California Lyme Disease Association (CALDA)
Great info about Lyme Disease from the California Lyme Disease Association.
Posts tagged ‘Awareness’
Evidence of Persistent Lyme Disease
The following link is a voluminous report showing multiple studies
and evidence of persistent lyme disease, even after abx treatment.
“Lyme on the Brain” word attachments with photos
Lecture Notes of Tom Grier: Tom Grier (Microbiologist from Minnesota) spoke at Lac Court Oreilles Convention Center in Hayward, WI. Tom’s life work is to do further research and bring awareness of this illness to everyone.
Previous posts have not included the photos and clip art which is helpful in understanding the lecture posts fully. You can find links to “Lyme on the Brain” documents in PDF form on the Wisconsin Lyme website.
“Lyme on the Brain” — by Tom Grier (part 4, lecture notes)
“Lyme On the Brain” continued…
Lecture Notes of Tom Grier: Tom Grier (Microbiologist from Minnesota) spoke at Lac Court Oreilles Convention Center in Hayward, WI. Tom’s life work is to do further research and bring awareness of this illness to everyone. For more info about Tom and his work checkout http://www.mibdec.com
If we look back and do a quick review of the lecture so far, we see some important points that keep repeating themselves in all stages and aspects of Lyme disease.
This is because of their fundamental importance in the disease process. To understand and make sense of the end stages of Lyme disease, we have to understand the fundamentals.
Key Lecture Points
Lyme on the Brain – Part 1
- Lyme was first misdiagnosed as Juvenile Rheumatoid Arthritis in Old Lyme, Connecticut.
- In 1975, Lyme disease was first described in print as primarily an arthritic disorder.
- The cause of Lyme was not known until 1982; yet a treatment protocol was suggested and used that we still mostly use today consisting of two weeks of antibiotics.
- This treatment protocol was initiated seven years before we knew that the actual cause of Lyme disease was caused by a spirochetal bacterium.
- Lyme disease is caused by a spirochete in the same Genus as Tick-Born Relapsing Fever (Borrelia) a genus with tremendous variation.
- Spirochetes are known to persist, and cause relapses.
- Borrelia can change forms from spirals to cysts, and can change their surface antigens quickly.
Part 2
1) The Lyme spirochete attaches to blood vessels and causes leaks to occur.
2) The blood brain barrier (BBB) can be breached early in infection and remain “leaky” for 10-14 days. Once the BBB closes, it sequesters the infection inside the brain away from the immune system and treatment
3) Borrelia can have many strain variations and can adapt and change quickly
4) The current Lyme serology tests that use strain B-31 are not representative of the wild strains found in nature. (Dr. Ron Shell, Madison, Wisconsin)
5) The new Western Blot Reporting criteria or Dressler Criteria turns a poor test into a nearly worthless test. Two-tiered testing further makes Lyme disease diagnosis less accurate.
6) Lyme bacteria can enter the blood vessel endothelial cells, and evade the immune system. (Sturrock and Ma)
7) Antibiotic treatment failure has been documented since 1979, and seven antibiotic treatment studies all demonstrated antibiotic failure ranging from 25% to 50%.
Part 3
1) Lyme disease is part of a larger pandemic called: Relapsing Fever
2) Neurogenic strains of Relapsing Fevers go to the brain and are deadly.
3) The Lyme bacteria can hide insidecells (fibroblasts, endothelial cells) and seeks tissues where it is protected from oxygen and the immune system.
4) Bb often hides inside connective tissue like tendons and the joints; Bb especially seeks the brain as prime target tissue.
5) There has been an extensive history of over 50 medical articles of spirochetes as one possible cause of MS published since 1911 in prestigious medical journals.
6) Dr. Gabriel Steiner demonstrated classical form spirochetes in MS patients in Germany since 1922, and again in Michigan MS patients in 1952.
7) In 1957, Dr. Rachael Ichelson, in Philadelphia, demonstrated spirochetes in MS patients and developed a culture technique to detect them.
8) Dr. Patricia Coyle tests 47 MS patients with an antigen/antibody complex test and finds that 15 of 47 MS patients have Lyme and respond to antibiotics, this refutes her prior published study where 20 random MS patients received an ELISA test and all tested negative. But her new 47 patient study was NEVER published.
