posted 26 April 2004 15:27            

>As I have said many times before ad nauseum - the overlap of symptoms between Sarc and Lyme are quite amazing.

It's hard to believe it when you read it. Some of the posts at SarcInfo look like they've be cut from Lymenet and pasted into the sarcinfo forum, and vice versa.

Scott said:

>So, the puzzle is coming together and I'm am very excited for all of us.

In trying to uncover the source of my misery I spent some time reviewing the information at SarcInfo and was very excited because it explained so much. Still, there were pieces missing. I then got mired down in a CFS/FM forum before dontlikeliver finally went there and clued me in to Lyme. Together lymenet and sarcinfo gave me, I think, the whole picture.

posted 26 April 2004 19:31            

>As I have said many times before ad nauseum - the overlap of symptoms between Sarc and Lyme are quite amazing.

I spent some time studying Dr. Marshall's paper "New Treatments Emerge as Sarcoidosis Yields Up its Secrets". It's an excellent paper.

First, even though lyme and sarc share many symptoms I believe they are different diseases. The SarcInfo FAQs states that once-a-day dosing of Benicar will make sarc symptoms worse. In my case I was using cozaar once per day and my symptoms improved dramatically. Thus I don't have sarc. I was also taking Zithromax and had no herx at that time.

Secondly, Dr. Marshall's Angiotensin Hypothesis is great work. Follow the pathway and you end up with a cascade of cytokines (which are known to cause inflammation). In the case of sarcoidosis the culprit seems to be Gamma Interferon. I'm speculating that lyme damage involves the same pathway, but another cytokine is involved. For ARBs to control symptoms in a wide variety of diseases (as is being reported) something in general is shared by all these diseases. The key could be A-II binding at receptors. Why are some diseases controlled with once-a-day dosing but others require 4 doses per day? Is Benicar that different from Cozaar? I don't think we are at the point of predicting which brand will work best, but I'll be the first to switch if Benicar is superior.

As to antibiotics. I was on IV rocephin for 10 weeks, followed by Doxy and Zithromax for an additional 12 months. If spirochetes are capable of forming alternate forms(as reported), we really don't know how to kill them. I never said I don't believe in antibiotics. I said they didn't cure me. Certainly I had enough antibiotics to have knocked the spirochetal population in body down and I should have felt much better until the population built back up. Since sarccoidosis is triggered or caused by different bacteria than lyme my statements do not apply to any disease other than lyme. There is so much variation in borrelia that my statements may only apply to my case. In the case of lyme I think a lot has to do with the timing. How long a person is infected prior to treatment is relevant. It may also have to do with genetics, both human and borrelia variation. Let's not forget the possibility of toxins. Maybe ARBs will control lyme without antibiotics. Time will tell.

I do have some relevant observations to relate concerning my experience on cozaar. I'll write later. It will deal with the 6-8 hour dosing issue.

For all of you who want to take antibiotics - do it. Everyone should make their own decisions. Please post the results. If you discover a cure and it's an antibiotic I'll take it and thank you from the bottom of my heart.

Go for it. Try an ARB.

posted 26 April 2004 19:36            

quote:

---

Originally posted by lymerx:
This discussion is very interesting. I have been taking zestril (an ace inhibitor) for 10 years now for HBP. I have had lyme for 4 years. I have taken antibiotics the whole time (also herbs and rife for 3 months). I had some joint pain early on but it subsided and left me with neuro symptoms and sinus symptoms. I wonder if the fact that I have been taking low doses of the ace inhibitor drug for HBP all this time may have been a help, may have limited my inflammatory symptoms. Any ideas? lymerx

---

This is good information. Can you tell us the dose - timing, # per day? What are your specific symptoms?

posted 26 April 2004 21:56            

25 mg once per day

No change in symptoms the first 6 days

Day 7-10 - much better, slight fatigue, some aching, ear ringing (it's normal for me to be slightly better some days - so I didn't consider this a cozaar effect)

Day 11- worse; fibromyalgia spots, ache, bad ear ringing, neck pain with headache, fatigue; symptoms worse at certain times of day (for days 7-11); realized cozaar effects may last only about 8 hours - made a mental note to pay attention to time of symptoms

Day 12 - woke with no pain (very unusual); took cozaar 9 am; 11 hours later I started aching; how do I test this idea that it lasts only 8 hours? (talking to myself)Decided to take the dose at a different time of day to see if the symptoms were delayed by an equal amount of time. And the answer is yes.

