Tuesday, 31 August 2010

WHAT DOCTORS ARE NOT TOLD

I have decided to post all 4 of Tom Grier's lectures which give us such an insight into what Doctors are not being told about Borrelia infections commonly referred to as Lyme Disease.


Lyme Disease is considered The Great Imitator not just presenting with Arthritis but neurological, psychiatric, heart block and digestive symptoms such that patients can be diagnosed with a whole range of illnesses Multiple Sclerosis, Parkinson's, Motor Neurons and many other neurological illnesses as well as fibromyalgia, ME/CFS, Arthritis, muscle weakness, Polymyalgia Rheumatica, Musculo skeletal disease, Crohn's disease and a host of other diagnosis.


Understanding your health problems is key, your doctor does not always know best if he isn't aware of all there is to know and hasn't the time or inclination to find out.



“Lyme on the Brain”
part 1 of 4
by Tom Grier
August 25, 2010



Introduction
Lyme disease was first recognized in Old Lyme, Connecticut, CT, in 1973 by two concerned mothers.


Judy Mensch and Polly Murray felt there were too many diagnosed cases of Juvenile Rheumatoid Arthritis in their neighborhood children.

Judy and Polly Murray who had backgrounds in public health collected over 200 local case histories and presented them to the CDC and CT health department.


Dr. Alan Steere, MD investigated the local cases of JRA and coined the misnomer "Lyme Arthritis" in his 1975 publication that first described Lyme Borreliosis as an arthritic disorder.

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

The infectious etiology of Lyme disease was not known until 1981 when Dr. Willy Burgdorfer, PhD from Rocky Mountain Labs in Colorado isolated the new species of Borrelia bacteria from a tick from Shelter Island.

The fact that "Lyme disease" was caused by a spirochete should have been a real concern and everything we thought we knew about Lyme disease should have been reevaluated at that time.

Borrelia was a family of bacteria not only associated with relapses and antibiotic treatment failures, but also is part of the same family of bacteria that causes [b]Tick-Borne Relapsing Fevers, a group of over 300 variant diseases that can be deadly within months:[/b]

(Borrelia duttonii and Borrelia crocidurai of Northeast Africa), or considered mild and often mislabeled as "self-limiting"; such as, Borrelia recurrentis found in the Southwest USA.

(Ron Ferris of Canada was diagnosed with Borrelia recurrentis and was sick for years despite treatment right up until the day he died).

In 1982 the Lyme bacteria was isolated from the "Lyme Bull's-Eye rash" from patients from New England.

With this new discovery causing so much excitement and demanding large sums of monies to investigate, no one wanted to admit that "Lyme" was just a new subclass of a larger world-wide disease spread by ticks that was well known for a century as tick-born-relapsing fevers.

We need to stop calling this disease Lyme disease and recognize that it is part of a worldwide problem called Borreliosis.
If we don't recognize Lyme disease as a larger worldwide health problem caused by bacteria that have a built in mechanism for variation, our health departments will define the disease out of existence.


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

Because if he had Borrelia in the brain that causes relapsing fever and that variant Borrelia lacks the Sop-A DNA sequence and we use a PCR Osp-A test to test his brain tissues:
he may test negative for Osp-A, but still have Neuroborreliosis that is an Osp-A deficient variant.

The report would say it is not "Lyme Disease" but is any Borrelia in the brain acceptable?

Ask his widow who had to fight this case to the Supreme Court just to get an autopsy.

But what good is an autopsy if they look for a species unlikely to be in Australia?

If a murderer kills you with a 44 caliber or a 38 caliber you’re still just as dead.

But our CSI people looking at Lyme need to be doing a better job if all they are going to look for is Borrelia burgdorferi (stricto sensu).

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


This has to change.

When Lyme was found to be caused by a spirochete, no serious reevaluation of treatment protocols ever took place.

Instead major medical institutions and universities made a mad rush to register patents for Lyme tests, Lyme vaccines, and patents on the bacteria's DNA sequences for PCR testing.
But what no one did including the CDC and NIH, they didn't do pathology studies to see if treatments were successful.

"Today when Lyme patients are told that they are cured, and that their continuing symptoms must be caused by something else:
I would like to know what is out there in nature that defies antibiotic treatment better than a spirochete?


Also if we keep discovering new infectious disease causing organisms like anaplasmosis, why do we assume that a patient with continuing symptoms that still responds to antibiotics is "cured"?

Are we so arrogant to think we have to keep our options limited only to diseases that only appear on a hospital lab-order test check-list?

Are we so sure Lyme is so easily curable?

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

But my question is:

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

Who has signed their guidelines in the blood of dying Lyme patients?"

Tom Grier
Lyme Lecture
Amery, Wisconsin
August 2010


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

Absolutes that changed:
Lyme was absolutely transmitted by a new tick species called Ixodes dammini.

Then it was discovered that this new species was the same as Ixodes scapularis ticks which had been around centuries and had a wider range than we first thought that Ixodes dammini had.

But in California, three major mountain ranges away from New England, Lyme was transmitted by Ixodes pacificus.

In Missouri, the Lonestar Dog Tick had a new Borrelia that caused Bull's-eye rashes and Lyme.

In Europe, it was the Sheep Tick, or the Sea Bird Tick that transmitted Lyme, and their host reservoirs were different from America's white-footed mouse thought at one time the only reservoir of Borrelia burgdorferi, and now just one of many rodents and possibly bird species.

