Thomas Grier - Borelioza.

Thomas Grier Executive Director
Dr. Paul H Duray Pathology Research
902 Grand View Ave
Duluth MN 55812 (218)728-3914
 
,,Piszę, bo jestem zaniepokojony  artykułem  niedawno opublikowanym ,a  napisanym przez profesora Jana Keppel Hesselink. Artykuł traktuje  o tym, ze  pacjenci i opinia publiczna  mają nieprawdziwe i przesadzone  obawy dotyczące  boreliozy i  nowoczesnych szczepionek. Jako ktoś, kto jest związany z boreliozą i badaniami nad borelioza od 1990 roku, mam obawy co do akademików, którzy wyrażają zdecydowane poglądy na ten temat oraz oferują niewielką lub żadną pomoc naukową w celu wspierania walki z Borelioza a uważają ze pacjenci starają się wpłynąć na medycynę w kierunku ujemnym.

Od 1991 - przez ponad 25 lat walczyłem do prawa o zamieszczania prawdy o Boreliozie.,,

,,Publiczne  fakty na temat boreliozy, są szczerze mówiąc nieprawdziwe i nigdy nie były prawdziwe. Wiele z tych nieprawdziwych faktów nadal są propagowane przez główne grupy lekarzy i placówki medyczne ale spójrzmy na fakty z pozycji zwykłego człowieka. Aby następnie zdecydować, co jest prawdą.,,

Powiedziano nam, że tylko kleszcze Ixodes dammini mogą przenosić boreliozę i że stwierdzono jedynie związek w  NE USA .Dlatego borelioza oficjalnie  była tylko w NE USA.

Prawda jest taka ze nigdy nie było Ixodes dammini .Trzeba zaznaczyć, ze dr Andrew Spielman Harvard błędnie zidentyfikował  kleszcza Black Legged i jego kilku bliskich kuzynów. Można te kleszcze znaleźć w całej Ameryce Północnej i na całej północnej półkuli Wszystkie one przenoszą  krętka boreliozy B. burgdorferi .

Powiedziano nam, że nigdy nie była Borrelia burgdorferi wewnątrzkomórkowa.

Prawda jest taka ze borelioza jest chorobą właśnie  wewnątrzkomórkową i załączam własne zdjęcia badawcze udowadniające iż  Borrelia przenika do mózgu, a następnie przenika do  komórek glejowych i ludzkich neuronów .

Wzywamy wszystkie kraje aby robiły  sekcje zwłok .A dokładnie sekcje ludzkiego mózgu, my to zrobiliśmy, wtedy można  zobaczyć całą prawdę o tej chorobie.

Powiedziano nam, że borelioza nie jest przenoszona z matki na płód.

Pierwszy dowód - (2006 Dr Gary Wormser Yale film dokumentalny ,,Under Our Skin  ,,)
Od 1989 osiem sekcji zwłok płodu pokazujące Borrelia w płynie pępowinowym, w łożysku, oraz niemal w każdym narządzie płodu . (mam zdjęcia)

Co jeszcze się stało?  

Dezinformacja o Lyme była najbardziej szkodliwa dla  tych, którzy mieli największy wpływ na środowisko medyczne czyli na :  CDC, Yale, SUNY, Harvard and Mayo Clinic, the ACP i  the IDSA

Inna  nieprawdziwa  informacja : powiedziano nam, że tylko jeden gatunek bakterii Borrelia powoduje boreliozę.

Czy nie wyciągnięto  lekcji z Relapsing Fevers?

Borrelia  ewoluuje jak żadne inne bakterie. Ciągle się zmienia i ewoluuje. Mamy obecnie 12 gatunków, które wywołują boreliozę i kilka gatunków, które nazywamy Lyme-like.

Inny fakt : powiedziano nam, że tylko jeden gatunek myszy roznosi te bakterie. 
Oczywiście teraz wiemy ze wiele gryzoni i ptaków jest nosicielami choroby i przekazują ja dalej.

W raporcie medycznym  Yale -  Marc Voortman mówi, że u pacjentów z dodatnim wynikiem testu ELISA ale negatywnym Western Blot może wystąpić rumień, porażenie Bella i obrzęk stawów, a leczenie nie jest konieczne. Ale jeśli test Western Blot jest dodatni można do 2 tygodni podawać Doksycyklinę.