Day 13 - extreme aching started in evening (about 12 hours after dose) couldn't sleep at all

Day 14- aching even after cozaar, but much worse after 10 hours. Ready to give up on cozaar!!

Day 15 - Much better; slight SOB, slight headache; 12 hours after cozaar upper back/chest muscles pulling

Day 16 - ear ringing; good day; 8 hours after cozaar muscles pulling; many muscles cramping; getting fibromyalgia like spot in left upper arm and shoulder blade.

Day 17 - woke with muscles hurting, etc bad headache after taking cozaar; ear ringing 10 hours after cozaar; In the past fibromyalgia spots would last 3+ days.

Day 18-20 - Same, but less intense symptoms

Day 21 - Very Good day; little pain; no SOB; slight headache in evening

Day 22 - Great day

Day 23 - Great day

Day 24 - noticed skin conditions are clearing up; patches of pimple like bumps are going away after years; my red, ugly, dirty elbows are even a little better (I've spent hours scrubbing them in the past); red tough patches on my ankles are normal looking again; leathery skin over areas of muscle loss are softer;
woke a little achy; Good day until 11 hours after cozaar- upper back pulling a little.

Day 25 - woke pain free; headache after cozaar; otherwise good

Day 26 - woke slightly cramped; felt good rest of day - have energy (very unusual), thinking better, no SOB, no fatigue, no pain; Was good in evening also

Day 27 - Fair day - some slight problems. Worked outside in hot sun (the sunny SE) and wasn't worn out. (That has never happened). Now I'm thinking maybe 2 doses per day would be better. I asked for medical advice and was told that there may not be a dose effect. I decided to try anyway and started with 25 mg morning and about 12 mg 12 hours later. Wanted to make sure it didn't drop my bp too much.

Day 28 - woke pain free (normally after working outside I'd hurt for days). Neck muscles tight, legs slight ache, but fair day

Day 29 - no pain; didn't take evening cozaar

Day 30 - L ear ringing; Great day - I mopped, vacuumed, cooked with no pain, no fatigue, no ache. Amazing - I haven't been able to be this active in years.

Day 31 - fibromyalgia trying to develop but never did. Good day

Day 32 - lower leg cramp, but only one. In the past I'd have cramp after cramp. Good day - no pain, no SOB or fatigue, have energy

Day 33 - another leg cramp; It's like the symptoms are trying to break thru but they aren't able to. Good day; lots of energy; no fatigue; no ache

Day 34 - good day; still going strong after working a 5 hour shift, working around house and being up 14 hours. (Ok - so I sat at the computer for 3 hours).

______

What have I learned?

1) It took a long time for it to kick in. You may have better results with ARBs if you follow Dr. Marshall's 3-4 doses per day protocol.

2) I don't think it lasts over 8-12 hours in the beginning at least. I have a lot to learn about dose.

3) It has not affected my headaches. Maybe they are less intense and maybe with more time they will clear up. I should mention that I have MS-like lesions in my brain.

4) Whatever you do - follow your doctor's advice

posted 26 April 2004 22:13            

>In answer to your question, I take 12 mgs of zestoretic (zestril with a diuretic) once a day.

Maybe you should ask your doctor if you could take a larger dose, or two divided doses. Or maybe try the newer ARBs - but if the ACE works why change a good thing...what you are doing is working for you! I think the ACE inhibitor may have played a role.

posted 27 April 2004 07:50            

The Sarclist posted the molecular diagrams a while back.

If the molecule is different, then it will probably latch on to receptors differently
than others. So while these are all ARBS they all aren't created equal.