Length of Tick Attachment:

A tick must be attached for at least 36-48 hours. WOW! How could you ever make that conclusion on the sparse veterinary and human data we have?

In fact the data suggests this is not true. Studies that looked at improper removal of a tick showed much shorter attachments are possible.

What child removes a tick properly?

Dr. Elizabeth Burgess, DMV, in Madison, Wisconsin: her work has been overlooked for decades.

Her preliminary work showed that the Borrelia species of spirochete possessed some mechanism and ability to penetrate mucous membranes suggesting transmission in cattle could be through urine to mouth contact putting cattle at a risk besides just ticks.

Dr. Burgess' veterinary work was harshly and unjustly criticized without investigation or inspection.

A decade later we see that Borrelia is a champion at penetrating mammalian blood vessels and endothelial cells that line the blood vessels.

How hard is it to imagine mucosa capillaries in cattle are exposed targets for Borrelia to penetrate on contact?

Since the introduction of the veterinary Lyme vaccines, we hear little about entire herds of cattle and horses being infected.

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

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

• If you suspect the tick was attached for at least 36 hours, observe the site of the bite for development of the characteristic skin rash, erythema chronica migrans (sic), usually a circular red
patch, or expanding "bull's eye," that appears between three days and one month after the bite.

Not all rashes at the site of the bite are due to Lyme disease. Allergic reactions to tick saliva are common.

Preventative antibiotic treatment is not necessary, is costly, and may cause side effects.

• If symptoms of later-stage Lyme disease develop, such as arthritic swelling of a joint, most often the knee, or facial nerve palsy, have a test done.

If the test is positive, have a more precise test done.
Only if this test proves positive should a course of antibiotic therapy begin.

Expect some symptoms to linger up to three months. No further antibiotic treatment is necessary.

His article suggests that treating a symptomatic patient with a negative Lyme test with antibiotics, may be more harmful than treating Lyme disease based on a single positive test and late stage symptoms.

It is clear that the Yale perspective on diagnosing Lyme disease is that late stage Lyme symptoms, including a swollen knee and Bell's Palsy, do not warrant antibiotic treatment despite a positive ELISA test!

It is suggested that delaying treatment in a
symptomatic Lyme patient with these late stage symptoms is better than risking antibiotics.

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

This statement tells us that Yale puts more faith in serology tests than in a patient's symptoms.

Even symptoms that include an expanding EM rash after a known tick bite, a swollen knee, Bell's Palsy, and a positive blood test must all be ignored because antibiotics are costly and could cause side effects!

(Apparently no one told this to dermatologists who often prescribe tetracycline for acne for years at a time at a cost of about $10 a month.)

I have to ask: What motivates these doctors to deny treatment to a symptomatic patient who has a rash and a positive ELISA serology?

(For full article and reference see canlyme.com)
==========================


What happens when a tick attaches?

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


In several mammal studies in the late 1980s, it was shown in many species including dogs that within hours of tick attachment that the Lyme organism is with every beat of the heart circulating through the entire body.

The spirochete's motility allows it to position itself into the cracks and folds of a blood vessel wall.

Borrelia burgdorferi has a tropism or an attraction to attach to the endothelial cells lining blood vessels.

Once the bacteria has attached, it traps tissue plasminogen that converts to plasmin and this begins the process of inflammation.

This irritation causes the endothelial cells to release digestive enzymes; such as,
basement membrane laminose, hyaluronidase, lipases, proteases.

White blood cells join in at the site releasing Metal-Matrix- Protease that facilitates cell penetration, and Tumor Necrosis Factor Alpha, and Il-1, Il-6 and TGF beta, all which play a role in cell communications and begin inflammatory cascades to begin.

The net result is within 24-48 hours we can measure the breakdown of the blood-brain-barrier in dogs that peaks at 48 hours and lasts for up to 14 days!

So are we really going to say that a tick has to be attached 48 hours?

This animal model suggests that the infection is potentially already established within the brain.

This study was done by tagging normal blood albumin with radioactive Iodine and tracking it into the CSF of the dogs.
(1989 Immunological Methods of Borreliosis Cold Spring Harbor).

If the Borrelia bacteria, which as a family has been known to be neurogenic and deadly since 1910, can penetrate blood vessels, then why do physicians who should know better still make public statements in the media that Lyme disease is not transmitted transplacentally to the fetus during pregnancy.

Nine published fetal autopsies since 1987 suggest otherwise, so what is their agenda for pretending to be ignorant of the facts?

END of Part 1 of LYME on the Brain by Tom Grier
**************************************


The above is posted by 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


and thanks to Betty G for contacting me with details on MD Junction here

Monday, 30 August 2010

RESEARCH TESTING PATIENTS WITH ME/CFS AND/OR LYME DISEASE

I had read about research on ME/CFS patients to be done by Stanford but hadn't really recognised how significant this is to those with ME/CFS and /or Lyme Disease, below is a list of some of the testing that will be done and according to details on SpiroChicks blog Igenex lab will be used for testing for Lyme Disease.

The full articles can be found on CALDA website here

SpiroChicks blog part one here and part two here

and ProHealth here

New ME/CFS Study at Stanford: Dr. Montoya to test for scores of Infections

'The testing is very extensive and includes some 60 different tests (viral, bacterial, etc.). They are still in the process of finalizing the list of tests but so far they have told me they're testing for:XMRV

EBV

HHV6

HHV1

HHV2

CMV (HHV5)

several strains of Lyme Disease

Chlamydia Pneumoniae

Babesiosis (several strains)

Bartonella (several strains)

Ehrlichiosis

Rickettsia

Mycoplasma

Enovirus,

...and much more!!'

