MOTOR NEURON DISEASE/ALS STABILIZED ON LONG TERM ANTIBIOTICS

Sharing from a friend with a link to a post on my blog about him here

The translation is thanks to Google so apologise for errors but you get the idea.

Dear Joanne 

would you please translate this to English? Its a column to have been underwritten wooden i will send to ILADS guys! borreliasyk I've been in 12 years. 

Like many others, I have not been believed that the Norwegian health care system that diagnosed me with ALS. I've driven trial twice. Lost both. This despite the fact that I tested positive on the Western Blot test, tested positive at the Vestfold Hospital and found Borrelia DNA in my blood in 2009. 

I sometimes have a feeling of being involuntary participant in an academic parlor game. It's as if most of the health care system sees this as a game - and not as a prolonged, intense and bitter struggle for life and health. , we have a large group of seriously ill patients who have good reason to believe that a Borrelia infection is the underlying cause - but are banned from using the device with a negative antibody test (often Elisa) as justification. 

In 12 years I have accumulated knowledge about the disease, but it seems that doctors have a monopoly on qualified opinions. Because of their status, they can decide what is the scope for credible evidence to justify saying their opinions. 

If they encounter documentation that goes across their opinions, they may with ease doubt about it. Or so they know not to studies and publications that make their arguments fall through. The latter is probably hard to recognize, so it will be easier to call documentation implausible. 

I refer to the magazine's story about how Borrelia among others Dr. Jon Sundal attended. He was also an expert witness against me in the trial. I'm not looking for the actual content of the program, but there are general attitudes Sundal have, I want to life! 

One tries to persuade public opinion that good western blot tests often give false positive responses, which is incorrect tests based on several numerical markers that identify Borrelia bacterium. Some markers are nonspecific and may cross react with other bacteria, while some markers are specific borrelia "fingerprint" - markers. Mon. require a certain number of markers to be regarded as positive for declaring the test as positive. 

This will make it easier to evaluate the tests. requirement to have a positive test, three of these specific markers. 

The American Health Authority (CDC) has recognized my test as secure positive. micrograms recombinant western blot (immunoblot) containing antigen that captures all strains of Borrelia bacteria. It does not Elisa! . Recommended Vestfold Hospital (SIV's) MIKROGEN recombinant western blot that is the best test.

 The problem is again money. The test is expensive and time consuming. This must be funded! SIV has expertise and a highly skilled specialists! 

Sundal also claims that one must have inflammatory cells in the spinal fluid of having neuroborreliosis. This Slovenian researcher Franck Strle proven wrong. He is with Hunfeld Fingerle Wilske and Stanek among tungtvektekterne in Europa.Også laboratories in Norway have discovered this! Unfortunately, doctors are not updated for this No, absolutely no Norwegian attending their seminars! Only a retired doctor, Per Bjarke. 

False negative tests dominate. Therefore, it is dangerous to allude that Elisa tests are good enough. Lori Bakken conducted a double-blind study showed that not only was Elisa inaccuracies between competing laboratories, but the same laboratory showed different results on the same sample. Only 45 laboratories had a score of 55 percent.

 Another study was conducted by the College of American Patholigists. The result was terrible. It was similar to the same number of false positives as false negatives. Only 45 percent of the 516 laboratories that tested showed the correct answer. It entered that stage I of the disease discovers Elisa 20-50 percent of cases and in stage II / III 70-100 percent, depending on the tests used. 

Some argue that sensitivity in stage II / III is not more than 20-80 per cent. The tests used in the cerebrospinal fluid in Norway today finds no more than 50 percent: 70 percent for garinii and 10 percent for afzelii, which is the most common borrelia strain circulating in Norway due to false negative results are numerous. 

The bacteria manipulate our immune system so that we do not produce antibodies. Antibodies are very late in forføpet. The bacteria can lie in niches inside the cells of the organs where it is hidden from the immune system. The bacterium converted to cyst forms with new antigens that are not found in the tests available today. 

The tests used today are quite specific as false positive is not a big problem. False negatives, however, problematic. This is why clinic and patients' own history is so important in the overall assessment. I think Western blot should be emphasized rather than as indirect Elisa test. The sensitivity has been discussed regarding western blot, but specific band in the test should be a clear indicator of Borrelia infection. 

ANTIBIOTICS For chronically ill have a pulsating regime (periodic time) high doses of ceftriaxone IV has been a success. This was published in the early 90's and was confirmed on MLDA Lyme congress in 2002. treatment should be individualized on both the dosage and length. 

Stricker refers to studies where long-term antibiotic treatment is far better than the standard treatment. Klempners standard (Dr Mark Klem opens conducted a study on the treatment of patients. Though the study had clear deficiencies, it has been accepted as standard. Probably why we have several cases of illness due under treatment) in a month ceftriaxone IV and two months of oral doxycycklin, had little effect on chronic borrelia or come late disease. 

Increased improvement the longer treatment duration was noticeable. This is published in the CID that is a IDSA (Infectious Disease Society of America). Looks like IDSA turns when they choose to publish this. So in these cases must be treated for months and even years with antibiotics. 