Benicar is also taken slightly differently when used in conjunction with abx (as compared to being taken just for BP).

If any one on a BP med is thinking of switching to Benicar as a trial (to see if it alleviates lyme symptom inflammation )- please contact Trevor Marshsll first, and have him consult with your Doc. as dosage and timing of dose is important.

posted 27 April 2004 08:07            

I even did 4.5 months of IV Rocephin 2gms daily and about 6 months of Flagyl included in the many abx I have tried.

The is a very interesting subject and we all need to familarize ourselves with this information.

I will be studying up on this and see if it is something that might be good for me. Especially, if this is something without narcotics, and it is, that will work for my severe and chronic pain.

Again, Thanks and I look forward to reading more about this...to google I go.

posted 27 April 2004 08:18            

Benicar has a mechanism by which inflammation is reduced, thereby allowing the immune system (and abx) to be more effective on the bugs, and the mucoid (or non mucoid) films they create around themselves.

The other BIG misunderstanding, is how the hormone 1,25-D (the component of the Vit D metabolism) works in the the body.

In the inflammation pathway of chronic disease, this hormone (1,25-D) is thought to be manufactured (nor only by UV exposure) but also by inflammation itself in certain cells and organs (like the kidney).

Take a look at the site listed below... it may read over your heads, but it's worth a read anyway.

This is a complicated subject, and alot of Drs. don't understand it - so don't feel bad if it's confusing.

Basically - Trevor Marshall is saying - reduce the inflammation the correct way (by limiting the over production of certain inflammatory hormones) and the abx will be able to work better to kill the pathjogen, and so will your immune system.

http://www.joimr.org/phorum/read.php?f=2&i=38&t=38

Http:// www.chestjournal.org/cgi/eletters/123/1/18

http://
clinmed.netprints.org/cgi/content/full/2003010001

http://
biochemistry.ucr.edu/faculty/norman.html

Barb

posted 27 April 2004 09:46               

I have a few questions, as I have started reading over the site and do not fully understand all the connections yet, but they are as follows:

1) A friend's son developed sarcoidosis some years ago, they spent summers on shelter island and even tho they religiously did tick checks i now wonder if he had a manifestation of lyme or rickettsia. Anyway, he took Hoxsey's formula and got well and has been well ever since. I want to go look at Hoxsey's formula agian, it's usually used for cancer, but it has powerful detox mechanisms. I'd like for us all to try and figure out why different methods of detox are working and what they might share in common. That would include herbs as in Hoxseys' formula. My reasoning is even though apparently you can take these arbs with low blood pressure, some people with lyme apparently have really bad neurally mediated hypotension...we don't know how this would affect them. Though there is overlap in the 2 diseases...they are not the same in most cases

2) WHy would Patricia Kane's therapy be working well in some cases--how does THAT therapy get rid of BLP's, as it apparently must be doing, and if Scott is talking to these doctors, does he mind asking them about that? Can we figure out how different approaches are affecting the same pathway? Is there any way to replicate Kane's therapy orally (seems not).

3) Why would a low-carbohydrate diet be so important? It seems to me it's not just because glucose feeds all kinds of bugs. There seems to be a more direct correlation. Can we speculate on that? How could insulin be tied in to this inflammatory pathway?

4) WHy did questran work in some? Did it just bind the BLP's? If so why didn't it work in all? Why did some get worse on questran?

5) WHy does bee venom work for some? And samento? Are either of these affecting this inflammatory pathway?

6) The sunlight problem--most lymies don't have it--so I assume that active form of Vitamin D is not involved for us.

I probably shoudl've waited to post until I'd read further and understand better.

Also, I'm going to link this thread to Byron's naturalhealthcare thread, I'd like to see what he thinks.

posted 27 April 2004 09:54            

quote:

---

Originally posted by treepatrol:
CWD forms its all LYME or cousins of it.