Sunday, 29 August 2010

MULTIPLE SCLEROSIS AND SPIROCHETES

The following is a particularly interesting extract from lecture by Tom Grier. Below he is talking about the history of Spirochetes in patients with Multiple Sclerosis. This should be of particular interest to those patients with Multiple Sclerosis, Parkinson's, Motor Neurons and other Neurological illnesses.
Lyme Disease is more prevalent in the UK than people realise so although this was presented in the USA it is just as relevant in the UK, other parts of Europe and Canada. Interestingly Scotland has one of the highest incidents of MS per capita in the World it has also been a known endemic area for Lyme Disease for many years.

Lyme on the Brain (Part 3-A)
Lecture Notes of Tom Grier
Tomgrier2001@yahoo.com

To read the full lecture visit Madison Area Lyme Support group here

MS and Spirochetes

In every Lyme disease support group in this country (and I have visited dozens), there have always been at least one multiple sclerosis, MS, patient who turned out to have Lyme disease, and was recovering on antibiotics.
But if this is true why is there is no documented connection between spirochetes and M.S.?
As it turns out there are more than 50 such MS-spirochete references prior to World War II and going back to as far as 1911, and published in such prestigious journals as the Lancet.
1911 Buzzard Spirochetes in MS Lancet
1913 Bullock MS Agent in Rabbits Lancet
1917 Steiner Spirochetes The Cause of MS Med Kiln
1918 Simmering Spirochetes in MS by Darkfield Micro
1918 Steiner G. Guinea Pig Inoculation with MS infectious agent from Human
1919 Steiner MS Agent Inoculation into Monkeys
1921 Gye F. MS Agent In Rabbits Brain 14:213
1922 Kaberlah MS Agent In Rabbits Deutch Med Works
1922 Sicard MS Spirochetes in Animal Model Rev Neurol
1922 Stepanopoulo Spirochetes in the CSF of MS Patients
1923 Shhlossman MS Agent in Animal Model Rev Neuro
1924 Blacklock MS Agent in Animals J. of Path and Bac
1927 Wilson The Rat as A Carrier of MS British Med Journal
1927 Steiner G Understanding the Pathogenesis of MS
1928 Steiner Spirochetes in the Human Brain of MS Patients
1933 Simons Spirochetes in the CSF of MS Patients
1939 Hassin Spirochete-like formations in MS
1948 Adams Spirochetes within the Ventricle Fluid of Monkeys Inoculated from Human MS
1952 Steiner Acute Plaques in MS and The Pathogenic Role of Spirochetes as the Etiological Factor Journal of Neuropathology and Exp Med 11: No 4:343 1952
1954 Steiner Morphology of Spirochaeta Myelophthora (Myelin Loving) In MS Journal of Neuropathology and Exp Neurol 11:4 343 1954
1957 Ichelson R. Cultivation of Spirochetes from Spinal Fluids of MS Cases with Negative Controls Procl. Soc. Exp. Biol Med 70:411 1957
If you follow the European Medical Literature concerning Multiple Sclerosis from 1911 to 1939, you find that in France, Germany and England; there were independent researchers all observing similar things and coming to similar conclusions:
1) Spirochetes are often found in conjunction with the lesions in the brains of patients who have died with MS.
2) These spirochetes can be isolated and can infect many mammalian animal models; including: mice, rats, hamsters, guinea pigs, rabbits, dogs, and primates.
3) The spirochetes could be re-isolated from the brains of the infected animals and be inoculated into more un-infected animals and re-isolated from their brains.
Why in the 21st century have spirochetes been ignored as infectious agents of the human brain?
The short answer is that to save time and money we no longer do things old school by which I mean:
no one does brain autopsies and physically stains or cultures for the bacteria.
Instead we have gotten lazy and cheap in our research and tried to rely on blood tests and CSF fluid to give us the answers.
But those tests are wholly inadequate to detect living spirochetes sequestered inside brain cells.
Now this is the important part about detecting spirochetes within human tissues.
First you cannot find spirochetes if you don’t properly stain the tissue for them.
Spirochetes are completely invisible under the microscope without special stains.
In 1911, chemists and microbiologists only had silver stains that stained nucleic acids, and for some reason these stains caused the entire spirochete to turn black and opaque.
(It turns out that Borrelia’s nucleic acid is nearly evenly distributed under its inner membrane like a web of DNA that fits the entire bacterium like a nylon stocking
surrounding the cytoplasm.
In other words the silver stain outlines the shape of the bacterium.)
The trouble with silver stains is that they cannot enter human cells. So for nearly a century it was reported that spirochetes were mostly extracellular and found outside all human cells.
Not only was this a wrong conclusion based on inadequate methods, but the consequences of not recognizing an intracellular infection was and still is dire. Why?
Because intracellular infections can be incurable or at the very least more difficult to treat; there is almost no way to determine an end point where a bacteriological cure has been obtained.
Next is that spirochetes are known to disappear by changing to cyst forms, and also by going intracellular.
So these puzzled researchers that were only seeing classical formed spirochetes in 1 in 20 MS patients, may have been seeing them all along and not realizing what they were seeing. How can we conclude this?
Researchers wanted to see if the infectious agent was still in MS lesions despite no visible spirochetes.
Researchers removed brain tissue at necropsy of human patients and inoculated the tissue into uninfected animals.
In some cases, this caused the infection to occur and show up in the brain of the animals; sometimes the classical-form spiral shaped spirochetes emerged.
All of this meticulous work was done prior to WW II, and completely untainted by today’s politics and special interests; yet this body of work is being wholly ignored.