Part 4 Lyme on the Brain Lecture Notes
Definition: L-form is a Lister Body named after Dr Joseph Lister (Listerine)who developed sterile surgical technique.
An L-form is a bacteria that can shed its cell wall and survive with just a membrane. It loses its structural shape and becomes spherical.
These L-forms resist cell-wall agents like amoxicillin because it survives the loss of its cell wall.
Well since this talk is called Lyme on the Brain, we better spend some time talking about what Woody Allen calls his second favorite organ, the brain.
Most of the time in microbiology, we don’t attribute intelligent behavior to bacteria; in science we generally try not to anthropomorphize.
But when it comes to the Borrelia genus of spirochetes that have evolved over thousands of years in close proximity to ticks and mammals, it becomes apparent that spirochetes have mechanisms of survival that almost mimic intelligent behavior and are not commonly seen in other classes of bacteria.
Some microbes like fungus are dimorphic. In other words, they have two forms of existence; the fungal or rhizome form, and the spore or yeast form.
The cyst-like yeast spores offer the fungus a chance to survive and proliferate when conditions are not favorable for its fungal form to survive.
In the deserts of the Southwest USA, the spores of deadly fungal illnesses float on the air until one comes to rest in the warm moist lungs of an unfortunate victim.
You can immediately see the advantage of this survival mechanism: one form tolerates dry desserts, the other prefers a living host.
Spirochetes are a conundrum and a mystery. In a general sense spirochetes seem to take on different forms depending on their environment.
Inside a tick spirochetes are usually seen as the spiral-classical forms, and are sometimes seen with an occasional bleb or cyst formation. These blebs still have cell walls.
Rarely, we have seen large spherical forms or L-forms that often seem to contain classical spiral forms, suggesting that the bacteria can go back and forth through at least three possible reproductive stages.
1) The spiral forms appear to divide by normal binary fission-division.
2) The spiral forms seem to be able to produce or pinch off cyst like blebs with cell walls that can become a large cell wall deficient spherical forms.
3) Spherical cell wall deficient forms seem to be able to produce classical forms inside themselves. We have seen this in other spirochete families beyond just Borrelia.
The question is what triggers these morphic changes in spirochetes?
When we have been looking for classical spiral forms in tissue; have we been missing the cell wall-deficient forms?
****Photos can be found in the word document version****
In this photo from Warthin and Olson 1954, we see that the spirochete that causes Syphilis takes on different forms depending on the tissue it is in.
The spirals are from the blood, and in Syphilis unlike Lyme, there are vast numbers of this form in the bloodstream that can be seen on blood smear.
As you proceed through the aorta of this patient, the spirochetes continue to change until finally all that can be isolated from the final vessel wall are tiny granules, yet these granules appear to be infective.
These atypical forms
from Dr. Judith Miklossey originally isolated from the brain of a dementia patient.
Show the polymorphism of Borrelia spirochetes.
When she placed the atypical cells into BSK-II culture (below), even the sphericals reverted back to classical formed spirochetes.
****Photos can be found in the word document version****
Cell Wall Deficient Form of Borrelia burgdorferi found in spinal fluid and stained with immunoflourescent stain.
What forms does Borrelia take on in different human tissues?
Work done by Dr. Judith Miklossey, MD, PhD, suggests that Borrelia may have developed some surface receptors that trigger the bacteria to change when it encounters certain brain cell types; conversely the brain cells may react themselves by producing by products in response to the infection.
In particular, human microglia cells when added to cultures of Borrelia burgdorferi in the presence of human neurons seem to produce excessive amyloid precursor protein APP .
This occurred when in contact in culture with Borrelia isolated from the brains of dementia patients:
APP is the first step or component necessary to create the hallmark marker for Alzheimer’s or Dementia.
To summarize, Dr. Mikklosey’s work is difficult because of the absolute life changing conclusions at each stage of her work that we have to come to terms with.
Here are some essential points looking back almost 20 years.