Change of combination treatments may be necessary. Must be individualized. It is vital to acknowledge this since late come and chronic Borrelia ill probably have chronic infection combined with additional infections. Therefore, required prolonged treatment. Therefore I genuinely sorry when doctors refuse patients treatment! There is no reason to doubt that prolonged treatment helps some. 

According to statistics I should have been dead 10 years ago! I'm probably the only one in the world who has lived with ALS diagnosis in 12 years, which can stand on their feet and do not need a respirator! Court, the appeal board patient and their experts find it more probable than that I have borrelia. 

Fortunately rescued antibiotics I received in the USA for 03 my life! I had to go. Here at home did not help! Health care is often concerned with the ethical dimension. As I see it, it is the exclusion of Lyme disease patients is the greatest ethical challenge. These patients (assuming they indisputably have very severe disease) are invited ME diagnosis or ALS without other evidence than that it can not be anything else. 

It may NOT be ethically problematic to make treatment studies in this group of patients. They get anyway no qualified help. I will fight for us, as long as there is life in me.

Eivind Markhus

TREATMENT TO REVERSE MOTOR NEURON DISEASE.

'Any therapy which is capable of reversing the untreated

natural history of Motor Neuron Disease is Press-worthy.'

inmacdonald

Posts: 548

Joined: Fri 13 Jan 2012 22:32

by inmacdonald » Fri 23 Nov 2012 17:22

ALS-like Lyme and ALS not related to Lyme Neuroborreliosis:

Let us reduce the discussion to progressive incapacitating Motor Neuron Disease.
Dr William Harvey ,now deceased from a Heart Attack in year 2012 an buried with honor at the Cemetery of the US Air force Academy, developed Motor Neuron disease,progressive type.
He diagnosed himself ..He started a course of Long term antiborrelia antiBabesial antimicrobialtherapy.
Dr. William Harvey experienced a reversal of his motor neuron disease after long term antibiotic therapy.

Dr David Martz developed progressive motor neuron disease. He was diagnosed by several consultant neurologists as "most consistent with Amotropic Lateral Sclerosis. His children searched the Internet
and found the newspaper reports of Dr William Harvey's results with the success of long term antibiotic
and antibabesia therapy in motor neuron disease. Dr David Martz became a patient of Dr Bill Harvey.
Long term Therapy with antiborrelia/antibabesial medications produced a reversal of his disease. but from time to time, Dr David Martz must restart the Dr Harvey Protocol to maintain his recovery.

Dr. David Martz and I had a conversation on Nov 3, 2012 in Boston. We discussed our "MarkTwain" moments. Dr.Martz has since his recovery, treated multiple patients with Antibiotics/antibabesial medications and has noted reversal of motor neuron disease in his patients. He is drafting a manuscript
to report these patients. It is likely that the completed manuscript will be published in a Scandinavian Neurology Journal, just as his case report was published. It is noteworthy that previous to the acceptance of
the Harvey Martz manuscript in a Scandinavian Journal, it was reviewed and rejected by multiple journals based in the USA and in the United Kingdom.

Any therapy which is capable of reversing the untreated natural history of Motor Neuron Disease is Press-worthy. The untreated natural history of Motor Neuron Disease is a short pathway to death by suffocation.
Above all , do no harm.
Best, 
Alan B> MacDonald MD

Motor neuron disease recovery associated with IV 
ceftriaxone and anti-Babesia therapy

Conclusion

We have documented the full neurological recovery in a patient 
with an unrecoverable MND. Thesuccessful clinical outcome was 
associated with antibiotic therapy in response to evidence of two 
concurrent infections. 

We suggest that MND may be associated with an infectious trigger
in certain cases. The use of antibiotic therapy in MND merits further evaluation.

The above comments by Dr MacDonald was posted on 
Lymenet Forum here  in response to my comments about 
an ALS/MND forum post.

Earlier posts about Dr Martz and his research can be found here  

LYME DISEASE SYMPTOMS - COMPREHENSIVE LIST.

Most doctors are unaware of the many ways that Lyme Disease can affect patients so I am copying and posting this open letter that Dr Alan B MacDonald sent to Carter Blakely on Wellness Guidelines which includes a comprehensive list of conditions that can be related to an infection of Lyme Disease. Thanks to Dr MacDonald for posting on Lymenet Europe link here

Carter Blakey

I write to support the inclusion of the ILADS Lyme Disease
Objectives for inclusion in Healthy People 2020.