_______________________________________

The above should be of interest to anyone suffering with Multiple Sclerosis, Parkinson's, Motor Neurons or any other Neurological Illness.

I have posted before about Multiple Sclerosis, Parkinsons and Motor Neurons, by putting Multiple Sclerosis in the search box in the right hand column you can read earlier posts or click here
Parkinsons here
Motor Neurons here

Saturday, 28 August 2010

DOES IT SOUND AS THOUGH A COUPLE OF WEEKS ANTIBIOTICS WOULD CURE THIS?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The above is a short extract from Lyme on the Brain (Part 3-A)
Lecture Notes of Tom Grier
Tomgrier2001@yahoo.com

The whole article can be found on Madison area support group here

Friday, 27 August 2010

BRAVO LE MONDE, SENSE AT LAST

Published yesterday in Le Monde the French National newspaper here

Translated with Google Translate apologise for the inaccuracies but far better than my ability to translate and sufficient to understand that for once a decent summary of the situation with Tick borne Disease, Borreliosis including Lyme Disease.

The last two paragraphs which I have highlighted in blue is the best I have read in a National newspaper yet.

There is not enough awareness of the dangers of Tick borne Illness. I thought Lyme Disease was unique to the USA until after 4 years of chronic arthrits and muscle weakness my GP suspected that it was caused by Lyme Disease. I had been diagnosed with Fibromyalgia, ME/CFS, Arthritis, Muscle Weakness, Musculo Skeletal Disease, Polymyalgia Rheumatica but finally recovered my health on long term antibiotics following ILADS guidelines. If I had been left treated following the IDSA guidelines which our Health Protection Agency insist our doctors follow, despite considerable evidence and research which supports ILADS, I have no doubt I would have remained chronically ill.


Tick-borne diseases, dilemmas and controversies

by Sylvie Rinaudo , Dr. Engineer, eco-consultant
26.08.10

The summer and the holidays we confront massive small as the attackers are the biting insects and arachnids. Among the arachnids, ticks, which thrive at the expense of warm-blooded animals, which includes humans. Ticks wait on blades of grass or a calf shank passes nearby to grab hold of, and locate their prey to the heat, and smell.

Is it global warming that increases the number of ticks, which does not die during winters become too soft? Is the increase in forest wildlife due to the decrease in consumption of game, which leads to a proliferation of deer and wild boar? The fact is that ticks are more numerous, and the number of bites increased accordingly.

During blood feeding, they are likely to transmit diseases to their host, the best known in our climate is the disease (borreliosis) Lyme.

What happens to those infected? If they develop a rash around the bite, and consult a doctor, they are likely to be diagnosed carriers of Lyme disease, and benefit from antibiotic treatment. However, we know statistically that about half of those infected by this disease do not develop this sign warning Pathognomonic.

The disease may then persist and spread throughout the body. She is particularly fond of the joints and the nervous system, but the whole body is potentially parasite. If the notion of tick bite is present, the doctor may use a serodiagnosis, which will highlight possible contact with the infectious agent of Lyme disease.

This is where the dilemma begins, because Serodiagnostics borreliosis are far from reliable ones are used, for example, to detect HIV. This means that a significant number of people may be falsely reassured, while patients without a diagnosis. Ideally, physicians compensate for this lack of reliability of Serodiagnostics asking a clinical diagnosis, from all the patient's symptoms.

New dilemma: Lyme disease mimics many other diseases, and many practitioners have never met a direct and certain. Difficult for them to identify a clinical presentation that differs from the archetypal taught, so they may miss in good faith a real patient of Lyme, the more easily it will present a doubtful serology.

The more the disease is detected late, it is more difficult to treat. This is where two opposing currents medical, because in addition to the dilemmas previous medical controversy. The famous Infectious Diseases Society of America Infectious Diseases Society of America (IDSA), which has an undeniable dominance in international medical publications on infectious diseases, says that several weeks of antibiotic treatment sufficient to rid of those infected with Lyme disease. If, according to the IDSA, the patient is not cured at the end of this short course is that it suffers from something else, or a "post-Lyme syndrome", body wave and incurable .

Another American ( mistake it is actually International) Medical Society, the International Lyme and Associated Diseases Society (ILADS) recommends treatment longer for older cases, and taking into account other illnesses that may have arisen in the course of the tick bite, and denies the notion of post-Lyme syndrome, which she said would only be the result of inadequately treated Lyme disease.

The IDSA complains that long-term antibiotics are treatments that can cause side effects,

ILADS argues that the damage caused by the disease, if it is poorly or inadequately treated, are irrelevant in terms of severity and disability, with the side effects of antibiotics.