Dr. Judith Miklossey, MD, PhD, Neuropathologist
Essential points on her collective body of work on Dementia Brain Autopsies and the Association with Spirochetes
1) The first 13 dementia patients that randomly came through her facility were autopsied and the families allowed brain samples to be taken and studied. All 13 or 100% of the patients had spirochetes in the brain (Miklossey, Switzerland)
2) Isolates of the bacteria retrieved in three of the autopsies were identified as Borrelia species.
3) One of the cultures could infect mice, and was used in in-vitro brain cell cultures.
4) Isolates from one dementia patient when cultured in mouse brain cultures, caused markers for Alzheimer’s to appear.
5) Amyloid precursor protein converted to Beta sheet amyloid, hyperphosphoralation of protein tau occurred as well as neurofibrillary tangles as well as several other significant Alzheimer’s markers.
6) This was the first in-vitro model for Alzheimer’s; it was created with Borrelia bacteria.
7) Atypical forms of Borrelia were seen in the brains of subsequent dementia patients. These forms included:
coiled forms, intracellular forms, bleb forms, cyst forms, cell wall deficient forms, slime films and biofilms, and classical forms.
8) Atypical forms could revert to classical forms when placed in culture.
9) No other bacteria or virus were seen or associated with any of the dementia patients.
****Photos can be found in the word document version****
1) Normal uninfected mice are inoculated with Borrelia burgdorferi in the tail vein.
2) One month later, blood is isolated from the tail of the same mouse, and the bacteria are isolated for tests.
3) The bacteria are also isolated from the brain of the same mouse, and kept completely separate for testing.
4) The antibodies from the mouse’s blood recognize and attack the bacteria that were isolated from the blood of the mouse.
5) The same antibodies fail completely to recognize the bacteria that were isolated from the same mouse’s brain; it is as if these bacteria were completely invisible to the mouse’s immune system.
****Photos can be found in the word document version****
What has happened to the bacteria in the mouse brain?
Once the bacteria were isolated within the brain, it was then cut off from the peripheral immune system. This allowed the bacteria to change with each new bacterial division, and without the mouse’s immune system recognizing the changes; it is just like a criminal getting a face-lift and wearing a disguise.
The immune system kept up with the bacteria trapped in the blood, but could not make antibodies to the Lyme bacteria trapped within the brain.
The antibodies that were being produced no longer recognized the bacteria because it was still looking for the original strain, and what were now in the mouse’s brain were several generations away from the strain that Dr. Andrew Pachner started with.
Basically in crude terms, the Lyme bacteria that became isolated within the brain, mutated.
The Lyme spirochete we started with that was originally injected into the tail, is no longer the same isolate that Dr. Andrew Pachner found in the brain of the same mouse.
You now begin to see how current Lyme tests that are created using a laboratory strain of bacteria; a strain not even found in nature, can hardly be expected to keep up with the over 200,000 possible variations that Borrelia are capable of producing.
If Borrelia enters the brain and can be associated with disorders that to date have unknown causes like:
Multiple Sclerosis, Alzheimer’s disease, Parkinson’s, Gullain-Barre, and autism; then why haven’t there been any CDC studies to look into whether the Lyme bacteria can enter human brains, and what happens when the bacteria is in contact with brain cells.
In my opinion, of all the millions of dollars that the CDC has spent or dispensed on Lyme disease research, the most significant study to date has not been a study on deer, mice or the pesticides, but rather one of the few truly elegant microbiology studies done looking at the pathogenesis of Borrelia burgdorferi were done by CDC researchers, Dr. Jill A. Livengoode and Dr. Robert Gilmore.
****Photos can be found in the word document version****
The Livengoode-Gilmore CDC Human Brain Cell Study
Doctors Gilmore and Livengoode recognized a flaw in 20th century microbiology that led ultimately to an incorrect conclusion that has been repeated many times by scientists who were trying to minimize Lyme disease as a serious infection.
The incorrect conclusion is that Lyme disease neither gets into the brain, nor is it an intracellular organism, nor does it penetrate brains cells. This was based on interpretation of limited tools and stains.
Livengoode and Gilmore went on to disprove all of these assumptions as completely incorrect.
At the turn of the century, the only stains available to detect spirochetes were silver stains.
