ALS or MOTOR NEURON DISEASE CAUSED BY LYME DISEASE

Dr. Al Miller Lyme Disease Intro
Differential Diagnosis of Lyme & Borreliosis

Published on Apr 19, 2017

This is the introduction to my 4 part series on Lyme Disease.

For more information contact me at lymediagnosis@gmail.com

The above was shared by a friend Dana Parish with the following information -'Iwas surprised and delighted to receive a call from retired Mayo Clinic rheumatologist, Dr. Alfred Miller, last week. He wanted to tell me about his daughter-in-law, also named Dana, who was struck by ALS at age 43. He could not imagine this happening to this beautiful, healthy woman and started investigating. 

Upon researching, he discovered links between Lyme and ALS and had her tested. WHAT DO YOU KNOW!!! She was POSITIVE! Remember, though, he had her tested at a proper lab, IGeneX, and NOT Quest or Lab Corp, which miss approx 50% of cases!

So, all the "best" doctors in the world sent her home to die with no hope and no proper investigation into the CAUSE of her ALS. Those of us in the Lyme community are well aware that the Mayo Clinic is the LAST place you want to go if you have Lyme.

Dr. Miller began treating her aggressively with IV antibiotics and they halted the progression of her illness. This does not happen with "real" ALS. 

He began contacting his patients who he had previously diagnosed with Fibromyalgia, Rheumatoid arthritis, and other inflammatory "auto-immune" arthritis and diseases and urged them to get properly assessed for Lyme and other tick-borne diseases known to cause these symptoms, like Bartonella. 

WHAT DO YOU KNOW!! Most of them had Lyme!!

I look forward to bringing you more from Dr. Miller soon. In the meantime, he is on a mission to educate doctors and patients about the ravages of this disease and his horror at the medical community's ignorance about it.

All Dr Miller's presentations are available on You Tube  

https://www.youtube.com/channel/UCD19kTsVBMH-F0BfV3335Ow 

Thank you Dr Miller for having an open mind, after a lifetime in Rheumatology you were still willing to learn and seek out answers, but more importantly thank you for speaking up and sharing your experiences.

Singer/songwriter Dana Parish was involved in the recent Fox5NY News 

LYME & REASON which I posted about https://lookingatlyme.blogspot.co.uk/2016/07/fox-5-lyme-and-reason.html 

Thrilled to share that FOX 5 / Fox5NY.com Lyme and Reason Special won the Emmy for Best Science/ Health program, as presented by Dr. Oz.