However, it appeared that among the experts who drafted the guidelines of the IDSA treatment for Lyme disease, mainly applied in the U.S., many had conflicts of interest. Some doctors engaged as consultants for private medical insurance who refuse treatment cost time, others have participated in developing patents for vaccines antiborréliens, as shown in the excellent documentary "Wilson" Under Our Skin

The Attorney General of the State of Connecticut, seized by the U.S. Lyme disease patients, has investigated the IDSA , And noting the shortcomings and conflicts of interest, requested that the medical society to change its treatment guidelines for Lyme disease, so far without success.

What have we, the French, to do with this dark affair medical pharmacofinancière, which seems purely American?

Unfortunately, everything.

Indeed, French treatment guidelines Lyme disease, established in 2006 a few months after those of the IDSA, follow these closely.

That is to say that the U.S. guidelines for medical treatment, defendants in their country by people suffering from this disease and some practitioners who care for them, indicted by the Attorney General of the State Historical pathology (the town of Lyme, which gave it its name, is located in Connecticut), have so far been applied in France, officially the French Lyme patients.

These guidelines have the merit of French exist and to encourage treatment. However, for old cases of Lyme disease, they incur the same criticism that their American counterparts.

In his book entitled "The Hell of Matignon, Raphaelle Bacqué, journalist at Le Monde, quoting Laurent Fabius, former prime minister Francois Mitterrand, speaking about the contaminated blood scandal:

"Must exist in society and state, sensors, enabling the political authority to make good decisions, even if these are not decisions that are recommended by the scientific community. Thus, at the time, those who held the truth have not been heard. But there must, in society and the functioning of the state sensors to a young researcher who says the opposite of a big shot, but we'll see five years later he was right can be heard. "

The France would do well by taking into account the two existing systems of medical guidelines, which would treat the few hundreds (thousands?) French Lyme patients left behind by the only system of guidelines being applied. Ultimately, it would probably be cheaper for health insurance, and incomparably less costly in human terms.

Tuesday, 24 August 2010

HGRV-XMRV-MLV NEWS







The Whittemore Peterson Institute would like to congratulate Harvey Alter, MD, and Shyh-Ching Lo, MD, PhD, on their publication of the replication study.

A quote from Dr Joe Burrascano for patients with Lyme Disease-

'Definitely stay tuned - the volume of new and important information about this virus and its disease associations is increasing rapidly and in my opinion should be a concern to every patient with chronic neuro-immune diseases, including those with chronic Lyme.'

The Wall Street Journal here

The Washington Post here

The New York Times here


CNN here

The LA Times here


The Scientist here

Pro Health here

VIP dx tests here

Living with Chronic Fatigue Syndrome many links here

CFS Central an excellent read here

CFIDS here

Other articles as posted by Life as we know it here

Fox10TV here




MSN Health here

Science here

Business week here

Monday, 23 August 2010

DETECTION OF MLV-RELATED VIRUS GENE SEQUENCES IN BLOOD OF PATIENTS WITH CHRONIC FATIGUE SYNDROME AND HEALTHY BLOOD DONORS

The long awaited Alter/Lo paper thanks to blog Life as we Know it.

http://cfs-facts.blogspot.com/2010/08/and-here-it-is-long-awaited-paper.html

http://www.pnas.org/content/early/2010/08/16/1006901107.full.pdf+html


Detection of MLV-related virus gene sequences in
blood of patients with chronic fatigue syndrome
and healthy blood donors
Shyh-Ching Loa,1, Natalia Pripuzovaa, Bingjie Lia, Anthony L. Komaroffb, Guo-Chiuan Hunga, Richard Wangc,
and Harvey J. Alterc,1

Chronic fatigue syndrome (CFS) is a serious systemic illness of
unknown cause. A recent study identified DNA from a xenotropic
murine leukemia virus-related virus (XMRV) in peripheral blood
mononuclear cells (PBMCs) from 68 of 101 patients (67%) by nested
PCR, as compared with 8 of 218 (3.7%) healthy controls. However,
four subsequent reports failed to detect any murine leukemia virus
(MLV)-related virus gene sequences in blood of CFS patients. We
examined 41 PBMC-derived DNA samples from 37 patients meeting
accepted diagnostic criteria for CFS and found MLV-like virus gag
gene sequences in 32 of 37 (86.5%) compared with only 3 of 44
(6.8%) healthy volunteer blood donors. No evidence of mouse
DNA contamination was detected in the PCR assay system or the
clinical samples. Seven of 8 gag-positive patients tested again positive
in a sample obtained nearly 15 y later. In contrast to the
reported findings of near-genetic identity of all XMRVs, we identified
a genetically diverse group of MLV-related viruses. The gag
and env sequences from CFS patients were more closely related
to those of polytropic mouse endogenous retroviruses than to
those of XMRVs and were even less closely related to those of
ecotropic MLVs. Further studies are needed to determine whether
the same strong association with MLV-related viruses is found in
other groups of patients with CFS, whether these viruses play
a causative role in the development of CFS, and whether they represent
a threat to the blood supply.

XMRV-HGRV ME/CFS/LYME DISEASE UPDATE

Posted on Madison area Lyme Support group see here

Second email:
Hello!Thanks for letting me know there is a buzz about this going on.I am not part of the WPI (Whittemore Peterson Institute) but I do have an interest in HGRV (formerly known as XMRV) because I strongly believe it is an important contributor to what we know as chronic Lyme. I also believe it is involved in some way with autism and CFIDS, and possibly other so-called “neuroimmune diseases”.What is needed to further the study of HGRV is to set up clinical trials, because so far, all formal work on this virus is being done in the labs. To accomplish this, we are in the process of setting up a clinical working group, to consist of an alliance between researchers and clinicians. I was invited to join this group- of course, I accepted.That is the scoop- please feel free to forward this note to any interested parties.Thanks!Dr. B…………………….!
Contact Colleen Nicholson 516-286-7196
Research Assistant to Dr. Burrascano, MD
burraj51@bigplanet.com

Saturday, 21 August 2010

XMRV - HGRV. ME/CFS PATIENT AWARENESS

My last post was on the suggested name change of XMRV to HGRV.

