Damage" is likely a long-term phenomena, IMO, only loosely related to the symptoms. 4. SPECT scans are of little use without analysis way beyond the means of a typical physician. 5. In answer to a direct question, how did anticoagulants seem to help the neurolyme, Brian said that the changes are not vascular, that they are metabolic, and opined that anticoagulants are not likely to do any longterm good 6. This study was so meticulous that they even matched education level of patients and controls, as well as age and sex. Further, Dr Fallon's group found from SPECT data that the main metabolic changes in the brain were in the region of the Parahippocampal Gyrus. This is responsible for receiving sensory input from the outside world, integrating it, and projecting it onto the Hippocampus (memory) and Amygdala (fear, aggression, mood).The Insula was also affected. Further, the Para-Lymbic dysfunction noted on SPECT 1. disrupts attention, memory and learning 2. alters emotional response to sensory stimuli 3. distorts links between visceral states and mood, and may lead to increased stress responses 4. depresses the immune response and alters endocrine function 5. alters perception and emotional valence of pain, smell and taste Six of the 37 patients and 37 controls had significant adverse events during the trial, including two cases of serious thrombus, one MRSA infection and one Gall Bladder removal. This was an amazing presentation, and made the whole conference a memorable one for me. I felt as though I was part of history - now we know the data on IV Rocephin, so we can start focusing on the 'why' of how this therapy affects the body in chronic Lyme. ============================================ Infection. 1996 May-Jun;24(3):218-26. Related Articles, Links Formation and cultivation of Borrelia burgdorferi spheroplast-L-form variants. Mursic VP, Wanner G, Reinhardt S, Wilske B, Busch U, Marget W. Max von Pettenkofer-Institut, Ludwig-Maximilians-Universitat Munchen, Germany. **As clinical persistence of Borrelia burgdorferi in patients with active Lyme borreliosis occurs despite obviously adequate antibiotic therapy**, in vitro investigations of morphological variants and atypical forms of B. burgdorferi were undertaken. In an attempt to learn more about the variation of B. burgdorferi and the role of atypical forms in Lyme borreliosis, borreliae isolated from antibiotically treated and untreated patients with the clinical diagnosis of definite and probable Lyme borreliosis and from patient specimens contaminated with bacteria were investigated. Furthermore, the degeneration of the isolates during exposure to penicillin G in vitro was analysed. Morphological analysis by darkfield microscopy and scanning electron microscopy revealed diverse alterations. Persisters isolated from a great number of patients (60-80%) after treatment with antibiotics had an atypical form. The morphological alterations in culture with penicillin G developed gradually and increased with duration of incubation. Pleomorphism, the presence of elongated forms and spherical structures, the inability of cells to replicate, the long period of adaptation to growth in MKP-medium and the mycoplasma-like colonies after growth in solid medium (PMR agar) suggest that B. burgdorferi produce spheroplast-L-form variants. With regard to the polyphasic course of Lyme borreliosis, these forms without cell walls can be a possible reason why Borrelia survive in the organism for a long time (probably with all beta-lactam antibiotics) and the cell-wall-dependent antibody titers disappear and emerge after reversion. PMID: 8811359 [PubMed - indexed for MEDLINE] |
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How to remove a tick (filelink) Here are step-by-step instructions on how to remove a tick. Click here for an evaluation of commercially available tick-removal devices. This article discusses controlled studies on the various methods of tick removal. Here are tips on tick removal from a veterinarian. Here is info on a tick remover device. The CDC website info on tick removal is surprisingly brief and reassuring. Perhaps this reflects their official stance the borreliosis/Lyme disease is not a big problem in the US. The general concensus seems to be to NOT use heat to try to make the tick come out. There is no agreement on the technique that works best and whether or not it is vital to ensure the head is removed. ======================================================== I have used the Pro-Tick Remedy Tool that is shown at the Ohio State University website.... http://www.biosci.ohio-state.edu/~acarolog/tickgone.htm It is the one on the right side without any name just below the picture of the three tools. I have had the opportunity to use it on adult size and nymph size ticks. It works excellently!!!! I highly recommend it!!! I do not have any faith in a tweezer type apparatus. There is too much chance that the gut will be squeezed, forcing bacteria into the person. George Howell Last edited on Mon Jan 9th, 2006 06:05 by Foundation Staff |