PROTOMYXZOA RHEUMATICA IMPLICATED IN CHRONIC ILLNESSES

Listen to internet radio with Focus on Health on Blog Talk Radio

1 Step Blood Test Discovers Protozoa under Biofilm Structure

by Focus on Health

in Health

Fri, May 20, 2011 Dr Stephen Fry Interview

Thanks to Better Health Guy for the following  here

Steve Fry MD

• Presented on FL1953 which is now called Protomyxzoa rheumatica.
• Has found Ivermectin, Flagyl, and a low-fat diet to be helpful.
• Studies that have been done on Multiple Sclerosis patients show that patients live longer when on low-fat diets.
• Likes testing from Infectolab from Dr. Armin Schwarzbach for Chlamydia and Mycoplasma.
• Biofilm is an aggregate of microorganisms in which cells adhere to each other or to a surface.  Bacterial biofilms are a structured community of bacterial cells enclosed in a self-produced matrix according to Bill Costerton, a world leader in biofilm research.
• Lipids (fats) play a role in biofilms.
• Biofilms impact teeth, drinking water, paper manufacturing, ship hulls, medical implants, food processing, cooling towers, oil recovery, and much more.
• Iron, calcium, and magnesium all play a role in biofilm formation; be careful about the minerals that you use as these may add to the biofilms.
• There are 1,000 organisms in normal oral flora found in biofilms.
• Biofilms consist of extracellular DNA, proteins, and polysaccharides.
• Biofilms are microbial cells and EPS (extracellular polymeric substances).  EPS may be 50-90% of the biolfilm.
• Microbes are quorum sensing – biofilm communities talk to each other.  Decision making is made by decentralized groups to coordinate behavior.  This is used to coordinate gene expression.
• When microbes come together in a group, it becomes a more complex entity.
• Biofilms play a role in many diseases including ear/nose/throat, dental, respiratory, urology, orthopedic, chronic wounds, medical devices, catheters, chronic inflammation and osteonecrosis.
• Many areas of disease in the body are related to biofilms.  Coronary artery disease, MS, ALS all have association with biofilm communities.
• 46/50 children with otitis media (ear infection) had biofilms.  Chronic rhinosinusitis is a combination of  biofilms and several microbes.
• Biofilm plays a role in cystic fibrosis.
• Nanobacteria can be a cause for kidney stones and generates biofilm.
• In chronic wounds, bacteria is protected from systemic antibiotics and host defenses by biofilms which makes infection difficult to clear.
• Actinomyces, Acinetobacter, Treponema, and others are found in dental biofilms.
• Pseudomonas aeruginosa is a bacteria that is a profound biofilm former.
• Biofilm infections are difficult to eradicate.
• The immune system recognizes the infection, but it cannot eradicate it.
• Items that have been researched in biofilm treatment: Manuka honey, enzymes, multiple antibiotics, bismuth thiols, restricting metals, botanicals, mechanical removal, and EDTA to help chelate magnesium.   Magnesium is a main stabilizing force in biofilms.
• Other substances that are of interest to biofilm researchers include: Lactoferrin, Xylitol, Gallium, Dispersin, Farnesol, RNAIII inhibiting peptide, and Furanone C30.
• Corneal eye disease may be Acanthamoeba infection (protozoan).
• Protomyxzoa rheumatica (FL1953) is an Apicomplexa.
• CCSVI is a very hot topic but is also quite controversial.  One has to suspect biofilm communities.
• Organisms living in biofilm communities are usually not culturable.
• Biofilms are the rule, not exception.  They are ubiquitous.
• Book – "Biofilm Primer" by Bill Costerton.
• There is a Center for Biofilm Engineering at Montana State University - http://www.biofilm.montana.edu/
• Silver is a well known biofilm inhibitor.
• Ozone is used in industry to reduce biofilms.  Not sure if it works in humans, but may break up biofilm communities.
• Fry Labs does microscopy, serology, and molecular diagnostics.
• Protomyxzoa is an inflammatory trigger and vascular pathogen.
• Louis Pasteur believed that all diseases are caused by infections.
• Some autoimmune conditions include Graves, Hashimoto’s, Insulin-Dependent Diabetes Mellitus, Insulin Requiring Diabetes Mellitus, Multiple Sclerosis, Myasthenia Gravis, ALS, Systemic Lupus Erythematosus, Rheumatoid Arthritis, Sjogren's.
• Thomas McPherson Brown suggested that autoimmune disease is infectious in nature; primarily Mycoplasma.  The book “The Arthritis Breakthrough” was written by Brown in 1992.
• Fry has seen Protomyxzoa and biofilm in CFS, Fibromyalgia, Scleroderma, Rheumatoid Arthritis, Lupus, Multiple Sclerosis, ALS, Parkinson’s, Autism, and other conditions.
