Madison Area Lyme Support Group

“Lyme on the Brain” — by Tom Grier (part 3-A, 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

Tomgrier2001@yahoo.com

We have talked about how the Lyme spirochete attaches to the endothelial cells in blood vessels, and creates “LEAKY” blood vessels. Due to the spirochete’s exceptional motility, this allows the bacteria to enter virtually any tissue in the human body.

The big questions are: Where is it going? Why does it want to go to specific places? What happens when it gets to places where it can hide and survive?

Bacteria don’t have brains, but they do have millions of years of evolution that improved their overall survival through shear trial and error. The bacteria wants to survive.

For good or bad Borrelia bacteria have made their homes in ticks and mammals. How has evolution affected their genetics in order to enhance their own survival in ticks and mammals?

Let’s look at Borrelia bacteria from the bacterium’s point of view.

All known species of Borrelia bacteria that cause Relapsing Fever and Lyme Disease enter the blood of humans either by way of an insect bite such as from an infected tick, head-lice, or through infected blood contact.

Relapsing Fever caused by Borrelia recurrentis enters the blood stream through open bleeding capillaries on the head caused by the host scratching at lice and themselves until they are bloody, and then accidentally crushing the head-louse allowing the bacteria direct entry into the blood stream.

Dr. Joseph Dutton was infected with Borrelia duttonii when he was performing an autopsy on an African native who died very quickly of neuroborreliosis-encephalitis after contracting Relapsing Fever through the bite of the moubatta tick.

Unfortunately Dr. Dutton cut himself during this field autopsy, was also infected, and died of encephalitis within two weeks of initial infection.

Below is an excerpt from Dr. Willy Burgdorfer’s lecture on the history of spirochetes related to Lyme disease.

Take special note about the disappearance of classical formed spiral spirochetes in favor of granular-cysts, and also the ability of Borrelia to invade epithelial cells and appear to have disappeared.

This is a history and research that we cannot ignore and cannot afford to forget.

If we had looked at this evidence in 1982, we would have understood the paradoxes we were seeing and incorrectly dismissing as artifacts, in our diagnosis, treatment, and relapses of Lyme patients.

At the turn of the century, 1903 through 1905, the British physicians Dutton (Joseph Everett) and Todd (John Lancelot) working in the Congo, found that the disease referred to as “human tick disease” by David Livingston as early as 1857, was caused by a spirochete transmitted by the African soft-shelled or argasid tick, Orhithodoros moubata (Fig. 3).

Both Dutton and Todd contracted the disease.

Dutton, a pathologist, infected himself accidentally during a post mortem and died.

He is remembered by having had named the East African relapsing fever spirochete Borrelia duttonii.

Also playing an important role in relapsing fever research was the German microbiologist Robert Koch. At the end of 1904, he was called to East Africa to investigate the widely distributed East Coast Fever in cattle.

He soon learned that most Europeans traveling into the interior regions had been suffering of recurrent fever first thought to be malaria.

Although Koch was not aware of the British findings in the Congo and Uganda, he confirmed the vector role of the Orhithodoros moubata.

He was the first to demonstrate that spirochetes were transmitted via eggs (transovarial transmission) to the progeny of infected female ticks.

Ever since it was demonstrated that the body louse (Pediculus humanus humanus) and the African O moubatawere the vectors of the relapsing fever spirochetes known today as Borrelia recurrentis and B duttonii, respectively, intense studies have been carried out on the development of these microorganisms in their vectors, and on the mode of transmission to humans.

Thus, in 1912, the French worker Charles Nicolle and coworkers studied the behavior of B recurrentisin lice and noted that the spirochetes had disappeared from the midgut 24 hours after they had been ingested; they were no longer detectable until days 6 to 8 when they suddenly reappeared in the hemolymph.

A similar “negative phase” had previously been reported for B duttonii in O moubata by:

• Dutton and Todd (1905-1907),
• Leishman and other investigators (1907-1920),
• Fantham (1911-1915),
• Hindle (1911),
• later also by Hatt (1929) and
• Nicolle and associates (1930).

According to these investigators, ingested spirochetes invade the gut epithelium where they lose motility and after 3 to 4 days develop into cysts (blebs, vesicles) that contain granules or chromatin bodies (Fig. 4).

Dutton and Todd postulated that these spherules are formed by protuberance of the spirochetes periplasmic membranes;they may occur at any point along the spirochete.

At some time during their development, these spherules or cysts were said to burst and release their granules.

By the 10th day after infectious feeding, Dutton and Todd no longer found morphologically typical spirochetes, but instead large numbers of granules from which eventually new spirochetes developed provided the ticks were maintained at temperatures above 25° C.

Hindle, in 1911, reported similar observations. In infected ticks held at 21° C, the spirochetes had disappeared from the midgut by the 10th day after infectious feeding.

They could no longer be detected either in the gut or in the tissues.

However, triturates of such ticks injected into mice regularly proved infective, and an increase in temperature to 35° C resulted in the reappearance of morphologically typical spirochetes.

This “granulation theory” — as it was referred to — received a significant boost in 1950 when Edward Hampp of the National Institute of Dental Research in Bethesdashowed by stained smears, darkfield and electron microscopy that oral treponemes and Borrelia vincenti in cultures produce blebs and granules that were considered “germinative units.”

His hypothesis was supported by the observation that 31- month old cultures containing only granules invariably resulted in typical spirochetes upon transfer to fresh medium.

DeLamater and coworkers also reported similar observations from the University of Pennsylvania Medical School.

They provided evidence for the occurrence of a complex life cycle in the pathogenic and nonpathogenic strains of Treponema pallidum.

Accordingly, these spirochetes multiply by:

(1) transverse or binary fission, and

(2) by producing gemmae (cysts in which a single or more granules appeared to be the primordia of daughter spirochetes).

Once the Borrelia Lyme bacteria enter the blood stream of a human, it is immediately susceptible to attack.