---

How do you know that?

posted 27 April 2004 11:22            

"People who take so-called ACE-inhibitors for the treatment of high blood pressure should not take magnesium supplements. ACE-inhibitor medications tend to

***concentrate magnesium in the body***

and by taking additional magnesium you could develop problems."
www.health24.co.za/
dietnfood/What_is
_in_food/ 15-1167
-1172,13249.asp

Am J Hypertens. 1997 Feb;10(2):145-51. Related Articles, Links

The alterations in insulin sensitivity during angiotensin converting enzyme inhibitor treatment are related to changes in the calcium/magnesium balance.

Haenni A, Berglund L, Reneland R, Anderssson PE, Lind L, Lithell H.

Department of Geriatrics, Uppsala University, Sweden.

The present analysis was undertaken to investigate the relations between alterations in mineral factors, especially the balance between serum calcium and magnesium concentrations (S-Ca and S-Mg, respectively), and variables reflecting glucose and lipid metabolism during angiotensin converting enzyme (ACE) inhibitor treatment.

A total of 96 patients with essential hypertension, participating in four double-blind studies with four different ACE inhibitors and similar protocols, were included.

At the end of the initial placebo period and at the end of the period of active drug treatment, a hyperinsulinemic euglycemic clamp test was carried out, lipoprotein status was assessed, and the concentrations of serum electrolytes were measured.

The serum ACE activity was determined in the group treated with fosinopril. Changes in insulin sensitivity index (M/I) were directly correlated to alterations in S-Mg (r = 0.24, P < .02), and inversely correlated to changes in S-Ca (r = -0.19, P = .07) and the ratio between serum calcium and magnesium concentrations (Ca/Mg) (r = -0.27, P < .008). The change in total serum triglycerides (S-Tg) was inversely correlated to the change in S-Mg (r = -0.35, P < .0005), and directly correlated to the change in Ca/Mg ratio (r = 0.36, P < .0004). The reduction in serum ACE activity correlated to a more pronounced increase in S-Mg r = -0.62, P < .002), and decrease in the Ca/Mg ratio (r = 0.73, P = .0002).

We conclude that the changes in the studied metabolic variables and serum ACE activity during ACE inhibitor treatment are related to alterations in mineral status and the balance between calcium and magnesium concentrations in serum.

Publication Types:
Clinical Trial
Randomized Controlled Trial

PMID: 9037321
www.healthy.net/scr/column.asp?ColumnId=10&ID=97

Generally speaking, the rule of thumb is: if you have high BP, you need more Mg than Ca; if you have low BP, you need more Ca than Mg. We need both.

Bb SIGNIFICANTLY lowers our Mg levels as evidenced by the recent abstract from Romania and as stated by microbiologist, Dr. Gary Kaiser.

When Mg levels are low, calcium and potassium will rise at first, but eventually these will be deficient also. You cannot hold onto Ca or K without enough Mg.

"The spectrum of magnesium activities is impressive, indeed. For instance, magnesium inhibits platelet aggregation (quite like aspirin); thins the blood (as does Coumadin); blocks calcium uptake (such as Procardia); and relaxes blood vessels (as do ACE inhibitors). Of note, magnesium increases oxygenation in the heart muscle by improving cardiac contractability. It is for this reason that it is used frequently in emergency rooms to manage atrial defibrillation."
http://www.vitaminretailer.
com/SIE/articles/
HeartHealth.htm

posted 27 April 2004 12:07               

quote:

---

Originally posted by J123:
How do you know that?

---

This is the same lady who can take blood from you and in three days tell you if you have lyme by raising spirochetes from your blood which had none in it ie (blebs,Lforms) are there they revert back to spirochetes at least thats what I make out of it. http://www.fourwinds10.com/news/06-health/B-disease/2003/06B-02-01-03-microbiologist-Mattman-closing-lab.html

SarcInfo.com - How a Pathologist can see Bacteria causing Sarcoidosis
I just spent a fascinating afternoon with Dr Alan Cantwell, one of the first to report that a special type of bacteria had been found in the tissue of sarcoidosis patients. His first paper reporting these special pleomorphic bacteria was published in 1981, and a second paper in 1982. His discovery was ignored by Pulmonologists, although a number of other physicians have continued this work, with a detailed study of 20 patients and 20 controls in 1996, which clearly implicated bacteria as a likely cause of sarcoidosis. It was a bacteria similar to Mycobacterium Tuberculosis, but with an evolutionary adaptation that allows it to live without having a cell wall.