Jest patologiczny dowód, że dwa tygodnie antybiotyku nie są wystarczające przy Boreliozie.Lista dezinformacji jest długa.

Najbardziej szkodliwa nieprawda o Boreliozie  to to ze z uporem twierdzono iż po krótkiej antybiotykoterapii nie ma bakterii w organizmie.

Dołączam  zdjęcia pacjenta, który mieszka zaledwie kilka mil ode mnie. Był chory przez ponad 30 lat. Był zdiagnozowany (borelioza) .Leczył się  agresywnymi  kombinacjami antybiotyków przez ponad siedem lat. Kiedy zmarł znaleźliśmy zarówno Borrelia burgdorferi jak i Borrelia miyamotoi w jego mózgu oraz  B.burgdorferi i B. mayoni w jego jądrach
Borelioza jest i trwa.

Dostaje się do mózgu i do wewnątrz komórek mózgowych. (w załączeniu zdjęcia patologii z autopsji mózgu) Ponadto mamy dowody ze wyhodowano B. burgdorferi  na mózgach osób z Alzheimerem.
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2016 - choroba Alzheimera ma etiologię zakaźną i jest związana  z Boreliozą.
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Choroba z Lyme utrzymuje się w mózgu ( bakterie), badanie serologiczne -brak infekcji mózgu

Matki w ciąży przenoszą  Borelioze  na płód

Transmisja choroby drogą seksualną - udokumentowano - bakterie Borrelia znajdywano w ludzkich jądrach  nawet po antybiotykoterapii,

Borelioza może zabijać, jak to miało miejsce w Nowym Jorku .Mężczyzna miał Borrelia w sercu.Więc, gdy pacjent nie zgadza się ze swoim lekarzem i wyjaśnia, że ​​jest nadal chory po leczeniu . Kto ma rację? Czy lekarz powołując się 30-letnią dogmat, czy pacjent, który umarł i miał zbadany mózg  a autopsja wykazała przewlekłe zakażenie mózgu pomimo wielu lat leczenia antybiotykami?

Thomas M. Grier (dyrektor Exec)