ILADS is an international society of physicians, researchers,and concerned
health care professionals whom are expert in the theory and in the practice
of Lyme Disease and Related Disorders ( Co-Infections which exist simultaneously
in some Lyme Patients). Lyme Disease has the potential to cause tissue 
in multiple organ systems of the human body. The first systems to be recognized
namely skin [Erythema Migrans], Joint [Lyme arthritis] , nervous system 
[Borrelia meningitis and Borrelia induced Bell's {facial nerve} Palsy], and 
Cardiac [ Borrelia induced Bradycardias and Tachycardias- with or without
Atrioventrio-ventricular conduction system "Heart block"] were all described
in the Pre Spirochetal Era [ in the era 1975-1980] before Dr Willy Burgdorfer
described the etiologic infectious agent of Lyme disease, namely Borrelia
burgdorferi. The expansion of Medical complications of Lyme disease
has burgeoned in the Post-Spirochetal Era to now include such diseases as
Mononeritis mutiplex, a Lyme Multiple Sclerosis-like demyelination illness,
a Lyme Amytrophic Lateral Sclerosis-like Motor Neuron Disease, Lyme 
disease in pregnancy with transplacental transmission of the spirochete
across the placenta from Mother to unborn fetus causing Miscarriage , stillbirth
at term pregnancy, and linked to several congenital malformations in the 
developing fetus, Lyme disease associated Neurocognitive disorders including
a Lyme disease Dementia closely resembling Alzheimer's disease, Lyme Disease
Parkinson's disease like illness, Lyme disease Cardiomyopathy, Lyme disease
Temporal arteritis-like illness with blindness, Lyme disease of the Eye with Uveitis,
Optic neuritis, and Ossifying myositis of the extra ocular muscles of the eye,
Lyme disease related Malignant lymphomas [similar in evolution to the
Lymphomas consequent to chronic Helicobacter pylori infection of the gastric 
mucosa] , Lyme disease Autonomic Nervous System Dysfunction, Lyme Disease
Endocrine dysfunction, Specially prominent in the thyroid gland and in the
Pituitary Adrenal Gland systems, Lyme Disease related Chronic Fatigue Illness,
Lyme Disease Myalgic Encephalomyelitis, Lyme disease Transverse Myelitis,
Lyme disease Muscle wasting Illness,Lyme Disease related Hepatitis, Lyme disease associated Hepatitis, Lyme Disease associated Destructive and deforming arthritis, Lyme Disease associated Squamous cell Carcinoma as a consequence of Acrodermatitis chronica Atrophicans, and Lyme Disease Neuropsychiatric Disorders.

Investigators in China have published evidence that the Lyme Disease spirochete
[chinese strain] is recoverable from some cases of Sarcoidosis in Chinese patients.
Investigators in Europe have published evidence that Lyme disease associated
Abdominal Aortic aneurysm exists in Europe.

Lyme Disease is more properly called Lyme borreliosis, because a variety of Borrelia
strains from all continents [except Antarctica] are now isolated, each with a different
strain name and each with a different potential to cause disease and or death
in human and mammalian patients.

Babesia infections [similar to Malaria- but tick transmitted] are co-travellers with
Lyme borreliosis. Borrelia exist as different strains, each with a potential to threaten
the safety of the human blood supply. Babesia infections may be diagnosed by blood smear examination by an expert pathologist. Alternatively, the detection of
antibodies which are specific to each of the strains of Babesia is possible if and only
if the test kits utilized are a perfect match for the suspected Babesia strain,based
on the geographic location where Tick transmitted Babesia infection was acquired.
For example, in the United States of America, Babesia infections on the East coast
are usually Babesia Microti, and on the West Coast Babesia duncani. In Missouri, babesia infections are Babesia strain MO. In Europe, Babesia infections may be due to a number of strains such as[but not limited to] Babesia strain Eo, strain divergens, and strain bigemina. In detection of blood antibodies - which are strain specific, the use of the proper test kit [ kit specificity restricted to one strain at a 
time] is essential to avoid missing the diagnosis of Babesiosis. For example,
test kits designed to detect antibodies to Babesia microti will produce NEGATIVE
results if the patient has Babesia Duncani in his/her blood. Undetected Babesia in Blood bank units , when transfused into human hosts may produce Fatal results. A
Registry of human fatalities due to Transfusion transmitted Babesiosis is on file
at the Centers for Disease Control and prevention. Over 100 cases of transfusion
transmitted babesiosis with a Fatal outcome in the recipients have been recorded
in a 10 year interval by the CDC.Ongoing surveillance for contamination of Blood
donor units from Asymptomatic Blood donors is aggressively being conducted
in New York State . Other States in the USA may have an unrecognized
threat to the blood supply because Babesiosis screening programs are not
in place in All of the 50 states. It is well known that residents of the USA
relocate their residence to other states every 6-7years. It is therefore a real concern that Babesia infections acquired in one state may produce potential blood supply
safety issues when Blood donors relocate their residence.

In addition to Babesiosis ,other Lyme Disease complex co-infections include:
Anaplasmosis,Human granulocytic Ehrlichiosis, Human Monocytic Ehrlichiosis,
Bartonellosis (various strains), and for the Amblyomma american tick [Lone Star Tick] vector: Francisella tularenesis {Tularemia}, Rocky Mountain spotted Fever, Coxiella burnetti infection.

Tick Transmitted infections to man are the fastest growing category of
infectious diseases in the United States of America today. The Statistical 
compilation of such infections, by the CDC, is admittedly an underestimate
of the true numbers of Tick tick transmitted infections in USA citizens and
in immigrants to the USA.

Respectfully,

Alan B. MacDonald MD, FCAP, FASCP
November 9,2012

inmacdonald

 

Posts: 522

Joined: Fri 13 Jan 2012 22:32

Top

SUCCESSFUL TREATMENT OF MOTOR NEURONES DISEASE, ALS, LOU GEHRIG'S

Dr. David Martz -- unedited footage from Bev Feldman on Vimeo.