I have been following comments on forum Phoenix Rising here

I was saddened to read how few patients suffering with ME/CFS seem to know anything about Lyme disease or Dr Joe Burrascano.

My diagnnosis of ME/CFS as well as many other diagnosis was found to be Lyme Disease and on appropriate antibiotics I have recovered my health and my life.

Eurolyme a forum for patients with Lyme Disease did a pole and found that 75% of patients were previously diagnosed with ME/CFS before being diagnosed with Lyme Disease.

Lyme Disease is rarely considered by our doctors as a differential diagnosis especially where I live in the UK.

Many of the top ME/CFS expertse in this field the likes of Nancy Klimas, Judith Mikovits, Kenny de Merlier, Garth Nicholson and many others recognise that some ME/CFS patients have Lyme Disease and respond to antibiotics.

If you put the words Kenneth Friedman in my search engine you will find I posted an e mail from him to me saying that research shows about 30% of ME/CFS patients do indeed have Lyme Disease.Or click here

Even the NICE Guidelines for ME/CFS say Lyme Disease must be excluded before diagnosing ME/CFS.

That is the key how do you exclude something when tests can miss 50% of cases.

Patients who are Chronically ill rarely suffer from just one micro organism at a time.

Below is a brief overview from Dr Burrascano on Lyme Disease but his full guidelines are in the links in the side bar on this blog.

LYME DISEASE THE NUTS & BOLTS
BY JOSEPH T. BURRASCANO, JR, MD
presented July 2010 in DePere, WISCONSIN
9 pages

WHAT IS LYME DISEASE?
Lyme disease is the illness that results from the bite of an infected deer tick

STATISTICS
• Fastest growing vector-borne infectious disease in the USA
• CDC estimates are over 200,000 new cases per year!
• In the USA, rate of new cases exceeds that of HIV/AIDS
• Anyone can get it- affects all ages, both genders, and even our pets

LYME IS NEARLY EVERYWHERE!
• Lyme has been reported in all 50 states
• Present worldwide- every continent except Antarctica
• In many areas, lawns have higher tick concentrations than the surrounding woods
• Ticks can survive down to 17 degrees below zero! (may still get tick bites in wintertime)• Most people are bitten during usual daily activities
• Tick bite is painless
• Tick is so tiny, it can be missed

BASIC FACTS
• Only 16% recall a tick bite
• “Classic” rash (Erythema Migrans) occurs in only 1/3 to ½ of cases
• Subtle onset of nonspecific “viral-like” symptoms often obscure the diagnosis
• Blood test may miss up to ½ of cases!!!
• Spinal fluid serology positive in only 9%!!! (91% false negative rate!!!!)

MORE NEW STRAINS OF BORRELIA IDENTIFIED
• A new strain of Lyme Borrelia called SCW-30h has been found in the USA, in all areas.
• Another new one, B. americana has been found in the South from Texas to the Atlantic
• These are being investigated to find out if they can make you ill, and if so, how best to treat it.
• ?atypical Lyme; seronegative Lyme

INCREDIBLY COMPLEX!
• Ticks may carry DOZENS of potential pathogens- NATURE’S DIRTY NEEDLE!
• One tick bite can result in simultaneous co-infections by different germs
– Spirochetes (Lyme)
– Parasites (Babesia)
– Bacteria (Ehrlichia, Anaplasma)
– Mycoplasmas (Gulf-War and Chronic Fatigue germs)
– Viruses (T.B.E., West Nile Virus)
– Worms (nematodes)?
XMRV- A New Retrovirus- Is This Another Co-Infection?
• Xenotropic murine leukemia virus-related virus (XMRV) was first isolated from prostate cancer patients
• Dr. Judy Mikovits looked for XMRV in CFIDS patients. She found it in only 3.7% of healthy controls but 95% of CFIDS cases were antibody positive and 68% were PCR-positive. Overall, 98% tested positive!
• Recently, the FDA has independently confirmed this study
• She and collaborating clinicians also found XMRV in Lyme, fibromyalgia, atypical MS and autism
• This is a retrovirus (as is HIV) and theoretically can cause or add to many symptoms and immune defects as seen in these illnesses, as well as in Lyme
• Three avenues of treatment are being studied:
– Anti-retroviral agents, as used in HIV
– Artesunate
– Antiviral herbs

LYME- WHY THE CONCERN?