These special bugs are called "Cell Wall Deficient Bacteria" (CWD), and they have been found not only in Sarcoidosis, but also a number of other diseases, including Crohn's disease. There is a well written description of these bacteria at 'The Lyme Alliance'.

<--- A clump of tiny, round, 'coccoid forms', resembling minute granules, is at the far left of this image of a sweat gland from the skin of a lung sarc patient.

Here are the 'rod' bacteria more commonly seen by a pathologist --->

Dr Cantwell came under intense criticism when he reported that he could also find these bacteria in cancer patients, and from that time onwards he was ostracized by many in the medical profession. Dr Lida Mattman has managed to plot a course through the medical politics, and she is still working and researching today. Dr Phyllis E Pease has also continued to publish. Dr EA Moscovic has also published about CWD in Sarcoidois.

These CWD bacteria grow very slowly. Sometimes it can take months to culture them in a lab. That is one of the reasons that the labs don't find them during their standard tests for fungi and bacteria. These CWD have also been referred to as mycoplasma, L-forms, mollicutes,and nanobacteria. Milton Wainright referred to them as 'pleomorphic' in his recent article.

Alan gave us the benefit of his decades of research on cell wall deficient bacteria, explaining how any pathologist could see them under a microscope, and which stains should be used to make the bacteria show up amongst the tissue. If you look at the two images above, on the left you have a microscope photo, at 1000 times magnification, of the tissue surrounding the sweat gland from the skin of a lung sarcoidosis patient. The orifice for the sweat gland is the large open space at the lower right, the clump of tiny bacteria (called a coccoid form) is at the middle left. Click the image for an enlarged view. It is not easy to see these bacteria, but a good pathologist should be capable of doing it.

Normally the stain would show up the bacteria as red, (like the 'bacterial rods' on the right from the University of Wisconsin). But they show up as light pink, or, as in this slide, a purplish violet (a mixture of pink and blue).

Your pathologist might even be able to find these bacteria in old biopsy slides (some hospitals keep these for years). Here is some info that will help him find these tiny bugs (include this with Doc's pathology request)

The stains that are most useful to view the bacteria are:
1. Intensified Kinyoun
2. Giemsa
3. Fite-Faraco (often used with Leprosy biopsies)

They must be viewed under oil using an "oil immersion lens" at a magnification of 1000.

There are several books that will help a pathologist recognise the cell wall deficient bacteria:
1. Mattman LH: Cell Wall Deficient Forms. ISBN 0-8493-4405-0 (info from B&N.com)
2. Domingue G: Cell Wall Deficient Bacteria. (info from Amazon)
3. Xalabarder C: Publicaciones del Instituto Antituberculoso Francisco Moragas, Caja de Pensiones Para La Vejezy de Ahorros, Paseo de San Juan, 20, Barcelona-10: "L-Forms of Mycobacteria and Chronic Nephritis". 1970

Dr Alan Cantwell's book is interesting reading, and extremely provocative. It has photographs of the sarcoidosis microbes in it.

Now of course this topic is a little more complex than I have made it sound. The University of Wisconsin has an excellent description of the importance of the cell wall to a microbe, and why certain antibiotics, such as the penicillins, attack the microbe's cell wall. Microbes that have evolved to live without a wall are immune to attack by the penicillins (but apparently not immune to Minocycline). In fact the existence of your CWD mutations may be due to the use of the Penicillins on microbes for which the Tetracyclines should have been chosen in the first place.

Additionally, species of the E-coli Bacterium, as well as the Strep bacterium, have been found in a cell-wall deficient form, not just the Mycobacteria.

Hopefully this tutorial will give you and your pathologist the information needed to verify that these microbes were in fact in YOUR biopsy tissue, and that therefore Doc had better darn well think about trying some antibiotics to get rid of them...