By nature of the large molecules and charged ions, the silver stain could not penetrate into human cells. So all spirochetes were seen outside of cells; it was assumed that spirochetes did not as a rule seek out intracellular locations like Malaria.
Livengoode and Gilmore had at their disposal a million dollar microscope that could do things no other microscope can.
It cannot only look inside of intact whole living cells in culture, but a computer video processor can create three-dimensional photos. The other advantage it had was it could uses different optical frequencies to detect different fluorescent stains.
More simply put, it could use one color stain to see spirochetes inside cells, another color for outside the cell and a computer could merge the images.
The result is some of the most beautiful imagery ever seen looking at living human brain cells in culture.
The confocal laser microscope could look inside cells but where do you start?
Since it had been reported that Borrelia could penetrate endothelial cells (Ma and Sturrock), and since this is the key to Borrelia entering the brain, the team started with endothelial cell cultures.
When they added Borrelia burgdorferi to endothelial cell cultures, there was an immediate attraction or tropism for the cells by the Borrelia.
The first images revealed spirochetes attached all over the cells, but further inspection revealed that within mere hours, spirochetes had gone inside the endothelial cells and were completely intracellular.
Exactly the very same thing that other researchers reported and many Lyme authorities claimed never happened.
Borrelia burgdorferi attached to the outside
of umbilical endothelial cells in c culture.
****Photos can be found in the word document version****
Merged photo of Borrelia burgdorferi on the outside and inside of an endothelial cell.
****Photos can be found in the word document version****
Livengoode and Gilmore then went on to add Borrelia burgdorferi to a culture of human glial cells, the cells that help mylenate and repair the brain.
Once again Borrelia exhibited a clear tropism for this cell type and attached extracellularly. Then within a few hours the bacteria found their way inside the Glial cells.
More importantly the very cells we use to process information and form thoughts with our neurons, were also easily infected.
Brain neurons since 1987 seem to have been recognized as target tissue for Borrelia burgdorferi and first noticed in fetal autopsies.
This cortex neuron clearly has Borrelia sequestered inside. The consequences of an untreated intracellular brain infection are unknown.
What is known from the Livengoode Gilmore study is that Borrelia burgdorferi seems to cohabitate within all of these cells without killing them and this was observed for a week.
To the right a neocortex
Neuron with a spirochete
beginning its entry into
the brain cell.
****Photos can be found in the word document version****
Although we cannot predict the final presentation of what intracellular brain infections with Borrelia would look or act like based on this in-vitro study; we can make some observations on the human diseases we have already seen where spirochetes have seemingly played a role.
In the MS patients where spirochetes have been associated, it appears that demyelination occurs allowing us to see bright spots or white matter lesions on MRI scans of the brain.
The clinical MS presentation can vary, but quite often in addition to MS central nervous system symptoms, we see peripheral symptoms consistent with Lyme disease.
In dementia patients where spirochetes have been isolated, it appears to be an Alzheimer’s like dementia in pathology, but the presentation of symptoms seems more consistent with Syphilis.
Yet Lyme does not seem to have a directly measurable sexual transmission that we can document.
The question we have to ask is:
Knowing what we do about these two presentations of symptoms, can we expect to find spirochetes in the brain autopsies of dementia patients and MS patients if we start looking with the right tools and stains?
Below is the brain autopsy of an Ashland, Wisconsin, man who had presented with an atypical dementia and had received in the course of his nursing home stay at least three courses of antibiotics that were consistent with the current IDSA guidelines for Lyme disease. He only had brief periods of remission and continued to decline after every treatment ended.
He was an avid hunter, fisherman, and operated a farm and an orchard. He had three sons.
Two of his sons were disabled from Lyme disease until they were diagnosed and treated. One was diagnosed with MS the other with rheumatoid Arthritis. They made good recoveries but not 100%. The third and youngest son got Lyme and was treated earlier but still had symptoms for years.
Thinking that their family was somehow more genetically susceptible to chronic Lyme, they pursued a Lyme diagnosis for their father in a nursing home.
The doctors refused to test for Lyme disease on the basis that he had already received antibiotics for pneumonia that would have been sufficient to kill any Lyme.