ILLNESS CAN VARY FROM MILD TO VERY SEVERE
– Early Lyme, if promptly recognized and appropriately treated, can be cured
– Untreated Lyme may progress, causing a very severe illness and disability
– Can be latent for months to years, and later result in catastrophic, permanent damage
– Deaths have been reported
• Most symptoms are non-specific
• Mild symptoms often are dismissed
• Many medical errors due to lack of diagnosis
• More medical errors from incorrect diagnoses and unnecessary or dangerous treatments
– Fibromyalgia, ME/CFS, depression, multiple sclerosis, ALS (Lou Gherig’s Disease), malingering, Munchausen
• Often, patients see literally dozens of doctors and undergo an encyclopedia of tests, Lyme is missed, and they still have no diagnosis
• When medical doctors cannot find a cause for the complaints, they refer patients to a psychiatrist (blame the patient for his/her illness!)
• Can be transmitted from mother to child

TYPES OF LYME DISEASE
• “Classic” Lyme (my definition) includes:
– Early localized
– Early disseminated
– Late disseminated
• Chronic Lyme Disease
– Illness present for one year or longer
– Is a totally different disease!
– May not be curable!

DIAGNOSING LYME A difficult task!
SYMPTOMS
• Headaches, photophobia, stiff neck
• Fatigue, intolerance of exercise
• Aches in and around joints
• Numbness, tingles, sense of vibration
• Poor coordination, imbalance, light-headed, need to sit or lie down, especially in afternoon
• Forgetful, confused, speech errors, ADD-like
• Sleep disturbance
• Neuropsychiatric- anxiety, panic attacks, depression, rage attacks, antisocial behavior
• Intolerance of stress, alcohol, sleep deprivation (any of these will make all symptoms worse)

BLOOD TESTING
• LYME (Borrelia burgdorferi)
– Serologic tests (ELISA, Western Blot)
– Sensitivity is poor: Commercial labs: 50% Private reference labs (Igenex): 70%
– PCR- also poorly sensitive- <30%
• Even a spinal tap serology will miss over 90% of cases!

• CO-INFECTIONS
– Situation is worse- pick up 30% at best!!!!
• Conclusion: LYME IS A CLINICAL DIAGNOSIS
ERYTHEMA MIGRANS- TYPICAL “BULLSEYE” RASH
• Expands over time, Painless, Raised, May be warm
RINGWORM
– Scaly center
– Not raised or warm
SPIDER BITE
– Painful!
– Necrotic center

MAKING A CLINICAL DIAGNOSIS: THE POINT SYSTEM
• Tick exposure in an endemic region 1
• History consistent with Lyme 2
• Systemic signs & symptoms consistent with Bb infection (other potential diagnoses excluded):
• Single system, e.g., monoarthritis 1
• Two or more systems 2
• Erythema migrans, physician confirmed 7
• ACA, biopsy confirmed 7
• Seropositivity 3
• Seroconversion on paired sera 4
• Tissue microscopy, silver stain 3
• Tissue microscopy, monoclonal IFA 4
• Culture positivity 4
• B. burgdorferi antigen recovery 4
• B. burgdorferi DNA/RNA recovery 4

INTERPRETATION
DIAGNOSIS
• Lyme Borreliosis Highly Likely: 7 or above
• Lyme Borreliosis Possible: 5-6
• Lyme Borreliosis Unlikely: 4 or below
CD-57 COUNT (Natural Killer Cells)
• Low counts seen in Chronic Lyme when the infection has been active > 1 year
• Reflects degree of infection
• CAN BE A SCREENING TEST!
• Predicts a relapse if low when antibiotics end
• Must use method of LabCorp (normal is >180)
– <20- severe illness
– 20-60- most common result in chronic patients
– >60- Lyme activity minimal
– >120- Relapse NOT likely after treatment ends
EARLY LYME
• Rapid diagnosis is critical- fully curable at this stage if treated properly
– Start treatment as soon as possible
– If a rash is present, start treatment immediately!
• Do not wait for blood tests- Tests may take weeks to become positive or may NEVER get a positive test!
– If no rash, but high suspicion, treat, observe clinically, and retest serially
TREATMENT OF EARLY LYME
Oral antibiotic for 4 to 6 weeks
• Shorter courses associated with a linear rate of treatment failures
• Be sure to use full doses!
– Lyme has already spread to other areas
– Already in the central nervous system
– Inadequate treatment may worsen later illness (“survival of the fittest”)
• APPROPRIATE TREATMENT OF EARLY LYME MAY PREVENT CHRONIC LYME

DISSEMINATED LYME
• By definition, present for more than six weeks, but less than one year
• Initial non-specific symptoms gradually change to involve multiple discrete organ systems:
– Joints (pain, stiffness, subtle swelling)
– Peripheral nerves (numbness, tingles, weakness, vibration)
– Central nervous system (“brain fog”, impaired short-term memory, confusion, mood disorders)
– Original, general symptoms may persist (headache, fatigue, sweats, etc.)
• Specific patterns develop:
– Monthly cycle of waxing and waning illness
– Symptoms affecting major organ systems “migrate”- move around

TREATMENT OF DISSEMINATED LYME
• Start with orals if possible
• If very ill, pregnant, or cannot tolerate oral antibiotics, then may need IV therapy for 6 to 12 weeks, followed by oral therapy if the infection is still active
• May need combination therapy (co-administration of two or more dissimilar antibiotics)
• Duration of treatment often mirrors duration of illness- treat for 6 weeks to 6+ months
• Must be free of signs of active infection before treatment ends