Dr Martz was diagnosed with Motor Neurones Disease ( Amyotrophic Lateral Sclerosis, ALS, Lou Gehrig's Disease) in 2003.

Above he talks about his journey in being tested for Lyme Disease but repeated negative serology until eventually a positive DNA test in Urine.

He was treated with aggressive IV antibiotics, he says the change was dramatic.

'Within 1 month the body pain that had required oxycodone had disappeared, the arthritis that had required Intramuscular Methatroxate had totally disappeared.

Within 1 month my energy went from half an hour to with 4 to 5 hours stamina.

By 2 months I was able to cross my legs without using my arms to assist them.

By 3 months I could get up out of a chair myself without anyone having to pull me up.

By 6 months my Neurological findings had disappeared.

I did not return to absolute complete normality but did return to about 70% of my base line self and was subsequently able to open a new practice to see if my response to antibiotics might be shared by others stricken down with the usually fatal diagnosis of ALS ( MND). 

Rocky Mountain Chronic Disease Specialists was opened in 2005 and we saw approximately 900 patients over the next 2 1/2 years.

 About 100 of them had ALS ( MND) we did identify that some patients did respond to antibiotic therapy regardless of the positivity or negativity of their Lyme Disease testing by any laboratories.

We found about 15% of people clearly got functionally better and probably 20- 30% had their disease stabilized, without progressing further.

This is unheard of and we are in the process of preparing this information for publication.'

________________________________

An earlier post on Dr Martz here

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.

PROBLEMS WITH TESTING

'Therefore using only ELISA as a screening test or for diagnosing Lyme borreliosis seems debatable.'

Well that is an understatement, but a step in the right direction, if only our Health Authorities would listen.


Arch Immunol Ther Exp (Warsz). 2011 Jan 22. [Epub ahead of print]

Serodiagnosis of Borreliosis: Indirect Immunofluorescence Assay, Enzyme-Linked Immunosorbent Assay and Immunoblotting.

Wojciechowska-Koszko I, Mączyńska I, Szych Z, Giedrys-Kalemba S.
Department of Microbiology and Immunology, Pomeranian Medical University, Powstańców Wielkopolskich 72, 70-111, Szczecin, Poland, IwonaKoszko@interia.pl.
Abstract
Lyme disease is an infectious, multi-system, tick-borne disease caused by genospecies of Borrelia burgdorferi bacteria sensu lato, characterized by remarkable heterogeneity. In this situation choosing an optimal antigen array for diagnostic tests seems problematic. The serological tests for borrelia routinely done in laboratories often produce ambiguous results, which makes a proper diagnosis rather complicated and thus delays the implementation of an appropriate treatment regimen. Thirty-seven outpatients and eight inpatients with suspected borreliosis diagnosis hospitalized at the Clinics of the Pomeranian Medical University (Szczecin, Poland), participated in the study. In order to detect the antibodies against Borrelia sensu lato three kinds of serological tests were used: indirect immunofluorescence assay (IIFA), enzyme-linked immunosorbent assay (ELISA), and immunoblot. The IIFA and immunoblot tests conducted on 45 patients (100%) produced positive results for both the IgM and IgG antibody types. In the case of ELISA, positive or borderline results were observed in only 24 patients (53.3%). The immunoblot test for IgM most frequently detected antibodies against the outer surface protein C (OspC) antigen (p25), and, in the case of IgG, against the recombinant variable surface antigen (VlsE). The IIFA screening test used for diagnosing Lyme borreliosis produced the highest percentage of positive results, which were then confirmed by immunoblot, but not by ELISA. Therefore using only ELISA as a screening test or for diagnosing Lyme borreliosis seems debatable.
PMID: 21258869 [PubMed - as supplied by publisher]


http://www.ncbi.nlm.nih.gov/pubmed/21258869

In fact there has been a considerable body of research over many years showing the problems over testing for Lyme Disease and not just the Elisa but also the Western Blot.

See Steven Phillips presentation to the IDSA review panel 25 studies on seronegativity and persistent infection. here

Interestingly Steven Phillips highlights on 18 occasions were the authors of the discredited IDSA Lyme Disease guidelines were involved in those studies but failed to include in their guidelines. When asked why by the Chairwoman at the end on the hearing Steere replies that he has changed his opinion. Yes OPINION is what is driving the IDSA guidelines for Lyme disease.

The recent Institute of Medicine workshop on the state of the science for Lyme Disease and other Tick borne diseases leaves the listener in no doubt that testing is just not reliable in any of these illnesses and that for some long courses of treatment are needed to deal with some chronic tick borne diseases.

The Video casts are still available to watch here

One of the most significant presentations was that of Ben Luft who recently Sequenced the Genome for Borrelia here he points out the difficulties over testing because of the various different strains of Borrelia but he also emphasises that it is a relapsing illness. You can read a phonetic translation of his presentation here

How many thousands of patients have had negative test results for Lyme Disease and been told by their doctors they don't have Lyme Disease, when in reality they do but the poor testing has missed the result.