Dear Editors: I am writing to express a concern about the article you recently published, written by Professor Jan Keppel Hesselink. The article was a position paper about how patients and the lay-public have exaggerated concerns or misrepresented the seriousness of Lyme disease and modern vaccines.
As someone who has been involved with Lyme disease and Lyme disease research since 1990, I have concerns about academics who express strong opinions on this subject, but offer little or no scientific support or research of their own to support that patients are trying to influence medicine in a negative direction.
Since 1991 I have fought for pathology based Lyme disease research to put certain myths and misinformation about Lyme-Borreliosis to rest. For over 25 years the lay-public has been told facts about Lyme disease that quite frankly are not true and were never true. Many of these untrue facts are still being propagated by major physician groups and medical institutions; but lets look at the facts from a position of human pathology. Then decide who is misleading whom?
We were told that only the Ixodes dammini tick could carry Lyme disease and that it was only found in the NE USA therefore Lyme disease was only in the NE USA. The truth is there never was an Ixodes dammini tick, Dr. Andrew Spielman of Harvard misidentified the Black Legged tick which is found throughout North America and several close cousins of this tick all carry the Lyme spirochete and B. burgdorferi is found all through the Northern Hemisphere.
We were told that Borrelia burgdorferi was never intracellular. In truth Lyme disease is very much an intracellular disease and I have attached our own research photos to support that Lyme disease enters the brain and then enter both glial cells and human neurons. We urge every country to do human-brain autopsies as we have done, to see the whole truth of this disease.
We were told for over two decades that Lyme disease is not transferred from mother to fetus. (2006 Dr. Gary Wormser Yale in Under Our Skin documentary.) Once again we have the pathology evidence from 1989 of eight fetal autopsies showing Borrelia in the umbilical fluid, in the placenta, and in almost every fetal organ at necrotopsy. (See attach images)
What else did they get wrong? (When I say they I generally mean in my opinion that the misinformation about Lyme was most damaging from those that had the most influence on the Medical Community which includes the CDC, Yale, SUNY, Harvard and Mayo Clinic, the ACP and the IDSA)
Another untrue truth we were told was that only one species of Borrelia causes Lyme disease. Did they learn nothing from Relapsing Fevers? Borrelia changes and evolves like no other bacteria. It is constantly changing and evolving. We now have 12 species that cause Lyme disease and several species that we call Lyme-Like.
Another non-fact is that we were told that there was only one reservoir host – the white footed mouse. Of course now we know many rodents and birds are carriers of the disease and transmit it to feeding ticks. The range of these animals is far beyond the NE USA where we were told was the only place Lyme disease could exist.
In the Yale medical Report by Marc Voortman it says that patients with a positive ELISA test but a negative western blot can ignore symptoms like a bull’s-eye rash, Bell’s Palsy, and swollen joints and no treatment is necessary, but if the Western Blot test is positive you can treat up-to 2 weeks with doxycycline. I have attached pathological proof that two weeks is not sufficient for late Lyme symptoms.
The list of misinformation shows that the medical experts from the very discovery of this disease got over a dozen major-critically important facts about Lyme Borreliosis completely wrong, and perpetrated misinformation long after pathology had proved them wrong.
The most damaging untruth about Lyme disease was the insistence that Lyme disease does not persist in the human body after antibiotic treatment.
Attached are photos from a patient that lives just a few miles from me. He was a logger who was sick for 30+ years. He was diagnosed with Lyme disease and treated with aggressive antibiotic combinations for over seven years. When he died we found both Borrelia burgdorferi and Borrelia miyamotoi in his brain, and we found live B.burgdorferi and B. mayoni in his testicle.
Lyme disease does persist. It gets into the brain and inside brain cells. (Attached pathology photos from brain autopsies) In addition we have cultured B. burgdorferi out of Alzheimer’s brains.
It is unfortunate to see a position paper like this in 2016 considering that this is the year that many major Universities are clamoring to be the first to publish that they have found an infectious etiology to Alzheimer’s disease, and Borreliosis is the front running contender as a brain pathogen. While we have been using pathology for over twenty-years to prove Borrelia and Alzheimer’s are related, others are just now waking up to the fact that having both a cause and a potential treatment for Alzheimers, is worthy of major recognition.
2016 is the year that the race for the Nobel Prize has begun in earnest, and the group that gets accepted recognition of Borrelia in human brain causes Alzheimer’s pathology will most likely win the prize. You will see papers by Harvard and other major Universities vying for the pole position to prove Alzheimer’s has an infectious etiology.
While others live in the past and criticize patients for their efforts to use pathology to prove their illness has been mismanaged, the medical community has moved on and accepted that the facts they once thought were true are now part of history, and that the Lyme patients were in fact more right than the experts.
Lyme disease persists in the brain, the serology tests are missing brain infections, pregnant mothers can transmit the disease to their unborn child, sexual transmission is likely now that we documented Borrelia in human testicles even after antibiotics, and Lyme disease is found through-out the Northern hemisphere caused by more than a dozen species of Borrelia and carried by many ticks, and Lyme disease can kill as it did in the New York man who had Borrelia in his heart.
So when a patient disagrees with their doctor and explains that they are still sick after treatment. Who is right? The doctor citing 30 year old dogma, or the patient that died and had a brain-autopsy done that revealed a persistent brain infection despite years of antibiotics?
Thomas M. Grier (Exec Director)
https://www.facebook.com/groups/Lyme.Nedeland/permalink/1827122577520254/
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Notes and Observations on Cell Wall Deficient Forms By Tom Grier