An immediate cellular response of neutrophils and macrophage will try and digest the bacteria, and also present markers for the bacteria to lymphocytes that will over the course of several weeks begin to turn out killer T-cells and B-cells that produce specific antibodies.

The first mechanism to survive is to leave the blood stream!

Borrelia can do this by either entering the blood vessel cells called endothelial cells, or transiting the blood-vessel through gaps it creates, and entering other tissues.

If the bacteria do this quickly enough, not enough bacteria will be present to cause an immune response. In other words, it tricks the immune system into thinking that there is no active persistent infection.

If the infection load in the blood is too low, the immune response is muted. But the bacteria can persist in low numbers in other tissues.

Often the first tissues the bacteria find themselves in; is back in the skin usually at the tick-bite-site.

The cellular response to attack the bacteria that is literally swimming through the skin cells, causes the redness, and the appearance of the rash.

Over time parts of the rash fade as the immune response lessens as the bacteria move away from ground-zero.

Another place Borrelia burgdorferi can hide is in the skin. We have seen in culture that fibroblast skin cells can safely harbor the bacteria, and prevent powerful drugs like IV ceftriaxone at high concentrations to have almost no lethal effect on the sequestered bacteria.

If we can’t kill the bacteria in in-vitro skin studies, why would we think we have any better luck in a living human when there are even better places to hide?

Georgilis K, Peacocke M, and Klempner MS. Fibroblasts protect the Lyme Disease spirochete, Borrelia burgdorferi from ceftriaxone in vitro. J. Infect Dis. 1992;166:440-444

It isn’t what we don’t know about Lyme disease that is causing patients to suffer. It is what we have known and chosen to ignore that is slowly killing patients by diminishing their quality of life until they have nothing left to fight with.

Once the bacteria enter the blood stream, with every beat of the heart the bacteria are dispersed throughout the body. These motile leech-like creatures use their ability to swim and their ability to attach to cells to their advantage to survive.

Dr. Russell Johnson PhD University of MN, reported at a Lyme research conference workshop I attended in Bloomington, Minnesota, that hamsters infected with Borrelia had live bacteria within their tendons within 4 days of experimental tick bite, and the bacteria was detectable in the brain of the rodents within a week.

But because this research was for a drug company with an antibiotic seeking an indication for use against Lyme disease, and the antibiotic failed to eliminate the infection from the hamsters unless dosed four times a day at twice the normal dose instead of just once a day dosing as the drug company desired; the research was never published and the drug for other reasons was later removed from the American market altogether.

How much other research useful to suffering Lyme patients has been lost because of the pursuit of patents, indications, and market share?

I can tell you after attending over 20 International Lyme conferences, that much of the best research information is never fully published.

Take for example the Nantucket Island Lyme Patient Treatment Study that lasted over five years. Although it was funded by public monies; only those who attended a research symposia saw the raw data about antibiotic failures and the overall failure and patient relapse rate of over 50 % after five years of follow-up.

Yet the conclusion of the published study said there were no long-term consequences that were serious: Serious to whom? Do you wonder what they will leave out in ten years?

So we know the bacteria can evade the immune system and sequester itself, but over time where does it want to be?

One suspected food source is N-Acetyl-Glucosamine, a component of connective tissue.

Coincidentally we see many joint and connective tissue problems in Lyme patients, and we have found the live Lyme bacteria within human patient’s ligaments despite aggressive antibiotic therapy.

Haupl T, Hahn G, Rittig M, Krause A, Schoerner C, Schonnherr U, Kalden JR and Burmester GR: Persistence of Borrelia burgdorferi in ligamentous tissue from a patient with chronic Lyme Borreliosis. Arthritis and Rheum 1993;36:1621-1626

Schmidli J, Hunzicker T, Moesli P, et al, Cultivation of Bb from joint fluid three months after treatment of facial palsy due to Lyme Borreliosis. J Infect Dis 1988;158:905-906

Once the Lyme spirochete has found a food source like inside a tendon or joint, it must also be protected. Since the tendons and connective tissue are poorly oxygenated and few immune cells circulate there, they have a safe haven.

Occasionally we see heart complications, and arrhythmia issues. This is because the bacteria is also attracted to nerve cells and related tissues.

Within the heart there is a web-like network of nerve cells called the purkinje fibers. These fibers regulate the controlled contractions of the heart by a coordinated conduction system that keeps the contractions even and regular.

Between each of these nerve fibers is a rich source of N-Acetyl-Glucosamine, and coincidentally on tissue biopsy and stain, we see the spirochete lined up parallel to the nerves and buried within this food source.

Sometimes this leads to myocarditis, myocardiopathy, and arrhythmias like atrial fibrillation, tachycardia, bradycardia, and 2nd degree-heart-block.

In our Duluth, Minnesota, Lyme disease Support group, we had a Lyme patient who was on the waiting list for a heart transplant.

After six months of oral amoxicillin for Lyme, his cardiomyopathy improved to the point where he was no longer disabled, no longer needed a heart transplant, and became a fish farmer on the Iron Range.

His $300 of amoxicillin saved him $100,000 and a life of always being on anti-immune, rejection drugs.

Goodman JL, Sonnesyn SW, Holmer S, Kubo S, Johnson RC.: Seroprevelence of Borrelia burgdorferi in patients with severe heart failure, evaluated for cardiac transplantation at the University of MN. Abstract # 49, presented at the Fifth International Symposia on Scientific Research on Lyme Borreliosis, Arlington, VA, 1992 *

13 % of patients awaiting heart transplant tested positive by ELISA test.

Now we saw earlier just how poor this test was at detecting Lyme disease and that false positives were low. Yet the prevailing explanation from university researchers for these positive patients was “false-positives”.

I guess I would believe that if we didn’t currently have another Lyme patient awaiting a heart transplant; he is also part of our 3-year documentary on Lyme disease in Minnesota/Wisconsin, and has requested an extensive autopsy to look for Lyme if he dies.