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Q: Why do some Lymies recover in just a few weeks on IV antibiotics? No Lymie has "gotten well" in just a few months of therapy. Never. There are two issues. The first is the definition of "gotten well." The problem here is that if there is no definitive agreement on how to measure the disease severity itself, then there is no way to measure the change in the disease itself. One is dependent on reports of patients "feeling better." And patient reports are inherently unreliable. Think of yourself - think what you would give to be able to have a week, or maybe two, of a clear mind. Able to think clearly again. Wouldn't you declare that you are "feeling much better?" You would still be far from cure, but just getting from day to day is your aim right now. But that is not our aim. Our aim is nothing short of cure - full recovery. The second problem is that many physicians, even experts, do not understand that all antibiotics do not necessarily kill all bacteria. Some antibiotics actually help bacteria survive. In fact, many antibiotics have been isolated from bacterial species, and their function is exactly that - to allow one species to survive while killing its competitors. For example, Demeclocycline, a close cousin of Minocycline, was first isolated from a mutant Strep species. It doesn't harm the Strep as much as it harms competitive species. So this lack of understanding has led to the concept that people taking IV Rocephin are in fact killing the bacteria which cause their chronic Lyme. But Rocephin does not do that. It actually protects the Th1 bacteria from the immune system, and in so doing, makes the patient feel better. But the patients relapse when they stop the Rocephin infusion. Brian Fallon's study at Columbia showed that definitively. Any benefits from IV Rocephin are lost within a few months after discontinuing treatment. One of my presentations at our upcoming June 2006 conference is going to be exactly on this topic - "Why do all Antibiotics not kill all Bacteria?" ..Trevor.. |
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Jun 04 2006 9:03 AM Pesky Lyme disease hangs on Medical professionals disagree on treatment By Robert Miller THE NEWS-TIMES If you get bitten by a black-legged tick, what's your next move? If you start showing symptoms of Lyme disease, one school of treatment argues you should take at least two months of antibiotics for the simplest case and much more for complicated ones. You can also expect the tick to be carrying more than the strain of bacteria that causes the disease. Dr. Richard Horowitz of Hyde Park, N.Y., president-elect of the International Lyme and Associated Diseases Society (ILADS), said "99.9 percent of the patients I see with Lyme disease are co-infected. There are 10 other diseases we should be looking for." Horowitz spoke last week at a forum held by the Newtown Lyme Disease Task Force. The second school of thought would argue that the longest you should ever take antibiotics is 28 days — even if you've got the painful arthritis that's a symptom of Lyme. It also questions whether there's a condition called chronic Lyme disease — a persistent infection that can last for years — and discounts the threat of omnipresent co-infection. "The evidence does not support that — far from it," said Dr. Gary Wormser, chief of the infectious diseases division at New York Medical College in Valhalla, N.Y., and vice-chairman of its department of medicine. The differences between the two approaches and the implications for the way patients are treated for Lyme disease are profound. And this comes at a time of increasing threat from the disease. Lyme disease is at the epidemic stage in the state. There were 1,810 cases reported to the state Department of Public Health in 2005, compared to 1,348 in 2004 — a 26 percent increase. Connecticut has the highest per capita rate of Lyme disease in the country with about 136 cases per 100,000 people. But by all accounts, the disease is underreported by a factor of 10 or more. "The Centers for Disease Control and Prevention reported there were 19,804 cases (nationwide) of Lyme disease in 2004," said Pat Smith, president of the Lyme Disease Association, a patient advocacy group, who also spoke at the Task Force meeting. "That means there were about 200,000 cases, and that doesn't count the ones that don't fit the CDC requirements." Lyme disease is caused by a cork-screw-shaped bacteria, Borrelia burgdorferi. The black-legged tick — also known as the deer tick — ingests the bacteria when it feeds on deer, white-footed mice and small rodents, which act as sort of moveable