Wouldn't it be nice if, when you're on safari and you're charged by a man-eating lion, you knew your gun was loaded with live ammo instead of blanks? I'd like to feel that way when I think about antibiotic treatment of Lyme disease. But what if we're just shooting blanks? At a recent Lyme disease conference in Detroit, Michigan, that fear of shooting blanks became palpable when I listened to Dr. Lida Mattman, Ph.D., speak about cell wall deficient forms (CWD) of bacterial pathogens, specifically B. burgdorferi, the cause of Lyme disease.  Dr. Lida Mattman, a professor emeritus from Wayne State University, has been studying spirochetes for over fifty years. She was a protégé of the great Gabriel Stiener, who was the first to establish, in a series of papers going back to 1918, that multiple sclerosis was associated in many cases with a spirochete. Since her association with Steiner, Lida Mattman has had a continued interest in spirochetes, but for the last seven years she has focused the bulk of her attentions on cell wall deficient forms.  This area of microbiology has long been neglected, and we are now paying a price for that neglect. Dr. Mattman's work suggests that cell wall deficient forms are prevalent, and pathogenic. Cell wall deficient forms of a mycobacterium may be thecause of sarcoidosis. Other diseases, such as Crohn's disease, coronary thrombosis, Kaposi's sarcoma, endocarditis, and MS, may all involve cell wall deficient bacteria. What were once thought of as anomalies and nonpathogenic are now proving to be insidious, deadly, and nearly invisible. Hence the name of her text book, Stealth Pathogens. (CRC Press) What are cell wall deficient bacteria? First; let's review some basic microbiology. For decades, students have been taught that there are three main types of bacteria: rods, spheres, and spirals. These shapes were maintained by a rigid cell wall that added structural integrity to the bacteria. Since human cells don't have cell walls, a good way to kill bacteria was to interrupt cell wall synthesis, because this would kill the bacteria, but not harm the human host.This is the basis of most bactericidal antibiotics, like cephalosporins (Rocephin, Suprax, Ceftin, Claforan) and penicillin's (amoxicillin, ampicillin..). The problem is, what happens if there is no bacterial cell wall to inhibit?  When a bacteria like a spirochete loses its cell wall, it becomes incapable of holding its spiral shape. It becomes a sphere surrounded by a thin semi-permeable membrane. This round sphere is like the evil counter pare to the classical spiral form. Why evil? Well, when the bacterium sheds its cell wall, it also sheds several proteins that are markers to the human immune system. In other words, the immune system has trouble finding and recognizing this new form of the bacteria. It's almost like a criminal using disguises to change identities after each crime. Only this disguise is also bullet proof because, without a cell wall, antibiotics like Rocephin are useless.  What is also intriguing is the fact that these cell wall deficient forms (also known as L-forms) can be seen from time to time as reverting back to the classical form. This means the Lyme spirochete appears to be capable of turning off the genes that create cell walls when it is convenient to do so, and the CWD form can then produce the classical spiral form when it needs to.* Does the bacteria do this to avoid antibiotic therapy? Probably not. It might be an evolved mechanism to dodge mammalian immune systems, but it is doubtful it has specifically evolved a defense mechanism against antibiotics. Survival against antibiotics just happens to be a consequence of this particular evolutionary morphologic development.  This appears to be borne out by some work done over sixty years ago on syphilis patients by Warthin and Olson. It was found that, as you sectioned a blood vessel of a syphilis patient, you found a progression from the classical spiral form to what appears to be the L-forms. As you entered the vessel wall and continued to enter other tissues, the shape of the spirochete gradually changed from a spiral to a sphere. This means that the Lyme spirochete may also favor one form over another, depending on what tissue it is in at the time. This evolutionary strategy makes a lot of sense. If it can survive better in the tissues in a CWD form, then the infection can continue even if its classical spiral counterpart is wiped out and eliminated from the blood stream. In the end, the death of one form of the bacteria is meaningless if the infection is ultimately maintained somewhere else m the host in its alternative form.  Dr. Mattman said she frequently isolates L-forms from Lyme patients with aseptic meningitis and endocarditis, How is this done? Traditional culture media is virtually worthless, as are traditional heat fixed blood smears. The answer is, in many cases, a simple technique that is rarely used any more in labs. A live wet mount is prepared using the patients blood or bully coat. This is a simple procedure, where the blood sample is placed on a wet slide with acrodine orange dye to stain the nucleic acids. Then a monoclonal antibody fluorescent stain that is specific for Borrelia burgdorferi is added. Then the slide is examined under a microscope. Although this is a simple procedure that most labs could easily do; it is not being done. Why? Simply because most labs have no real understanding of CWD forms.  