Interestingly Doctors are not warned about the possible seronegative results even though here in the UK the makers of those test kits Trinity Biotech say-

'Negative results (either first or second-tier) should not be used to exclude Lyme disease.'

How many patients with Fibromyalgia, ME/CFS, Arthrits, Muscle weakness, Polymyalgia Rheumatica, Neurological illnesses like Multiple Sclerosis, Motor Neurons, Parkinson's and many more health problems are properly assessed for Lyme Disease or other tick borne diseases?

335 EMERGING INFECTIOUS DISEASES SINCE 1940-60% ZOONOTIC

A Systems Approach in Understanding Tick-Borne Diseases: People, Animals, and the Ecosystem
Richard Ostfeld, Ph.D. Disease Ecologist
Cary Institute of Ecosystem Studies

'We live in an age of emerging infectious diseases. A recent study by Jones et al demonstrates that no fewer than 335 new infectious diseases of humans have emerged since 1940.

Of those Infectious Diseases about 60% of them are Zoonotic, meaning that the pathogen replicates within and is transmitted from non humans vertebrate species to humans.

Of these Zoonotic diseases about 72% are from wildlife with the remainder coming from domestic animals of various kinds.

Fully 30% of the newly emerging diseases are vector borne including most of the Tick borne diseases we will be talking about today and tomorrow and throughout the 20th Centuray and into the 21st Century the rate of emergence of new Infectious Diseases of humans has increased.'

The above were the opening remarks by Richard Ostfeld at A Workshop on the Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-borne Diseases: the Short-Term and Long-Term

To view and listen to the whole presentation click here

*****************************************************************************
Much of the controversy over diagnosis and treatment of Lyme Disease comes back to the old problem of definition of Lyme Disease and it is interesting to see how the ILADS conferences (London and USA) moved away from that narrow definition of Lyme Disease, (Dr Bransfield's presentation of the Decade of the Microbe) as they are finding many of their patients are multiply infected with different organisms.

Dr Richard Horowitz interviewed for a TV program here refers to MCIDS - Multiple Chronic Infectious Diseases Syndrome found through CALDA website here

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

I was lucky that my Chronic symptoms of Arthritis and muscle weakness which developed following tick bites and Bulls eye rashes responded so well to long term antibiotics although it took 4 years for my GP to realise the connection to the tick bites.

I never tested fully positive on any of the two tests given but listening to the Institute of Medicine Workshop it seems that many of the tick borne illnesses have problems over testing and many of the available tests are not given to patients like myself who are chronically ill.

Through Eurolyme I am in touch with patients who have Neurolgical symptoms, some diagnosed with Multiple Sclerosis, Parkinson's and Motor Neurons who are responding well to long term antibiotics.

So whilst science is still evolving over these complex emerging diseases it is best to keep an open mind and see what works well for us as individuals.

MICRO ORGANISMS AND CHRONIC ILLNESS

'According to Dr. Brewer, XMRV is potentially associated with Parkinson's, chronic Lyme disease, MS, ALS - as well as ME/CFS. In his practice, 90% of his XMRV+ patients are Lyme Disease. (The Patient Advocate had heard previously that all of Dr. Brewer's Lyme patients are XMRV+) Four our of four of his MS patients are XMRV+, 1 out of 1 ALS patient is XMVR+, and 1 out of 1 Parkinsons patient is XMRV+.'

The above was posted on CFS Patient Advocate blog here

(Another great read about Judith Mikovits presentation here
and more here although you may need to follow this on Facebook to read it or follow me on facebook where there is a link.)

Read the full post for more information about the presentation at the recent ILADS conference.

For further posts about ALS or as we call it in UK Motor Neurons, MS, Multiple Sclerosis, or any of the other illnesses mentioned put the name in the search box on the right of this blog for earlier posts.

MULTIPLE SCLEROSIS, PARKINSON'S, ALZHEIMER'S, GULLIAN-BARRE, AUTISM

Lyme on the Brain
Lecture Notes by Tom Grier
August 28, 2010

If we look back and do a quick review of the lecture so far, we see some important points that keep repeating themselves in all stages and aspects of Lyme disease.

This is because of their fundamental importance in the disease process. To understand and make sense of the end stages of Lyme disease, we have to understand the fundamentals.

Key Lecture Points

Lyme on the Brain - Part 1

1) Lyme was first misdiagnosed as Juvenile Rheumatoid Arthritis in Old Lyme, Connecticut.

2) In 1975, Lyme disease was first described in print as primarily an arthritic disorder.

3) The cause of Lyme was not known until 1982; yet a treatment protocol was suggested and used that we still mostly use today consisting of two weeks of antibiotics.

4) This treatment protocol was initiated seven years before we knew that the actual cause of Lyme disease was caused by a spirochetal bacterium.

5) Lyme disease is caused by a spirochete in the same Genus as Tick-Born Relapsing Fever (Borrelia) a genus with tremendous variation.

6) Spirochetes are known to persist, and cause relapses.

7) Borrelia can change forms from spirals to cysts, and can change their surface antigens quickly.

Part 2

1) The Lyme spirochete attaches to blood vessels and causes leaks to occur.

