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Tick-Borne-Disease Pathology Fellowship(A self-funded research group) Thomas Grier (Study Coordinator) donatebrin@gmail.com / 218-216-5670

Dear Legislators

Why the medical community’s perspective on Lyme disease is different from a pathologist’s perspective.

Lyme Disease Blood-Tests VS Tissue Pathology and Culture

Lyme disease is a collection of many species of bacteria not just one species!

1. Since 1982 when the cause of “Lyme-disease” was discovered to be cause by a spiral shaped bacterium called Borrelia burgdorferi, almost all conclusions about Lyme disease from that time to the present was based on flawed blood tests that were designed using only Borrelia burgdorferi. (See slide #1)

Lyme disease is not caused by just one species of Borrelia bacteria, but we now know of 17 species of Borrelia that have been discovered in the last 10 years that cause human-Lyme disease. (See slide #2)

Lyme disease blood tests are all made with a laboratory strain (B-31 strain) of just the original Borrelia species and cannot detect the other 16 species or any newly emerging species being discovered at a rate of about one per year. New species of Lyme causing Borrelia are appearing at a rate of about one new Lyme-disease species per year.

The tests that are made with B-31 Borrelia burgdorferi strain are less sensitive than tests made with the Lyme-species found in ticks found in nature. (Pasteur Institute). B-31 is not identical to the human pathogens and lab-strain is used only because of cost and convenience.

All antibody-based Lyme-disease blood tests are indirect-tests as they only detect our antibody response and not the presence of actual bacteria.

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The absence of anti-Lyme antibodies does notmean a symptomatic patient is not infected.

Our antibody response can vary widely fromPatient to patient for several reasons such as:

A) The initial infection load may be below immune cell thresholds to initiate B-Cells to change into antibody producing plasma cells.(If not enough bacteria are detected and deemed a threat, then the cells that make antibodies stay resting)

B) The blood-tests using B-31 Strain do not detect all species of Lyme pathogens.

C) The Bacteria have an early mechanism of blocking our immune system’s effectiveness.

D The infection moves quickly out of the bloodstream where our immune system resides. The bacteria then enters tissues where the human immune system is not allowed or is limited such as the: Brain, Eyes, Testicle, tendons, but most insidious and effective is Borrelia spirochete’s abilities to hide inside human cells.

E) Borrelia can live inside human cells including blood-vessel wall cells, liver cells, macrophage, skin cells, and most deleterious is the fact that Lyme can reside inside the human brain inside both neurons and glial cells. (See slide 4)

This disease enters tissues including the human brain and blood vessels quickly.

2. The family of bacteria that comprises both Lyme disease species and Tick-Borne-Relapsing-Fever species, penetrates and transverses blood vessels quickly.

From tick-bite to the human brain, may take less than a single day for Lyme disease to move from the tick to vital human organs including our brain.

In cultures with Lyme disease containing living blood-vessels (human umbilical vein), gaps between blood-vessel-wall cell junctions can be seen forming in mere hours. (See slide 5)

Using living mouse blood-vessels in the mouse ear, we can see penetration of the Lyme disease spirochetes from vessel attachment to entering tissues in mere minutes. (See slide 6)

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The CDC researchers Jill Livengoode and Robert Gilmore showed in a taxpayer paid elegant experiment, that Borrelia Lyme disease spirochetes penetrate and inhabit human neurons, glial brain-cells, and blood vessel endothelial cells. (CDC Slides listed)

(The Blood-Brain-Barrier or BBB)

The human blood-brain-barrier of our brain is meant to protect us from infections, but it also acts as a barrier to effective detection of active brain infections and inhibits antibiotic treatments by blocking drug penetration.

3. Some species of Borrelia are neurotropic. This means that once the infection settles in the brain, the infection tends to stay behind the BBB, because the infection can survive and thrive and not be attacked by our immune system.

While the BBB is meant to protect us, it is a very real barrier that inhibits both against our blood-tests detecting Lyme disease, and the BBB also prevents many drugs including antibiotics from entering.

The BBB is so selective that our disease-fighting immune cells are not allowed to enter the human brain. The blood-brain-barrier is a protective mechanism against brain inflammation caused by our immune cells. (See slide 7)

Once Lyme disease enters the human brain it has several layers of protection. Once inside the brain, the infection has isolated itself from our immune system, the bacteria are behind the Blood-Brain-Barrier where antibiotics are less effective and several Borrelia species including Lyme disease can enter and inhabit our brain cells. But there is one more trick Borrelia bacteria has to survive inside the human brain undetected.

Biofilms and Amyloid!

We once thought that amyloid was a marker for Alzheimer’s disease, but beta amyloid plaques may indeed have a protective role against brain infections.

What are biofilms???

4. We now know that Borrelia spirochetes are good formers of biofilms. Biofilms protect colonies of bacteria from the human immune system and from antibiotic penetration. If the antibiotics can’t reach the bacteria, they can’t inhibit the infection.

For an antibiotic to work it must have contact with the bacteria and be absorbed. Once inside the bacteria, antibiotics can inhibit bacterial metabolism by blocking bacterial

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protein making machinery called ribosomes. Antibiotics are not antiseptics that kill on contact. Antibiotics work by inhibiting bacterial metabolism through enzyme pathways.