Frustrated and confused, the eldest brother arranged for a brain autopsy at the time of death.
****Photos can be found in the word document version****
The entire brain was sent to Dr Alan MacDonald. The results were stunning and conclusive.
****Photos can be found in the word document version****
Yale Medicine Special report May 15, 1996
- Tick must be attached 36 hours or more.
- Do not treat any rash with antibiotics.
- Symptoms like Bell ’s palsy, a swollen knee, requires an ELISA test before treating with antibiotics.
- If this test is negative don’t treat.
- If the test is positive do not treat, give a Western Blot and only treat if it is positive.
- Treat for two weeks with doxycycline
- Any lingering symptoms will take up to 3 months to dissipate
- Do not treat with antibiotics again.
****Photos can be found in the word document version****
END OF PART 4
LYME ON THE BRAIN
LECTURE NOTES
By TOM GRIER
“Lyme on the Brain” — by Tom Grier (part 3-B, lecture notes)
“Lyme On the Brain” continued…
Lecture Notes of Tom Grier: Tom Grier (Microbiologist from Minnesota) spoke at Lac Court Oreilles Convention Center in Hayward, WI. Tom’s life work is to do further research and bring awareness of this illness to everyone. For more info about Tom and his work checkout http://www.mibdec.com
Also in modern Lyme disease mouse model; the infection appears to have disappeared, but ticks that feed on the mice can then infect other mice. We might be looking for spirals, but that doesn’t mean that’s what we will find in every case.
Spirochetes are masters at morphing and changing forms. It helps them survive or another way of putting it; it contributes to relapses occurring even after aggressive antibiotic therapy.
What these early MS researchers found was amazing. First most isolated the bacteria from the human MS lesions, but just like Syphilis, they found it was only possible to keep them alive in animal models. Culturing Borrelia in 1911 was just not yet possible.
Once the organism was introduced to various animal models, it was often and many times re-isolated from the brains of the animals and reintroduced to new uninfected animals with exactly the same results.
The bacteria found its way to the brain of the animals, and the brain tissue could cause infection in uninfected animals.
The research became so established that the researchers often communicated with each other and commonly referred to the organism as “The MS Spirochete” which was eventually named Myela phethora or “myelin loving” by Dr. Gabriel Steiner from Germany.
Dr. Steiner was the most fastidious and persistent of all the MS/spirochete researchers, and wrote several position papers on the position, that MS was caused by an unidentified species thought most likely to be in the Borrelia family of spirochetes.
Steiner transferred the MS agent to many animals including monkeys. He created a better silver-stain, which we still use, today and is called Steiner-Silver-Stain.
When things got dicey for Jewish scientists in Germany in the mid 1930s, Steiner fled Germany and resettled in Ann Arbor, Michigan.
Steiner did not publish again for over a decade, and was amazed that America had nearly no knowledge of the European spirochete model of MS, so he wrote an article in 1952 called: “The Pathogenic Role of Spirochetes in the Etiology of Acute Plaques in MS”.
What Steiner found in American MS patients was the same as other parts of the world. MS lesions sometimes contained spirochetes that could infect animal models.
Compare below the photo of a spirochete from the lesion of a German MS patient in 1922, compared to the spirochete isolated from an American MS patient in 1952 from Michigan.
His work was completely corroborated by an American scientist Dr. Rachael Ichelson, who worked in public health in Philadelphia for 40 years.
She was written up in a column by First Lady Eleanor Roosevelt as the pre-eminent female scientist of her decade, and this was ten years before she studied MS.
Her outstanding work on MS which she did on her own time and her own money was eventually noticed by TIME magazine which did and article on her in 1957.
But an unfortunate twist of fate occurred. In 1957, Rachael was written up in TIME magazine as having a possible cause and treatment for MS, but the latest rage in 1957 on the heals of Polio, was everything undiscovered was caused by a virus.
When TIME magazine went to get a quote from the newly established MS society of the time, they merely stated that MS was not an infection.
If it was an infection, then sisters would be infecting brothers, parents would infect their children, and wives would infect husbands.