2) The blood brain barrier, BBB, can be breached early in infection and remain “leaky” for 10-14 days.

Once the BBB closes, it sequesters the infection inside the brain away from the immune system and treatment.

3) Borrelia can have many strain variations and can adapt and change quickly.

4) The current Lyme serology tests that use strain B-31 are not representative of the wild strains found in nature. (Dr. Ron Shell, Madison, Wisconsin).

5) The new Western Blot Reporting criteria or Dressler Criteria turns a poor test into a nearly worthless test. Two-tiered testing further makes Lyme disease diagnosis less accurate.

6) Lyme bacteria can enter the blood vessel endothelial cells, and evade the immune system. (Sturrock and Ma).

7) Antibiotic treatment failure has been documented since 1979, and seven antibiotic treatment studies all demonstrated antibiotic failure ranging from 25% to 50%.

Part 3

1) Lyme disease is part of a larger pandemic called: Relapsing Fever.

2) Neurogenic strains of Relapsing Fevers go to the brain and are deadly.

3) The Lyme bacteria can hide inside cells (fibroblasts, endothelial cells) and seeks tissues where it is protected from oxygen and the immune system.

4) Bb often hides inside connective tissue like tendons and the joints; Bb especially seeks the brain as prime target tissue.

5) There has been an extensive history of [b]over 50 medical articles of spirochetes as one possible cause of MS published since 1911 in prestigious medical journals.

6) Dr. Gabriel Steiner demonstrated classical form spirochetes in MS patients in Germany since 1922, and again in Michigan MS patients in 1952. [/b]

7) In 1957, Dr. Rachael Ichelson, in Philadelphia, demonstrated spirochetes in MS patients and developed a culture technique to detect them.

8) Dr. Patricia Coyle tests 47 MS patients with an antigen/antibody complex test and finds that 15 of 47 MS patients have Lyme and respond to antibiotics, this refutes her prior published study where 20 random MS patients received an ELISA test and all tested negative. But her new 47 patient study was NEVER published.

Part 4 Lyme on the Brain Lecture Notes

Definition: L-form is a Lister Body named after Dr Joseph Lister (Listerine) who developed sterile surgical technique.

An L-form is a bacteria that can shed its cell wall and survive with just a membrane. It loses its structural shape and becomes spherical.

These L-forms resist cell-wall agents like amoxicillin because it survives the loss of its cell wall.

Well since this talk is called Lyme on the Brain, we better spend some time talking about what Woody Allen calls his second favorite organ, the brain.

Most of the time in microbiology, we don’t attribute intelligent behavior to bacteria; in science we generally try not to anthropomorphize.

But when it comes to the Borrelia genus of spirochetes that have evolved over thousands of years in close proximity to ticks and mammals, it becomes apparent that spirochetes have mechanisms of survival that almost mimic intelligent behavior and are not commonly seen in other classes of bacteria.

Some microbes like fungus are dimorphic. In other words, they have two forms of existence; the fungal or rhizome form, and the spore or yeast form.

The cyst-like yeast spores offer the fungus a chance to survive and proliferate when conditions are not favorable for its fungal form to survive.

In the deserts of the Southwest USA, the spores of deadly fungal illnesses float on the air until one comes to rest in the warm moist lungs of an unfortunate victim.

You can immediately see the advantage of this survival mechanism: one form tolerates dry desserts, the other prefers a living host.

Spirochetes are a conundrum and a mystery. In a general sense spirochetes seem to take on different forms depending on their environment.

Inside a tick spirochetes are usually seen as the spiral-classical forms, and are sometimes seen with an occasional bleb or cyst formation. These blebs still have cell walls.

Rarely, we have seen large spherical forms or L-forms that often seem to contain classical spiral forms, suggesting that the bacteria can go back and forth through at least three possible reproductive stages.

1) The spiral forms appear to divide by normal binary fission-division.

2) The spiral forms seem to be able to produce or pinch off cyst like blebs with cell walls that can become a large cell wall deficient spherical forms.

3) Spherical cell wall deficient forms seem to be able to produce classical forms inside themselves. We have seen this in other spirochete families beyond just Borrelia.

The question is what triggers these morphic changes in spirochetes?

When we have been looking for classical spiral forms in tissue; have we been missing the cell wall-deficient forms?

In this photo from Warthin and Olson 1954, we see that the spirochete that causes Syphilis takes on different forms depending on the tissue it is in.

The spirals are from the blood, and in Syphilis unlike Lyme, there are vast numbers of this form in the bloodstream that can be seen on blood smear.

As you proceed through the aorta of this patient, the spirochetes continue to change until finally all that can be isolated from the final vessel wall are tiny granules, yet these granules appear to be infective.

These atypical forms from Dr. Judith Miklossey originally isolated from the brain of a dementia patient.

Show the polymorphism of Borrelia spirochetes.

When she placed the atypical cells into BSK-II culture (below), even the sphericals reverted back to classical formed spirochetes.

Cell Wall Deficient Form of Borrelia burgdorferi found in spinal fluid and stained with immunoflourescent stain.

What forms does Borrelia take on in different human tissues?