Only metabolically active bacteria uptake the antibiotics. So “dormant” bacteria cannot be killed until the dormant bacteria regain metabolic activity in the presence of antibiotics, and then must be in direct contact of the antibiotics at bactericidal levels. But the blood-brain-barrier combined with intracellular locations, and bacterial biofilms and amyloid sequestration prevent bacterial contact with both immune cells and antibiotics.

Now we add the final straw to the camel’s back.

5. AMYLOID, Alzheimer’s and Borrelia

A bacterial biofilm is where clumps and colonies of spirochetes coalesce into groups by secreting a protective gel that binds them together. In patient autopsies we can actually detect Borrelia tissue infections by using stains specific for the molecular components of the biofilm gel. (Then we can re-stain the biofilm areas with Borrelia stains to confirm the presence of Borrelia spirochetes. (Borrelia species are nearly invisible in tissue without proper stains.)

Interestingly when we do brain-autopsies on dementia patients, we almost always see Borrelia associated with the Alzheimer’s amyloid plaques. Many researchers now believe that instead of amyloid being the cause of Alzheimer’s Dementia, that the amyloid is produced in response to infections and sequester infections of the brain. We now know many bacterial diseases can stimulate amyloid production and in the lab the amyloid engulfs the infections.

Whereas other infections may be easily killed, the Borrelia infections seem to thrive and may survive in a semi-dormant state for decades. (See slide group 8)

More monies and research are needed to investigate infectious etiologies of Alzheimer’s dementia and MS. We now have tools that can detect spirochetes in the brain that we didn’t have 10-years ago. We also have at our disposal brain banks that have specialized in dementia brains, and these stored tissues have proven to be a boon to Lyme disease research.

Why did we adopt a serology only perspective of Lyme disease?

6. In 1982 researchers found Borrelia burgdorferi difficult to work with. It was difficult to culture and it was always changing its surface proteins so using these ever-changing proteins as a source for Lyme-disease antibody tests, proved to be inconsistent. Currently we still use Borrelia-Surfact-Proteins to make Lyme tests, but using lab strain B-31 means the Lyme tests are always consistent. (Consistently flawed!)

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7. The bacterial surface proteins are the proteins that we need to make our two major Lyme disease tests: ELISA antibody tests and Western Blot antibody tests.

Borrelia surface proteins are isolated and put in little wells on a plastic card, and the wells have a color changing indicator dye that changes in a positive reaction.

A patient’s serum is added to the dozens of wells at various dilutions. Any serum diluted to about 500 parts water to one part serum that shows a significant color change is deemed a positive reaction.

The cut off point for dilution is different in different labs, Mayo Clinic requires 1024 parts water to one-part patient’s serum to be positive. (That is an extremely high cut off point, some labs use as low as 1:125 dilutions. At low dilutions below 125 parts water to one part serum can result in false positives. Independent researchers not financially linked to the blood tests have found there are more false negatives than positives. (See Dr. Lori Bakken Madison Pathology Testing)

The point is when Lab Strain B-31 was introduced by Dr. Alan Barbour, it was easily grown and cultured and unlike natural strains, B-31 never showed surface-protein variability. So labs across America and the CDC adopted this cheap and easy source of bacterial proteins for their blood tests.

But B-31 strain is not found in nature. It is not a fair representation of the wide variety of Borrelia species that causes Lyme disease and certainly not a closely related group of diseases caused by Borrelia species.

There is a disease found in the same species of ticks that harbors Lyme disease. This related disease is called Borrelia miyamotoi which is a Tick-Borne Relapsing Fever and appears to prefer the human brain as its target tissue of choice.

The final and biggest reason for using flawed Lyme-disease blood tests are the numerous financial conflicts of interests trying to create a low cost product with a high profit margin.

Many patents for the CDC Lyme testing are owned by the CDC officers in charge of tax-payer paid Lyme disease research. Not one taxpayer dollar has ever been spent on human pathology such as looking at brain-bank tissues and staining for Borrelia spirochetes. But our monies have been spent repeatedly to produce Lyme disease tests only to see the patents put in the names of CDC officers.

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The rogue Borrelia. Borrelia miyamotoi.

8. Borrelia miyamotoi is found in the same tick as Lyme disease. But unlike Lyme disease it can be transmitted from an infected Deer-Tick in just 20 minutes, and brain autopsies indicate that it likes the human brain and in a limited number of brain autopsies (112 brain autopsies) B. miyamotoi and Lyme disease is associated with Alzheimer’s Dementia in a large percentage of dementia brains that were tested. (See slide group 9)

Although the spirochete looks the same as Lyme disease, it is not even in the same genetic grouping. Although the symptoms of B. miyamotoi are similar to Lyme disease, and is in the same family and genus of bacteria (Borrelia), they are different enough that Lyme disease blood tests cannot detect Borrelia myamotoi in the human brain or blood.

Rather than address the shortcomings of testing for B. myamotoi, and Lyme-like diseases of the south caused by B. lonestarrii, the CDC mostly ignores these diseases as well as newer species of Borrelia, and continues to use the same outdated one-size-fits-all recommendations for Lyme disease testing.

The medical community acts as though there are no other Lyme species other than Borrelia burgdorferi. But Borreliosis in America is far more complicated, and more serious than what is being told to American doctors. (See Autopsy Slides Group 10)

Sincerely.

Thomas Grier 218-216-5670 / donatebrain@gmail.com

Pathology Study Coordinator for the Paul Duray Pathology Fellowship ( A self-funded organization of volunteer scientists)