reservoirs of Borrelia. When an infected tick bites a human, the human can get infected as well. The initial symptoms of the disease can include a bull's-eye rash, fever, headache and sore joints — like a case of the flu without a cough. If the disease is diagnosed early, it can usually be treated successfully with a month of antibiotics. "We've found there's a six-week window where treatment is really successful," said Thomas Forschner, executive director of the Lyme Disease Foundation based in Tolland, Conn. But only about half the people infected by a tick bite get the telltale rash. Some have no symptoms at all. Others are treated with antibiotics, but relapse. They can develop much more severe symptoms, including swollen joints. But because the most common blood tests for Lyme disease are highly inaccurate, doctors who rely on them can easily misdiagnose or disregard the symptoms. The CDC says doctors should not base a diagnosis on those tests but on clinical observations. "You only use the blood tests to support your diagnosis," said Horowitz of ILADS, whose members are often doctors whose practices are devoted to treating the disease. What's most controversial is the diagnosis of chronic Lyme disease. Doctors in the ILADS and patient advocates like Smith insist that people can develop long-term, recurring Lyme infections that can manifest themselves in a host of symptoms — chronic fatigue, sight and hearing loss, memory loss, depression and personality changes, heart damage and arthritic pain that can flare up in different places. "It's a multi-system bacterial infection," Horowitz said at the Newtown Lyme Task Force meeting. "There are 300 different strains of Borrelia burgdorferi internationally and 100 in the United States. The symptoms can come and go and they can migrate. It's a gestalt of symptoms." Doctors who are convinced chronic Lyme disease exists treat those patients with long-term courses of antibiotics, often lasting months or years. The ILADS criteria do not limit how long patients should be on antibiotics, leaving that up to the doctors' discretion. Horowitz said his rule of thumb is to continue antibiotics until a patient is symptom-free for two months. Horowitz also said ticks carry several other illnesses, including anaplasmosis, the malaria-like babesiosis, and bartonella, commonly known as Cat Scratch fever. All of these come with their own set of symptoms, which must be treated as well. This means patients must get a mix of antibiotics. "When I see a patient with chronic Lyme disease, I see a patient with chronic Lyme and co-infection," he said. But Wormser of New York Medical College follows the guidelines of the Infectious Diseases Society, or IDSA. He said there's no evidence for so much co-infection in Lyme patients. IDSA also says there's no scientific proof for a diagnosis of chronic Lyme disease, and thus no need whatsoever for long-term antibiotic therapy. "Study after study has shown this," he said. They've tested patients who claim they have chronic Lyme disease. Half never had Lyme disease to begin with. "Another study at Yale showed that half the people being treated for chronic Lyme actually had other treatable diseases," Wormser said. Wormser co-authored the IDSA Lyme disease guidelines. The society represents about 8,000 infectious disease specialists in the United States. The society is now rewriting those guidelines. Wormser said he does not expect them to be substantially different than they are now . But proponents of more liberal use of antibiotics to treat Lyme said last week that they expect, if anything, the new IDSA guidelines will be even more conservative than they are now. "It doesn't make any sense," said Forschner of the Lyme Disease Foundation about any reduction in the IDSA guidelines, which now allow 14 to 28 days of antibiotic treatment. "What difference does a little bit more of antibiotics make?" Forschner said the scientific literature does not support long-term antibiotic therapy for early Lyme disease, which some doctors now prescribe. "I think the new IDSA guidelines are in reaction to that. But why swing the pendulum so far in the other direction?" Forschner said. There is one substantial change to the IDSA guidelines, Wormser said. It will advise doctors that, on a selective basis, they can prescribe a single large dose of antibiotics to a patient immediately after a black-legged tick bite, before the patient starts exhibiting any symptoms of the disease. A 2001 study in the New England Journal of Medicine showed that such treatment, given within three days of a deer tick bite, was 87 percent effective in stopping the disease in its tracks. Smith of the Lyme Disease Association said what her group would like is for doctors to tell patients with Lyme disease that there are two established standards of care — the conservative one