It never occurred to them that this infection was not passed from person to person, but rather from tick to human! An incorrect and capricious assumption led to the discontinuation of work of immense importance.
During this time an ambitious scientist who said his viral theory was correct discredited Rachael Ichelson’s work.
He went on to say that spirochetes were not the answer because in his experience, only 5 % of MS patients had evidence of spirochetes.
To date, no VIRAL theory of MS has panned out, while more evidence grows each year for a connection to spirochetes.
This story of a politically powerful scientist crushing a public health worker for his own glory is almost an exact plot-line from Ayn Rands “The Fountainhead”, it is an epic tale and a tragic one.
Rachael died of cancer just a few years later ruined not by science, but by politics.
In 1995, we conducted an antibiotic treatment study for MS patients from Lyme Endemic Areas of the Midwest.
Most of the patients were from St. Louis County, Pine County, and Beltrami County in Minnesota and a few patients were from Wisconsin and Minnesota.
It was a preliminary study just to get an idea if some local MS patients were actually Lyme patients, and if so, would they would respond to three months of antibiotics.
It was called the Lyme Endemic Area MS Study or LEAMSS.
In our study we pre-tested all MS patients for Lyme disease by Western Blot and ELISA; we only accepted seronegative patients that had been diagnosed with MS either by MRI or spinal fluid markers.
But our study was skewed in one aspect, we required all MS patients in our study to have at least three symptoms consistent with late stage Lyme and affect more than just the CNS.
We only accepted seronegative MS patients because we wanted to establish that in this late stage of MS/Lyme, those Lyme patients were seronegative for antibodies.
More importantly, we felt it was only ethical that anyone who tested positive for Lyme disease had to get treated immediately, so seropositive patients were not accepted; they were treated.
Accepting them into our study would have made our final numbers look more favorable, but we stuck to our decision to exclude all Lyme seropositive patients from our data.
Out of 26 patients, only three seroconverted; all were positive by IgM Western Blot at 4-6 weeks. These patients responded to antibiotics but not dramatically.
Five more patients had favorable response to the three months of antibiotics, but again there were no dramatic cures or immediate responses.
What is most important in this study was the fact that we got 3 definite seroconversions after six weeks of antibiotics, and that a treatment failure patient named Judy from Bemidji, Minnesota, stayed on amoxicillin for 15 months after the study ended.
Judy had not responded in any favorable way to her three months of doxycycline. In the last week of the study she was switched to amoxicillin.
We followed our study protocol to the letter, but our length of treatment was grossly inadequate.
When we did the year follow-up, Judy had made a nearly complete recovery, and was back after years of being disabled to a full-time mail carrier in Northern Minnesota.
It then was obvious that we had not treated long enough to overcome years of brain damage cause by the bacteria, and that cell wall agents like amoxicillin might be a better choice for treating neurological Lyme disease than a bacteristatic drug like doxycycline which can diminish metabolic function of spirochetes and perhaps make them even more dormant.
Doxycycline acts on the 30s ribosome in the bacteria, and diminishes metabolic activity without killing the bacteria. The body’s immune system then has a chance to finish the job. We call this a BACTERISTATIC antibiotic.
The cyclines class of antibiotics or macrolides, inhibit high metabolic activities like bacterial division.
Penicillin class antibiotics work on the 50s ribosome and block cell wall synthesis of dividing bacteria. This usually leads to bacterial death by structural failure.
However if the bacteria don’t divide or are slow dividers or are intracellular, the antibiotics often fail.
Macrolide antibiotics like clarithromycin can get in the brain and inside cells but does it kill the bacteria?
Cephalosporin’s can get in the brain but not inside human cells, so does it kill intracellularly and what about the dormant bacteria that these drugs cannot in anyway affect or kill?
This is not an infection we want to linger in our body and find hiding spots.
At the conclusion of our MS antibiotic treatment study, we brought our results to the state health department and to local MS experts.
We were amazed at the total lack of interest and hostility that we were met with. We were passed to the lowest possible echelon of bureaucrats who had little or no understanding of our work, and no one took even ten minutes to understand the history of spirochetes and MS.
They had made up their minds already, and we were not to be taken seriously.