The hard truth is that patients are willing to die to find the truth, but our health care system refuses to do any autopsy studies on Lyme disease? Why? It is the gold standard.

Autopsy is the answer to all our questions. Not to do a national multi-center autopsy study is a way of saying “We don’t really want to know the truth.”

The joints, heart, and skin are good places to hide, but this bacterium is seeking a better place to survive.

We have seen that over time untreated Lyme rashes go away all by themselves. This is because the immune system has suppressed or eliminated the bacteria, or exposure to severe heat like saunas has killed the heat labile organism.

(Borrelia cannot tolerate temperatures above 108 F for more than twenty minutes.

But to get our core temperature and brain to that temperature would kill us, so all we can do is use heat as an adjunct to kill the bacteria in our skin and help deliver more antibiotic deeper because of vasodilatation of blood vessels.

This was done to treat Syphilis, and when penicillin came out commercially in the mid 1940s, hot springs across the nation went out of business. ) See Dr. Bundeson in the book by: DeKruif, Paul: Life among the Doctors. Pp140-168

This place where the Lyme bacteria seeks is ideal. The human brain is so selective to what it allows in that it even keeps out white blood cells. Without white blood cells the bacteria has no enemies.

The bacteria swims through the blood-brain-barrier blood vessels early in infection, and then when the barrier reseals itself, the bacteria is not only safe from immune assault, but also antibiotics have trouble getting into the brain.

Some antibiotics like IV-ceftriaxone and other cephalosporin’s get into the brain but they don’t penetrate inside brain cells. Why is this important?

Well it turns out that Borrelia burgdorferi can penetrate into brain cells quickly and easily, and once they do; they can sit quietly in a non-metabolic dormant state. No amount of antibiotic can kill a dormant spirochete.

Now put it inside a cell, inside a brain behind a protective barrier, now keep out the immune system, and make sure the temperature stays nice and low like the brain prefers.

Now you have an incubator for long-term bacterial survival and eventual neurological problems that may take years to develop.

If what I am telling you is true, then surely we have seen spirochetes associated with neurological disease before? Yes, Syphilis dementia and paresis is well documented, but what else are we missing?

MS and Spirochetes

In every Lyme disease support group in this country (and I have visited dozens), there have always been at least one multiple sclerosis, MS, patient who turned out to have Lyme disease, and was recovering on antibiotics.

But if this is true why is there is no documented connection between spirochetes and M.S.?

As it turns out there are more than 50 such MS-spirochete references prior to World War II and going back to as far as 1911, and published in such prestigious journals as the Lancet.

• 1911 Buzzard Spirochetes in MS Lancet
• 1913 Bullock MS Agent in Rabbits Lancet
• 1917 Steiner Spirochetes The Cause of MS Med Kiln
• 1918 Simmering Spirochetes in MS by Darkfield Micro

• 1918 Steiner G. Guinea Pig Inoculation with MS infectious agent from Human

• 1919 Steiner MS Agent Inoculation into Monkeys
• 1921 Gye F. MS Agent In Rabbits Brain 14:213
• 1922 Kaberlah MS Agent In Rabbits Deutch Med Works
• 1922 Sicard MS Spirochetes in Animal Model Rev Neurol
• 1922 Stepanopoulo Spirochetes in the CSF of MS Patients
• 1923 Shhlossman MS Agent in Animal Model Rev Neuro

• 1924 Blacklock MS Agent in Animals J. of Path and Bac

• 1927 Wilson The Rat as A Carrier of MS British Med Journal

• 1927 Steiner G Understanding the Pathogenesis of MS

• 1928 Steiner Spirochetes in the Human Brain of MS Patients

• 1933 Simons Spirochetes in the CSF of MS Patients

• 1939 Hassin Spirochete-like formations in MS

• 1948 Adams Spirochetes within the Ventricle Fluid of Monkeys Inoculated from Human MS

• 1952 Steiner Acute Plaques in MS and The Pathogenic Role of Spirochetes as the Etiological Factor Journal of Neuropathology and Exp Med 11: No 4:343 1952

• 1954 Steiner Morphology of Spirochaeta Myelophthora (Myelin Loving) In MS Journal of Neuropathology and Exp Neurol 11:4 343 1954

• 1957 Ichelson R. Cultivation of Spirochetes from Spinal Fluids of MS Cases with Negative Controls Procl. Soc. Exp. Biol Med 70:411 1957

If you follow the European Medical Literature concerning Multiple Sclerosis from 1911 to 1939, you find that in France, Germany and England; there were independent researchers all observing similar things and coming to similar conclusions:

1) Spirochetes are often found in conjunction with the lesions in the brains of patients who have died with MS.

2) These spirochetes can be isolated and can infect many mammalian animal models; including: mice, rats, hamsters, guinea pigs, rabbits, dogs, and primates.

3) The spirochetes could be re-isolated from the brains of the infected animals and be inoculated into more un-infected animals and re-isolated from their brains.

Why in the 21^st century have spirochetes been ignored as infectious agents of the human brain?

The short answer is that to save time and money we no longer do things old school by which I mean:

• no one does brain autopsies and physically stains or cultures for the bacteria.
• Instead we have gotten lazy and cheap in our research and tried to rely on blood tests and CSF fluid to give us the answers.
• But those tests are wholly inadequate to detect living spirochetes sequestered inside brain cells.

Now this is the important part about detecting spirochetes within human tissues.

First you cannot find spirochetes if you don’t properly stain the tissue for them.

Spirochetes are completely invisible under the microscope without special stains.

In 1911, chemists and microbiologists only had silver stains that stained nucleic acids, and for some reason these stains caused the entire spirochete to turn black and opaque.

(It turns out that Borrelia’s nucleic acid is nearly evenly distributed under its inner membrane like a web of DNA that fits the entire bacterium like a nylon stocking

surrounding the cytoplasm.

In other words the silver stain outlines the shape of the bacterium.)