• In their smear testing, they originally identified Hemobartonella which included Hemoplasma. Today, they suggest that Epierythrocytic bacteria is a better term.  They rarely find actual Bartonella when doing PCR testing but have found cousins.
• Even a single organism can protect itself with biofilm.
• People with parasitic infections are immunocompromised.
• They have found a host of different types of bacteria in biofilms – Ralstonia, Acinetobacter (commonly seen in many patients).
• Protomyxzoa is a slime forming protozoa.  It produces biofilm.
• In ALS, 6 of 6 tested had Protomyxzoa.  5 of 6 tested has Ralstonia which is also a biofilm former.  They see profound biofilm communities.
• When one is infected with Plasmodium as a child, it reduces later incidence of Multiple Sclerosis.  The efficacy of quinine in the treatment of MS supports this connection.
• They are able to culture Protomyxzoa now.  The entire thing becomes like gelatin and they cannot get it off the microtiter plates.
• They have seen filaments as long as 3 or 4 inches in some blood samples.  When sticky stuff is coming out during a blood draw, it may not be a clot, but may be a filament or biofilm.
• In CCSVI, filaments of Protomyxzoa may be involved.  It is a vascular disease and may lead to inflammation of the vessel or vasculitis.
• Protomyxzoa has been isolated from Culex tarsalis and Culex quinquefasciatus mosquitoes.  81% by PCR carried Protomyxzoa.
• Dogs have Protomyxzoa more than cats and the older the dog, the more likely they are to have Protomyxzoa.
• Diseases are infectious and a biofilm forming protozoan could be at the heart of the problem.
• Treatment may include Tetracyclines, Plaquenil, Flagyl, herbs, enzymes, McDougall diet, and mechanical interventions such as CCSVI venoplasty.
• One should generally not consume arginine, folic acid, or magnesium as these may strengthen the protozoan and thus the biofilm.
• As for folic acid supplementation, some breads have 5% folic acid by weight.  Folic acid may increase cancer risk.  Protozoans love folic acid.
• For autoimmune conditions, antimalarials, antibiotics, anti-protozoals, anti-fungals, anti-biofilm agents, biologics, and dietary modifications may be beneficial.
• Enbrel may be helpful in some for reducing the inflammatory response.
• Fry Labs is now working on drug sensitivity studies.
• CCSVI treatment includes a mechanical clearing or balloon procedure.  It runs about 10K.  There was reportedly one death from a CCSVI procedure.
• Stents do not do very well in veins.
• From the Hubbard Study, about 1/3 feel worse, 1/3 feel nothing, and 1/3 get better with some significantly better.  One bedridden runner was running again after the procedure.
• Protozoans love lipids (fats).  The McDougall diet is used as part of treatment.  Doxycycline and tetracyclines may target the fatty acid synthesis machinery.
• Toxoplasmosis is also dependent on fats.
• Protomyxzoa grows 100 times faster with fats than without.
• There is a reduction in relative biofilms with the McDougall diet.
• In some people where they had seen the organism and biofilms, they could not find the organism after being on the McDougall diet.  Unfortunately, after starting to eat higher fat content, the microbe was again present and visible.
• They did a test in people with Protomyxzoa using a 12.5 day water fast and levels of Protomyxzoa dropped to undetectable.  Within 2 days of eating again, it was back.
• Protomyxzoa is found in CFS, Fibromyalgia, Rheumatoid Arthritis, Lupus, Crohn’s, MS, Parkinson’s, ALS, Autism, Scleroderma, and others.
• Protomyxzoa is Public Enemy #1.
• Protomyxzoa loves fat.  It is complex.  It is drug-resistant.
• Antiprotozoals or anthelmintics may be good options.
• Roy Swank Diet – 0 people on a regular diet lived with MS for 30 years.  In those on low fat diets, all but 1 was still alive.
• Protomyxzoa leads to vascular disease and chronic inflammation.  There are coagulation impairments and retrograde venous blood flow.
• Many systemic diseases can be explained as vascular phenomenon.
• Protomyxzoa is likely transmitted by mosquitoes.  Ticks are being analyzed.
• The protozoan is believed to be the foundation pathogen.
• It is not an intracellular bug; it is a big bug.  Likely exists more on the surface of the RBC, not inside.
• Patients often get worse when on magnesium.  He does not support the use of topical magnesium either.
• Bismuth may play a role as a biofilm inhibitor.
• Omega fats from chicken and plants are probably the best.
• Interestingly, it may be that magnesium is sequestered in the body and not always low as magnesium levels seem to go back to normal when the Protomyxzoa is treated.
• Dr. Fry previously had a success rate of over 70% with his patients.  Since introducing dietary modifications, this has now gone to over 90%.
• http://www.frylabs.com