Work done by Dr. Judith Miklossey, MD, PhD, suggests that Borrelia may have developed some surface receptors that trigger the bacteria to change when it encounters certain brain cell types; conversely the brain cells may react themselves by producing by products in response to the infection.

In particular, human microglia cells when added to cultures of Borrelia burgdorferi in the presence of human neurons seem to produce excessive amyloid precursor protein APP.

This occurred when in contact in culture with Borrelia isolated from the brains of dementia patients:

APP is the first step or component necessary to create the hallmark marker for Alzheimer’s or Dementia.

To summarize, Dr. Mikklosey’s work is difficult because of the absolute life changing conclusions at each stage of her work that we have to come to terms with.

Here are some essential points looking back almost 20 years.

Dr. Judith Miklossey, MD, PhD, Neuropathologist

Essential points on her collective body of work on Dementia Brain Autopsies and the Association with Spirochetes

1) The first 13 dementia patients that randomly came through her facility were autopsied and the families allowed brain samples to be taken and studied. All 13 or 100% of the patients had spirochetes in the brain (Miklossey, Switzerland)

2) Isolates of the bacteria retrieved in three of the autopsies were identified as Borrelia species.

3) One of the cultures could infect mice, and was used in in-vitro brain cell cultures.

4) Isolates from one dementia patient when cultured in mouse brain cultures, caused markers for Alzheimer’s to appear.

5) Amyloid precursor protein converted to Beta sheet amyloid, hyperphosphoralation of protein tau occurred as well as neurofibrillary tangles as well as several other significant Alzheimer’s markers.

6) This was the first in-vitro model for Alzheimer’s; it was created with Borrelia bacteria.

7) Atypical forms of Borrelia were seen in the brains of subsequent dementia patients.

These forms included:

coiled forms, intracellular forms, bleb forms, cyst forms, cell wall deficient forms, slime films and biofilms, and classical forms.

8) Atypical forms could revert to classical forms when placed in culture.

9) No other bacteria or virus were seen or associated with any of the dementia patients.

PACHNER MOUSE BRAIN MODEL

1) Normal uninfected mice are inoculated with Borrelia burgdorferi in the tail vein.

2) One month later, blood is isolated from the tail of the same mouse, and the bacteria are isolated for tests.

3) The bacteria are also isolated from the brain of the same mouse, and kept completely separate for testing.

4) The antibodies from the mouse’s blood recognize and attack the bacteria that were isolated from the blood of the mouse.

5) The same antibodies fail completely to recognize the bacteria that were isolated from the same mouse’s brain; it is as if these bacteria were completely invisible to the mouse’s immune system.

What has happened to the bacteria in the mouse brain?

Once the bacteria were isolated within the brain, it was then cut off from the peripheral immune system.

This allowed the bacteria to change with each new bacterial division, and without the mouse’s immune system recognizing the changes; it is just like a criminal getting a face-lift and wearing a disguise.

The immune system kept up with the bacteria trapped in the blood, but could not make antibodies to the Lyme bacteria trapped within the brain.

The antibodies that were being produced no longer recognized the bacteria because it was still looking for the original strain, and what were now in the mouse’s brain were several generations away from the strain that Dr. Andrew Pachner started with.

Basically in crude terms, the Lyme bacteria that became isolated within the brain, mutated.

The Lyme spirochete we started with that was originally injected into the tail, is no longer the same isolate that Dr. Andrew Pachner found in the brain of the same mouse.

You now begin to see how current Lyme tests that are created using a laboratory strain of bacteria; a strain not even found in nature, can hardly be expected to keep up with the over 200,000 possible variations that Borrelia are capable of producing.

If Borrelia enters the brain and can be associated with disorders that to date have unknown causes like:

Multiple Sclerosis, Alzheimer’s disease, Parkinson’s, Gullain-Barre, and autism; then why haven’t there been any CDC studies to look into whether the Lyme bacteria can enter human brains, and what happens when the bacteria is in contact with brain cells.

In my opinion, of all the millions of dollars that the CDC has spent or dispensed on Lyme disease research, the most significant study to date has not been a study on deer, mice or the pesticides, but rather one of the few truly elegant microbiology studies done looking at the pathogenesis of Borrelia burgdorferi were done by CDC researchers, Dr. Jill A. Livengoode and Dr. Robert Gilmore.

The Livengoode-Gilmore CDC Human Brain Cell Study

Doctors Gilmore and Livengoode recognized a flaw in 20th century microbiology that led ultimately to an incorrect conclusion that has been repeated many times by scientists who were trying to minimize Lyme disease as a serious infection.

The incorrect conclusion is that Lyme disease neither gets into the brain, nor is it an intracellular organism, nor does it penetrate brains cells. This was based on interpretation of limited tools and stains.

Livengoode and Gilmore went on to disprove all of these assumptions as completely incorrect.

At the turn of the century, the only stains available to detect spirochetes were silver stains.

By nature of the large molecules and charged ions, the silver stain could not penetrate into human cells. So all spirochetes were seen outside of cells; it was assumed that spirochetes did not as a rule seek out intracellular locations like Malaria.