The trouble with silver stains is that they cannot enter human cells. So for nearly a century it was reported that spirochetes were mostly extracellular and found outside all human cells.

Not only was this a wrong conclusion based on inadequate methods,but the consequences of not recognizing an intracellular infection was and still is dire. Why?

Because intracellular infections can be incurable or at the very least more difficult to treat; there is almost no way to determine an end point where a bacteriological cure has been obtained.

Next is that spirochetes are known to disappear by changing to cyst forms, and also by going intracellular.

So these puzzled researchers that were only seeing classical formed spirochetes in 1 in 20 MS patients, may have been seeing them all along and not realizing what they were seeing. How can we conclude this?

Researchers wanted to see if the infectious agent was still in MS lesions despite no visible spirochetes.

Researchers removed brain tissue at necropsy of human patients and inoculated the tissue into uninfected animals.

In some cases, this caused the infection to occur and show up in the brain of the animals; sometimes the classical-form spiral shaped spirochetes emerged.

All of this meticulous work was done prior to WW II, and completely untainted by today’s politics and special interests; yet this body of work is being wholly ignored.

Here is a lesson from history that we should learn:

During our bicentennial year in Philadelphia in 1976, a new disease emerged. An infectious pulmonary disorder suddenly infected and ravaged many people who attended a hotel where there was an America Legion convention that was being held.

When 180 people got sick; 29 of them despite early and aggressive supportive therapy died; it was clear that this was no ordinary flu or pneumonia.

Because it appeared that the mystery illness might be being passed from person to person; immediately it was given epidemic status and the CDC stepped in.

But they were flabbergasted to say the least. Since they could not see bacteria in the lungs of the victims they assumed it had to be a virus, but all their time consuming virus searching did not yield a single clue.

Desperate to find answers at any cost, tissues especially lung tissues were sent to many scientists. Despite nearly an estimated 500,000 man-hours, the cause of the mystery illness was still unknown. It remained seemingly invisible under the microscope.

It is amazing to me that in the annals of medical history; we do not recognize the role of serendipity and credit people who made a difference. You have to look long and hard to find the real story of solving Legionnaire’s Disease.

To look back, you would think the CDC just walked in and solved it with a faceless team of experts and credit given to a government agency; not the work of an individual workaholic microbiologist poking around hot springs and an expert in soil bacteria.

Dr. Carl Fliermans solved the first part of the puzzle when he discovered that Legionella pneumophila lipids resembled those of the thermophilic bacteria he’d found in the thermal regions of the Yellowstone National Park, and that this bacteria tended to live as biofilm (scum) associated with certain species of algae.

Subsequently, Fliermans began poking around aquatic habitats and found – guess what? – this bacteria was residing in thermal waters discharged from a nuclear reactor at Savannah River Laboratory.

This bacteria was later found to be living in natural hot springs all over the United States and, most importantly, in air-conditioning cooling towers.

Once the bacteria were known, special stains for soil bacteria, and special culturing techniques solved the Legionnaire’s mystery.

What was invisible to hundreds of microbiologists could now be seen because of the right stain and right culture technique that was outside the realm of the CDC’s medical team.

Lecture Cyst References

Lecture MS references

Updated Lecture references part 5 (109 pages)

“Lyme On The Brain” (part 2) by Tom Grier

“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

Tomgrier2001@yahoo.com

The heart and soul of the mechanism of infection, or the pathogenisis of Borrelia bacteria that cause Relapsing Fever and Lyme Disease is its ability to attach to the lining of blood vessels and cause gaps or holes to appear between the endothelial cells.

The endothelial cells themselves release digestive substances, as well as our own white blood cells releasing blood-born immune factors such as tissue plasminogen, TNF-alpha, IL-1, Il-6, histamines, vaso-active amines and MMP-9 that facilitates cell penetration through any and all blood vessels, but especially important is the immediate transit of Borrelia burgdorferi through the blood-brain-barrier.

Animal models including dogs and primates show conclusively that this is not just a random occurrence, but rather a very specific mechanism that facilitates both the immediate and long-term survival of Borrelia within mammalian systems. In dog-models, the uninfected dog’s blood protein albumin was tagged with radioactive Iodine, and then traced using radio-detection of entering the brain and spinal-fluid. After infected ticks were allowed to feed on the dogs, this “leaky-brain-effect” took less than 24-48 hours to reach its full potential.

We can measure and observe this leaky-brain-effect in dogs, hamsters, rabbits, and primates within hours, and we can see and detect in many other animal models including guinea pigs, mice, hamsters, and rabbits the actual transit of Borrelia into the brain of these animals within days of tick-bite, yet our own USA health-care experts are saying without equivocation that infected ticks have to be attached for at least 36-48 hours (YALE Medical Report, IDSA-Lyme Treatment Guidelines)

Why is there such an absolute dictatorship in our guidelines when we have direct animal studies since 1989 that suggest that not only does Borrelia bacteria penetrate blood vessels and enter the brain, but once the blood-brain-barrier closes up 10-14 days after initial infection; the sequestered bacterial infection within the brain is undetectable by serology tests.

Our current serology tests that detect antibodies to the Lyme bacteria; require at least 4-6 weeks after exposure to produce significant antibodies to the Lyme bacterium. By then the infection can be resting dormant and quiescently within the host’s brain, undetected, undetectable, and creating changes within the brain that are subtle and perhaps for awhile negligible.

*******************************************

Consider these other short-comings of the

current antibody based Lyme serology tests:

1. To create these tests we need a representative source of the wild bacteria as a source for specific antigens that can be used to detect the specific antibodies that patients produce as a result of an infection from their local area.