For information about the work of Dr Brown which Dr Fry refers to see The Roadback Foundation here  and an earlier post here  with a video of Dr Brown and his work.

ONE CAUSE OF ALZHEIMER'S DISEASE AND OTHER NEUROLOGICAL DISEASES - ALS, MOTOR NEURONE, MULTIPLE SCLEROSIS, PARKINSON'S

Dr Alan MacDonald has been posting some excellent and informative posts on Lymenet Europe of late


Many patients with Chronic lyme Disease will remember Dr MacDonald from scenes in Under our skin As you can see in the above video Borrelia has not just been found in patients with Alzheimer's but also patients with other Neurological Diseases - ALS, Motor Neurone, Multiple Sclerosis and Parkinson's.


According to Under Our Skin news clip Dr MacDonald became ill with an Alzheimer's like illness and had to retire. He says on the Lymenet forum that he is doing well providing he is on medication, clearly reading his posts there is not a lot wrong with his cognitive abilities and I was delighted to read the following.


'My research was interrupted by several years when I was ill. I have now returned to limited Alzheimer's disease Research as an Affiliated Researcher at the Harvard University McLean Brain Bank.'


Taken from the comment below:-


I am glad that you asked:
Dr Judith Miklossy has always worked independently commencing her studies on Neuroborreliosis and Alzheimer's Disease in 1993 with her initial publication in Neuroreport.
She is presentlythe President of a Foundation which is devoted to Alzheimer's research and connections
to neuroborreliosis. She operates her own website, which contains her credentials and her biblography.


I have always worrked independently commencing my Studies of Alzheimer's disease and connections
between Neuroborreliosis and Alzheimer's disease in 1986 with my publication in the Journal of the American Medical Association "Borrelia inthe Brains of patiens dying with Dementia", followed by the 1987
article "Concurrent Neocortical Borreliosis and Alzheimer's Disease" published in Human Pathology,
and then"Concurrent Neocortical borreliosis and Alzheimer's Disease - Description of a spirochetal cyst form", in 1988 in the Annalsof the New York Academy of Sciences.


Although Dr Miklossy and I have a close friendship, we beleive that maintaining independent
research Laboratories ( In New York and in Switzerland) is the ideal pathway to establish 
a bibliographic base of independently produced papers to support th concept of an infectious
pathway to future development of some ( but not all) cases of Alzheimer's Disease.


I have never been a reviewer nor referee for the peer review of any of Judith's papers.
Judith has never been a reviewer or referee for the peer review of any of my papers.


My Last published works were reviewed and accepted for presentation at the Alzheimer's Disease
and Related Disorders International conference in 2006 Madrid Spain. My research was interrupted by
several years when I was ill. I have now returned to limited Alzheimer's disease Research as an Affiliated
Researcher at the Harvard University McLean Brain Bank.


What commonalities have been gleaned by two independent investigators working on the Chronic
Neuroborreliosis /Alzheimer's disease connection:
1. Identification of Borrelia burgdorferi spirochetes in Autopsy Alzheimer's brain tissue by
Silver staining ( Miklossy+ MacDonald+)
2. Culture of Autopsy Alzheimer's Brain tissue to yield growth of Borrelia burgdorferi spirochetes
(Miklossy + MacDonald +)
3. Idenification of argyrophilic plaques in Autopsy General Paresis brain tissue 
which are exactly the same size, density and distribution as argyrophilic plaques in
Alzheimer's disease autopsy tissue ( Miklossy + MacDonald +)
4. Identification of bacterial peptidoglycan staining in Alzheimer's plaques
(Miklossy + MacDonald -not studied)
5. Indentification of Intracellular borrelia burgdorferi spirochetes within diseases neurons
inautopsy Alzheimer's Brain tissue ( Miklosssy + macDonald+)
6. Identification of the role of the granular form of borrelia burgdorferi as a contributor to
the classical finding of "granuolo-vacuolar" degeneration of Neurons in Alzheimer's disease
(Miklossy +( immunohistochemistry) MacDonald + (In Situ DNA hybridization))
7. The use of highly specific molecular beacons to pick up evidence of Borrelia burgdorferi DNA
sequences in Alzheimer's disease Plaques ( MacDoanld +)
8. The use of PCR performed on total Alzheimer's frozen brain tissue from the Harvard Brain Bank
to amplify borrelia specific DNA sequences from Orf BB0147 and to confirm the DNA structure
by DNA sequence analysis of PCR amplified products. (MacDonald +)


We seek to analyze Cerebrospinal fluid from Alzheimer's Disease patients for the following:
a. Borrelia burgdorferi Specific DNA
b. Whole proteome analysis using Dr Steven Schutzer's MASS spectroscopy analysis
protocol which was published in PlosONE. Dr Schutzer's program is able to
reliably distinguish CSF specimens from Chronic Lyme Disease patients
and to separate such patients from those with Chronic Fatique (notlyme),
Based on State of the art Proteome analysis via Mass Spectrographic Analysis.
Respectfully,
Alan B.MacDonald MD
PS: Ifyou have a moment,please read Dr Hideyo Noguchi and J E.Moore's paper in the Journal of Experimental Medicine from their lab at the Rockefeller Research Institute in New York City
(Link: http://jem.rupress.org/content/17/2/232.full.pdf+html ) and you will read about the "politics of Paresis" which prompted heated debates between Noguchi and Professor Max Nonne.