Livengoode and Gilmore had at their disposal a million dollar microscope that could do things no other microscope can.

It cannot only look inside of intact whole living cells in culture, but a computer video processor can create three-dimensional photos. The other advantage it had was it could uses different optical frequencies to detect different fluorescent stains.

More simply put, it could use one color stain to see spirochetes inside cells, another color for outside the cell and a computer could merge the images.

The result is some of the most beautiful imagery ever seen looking at living human brain cells in culture.

The confocal laser microscope could look inside cells but where do you start?

Since it had been reported that Borrelia could penetrate endothelial cells (Ma and Sturrock), and since this is the key to Borrelia entering the brain, the team started with endothelial cell cultures.

When they added Borrelia burgdorferi to endothelial cell cultures, there was an immediate attraction or tropism for the cells by the Borrelia.

The first images revealed spirochetes attached all over the cells, but further inspection revealed that within mere hours, spirochetes had gone inside the endothelial cells and were completely intracellular.

Exactly the very same thing that other researchers reported and many Lyme authorities claimed never happened.

Borrelia burgdorferi attached to the outside
of umbilical endothelial cells in culture.


Merged photo of Borrelia burgdorferi on the outside and inside of an endothelial cell.

Livengoode and Gilmore then went on to add Borrelia burgdorferi to a culture of human glial cells, the cells that help mylenate and repair the brain.

Once again Borrelia exhibited a clear tropism for this cell type and attached extracellularly. Then within a few hours the bacteria found their way inside the Glial cells.

More importantly the very cells we use to process information and form thoughts with our neurons, were also easily infected.

Brain neurons since 1987 seem to have been recognized as target tissue for Borrelia burgdorferi and first noticed in fetal autopsies.

This cortex neuron clearly has Borrelia sequestered inside. The consequences of an untreated intracellular brain infection are unknown.

What is known from the Livengoode Gilmore study is that Borrelia burgdorferi seems to cohabitate within all of these cells without killing them and this was observed for a week.

To the right a neocortex Neuron with a spirochete
beginning its entry into the brain cell.

Although we cannot predict the final presentation of what intracellular brain infections with Borrelia would look or act like based on this in-vitro study; we can make some observations on the human diseases we have already seen where spirochetes have seemingly played a role.

In the MS patients where spirochetes have been associated, it appears that demyelination occurs allowing us to see bright spots or white matter lesions on MRI scans of the brain.

The clinical MS presentation can vary, but quite often in addition to MS central nervous system symptoms, we see peripheral symptoms consistent with Lyme disease.

In dementia patients where spirochetes have been isolated, it appears to be an Alzheimer’s like dementia in pathology, but the presentation of symptoms seems more consistent with Syphilis.

Yet Lyme does NOT seem to have a directly measurable SEXUAL transmission that we can document.

The question we have to ask is:

Knowing what we do about these two presentations of symptoms, can we expect to find spirochetes in the brain autopsies of dementia patients and MS patients if we start looking with the right tools and stains?

Below is the brain autopsy of an Ashland, Wisconsin, man who had presented with an atypical dementia and had received in the course of his nursing home stay at least three courses of antibiotics that were consistent with the current IDSA guidelines for Lyme disease. He only had brief periods of remission and continued to decline after every treatment ended.

He was an avid hunter, fisherman, and operated a farm and an orchard. He had three sons.

Two of his sons were disabled from Lyme disease until they were diagnosed and treated. One was diagnosed with MS the other with rheumatoid Arthritis. They made good recoveries but not 100%. The third and youngest son got Lyme and was treated earlier but still had symptoms for years.

Thinking that their family was somehow more genetically susceptible to chronic Lyme, they pursued a Lyme diagnosis for their father in a nursing home.

The doctors refused to test for Lyme disease on the basis that he had already received antibiotics for pneumonia that would have been sufficient to kill any Lyme.

Frustrated and confused, the eldest brother arranged for a brain autopsy at the time of death.

The entire brain was sent to Dr. Alan MacDonald. The results were stunning and conclusive.

Yale Medicine Special report May 15, 1996

END OF PART 4
LYME ON THE BRAIN
LECTURE NOTES By TOM GRIER
August 28, 2010

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The above is posted by kind permission of Tom Grier the author.Tom requested that I make available the supporting references, these total over 100 pages. I can't seem to add links to this post but should anyone wish these references I will e mail them with attachments so contact me, my e mail can be found in my profile in the right hand column of this blog.

Thanks to Madison Area Lyme Support Group for posting here

From Tom :-Thanks to BettyG, Iowa Lyme Activist and group leader of www.mdjunction.comLyme board,

for all her hours of work breaking up my work making it user-friendly for severely neuro lyme patients to be able to read and comprehend, proof reading it, and for its finished appearance.

Found on mdjunction here

I have long been interested in the work of Judith Miklossy a link into her website can be found in the right hand column of my blog or by clicking here

I had the privaledge to meet Judith Miklossy last year at the Lyme Disease Action conference in the UK and listen to a fascinating presentation by her on her work.

Anyone with a family member with Alzheimer's would do well to read Judith Miklossy' website.

The science is still evolving and much more attention and research needs to be done in this field.