Since Borrelia bacteria are genetically equipped to change their antigenic appearance (strain variation) it is important to use tests that are designed using the best representation of the bacteria that is found in the local area. There can be tremendous variation in Borrelia isolates even those found within close proximity to each other. There are well over 1000 Borrelia isolates of Borrelia burgdorferi that are strain variations in the USA alone. This is not even counting the greater variation that we see if we look at other related geno-species such as Borrelia lonestarrii in Missouri, or Relapsing Fever Borrelia in the SW USA, or the genospecies Borrelia garinii and Borrelia afzelii found in Europe, or the dozens of other related bacteria in the world that cause Lyme-like or Relapsing-Fever-Like diseases caused by various variant strains of Borrelia bacteria. Once you see this global picture you can never look at Lyme as an isolated disease ever again. It is part of a global-pandemic called Borreliosis.

But the tests that have been chosen for us, and dictated that we use are not based on any Borrelia found in nature! Why?

Since Borrelia identity changes quickly by inserting variant plasmid genes into its larger linear chromosome, the bacteria will always have built in variation unless you eliminate plasmids.

(Borrelia burgdorferi has about 31 circular or linear plasmid-chromosomes that facilitate genetic variation, it is estimated that over 60 genes can insert in at least three different chromosome loci resulting in over sixty to the 3^rd power variations in the bacteria or potentially over 200,000 possible variations that could be predicted based on what we currently know.)

This creates an economic and practical dilemma for manufactures of Lyme serology tests who want consistency and reproducibility without the expense of isolating local bacteria from local ticks and growing them in the lab which is very difficult, time consuming, inconsistent and expensive. For this reason manufacturers use a strain that was developed in a lab that resists variation.

Strain B-31 that was originally isolated from the NE USA ticks, and was created through high-passage selection until it remained consistent from division to division.

B-31 is never found in nature, and when B-31 tests were compared and tested by independent researchers in Madison WI, France, Austria, and United Kingdom, B-31 had short comings and never had the essential antibody detection that the tests developed from local wild-strains produced. One can make an argument for B-31 consistency, but never for its local strain selectivity.

What makes this discussion about what strain we use to make Lyme serology tests completely moot; is the one fact that we completely ignore in the United States:

Once Borrelia bacteria breach the brain’s defenses, absolutely no Lyme serology test short of an autopsy can rule out infection within the human brain!

Here are some other considerations about Lyme test shortcomings:

1. Dr. Lori Bakken Madison WI tested 516 labs across the USA using Lyme ELISA tests, and found them seriously lacking and only about 50 % accurate in consistency of positive tests. She used triple paired identical blinded samples. This independent test illustrates the fallibility of the Lyme ELISA test yet incredibly the ELISA is demanded by so called experts and medical authorities to be used as one of two screening tests used for the diagnosis of Lyme disease.

(Bakken LL, Callister SM, Wand PJ, Schell RF. Interlaboratory Comparison of Test Results for the Detection of Lyme Disease by 516 Participants in the Wisconsin State Lab of Hygiene/College of American Pathologists Proficiency Testing Progrm. J Clin Microbiol 1997; Vol 35, No 3:537-543

Bakken LL, Case KL, Callister SM et al. Performance of 45 Laboratories participating in a proficiency testing program for Lyme disease serology. JAMA 1992;268:891-895

Now consider the second screening test: The Western Blot was once a useful tool for diagnosing Lyme disease when used properly, but the National Western Blot Criteria meeting held in Dearborn MI changed this test from somewhat useful to useless and the logic and science behind it is so poor we have to ask ourselves what agenda did the committee of state epidemiologists and concerned patent-owners have? Yes people and institutions who had conflicts of financial interest had input into the two-tiered system of diagnosis that we currently use.

The nearly arbitrary decision to eliminate species specific antibody-bands from the reporting of the Western Blot tests definitely made the Western-Blot test less accurate. This change in accuracy did not come about from changing the actual test but rather by enforcing a reporting-bureaucracy that made the test less sensitive. Make no mistake the labs that do this test still see the positive bands that are banned from reporting, but are legally unable to report them.

Then to further cloud the already muddy waters of accuracy it was decided that all laboratories across the USA have to report all Western Blots as either positive or negative and not report the essential bands.

Not reporting significant Western Blot Band is to a scientist, tantamount to saying:

There are no contaminates in

your drinking water, so please don’t waste your time testing the well water, and if you do test the waters and find something that we haven’t reported, we have already deemed that the contaminates are unimportant and benign.

Well the contaminates (bands 31, and 34) aren’t as benign as we are told. Let’s look at the old Western Blot reporting criteria on 66 kids with a tick-bite and bull’s-eye rash compared with the new reporting criteria. This is the same test and same patients, but we are now using the Dearborn MI “Dressler” criteria for Western Blot reporting.

Western Blot and False Negatives in Children: 1995 Rheumatology Symposia Abstract # 1254 Dr. Paul Fawcett et al. 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. Under the newly proposed criteria only 20 were now considered positive. That means 46 children who were all symptomatic, would probably under the previously mention YALE Criteria be denied treatment! That’s a success rate of only 31 %.

66 Children with Bull’s Eye rash Old W. Blot Criteria 100 % positive

New NIH Criteria 31% positive

The number of false positives under both criteria was ZERO %

* Note: A misconception about Western Blots is that they have as many false positives as false negatives. This is not true. False positives are rare.

The conclusion of the researchers was: “the proposed Western Blot Reporting Criteria are grossly inadequate, because it excluded 69% of the infected children.”

More issues with serology testing in Lyme:

1. The human body starts to make IgM antibody at 4-6 weeks after exposure to the pathogen, and does not make IgG antibodies for many months, yet some “Lyme Experts” want to eliminate IgM Western Blot reporting completely. This would almost certainly mean less early Lyme disease detection because most doctors who use “Two-Tiered” testing protocols will test within the first two months of tick bite and the negative Western Blots will demand that they not treat. (See Yale treatment protocols above)

D) The Lyme bacteria can hide almost immediately within the human body.

Without a large enough number of bacteria (infection load) that remains in the

bloodstream for a sufficient time for the immune system to recognize the

pathogen, the human immune response will be minimal or absent.