Lymenet Europe forum here


Dr Alan Macdonald was the first person to find Borrelia spirochetes in the brains of patients who had diesd from Alzheimer's I have posted before about him and his work here 





Dr MacDonald is the first person I have heard of diagnosed with an Alzheimer's type illness retired from work who has sufficiently recovered to return to work, albeit limited and for that work - to be research into Alzheimer's Disease this most important research area.

ARTHRITIS, MUSCLE WEAKNESS ANTIBIOTICS, MONKEY BUSINESS - WHO KNEW WHAT AND WHEN?

The recent Embers study on persistence of Borrelia Burgdorferi in Rhesus Macaques following antibiotics treatment  here is opening up much needed debate.

Recently Lyme Policy Wonk has been running a series of posts about this research available here 

The comments are well worth reading to the latest post on the above link.

So many questions need answering and Philip Baker doesn't seem to be convincing many in his answers.

Hopefully this Embers study proving persisters will start the process of who knew what and when?

No matter that Baker says 'Furthermore, the significance of the results reported by Embers et al. with respect to human disease are far from clear and remain to be established. Sufficient information was not provided to indicate that the antibiotic regimen used was adequate to clear the disseminated infection, specially since ceftiofur — not ceftriaxone — was used. Since ceftiofur differs significantly from ceftriaxone in structure, one can not assume that it has the same PK/PD properties or even the same MID. Furthermore, ceftiofur has not been approved for use in human studies and its efficacy for the treatment of borreliosis — in humans and/or in animals– has not been established. More important, no evidence is provided to indicate that “persistors” — even those taken up by ticks in the xenodiagnosis experiments are infective and cause disease.'
There has been an amendement to the original study saying that in fact it was Ceftriaxone that was used not Ceftiofur see PLoS ONE here 
He might argue about the subtle differences of Ceftiofur and Ceftriaxone but he cannot argue over the fact that 60 days of Doxycycline followed 30 days of Ceftiofur and even with that was unable to clear persisters. Here in the UK even if you are lucky enough to be diagnosed you rarely get prescribed more than one or two weeks antibiotics.


Furthermore he questions if persisters -----are infective and cause disease. Patients are sick and some of us respond well to antibiotics given long term we didn't have time to wait for research to prove how and why.


Most importantly the study itself says 'Finally, the use of variable and pulse-dosing regimens of antibiotics may improve efficacy [43] and this warrants testing in an appropriate model.'


 Allen Barbour  one of the authors of this study is sufficiently convinced in the persistence of this organism that he quotes it in his applications for vaccines '[0145]“This mechanism of genetic switching appears to be different from any other antigenic variation mechanism described in bacteria or protozoa and has important implications in Lyme disease. By combining different regions of the silent vls cassettes, it is possible for many different vlsE serotypes to coexist the same patient. It may be impossible for the host to mount a protective response against any one of these clonal populations, because of the small number of each type. Even mounting a response against one serotype would not protect against rapidly evolving, new serotypes.”
Application number: 12/853,019
Publication number: US 2010/0317026 A1
Filing date: Aug 9, 2010


Anyway less of my comments go to Lyme Policy Wonk  here to get an idea of who knew what and when. 


What has allowed this research to be suppressed for 12 years whilst patients have been denied treatment?


Here in the UK there are a growing number of patients being diagnosed with Lyme Disease and yet what efforts have been made by our Department of Health to raise awareness of this disease which can be avoided with simple precautions and can be treated more easily if caught in the early stages?


I was lucky my arthritis and muscle weakness responded well to antibiotics and led my GP to consider Lyme Disease as a differential diagnosis. I recovered, how many patients with Arthritis and muscle weakness get better on just oral antibiotics.


I was diagnosed with Fibromyalgia, ME/CFS, Musculo Skeletal Disease Polymyalgia Rheumatica none of the medications given for those illnesses made much difference thankfully antibiotics did.


How many more people will suffer while those responsible for our health play 'monkey business' with the science?