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Aussie Barb
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Posted: Sat May 28th, 2005 01:55 |
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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.
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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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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Aussie Barb
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Posted: Sat May 28th, 2005 01:56 |
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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! ~Joyful
Patient 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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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Aussie Barb
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Posted: Sat May 28th, 2005 02:05 |
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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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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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Posted: Thu Jun 23rd, 2005 14:17 |
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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
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Posted: Thu Jun 23rd, 2005 19:07 |
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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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Posted: Fri Jun 24th, 2005 06:54 |
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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.
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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 
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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)
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When you say "titer 31", I don't know what you're referring to. Is it one of the bands on the Western Blot?
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Yes, titer is another name for band. Titer #31 is band 31.
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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
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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
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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
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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 Tests
Like 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
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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..
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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
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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..
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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.
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"...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
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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)
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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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Posted: Fri Jun 24th, 2005 07:00 |
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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
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Posted: Fri Jun 24th, 2005 20:35 |
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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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Posted: Thu Jun 30th, 2005 04:54 |
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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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Posted: Fri Jul 1st, 2005 15:15 |
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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..
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Does Elisa test and western blot drop down after or while progressing on MP?
Yes
..Trevor..
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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..
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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.
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"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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Posted: Fri Jul 1st, 2005 15:21 |
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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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Posted: Mon Jul 4th, 2005 18:15 |
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LYME/BORRELIOSISlink
Tick-Borne and Other Emerging Infectious Diseases
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Posted: Wed Jul 20th, 2005 04:50 |
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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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Posted: Wed Jul 20th, 2005 07:42 |
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Plasmids and resistance
http://tinyurl.com/8lf88
Borrelia has 17 of these
..Trevor..
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Posted: Fri Jul 29th, 2005 19:26 |
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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
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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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Posted: Sat Aug 6th, 2005 03:58 |
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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)
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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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Posted: Tue Aug 9th, 2005 06:19 |
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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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Posted: Thu Aug 11th, 2005 18:45 |
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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 
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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
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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.
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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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Posted: Thu Aug 18th, 2005 22:23 |
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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
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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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Posted: Fri Aug 19th, 2005 03:21 |
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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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Barb: Dx Inflammatory Disease Endocrine Imbalance 2003| Depression| 24+ years not Dx| MP Aug04| ABC of MP| MP Search|
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