Intracellular localization of Borrelia burgdorferi within human endothelial cells. Ma Y, Sturrock A, Weis JJ. Infect Immun 1991 Feb; 59(2): 671-8. PMID:

Characterization of Borrelia burgdorferi invasion of cultured endothelial cells. Comstock LE, Thomas DD. Microb Pathog 1991 Feb; 10(2): 137-48. PMID:

Penetration of endothelial cell monolayers by Borrelia burgdorferi.
Comstock LE, Thomas DD. Infect Immun 1989 May; 57(5): 1626-8. PMID:

Although the antibody tests would be negative possibly for years, the infection can still be alive and cause problems where it survives such as in the: joints, heart, inside endothelial cells, and inside the brain and more specifically inside brain neurons and glial cells. These bacteria cannot be detected with indirect methods like Lyme antibody test including ELISA and Western Blots, nor is it likely that DNA-PCR can detect these infections without heroic efforts to obtain proper sampling that goes far beyond just blood and urine. Time, money and expediency has forced doctors to use tests that are inadequate for the task of determining the worst possible scenario which is a persistent infection within the brain.

For the simple reason that most patients are not obviously or immediately affected by their neurological infection, the medical system has ignored these ticking time-bomb patients that are seronegative, and symptom free. But the neuro-lyme patients will pay a severe price for having doctors who refuse to go back and connect all the dots after these patients reappear in their offices with severe disabling symptoms.

Untreated and improperly treated tick bites can lead to patient disasters. Yet the treatment guidelines are so black and white that we have to now ask ourselves: Are we going to hold the users of these treatment guidelines accountable for their lack of any flexibility?

Patients are not paid to be experts in any disease, but when an entire medical community has limited all the options for sick patients both in diagnosis and treatment, then can we not hold these professionals to the same standards we would expect from a plumber? If the pipes leak, at least try and understand why?

Here is an example of unrealistic expectations from the medical community. In Valhalla New York a temporary Lyme treatment center was created that used the ELISA test to screen patients. Using this inadequate test it was determined that about 30 % of all walk in patients had Lyme disease. But here is what one of the coordinators had to say about it:

There is great hysteria about Lyme disease… less than a third of the patients who walked in to our center actually had Lyme disease.

Would we hold the same standards of accurate self-diagnosis to cancer patients, or heart patients? Do we publicly chastise patients walking into a sexually transmitted disease center and say: “These people are wasting my time! Only a third of them have VD!!!”

Why then is there a double standard for people who are losing their jobs, their marriages and quality of life who are just seeking answers. No wonder so many patients turn to alternative treatments. The options for Lyme disease patients to get diagnosed and aggressively treated in America is extremely limited and only getting worse every year!

Now consider this: Recently a Lyme disease expert stated nationally that there is no evidence of transplacental transfer of active infection from mother to fetus.

We have actually observed in culture Borrelia burgdorferi penetrating umbilical vein.

We also have nine case histories 1987-1989 that confirmed by either culture or direct tissue staining that in fact Borrelia burgdorferi does cross the placenta, and has caused still-births including infections within the fetal brain.

(See work and photo by Dr. Andrew Szycpanski Stony Brook Dept. of Pathology New York of Borrelia creating holes in umbilical vein.)

If I was a Obstetric Nurse or OB-GYN and told to repeat this factoid that Lyme does not cross the placenta as stated by our guiding experts on Lyme disease concerning pregnant patients, and then to also be forced by clinic administrations, insurance companies and peer pressure to rely on two-tiered testing, and follow published treatment guidelines that ignore our entire encyclopedia of knowledge on spirochetes, I would be worried! I would be worried that when the next fetal autopsy is done that I would be called to be accountable.

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This is a silver stained image of a Borrelia burgdorferi penetrating a fetal brain neuron at necropsy of a still-born fetus from a mother thought to be at low risk for Lyme disease and seronegative for Lyme antibodies on several lyme serology tests. Alan MacDonald

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If Lyme disease patients have early undetectable neurological infections that resist current antibiotic treatment regimens, then why haven’t we seen evidence of this?

First of all if you define treatment success by merely saying that the patient’s Lyme tests are now negative after treatment, you will by virtue of incredibly bad science never see treatment failures. This is because eliminating the infection from the blood is not the same as eliminating it from the heart, brain and joints. But serologies will fail to detect these areas of sequested infection where the bacteria fails to stimulate antibody production.

Next you have to look at follow-up. If you do a study that compares doxycycline to IV ceftriaxone and the only symptom is a bull’s-eye rash and your only determination of cure is the absence of rash and a negative ELISA test, and your only follow-up post treatment is two weeks. You will probably conclude that doxycycline is as effective as IV ceftriaxone, and insurance companies will smile and love you. (See M. Eckman )

Two things have been consistently true in nearly one dozen antibiotic treatment studies: The longer you treat the fewer relapses you have, and the sooner you treat after tick bite the better, and the longer you follow patients after treatment the higher the relapse rate will be. We have patients from Nantucket Island that were followed over five years after months of antibiotic treatment and still relapsed and it didn’t matter if intravenous drugs were used. What was more important was How long you treated and how soon after tick bite you treated. Overall the relapse rate after 5 years approached 50 %, but to get all the facts you had to go to a Lyme Conference because this final relapse rate was never published and conveniently left out

How antibiotics work:

In most cases bacterial lethal exposure occurs only during cell division. For a spirochete like Borrelia that is a slow divider (24 hours under good conditions) to get the same lethal exposure during cell-wall synthesis as say treating strep bacteria, you would have to treat for one year and five months. Using the old microbiology formulas for tuberculosis from the 1950s, we would expect both TB and Lyme disease to require in many cases over one year of antibiotics including combination therapy. Well we learned our lesson with Tuberculosis but not yet with Lyme disease.

Relapse or Failure %

Logigian (1990) 37% After 6 months, 10 of 27 patients treated relapsed or failed treatment. 17 (63%) improved, 6 (22 percent) improved, then relapsed, 4 (15%) had no response.”