Click on the images to get enlarged versions.

CWD Bacteria in the connective tissue of the skin biopsy sample taken from a skin sarcoidosis patient

Culture of CWD staph bacteria from this patient (cultures of these CWD bacteria typically take months to grow)

Bacteria in the lung tissue of a patient with systemic sarcoidosis

Bacteria in a sweat gland of the skin of the same (lung sarc) patient

Culture from the second patient
The Mattman Study
Jo Anne Whitaker, M.D.,’ Eleanor G. Fort, B.G., M.T.’ Minter H. Dopson,” Lida H. Mattman, Ph.D.,“Sally M. Marlowe,N.P."
’Bowen Research and Training, Tarpon Springs, FL, USA, ” Chisolm Biological Laboratory,
Aiken, SC, USA “ Nelson Medical Research, Warren, MI, USA (4) Arthritis Pain Treatment Center, Clearwater, FL, USA
INTRODUCTION
Health is a state of balance. Because humans and microbes are often competitors, interactive co-evolution has resulted in multiple and varied defense mechanisms on the part of both. The body must juggle and perform delicate balancing acts to maintain adaptive successes in spite of constantly changing life situations.
Lyme Disease (LD), Fibromyalgia (FMS), Chronic Fatigue Syndrome (CFS), Gulf War Syndrome (CWS), and many similar chronic conditions affect multiple body systems often accompanied by extreme morbidity. Laboratory diagnostic methods presently in use are often undependable. We believe The Gold Standard Culture method developed by Lida Mattman, Ph.D. is the only consistently dependable procedure for the demonstration of the spirochete, Borrelia burgdorferi (Bb), the causative agent of LD. It is becoming increasingly obvious that the plethora of multiple clinical signs and symptoms associated with LD are also common to patients with FMS, CFS, GWS, and other commonly referred to as immune diseases. Most physicians do not consider LD to be a cause of these syndromes, thus, allowing untold numbers of direly ill patients to suffer without the antibiotic treatments which will improve their clinical situation, and, in some cases, cure their disease (acute LD).
MATERIALS AND METHODS
(1) The Mattman Blood Culture Technique for identification of BB was used. Her success in producing positive cultures involved initiating growth in cell-wall deficient forms of the spirochete.
(2) LUAT (Lyme Urine Antigen Test) performed at Igenex.
(3) Peripheral Blood Smears with Giemsa Stain (4) Live cell analysis.

Results
103 subjects exhibiting clinical evidence of multiple body system involvement were studied. The Mattman Blood Culture was positive for Bb in 94 subjects. 37 subjects were tested by LUAT for Bb antigen and 19 of the 37 tested positive. Smears were done on blood taken from the subjects. There was evidence of bone marrow stimulation characterized by hypochromia, red blood cells (RBCs) inclusions (stippling or parasites) and large polychromatic RBCs Platelets and white blood cells appeared normal. Extreme fragility of RBCs was detected in many (nonspherocytic). Live Cell Analysis was also performed on the blood of the subjects and followed over 4 days ( same preparation). Upon standing, most striking was parasitization of RBCs by ring forms, and in many cases spirochetes emerging from RBCs. There existed extreme degradation of red blood cell membranes. Cystic and large L-Body forms were frequent.
Breakdown of diagnosis and the number of subjects:
Fibromyalgia - 30
Osteoarthritis - 1
Mixed Connective Tissue Disease - 3
Polymyalgia Rheumatica - 1
Ankylosing Spondylitis - 1
Lupus Erythematosus - 1
Palindromic Rheumatism - 1
Chronic Fatigue Syndrome - 8
Multiple Sclerosis - 40
Amyotrophic lateral Sclerosis - 17

DISCUSSION
When Fleming discovered the miracle drug, penicillin by mistake, he observed that it worked by altering the cell wall, thus, preventing replication. The Mattman Culture Method induces positive growth by supporting the cell-wall deficient forms. These forms are extremely stealthy in their proclivity for pleomorphism, suggesting other genera. The ambiance of their surrounding medium is probably responsible for these changes and migration to all part of the body in the interest of self-preservation. Without intact cell walls their receptors are disadvantaged.