The health department seemed irritated with us and had no time or interest to discuss it.
Our only request of them was to make MS in Minnesota a reportable disorder for five years so we could look for incidence and patterns of infection, and to inform doctors that current Lyme tests could not detect the infection in MS patients.
Their response was that MS is not an infectious disease so therefore was not reportable.
To me this seemed like a total lack of scientific curiosity; frankly a belligerent attitude from people who are paid with public monies and whose job it was to keep Minnesotans well.
When the state’s foremost expert on MS was given the data, he merely dismissed us with a short factoid:
“Patricia Coyle tested 20 MS patients for Lyme disease and not one had Lyme! MS is NOT LYME!” Now there’s an all or nothing black and white determination based on one poorly designed study.
What he never saw from Dr. Patricia Coyle was just one year after our study, Dr. Coyle, MD, PhD presented at the San Francisco International Lyme conference a 47 patient MS study where 15 patients did in fact turn out to have Lyme, and responded favorably to treatment.
A nearly identical finding to what our study showed one year earlier.
What she did different from her first study or our study was that she did not use blood serologies, but used tests that could detect bacterial proteins in CSF and urine. A test not available to doctors or patients outside of an advanced research project.
So today in Minnesota, we do not have five years of useful MS reporting data, nor are patients informed that they may have as much as a one in three chance of responding to long term antibiotics.
MS patients are in fact often told by National Organizations to not pursue Lyme disease as a cause as it was a waste of time and money.
If you had a 1 in 20 chance of being cured of MS by taking less than $1000 worth of amoxicillin, would you do it? MS patients are not being given that chance or choice.
What I consider a waste of time and money is, the MS medications that have been tried for the past twenty years. We have not seen in my opinion any substantial lasting improvement. They cost as much as $100,000/year, are painful, and seem to lose their usefulness after a few months.
What I would advocate for MS patients who also have symptoms consistent with Lyme disease is exactly what I did for myself:
I sought out antibiotic treatment because the option of doing nothing was leaving me no other choice other than unbearable pain, suffering, and ending my life in an assisted living home.
In 1991, when I collapsed and was brought to the hospital, my diagnosis had been and still was Progressive-Relapsing MS.
My doctor was on vacation and the neurologist who saw me at 6 AM on a Monday morning had been only a few hours earlier attending an International Symposium on Lyme disease.
She looked at my chart for five minutes and said she couldn’t believe I had not been tested for Lyme disease.
My doctor treated me with 20 days of IV Rocephin; I was hallucinating, breaking into tremors and sweats, and the pressure inside my head was unbearable.
She said if I didn’t respond to treatment she had already placed my name on a waiting list for a bed in a nursing home.
Needless to say, when after 20 days I was worse than ever, she wanted to stop antibiotics completely bamboozled by my lack of a 100% recovery, I chose to self medicate on antibiotics rather than go to the Nursing Home.
So a doctor made the right diagnosis eventually but she had absolutely no experience with treatment or what to expect from a patient as sick as I was.
I had difficulty driving any distance for years, and reading was absolute agony.
The deficits Lyme left me with were great, but at least the agony of muscle pain, joint pain, fevers, atrial fibrillation, and the unrelenting pressure in my head were under control and manageable.
People ask me how long I treated myself.
It took an entire year of antibiotics just to rid myself of the pressure in my head, and another two years to be able to read without seizures, and to drive without risking lives.
No antibiotic seemed to help my neurologic symptoms especially pressure in my head, until I took roxrithromycin 300 mg twice a day with Bactrim DS for two months, followed by Biaxin 500 mg twice a day with Flagyl 500 mgs twice a day for six months.
After that amoxicillin seemed to work the best for peripheral symptoms.
It is always amazing to me how quickly we forget how things were and how much things can change, but in 1991; it was not as easy as it is now to get medications from Mexico especially unapproved medications.
We owe a great deal of thanks to a politically savvy group of people who helped facilitate the ability to get drugs for Americans when they are not available within our healthcare system.
I am talking about the People with AIDS national organization or PWAs.
When AIDS patients could not get medications that were not yet approved for AIDS, the PWA organizations got special laws passed, and they were able to import medications not approved in America and distribute them without prescriptions.