Pfister (1991) 37% 33 patients with neuroborreliosis treated. After a mean of 8.1 months, 10 of 27 were symptomatic and borrelia persisted in the CSF of one patient:

Asch (1994) 28% 3.2 years after initial treatment: 28% relapsed with major organ involvement; 18% were reinfected. Persistent symptoms of arthralgia, arthritis, cardiac or neurologic involvement, were present in 114 (53%) patients.”

Shadick (1994) 26% 10 of the 38 patients …relapsed within 1 year of treatment and had had repeated antibiotic treatment.”

Shadick (1999) >37% 69 of 184 previously treated patients (37%) reported a previous relapse.

Treib (1998) >50% After 4.2 years, more than ½ of 44 treated patients with clinical signs of neuroborreliosis and specific intrathecal antibody production were symptomatic.

Valesova (1996) 38% At 36 months, 10 of 26 had relapsed or progressed: complete response or marked improvement in 19, relapse in 6, and new symptoms in 4.

End of Lecture Notes for Lyme on the Brain Part 2 by Tom Grier

COMING UP NEXT… Part 3 – A history of spirochetes in MS since 1911 to present day.

Lecture Cyst References

Lecture MS references

Updated Lecture references part 5 (109 pages)

“Lyme On the Brain” (Part 1) by Tom Grier’s

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

Tomgrier2001@yahoo.com

Introduction

Lyme disease was first recognized in Old Lyme CT in 1973 by two concerned mothers. Judy Mensch and Polly Murray felt there were too many diagnosed cases of Juvenile Rheumatoid Arthritis in their neighborhood children. Judy and Polly Murray who had backgrounds in public health collected over 200 local case histories and presented them to the CDC and CT health department.

Dr. Alan Steere M.D. investigated the local cases of JRA and coined the misnomer “Lyme Arthritis” in his 1975 publication that first described Lyme Borreliosis as an arthritic disorder.

Although the actual cause of Lyme Arthritis that was sometimes associated with a bull’s-eye rash was not yet known, a treatment protocol of two weeks of tetracycline was already being recommended.

The infectious etiology of Lyme disease was not known until 1981 when Dr. Willy Burgdorfer PhD from Rocky Mt Labs isolated the new species of Borrelia bacteria from a tick from Shelter Island. The fact that “Lyme Disease” was caused by a spirochete should have been a real concern and everything we thought we knew about Lyme disease should have been reevaluated at that time.

Borrelia was a family of bacteria not only associated with relapses and antibiotic treatment failures, but also is part of the same family of bacteria that causes Tick-Bourne- Relapsing Fevers, a group of over 300 variant diseases that can be deadly within months (Borrelia duttonii and Borrelia crocidurai of Northeast Africa), or considered mild and often mislabeled as “self-limiting” such as Borrelia recurrentis found in the Southwest USA. (Ron Ferris of Canada was diagnosed with Borrelia recurrentis and was sick for years despite treatment right up until the day he died).

In 1982 the Lyme bacteria was isolated from the “Lyme Bull’s-Eye rash” from patients from New England. With this new discovery causing so much excitement and demanding large sums of monies to investigate, no one wanted to admit that “Lyme” was just a new subclass of a larger world-wide disease spread by ticks that was well known for a century as tick-born-relapsing fevers.

We need to stop calling this disease Lyme disease and recognize that it is part of a worldwide problem called Borreliosis.

If we don’t recognize Lyme disease as a larger worldwide health problem caused by bacteria that have a built in mechanism for variation, our health departments will define the disease out of existence.

Technically the MS/Lyme patient that recently died in Australia (a high ranking tennis player) may not have had Lyme disease even though he tested positive on two serology tests.

Why?

Because if he had Borrelia in the brain that causes relapsing fever and that variant borrelia lacks the OSP-A DNA sequence and we use a PCR osp-A test to test his brain tissues: he may test negative for osp-A, but still have Neuroborreliosis that is an osp-A deficient variant. The report would say it is not “Lyme Disease” but is any Borrelia in the brain acceptable? Ask his widow who had to fight this case to the Supreme Court just to get an autopsy. But what good is an autopsy if they look for a species unlikely to be in Australia? If a murderer kills you with a 44 caliber or a 38 caliber your still just as dead. But our CSI people looking at Lyme need to be doing a better job if all they are going to look for is Borrelia burgdorferi (stricto sensu)

Despite documented case histories of Lyme patients still being in the rash stage and yet progressing on to serious late stage complications while on tetracycline- class antibiotics, the use of cyclines for 2 weeks is still the recommended Lyme treatment. This has to change.

When Lyme was found to be caused by a spirochete, no serious reevaluation of treatment protocols ever took place. Instead major medical institutions and universities made a mad rush to register patents for Lyme tests, Lyme vaccines, and patents on the bacteria’s DNA sequences for PCR testing.
But what no one did including the CDC and NIH, they didn’t do pathology studies to see if treatments were successful.

“Today when Lyme patients are told that they are cured, and that their continuing symptoms must be caused by something else: I would like to know what is out there in nature that defies antibiotic treatment better than a spirochete? Also if we keep discovering new infectious disease causing organisms like anaplasmosis, why do we assume that a patient with continuing symptoms that still responds to antibiotics is “cured”? Are we so arrogant to think we have to keep our options limited only to diseases that only appear on a hospital lab-order test check-list?

Are we so sure Lyme is so easily curable?

Just one brain-autopsy that finds spirochetes post antibiotic treatment, can disprove the misguided position that a few weeks of antibiotics is sufficient to “cure” Lyme disease, and that work has already begun.

But my question is:

Who do we hold accountable? The answer has to be who ever it is that is withholding or restricting antibiotic treatment from symptomatic patients.

Who has signed their guidelines in the blood of dying Lyme patients?”
Tom Grier Lyme Lecture Amery WI

Early on doctors and scientists seemed to want to talk about Lyme disease in absolutes.