There are some scientists who oppose the idea that CWD forms are the cause of persistent infections. They assert that if CWD forms exist, why can't we detect them by PCR? Even in absence of cell wall, these bacteria still have to contain DNA. Yet no published studies exist that compare PCR/DNA amplification results to CWD culturing techniques. Although culturing has long since been the gold standard in proof of infection, there seems to be a double standard when accepting culturing as proof when it comes to CWD forms. Unfortunately, both PCR and L-form culture techniques are in their infancy, and are far from perfected or standardized.  Dr. Mattman also has a greater success with culturing the classical forms than most other researchers that I have met. Mostly, this is due to her fifty years of experience with spirochetes, but it also has to do with economics Dr. Mailman is a researcher, and as such, the priority of her lab is not to make money, but to produce data. As a result, Dr. Mattman mixes her own culture media, which is considerably different from the commercially available medias. Since modern hospital labs have long since stopped mixing their own medias, the only medias which are ever used are those which are commercially marketed to the labs through medical suppliers. Since Dr. Mattman's media is not commercially available, labs will never have the success rate at culturing spirochetes that they should. Labs are in the business of making money, and mixing up media is too hard, too time consuming, and too costly. If it isn't on the shelf, it's being used.  More than likely, Dr. Mattman's culture media will one day be commercially available, but its success has always depended on a couple of freshly made components, so bringing it to market isn't as easy as it sounds. Although there are better culture medias out there to detect Lyme disease than the commercially available preparations, it is the commercial availability of the other media that wins the day. Thus, modified Kelly media and B 5K-lI are the current standards for culturing the Lyme spirochete.  Treatment: What does this new information on CWT Borrelia mean to chronic Lyme patients? A medical advisor to Dr Mattman, Dr Steven Philips, MI), suggested that when a patient's therapy with a bactericidal antibiotic hits a plateau, it may be time to switch to a different regimen of protein inhibitors, such as the combination of doxycycline and Biaxin. These also appear to be the drugs of choice when a patient presents with symptoms of multiple sclerosis. These drugs do not depend on cell division and disruption of cell wall synthesis to kill the bacteria. Instead, they affect bacterial metabolism through inhibition of protein synthesis.  Dr. Mattman made it very clear that a second spirochete has been implicated in causing multiple sclerosis (MS). Her old mentor, Dr. Gabriel Steiner, first isolated spirochetes from MS lesions in 1918, and today the continuation of that work is being pursued by at least three researchers. The suspected organism has been tentatively dubbed Spirochaeta myelophthora. Since multiple sclerosis is a collection of symptoms of an unknown cause, it is possible that more than one cause will eventually be found. One undeniable fact is that many Lyme patients have been previously diagnosed as having MS. Perhaps Dr. Mattman's continued work will someday make that tragedy a rare occurrence!  Are CWD forms responsible for persistent chronic Lyme disease and negative tests? The possibility is quite real, but the answers will not be forthcoming until more labs agree to test for CWD forms. For this to happen, the benefits of doing tests for CWD forms as a means to save money in patient care must become apparent. The cost effectiveness of routinely using this type of laboratory test would most certainly benefit both patients and health insurers. Development of a test that can be used by commercial laboratories is the next step. *As a side note: This process of reversion back to the classical form is a different process than normal bacterial replication, which is binary fission, which involves a cell wall separating the parent cell, thus creating a clone cell This process does not occur in the Lyme spirochete when creating an L-form. This means we really don't understand the reproductive capabilities of this bacteria.

https://www.lymeneteurope.org/info/cell-wall-deficient-bacteria
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This means what Mr. Grier is presenting is all new and it is prima-fascia evidence that:

• Lyme disease bacteria enters the brain quickly
• Lyme Bacteria persists in the human brain despite antibiotics
• Borrelia bacteria are associated with the amyloid plaques of Alzheimer’s disease
• That parasitic worms called nematodes are a common pathogen in dementia
• Several species of Borrelia bacteria are involved in what we refer to as Lyme disease
• Lewy-Body Dementia and some Parkinson’s Disease cases have been associated with Borrelia
• MS Spinal fluids were found to contain nematode worms and patients have responded to antiparasite medications
• Glio-Blastoma a rare and fatal brain cancer is related to the presence of Borrelia.
• Both the Lyme spirochete and the Mayo Clinics newly discovered Borrelia mayonii have been found in the human testicle suggesting a loaded gun for sexual transmission.

https://madisonarealymesupportgroup.com/2017/04/03/microbiologist-tom-grier-talk-reminder-april-19-2017/

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