It is essential that the "medical world" question the validity of present laboratory methods in detecting Bb and recognizes that Lyme disease, sometimes a killer but almost always a disabler, is a disease just as fearsome as "The Great Imitator", syphilis, and about to become just as widespread. Success in treating LD can best be achieved with early clinical diagnosis and the initiation of proper long-term antibiotic and antigen-specific Transfer Factor therapies. Until this is achieved, there will continue to be great cost not only to patients progressing to chronic neuroborreliosis, but also to the public health community. One of the most crucial diagnostic tools, the initiation of a trial antibiotic regimen and antigen-specific Transfer Factor therapies, and the resulting Herxheimer reaction (belived by may "Lyme Savvy" practitioners to be the best indicator of LD response) must be embraced and practiced. It is paramount to accept the fact that Lyme disease is the most common and rampant vector- borne infectious disease in the US.

Its not a far leap to think that lyme or one of it buddies is the cause of all this suffering.TBD
Heres some more. http://www.mercola.com/2001/jul/25/lyme_disease.htm
http://www.lymenet.de/mattms.htm

Update on Research Activities

Bowen Research and Training Institute, Inc. is a research facility in Palm Harbor , Florida . After finding that there were few accurate tests for Borrelia burgdorferi (Bb), researchers at Bowen Research and Training developed a new direct immunofluorescent test that identifies the Borrelia burgdorferi (Bb) antigen.

This research project has found the Bb antigen in whole blood, breast milk, amniotic fluid, placental tissue, semen, eye fluid, tooth, foot nodule, shoulder fluid, spinal fluid, finger joint fluid and African dust. This test, called the Rapid Identification of Borrelia burgdorferi (RIBb) test, looks for an antigen of the Bb spirochete. Findings are documented with digital photography.

This method of testing is of particular importance for Bb because current serology tests measure only antibody response beginning three to four (3-4) weeks following onset of active Lyme disease, whereas the antigen of Bb is present within twenty-four (24) hours of contracting the disease. In addition to the RIBb test, a buffy coat blood smear stained with Wright Giemsa is examined to identify other tick borne bacterial infections such as Human Granulocytic Ehrlichia (HGE), and Human Monocytic Ehrlichia (HME), which are seen in the white blood cells (WBC). The parasite Babesia is often seen intracellularly in the red blood cell (RBC). All three infections can be identified in the same individual.

We have now tested over 2900 specimens including over 700 very sick children from all geographic areas and, as previously described, all are positive for the Bb antigen. The RIBb test has been validated by Mattman's culture method, yielding the same results on over three hundred (300) same draw blood specimens. An independent laboratory using thirty (30) same draw blood specimens has also confirmed the RIBb test. Appropriate, specific and non-specific positive and negative controls are performed on each specimen.

We have recently developed a titration serial dilution method for quantitating the amount of Bb antigen in the blood. This may help to differentiate the carrier state from the patients with serious disease by comparing persistence of fluorescing structures. This method will also help us to determine the efficacy of antibiotic and other treatment therapies. We strongly recommend that physicians order the serial dilution RIBb test pre and post antibiotic therapy to determine the efficacy of treatment.

In 1998 Dr. Lida Mattman cultured Borrelia burgdorferi by supporting the growth of cell wall deficient organisms in 43 out of 47 blood samples from patients with the signs and symptoms of chronic Lyme disease. In that study there were 23 out of 23 negative controls in patients without signs and symptoms of Lyme disease. For the last four years Dr. Mattman has not had a negative culture for Borrelia burgdorferi. All specimens have cultured out cell wall deficient Borrelia burgdorferi organisms.

A large epidemiological study needs to be done with a sensitive specific test for Borrelia burgdorferi to help understand its many complexities.

This study should alert us that Lyme disease is a very serious problem, quite possibly the fastest growing epidemic in the world, and one that is very difficult to diagnose and treat. The RIBb test as well as the identification of the presence of other tick borne infections is vitally important so that the disease can be diagnosed early in order for treatment to be started immediately to prevent the morbidity of chronic Lyme disease and other tick borne diseases.