endorsed by the infectious diseases association, and the liberal one written by the International Lyme and Associated Diseases Society. Then, at the very least, she said, patients would know the options. "We need to make sure the patients are aware of this." Smith praised a bill in the U.S. Congress sponsored by Sen. Christopher Dodd, D-Conn., and Sen. Rick Santorum, R-Pa., that would provide an additional $100 million in federal funding for Lyme research over the next five years. Smith said the federal government currently spends about $32 million a year for research on the disease and all its manifestations. "Another $20 million a year will be a significant increase," she said. The funding is also tied to specific goals, including finding a reliable blood test for Lyme infection. "It took researchers five or six years to find a reliable blood test for AIDS," she said. "We've know about Lyme disease for 30 years and we still don't have a reliable blood test. That's outrageous." Contact Robert Miller at bmiller@newstimes.com or at (203) 731-3345. |
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Is Lyme disease always poly microbial?-The jigsaw hypothesis. (filelink) Med Hypotheses. 2006;67(4):860-4. Epub 2006 Jun 30. University of Wales, College of Medicine, Accident and Emergency, Heath Park, Cardiff United Kingdom, Cardiff, United Kingdom. Lyme disease is considered to be caused by Borrelia species of bacteria but slowly evidence is accumulating which suggests that Lyme disease is a far more complex condition than Borreliosis alone. This hypothesis suggests that it may be more appropriate to regard Lyme disease as a tick borne disease complex. Over recent years numerous different microbes have been found in ticks which are known to be zoonotic and can coinfect the human host. The hypothesis suggests that multiple coinfections are invariably present in the clinical syndromes associated with Lyme disease and it is suggested that these act synergistically in complex ways. It may be that patterns of coinfection and host factors are the main determinants of the variable clinical features of Lyme disease rather than Borrelia types. An analogy with a jigsaw puzzle is presented with pieces representing Borreliae, coinfections and host factors. It is suggested that many pieces of the puzzle are missing and our knowledge of how the pieces fit together is rudimentary. It is hoped that the hypothesis will help our understanding of this complex, enigmatic condition. PMID: 16814477 [PubMed - in process] |
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The politics of Lyme disease (politicslymelink) "Lyme is one of the infections found in Th1 immune dysfunction." I don't want any patients to argue with me on this issue. It is a complex issue and currently closed to your participation. Please argue on the boards where Lyme dogma is discussed. However, this is the current thinking of others, not just myself, including physicians who are well known in the Lyme community. As time goes by we will be able to develop the thinking behind the statement so that its support becomes obvious. Nevertheless, at this point I want to make it entirely clear that, for a host of reasons, Borrelia is not the sole cause of Th1 immune disease. Indeed, it might even just be a co-infection, like EBV. Time will tell. ..Trevor.. |
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Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi. (filelink) Microbes Infect. 2006 Sep 22; [Epub ahead of print] Livengood JA, Gilmore RD Jr. Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA. Human infection by Borrelia burgdorferi, the etiological agent for Lyme disease, can result in serious acute and late-term disorders including neuroborreliosis, a degenerative condition of the peripheral and central nervous systems. To examine the mechanisms involved in the cellular pathogenesis of neuroborreliosis, we investigated the ability of B. burgdorferi to attach to and/or invade a panel of human neuroglial and cortical neuronal cells. In all neural cells tested, we observed B. burgdorferi in association with the cell by confocal microscopy. Further analysis by differential immunofluorescent staining of external and internal organisms, and a gentamicin protection assay demonstrated an intracellular localization of B. burgdorferi. A non-infectious strain of B. burgdorferi was attenuated in its ability to associate with these neural cells, suggesting that a specific borrelial factor related to cellular infectivity was responsible for the association. Cytopathic effects were not observed following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable. Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells during infection of the CNS. PMID: 17045505 [PubMed - as supplied by publisher] |
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