This eventually helped open up the Mexican border to allow people to have access to medications as long as they were not controlled-substances.
I was as current as any Lyme patient could be with research; I knew about medications available in other countries, and some that were still new to human testing.
I had read about an Argentina brain study where patients with brain tumors were give antibiotics before open brain surgery.
No antibiotic before or since entered the brain as well as roxrithromycin. It accumulated up to 50 xs more in the brain than its related cousin erythromycin.
I figured what was preventing my pressure in the head and visual problems from getting better were the lack of antibiotic getting to the brain.
But the only people who could get Rulid legally in 1991 were the PWA buying groups.
So I called one in Colorado Springs and spoke to Ken, a very intelligent and medically savvy AIDS patient. He told me all about Rulid and eventually sent me articles to research.
(The Internet was rudimentary at this time, so Xeroxed hard copies ruled the day!)
He said he could not legally help me because I was not an AIDS patient, but he wanted my address to send me the articles.
The next day I received by Federal Express 120 tablets of Mexican Rulid from Hoerchst-Russel manufacture. A $500 care-package sent on faith that I would pay.
Within days of treatment, I could feel gurgling inside my brain. I had experiences that to this day I cannot describe nor care to repeat.
I knew that I had been right. It wasn’t just the right drug that was needed; it was delivering the drug to the brain in high enough dose that was important.
To this day 18 years later, we do not have any better drugs or drug delivery systems to get antibiotics into the brain. I am convinced that this alone would make a huge difference in Lyme disease treatments.
If we establish through research and brain biopsy that Lyme disease survives traditional antibiotic treatments, perhaps then pharmaceutical manufactures will see the need for this research, but it may take orphan drug status to make it worthwhile.
That can’t happen when our own CDC talks about Lyme disease as if it were a minor annoyance and still believes in Lyme testing.
Lyme patient with MS-like lesions on MRI
An MRI of an MS patient’s brain seen with white matter lesions that are similar to what is seen in Lyme patients diagnosed with MS.
The blood brain barrier that normally protects the brain from most pathogens, can become leaky in early Lyme disease, and even begin to leak before a tick is through feeding.
This can allow undetected organisms to enter the brain early and evade both the immune system and standard Lyme testing.
In microbiology to determine the cause of disease without question, we want to fulfill Koch’s Postulates.
Prior to 1942, every attempt that was possible within ethical guidelines, was made to complete Koch’s Postulates to show that the MS spirochete named Myela phethora was responsible for causing MS.
Here is what early MS researcher accomplished:
- The organism was isolated from human MS lesions during autopsy.
- The spirochetes could only be kept alive in animal models.
- Inoculations of brain lesions from MS patients into animal peripheral blood caused the animals to become sick.
- The infected animals sometimes had spirochetes that could be re-isolated from the brain of the animal.
- The isolates could then infect more uninfected animals.
- The numbers of spirochetes found was extremely low, and sometimes they disappeared in animal models.
- Lesions from MS patients without observable classical form spirochetes occasionally caused infections in inoculated animals. Then spirochetes could be seen in those animal’s brain or tissues. Suggesting that spirochetes had a dimorphic life cycle meaning it could be a spirochete or something that was different from a spirochete.
Koch’s postulates are:
The microorganism must be found in abundance in all animals suffering from the disease, but should not be found in healthy animals.
- The microorganism must be isolated from a diseased animal and grown in pure culture.
- The cultured microorganism should cause disease when introduced into a healthy animal. The microorganism must be reisolated from the inoculated, diseased experimental host, and identified as being identical to the original specific causative agent.
End of Part 3
Lyme on the Brain
By Tom Grier
Next: Lyme on the Brain Part 4
Dr. Jill Livengoode and Robert Gilmore use a confocal laser microscope to look inside human brain cells infected with Borrelia burgdorferi
Dr. Judith Miklossey finds spirochetes in the brains of dementia patients and creates a mouse model of Alzheimer’s using Borrelia isolates from dead patients.
Local Autopsies of Lyme patients and what they mean.
Madison Area Lyme Support Group 