Jo Anne Whitaker, M.D.

That should keep ya busy

posted 27 April 2004 12:19            

TNF alpha is not all "bad":

Thus, one mechanism of action of TNF-alpha, SMase, and ceramide on thyroid FRTL-5 cells is to INHIBIT CALCIUM ENTRY.

PMID: 10092616

"We wanted to know if TNF-alpha was regulating the number of receptors on the cell surface," Bresnahan explained. "If the number of receptors increased, and if there was glutamate nearby to bind to them, that would allow more calcium into the cells, killing them."

Experiments at the Stanford lab were able to show that controlling the presence or activity of TNF-alpha had a direct relationship to the numbers of glutamate receptors on the cell surface and therefore on the amount of synaptic transmission.

"This showed that TNF-alpha, this cytokine that is supposed to come from the immune system and not have a role in transmitting information,

is actually a potent modulator of neurotransmitter interaction,"

Beattie said.

hdlighthouse.org/see/immune/tnf.htm

Through their ability to induce TNF production by macrophages, spirochete lipoproteins may play important roles in the development of the local inflammatory changes and the systemic manifestations that characterize syphilis and Lyme disease.

PMID: 1890308

Naturally...if Mg is "unavailable" the first thing to happen is Ca will try to go into the cells. The body tries to stop this. Ca levels rise, histamine kicks in, etc.

Need to get to the ROOT of the problem. Bb depletes a LOT of Mg. Restore the balance and maintain it so own healthy antibodies can do the job.

There is risk of cyst formation when Bb is in a nutrient deficient environment:

Cystic forms of Borrelia burgdorferi sensu lato: induction, development, and the role of RpoS.

Murgia R, Piazzetta C, Cinco M.
Dipartimento di Scienze Biomediche, sez. Microbiologia, Universita degli Studi di Trieste, Trieste, Italy. rmurgia@dsbmail.units.it

It has been demonstrated recently that cells of Borrelia burgdorferi sensu lato, the etiological agent of Lyme disease, transform from mobile spirochetes into nonmotile cystic forms in the presence of certain unfavourable conditions, and that cystic forms are able to reconvert to vegetative spirochetes in vitro and in vivo.

The purpose of this study was to investigate the kinetics of conversion of borreliae to cysts in different stress conditions such as starvation media or the presence of different antibiotics.

Using the same experimental conditions we also investigated the possible role in cyst formation of RpoS, an alternative sigma factor that controls a regulon in response to starvation and transition to stationary phase.

We observed that beta-lactams penicillin G and ceftriaxone, the antibiotics of choice in Lyme borreliosis treatment, favoured the production of cysts

when used with serum-depleted BSK medium.

In contrast, we observed a low level of cyst formation in the presence of macrolides and tetracyclines. In order to elucidate the role of the rpoS gene in cyst formation we analyzed the reaction of the rpoS mutant strain in comparison with its wild-type in different conditions.

Under the same stimuli, both the wild-type borrelia and the rpoS knock-out isogenic strain produced cystic forms with similar kinetics, thus excluding the participation of the gene in this phenomenon.

Our findings suggest that cyst formation is mainly due to a physical-chemical rearrangement of the outer membrane of Borrelia burgdorferi sensu lato leading to membrane fusion and controlled by different regulation mechanisms."

This may be why the Romanian's treatment plan worked. They gave abx. ALONG WITH restoring the very deficient level of Mg.

posted 27 April 2004 12:38               

Is this BLP, TNF, pathway, cytokines, ARB all summed up somewhere in a book or something?

Im sure there are A LOT of people this would help, but PLEASE break it down!

I think I do understand about BLP, etc. If you want to get the word out, that is more than fascinating

but laymens terms might help for some people. I *can* research it to figure it all out. Some other people may be too sick to do that.. and some

people like me might try REALLY hard to understand only to go WHAT???

Mind the small people, will ya?