Absolutes that changed:

Lyme was absolutely transmitted by a new tick species called Ixodes dammini, then it was discovered that this new species was the same as Ixodes scapularis ticks which had been around centuries and had a wider range than we first thought that Ixodes dammini had. But in California three major mountain ranges away from New England, Lyme was transmitted by Ixodes pacificus. In Missouri the Lone Star Dog Tick had a new Borrelia that caused Bull’s-eye rashes and Lyme, in Europe it was the Sheep Tick, or the Sea Bird Tick that transmitted Lyme, and their host reservoirs were different from America’s white footed mouse thought at one time the only reservoir of Borrelia burgdorferi and now just one of many rodents and possibly bird species.

Length of Tick Attachment: A tick must be attached for at least 36-48 hours. WOW! How could you ever make that conclusion on the sparse veterinary and human data we have? In fact the data suggests this is not true. Studies that looked at improper removal of a tick showed much shorter attachments are possible.

What child removes a tick properly?

Dr Elizabeth Burgess DMV Madison: her work has been overlooked for decades. Her preliminary work showed that the Borrelia species of spirochete possessed some mechanism and ability to penetrate mucous membranes suggesting transmission in cattle could be through urine –to- mouth contact putting cattle at a risk besides just ticks. Dr Burgess’s work veternary was harshly and unjustly criticized without investigation or inspection. A decade later we see that Borrelia is a champion at penetrating mammalian blood vessels and endothelial cells that line the blood vessels. How hard is it to imagine mucosa capillaries in cattle are exposed targets for Borrelia to penetrate on contact? Since the introduction of the veternary Lyme vaccines, we here little about entire herds of cattle and horses being infected.

Absolute treatment:

Two weeks of doxycycline is adequate despite persisting symptoms: I am curious: Has two weeks of tetracycline ever cured a case of acne???

Let YALE defend their own position:

A synopsis of this view point can be found in the Yale Medicine
Report, May 15, 1996 in an article by Marc Woortman states that:
(Excerpts from page 11, Yale Medicine, May 15th, 1996)

· If you suspect the tick was attached for at least 36 hours,
observe the site of the bite for development of the characteristic
skin rash, erythema chronica migrans (sic), usually a circular red
patch, or expanding “bull’s eye,” that appears between three days and
one month after the bite. Not all rashes at the site of the bite are
due to Lyme disease. Allergic reactions to tick saliva are common.
Preventative antibiotic treatment is not necessary, is costly, and
may cause side effects.
· If symptoms of later-stage Lyme disease develop, such as
arthritic swelling of a joint, most often the knee, or facial nerve
palsy, have a test done. If the test is positive, have a more precise
test done. Only if this test proves positive should a course of
antibiotic therapy begin. Expect some symptoms to linger up to three
months. No further antibiotic treatment is necessary.

This article suggests that treating a symptomatic patient with a
negative Lyme test with antibiotics, may be more harmful than
treating Lyme disease based on a single positive test and late stage
symptoms. It is clear that the Yale perspective on diagnosing Lyme
disease is that late stage Lyme symptoms, including a swollen knee
and Bell’s Palsy, do not warrant antibiotic treatment despite a
positive ELISA test! It is suggested that delaying treatment in a
symptomatic Lyme patient with these late stage symptoms is better
than risking antibiotics.

The statement from the second paragraph tells us the
intentions, “Only if this [second] test proves positive should a
course of antibiotic therapy begin.”

This statement tells us that Yale puts more faith in serology tests
than in a patient’s symptoms, Even symptoms that include an expanding
EM rash after a known tick bite, a swollen knee, Bell’s Palsy, and a
positive blood test must all be ignored because antibiotics are
costly and could cause side effects! (Apparently no one told this to
dermatologists who often prescribe tetracycline for acne for years at
a time at a cost of about $10 a month.) I have to ask; What motivates
these doctors to deny treatment to a symptomatic patient who has a
rash and a positive ELISA serology?

(For full article and reference see canlyme.com)

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What happens when a tick attaches?

This is the essence of the pathogenisis of Lyme disease: if you understand this concept of infection, you begin to understand why the conservative viewpoint of Lyme is causing latent morbidity and mortality.

In several mammal studies in the late 1980s, it was shown in many species including dogs that within hours of tick attachment that the Lyme organism is with every beat of the heart circulating through the entire body. The spirochete’s motility allows it to position itself into the cracks and folds of a blood vessel wall.

Borrelia burgdorferi has a tropism or an attraction to attach to the endothelial cells lining blood vessels. Once the bacteria has attached it traps tissue plasminogen that converts to plasmin and this begins the process of inflammation. This irritation causes the endothelial cells to release digestive enzymes such as basement membrane laminase, hyaluronidase, lipases, proteases. White blood cells join in at the site releasing Metalo-Matrix- Protease that facilitates cell penetration, and Tumor Necrosis Factor Alpha, and Il-1, Il-6 and TGF beta, all which play a role in cell communications and begin inflammatory cascades to begin.

The net result is within 24-48 hours we can measure the breakdown of the blood-brain- barrier in dogs that peaks at 48 hours and lasts for up to 14 days! So are we really going to say that a tick has to be attached 48 hours? This animal model suggests that the infection is potentially already established within the brain. This study was done by tagging normal blood albumin with radioactive Iodine and tracking it into the CSF of the dogs. (1989 Immunological Methods of Borreliosis Cold Spring Harbor)

If the Borrelia bacteria which as a family has been known to be neurogenic and deadly since 1910 can penetrate blood vessels, then why do physicians who should know better still make public statements in the media that Lyme disease is not transmitted transplacentally to the fetus during pregnancy. Nine published fetal autopsies since 1987 suggest otherwise, so what is their agenda for pretending to be ignorant of the facts?

END of Part 1

Lyme Lecture Notes From

Lyme On The Brain by Tom Grier

Lecture Cyst References

Lecture MS references

Updated Lecture references part 5 (109 pages)