CHRONIC LYME DISEASE
DEFINITION- ILL WITH LYME FOR ONE OR MORE YEARS
• Is the start of clinically significant immune breakdown
– Decreased function and numbers of all three arms of immunity: B, T and NK cells
– Elevated cytokine levels cause many of the symptoms, and further impair the immune response
– Because most Lyme tests are serologies, which measure immune response to B. burgdorferi, a weakened immune system may result in more false negative tests
• PARADOX: The sicker patient is more likely to have a negative (non-reactive) Lyme serology!
CLINICAL FEATURES Very complex disease:
• Difficult to diagnose
• Broad spectrum of illness, from subclinical to severely debilitating, and rarely, can be fatal
• Extremely difficult to treat the infections
• Extremely difficult to manage totality of complaints
• May not be curable in some- why is a chronic illness

CHRONIC LYME
• Primary symptoms of Chronic Lyme are NEUROLOGICAL (nearly every patient)
– Encephalopathy and encephalitis, Peripheral and autonomic neuropathy, Demyelination- central and peripheral
• Inflammatory arthritis in only 5%
• Myositis (muscle inflammation) rare, and Carditis (heart inflammation) also rare
• Immune suppression allows co-infections to flourish, and opportunistic infections (yeast, etc) become more of a problem
CHRONIC LYME IS MORE THAN AN INFECTION
• Immune “Dysregulation”: Immune activation & Immune suppression
• Neurotoxins, Hormonal disturbances, Damage to organs, tissues, cells and DNA
• Nutritional disturbances, Metabolic effects
TREATMENT OF CHRONIC LYME
• Antibiotics, usually in combinations
– Antibiotic synergism, cover all infected tissues, cover alternate forms of Bb, and co-infections
• Nearly every chronic Lyme patient is a candidate for IV antibiotics
• Supportive treatments
– Vitamins, probiotics, exercise, low carb diet, no alcohol, enforced rest
• If neurologic symptoms do not clear, there is the option to treat with IVIG

INDICATIONS FOR INTRAVENOUS THERAPY
• Abnormal spinal fluid (↑WBC, ↑Protein)
• Synovitis with high ESR
• Illness for more than one year
• Age over 60
• Acute disseminated illness in first trimester
• Acute carditis
• Documented immune deficiency
• Prior use of steroids or other immunosuppressants
• Failure or intolerance of oral therapy

DURATION OF ANTIBIOTIC THERAPY- CONTROVERSIAL!
• Restrictive guidelines by Infectious Disease Society of America (IDSA)
– Maximum is one month; rarely will repeat
– No allowance for physician’s clinical judgment or degree of illness of the patient
– No consideration of co-infections
– Under investigation by the Connecticut Attorney General!
• More realistic guidelines by International Lyme and Associated Diseases Society (ILADS)
– Treatment is individualized, based on patient need and response, and may have to be given for months to years

CHRONIC LYME- Treatment Issues
• In chronic Lyme Disease, active infection may persist despite prior antibiotic therapy
• Relapses do occur and retreatment is often needed
• Repeated or prolonged antibiotic therapy usually is necessary
• High doses of antibiotics are needed, and blood levels should be confirmed wherever possible
• Antibiotic combinations usually are necessary
• Check for co-infections and immune status, and treat appropriately
• May need to rotate through different regimens based on response
• If the CD-57 count is not normal at the end of treatment, then continued illness or a relapse is likely
• May not cure the infection, and may need repeated or open-ended maintenance therapy
• Signs of persistence of infection:
– continued fevers, synovitis
– four week cycles, migrating symptoms
– PCR positivity and low CD-57 counts
• As symptoms wind down, I DO NOT cut the dose, for resistance may develop
• Aggressive supportive therapy is required- and search for any other possible cause of a weakened host:
– Toxin exposure, heavy metal poisoning, malnutrition, endocrine dysfunction, other illnesses, severe or ongoing stress
• Progressively increase exercise program as the symptoms of Lyme decrease
– Exercise is vital and required, or a full recovery will not occur
– Not exercising will increase risk of a relapse

CO-INFECTIONS IN LYME
Nearly universal in chronic Lyme
• Symptoms more vague, and overlap
• Diagnostic tests LESS reliable
• Co-infected patients are more ill and more difficult to treat
• Lyme treatments do not treat Babesia, Bartonella or viruses
• One reason for “treatment-resistant” Lyme
• Bartonella, Babesia, Anaplasma, Ehrlichia, Mycoplasma, Viruses, Nematodes?
• ?Others

BARTONELLA-LIKE ORGANISMS (“BLO”)
• More prevalent in NJ ticks than even Borrelia!
• Clinically, seems to be a different species than “cat scratch disease” (?Tularemia)
• Persistent CNS symptoms despite Lyme Rx
• CNS symptoms out of proportion to physical
– Irritability, anxiety, insomnia, seizures, rage attacks, encephalopathy-encephalitis, psychiatric syndromes,
– Also gastritis, rashes, tender skin nodules, sore soles, AM fevers, light night sweats
• CSD serologies and PCR tests are insensitive!
– Miss up to 80% of clinically defined cases
• Bartonella FISH soon to be available

BARTONELLA-LIKE ORGANISMS- TREATMENT-
• Levofloxacin (Levaquin) is drug of choice- 500 mg daily, and consider adding a proton pump inhibitor
• Cell wall drugs suppress but do not kill BLO, but may synergize with fluoroquinolone
• Rifampin and metronidazole may be alternatives
• Erythromycins alone totally ineffective, and may inhibit concurrent fluoroquinolone. However, may work if given with rifampin
• Response to doxycycline alone variable but usually poor- may be combined with rifampin
• Combination of rifampin + Bactrim has had some success
• Treat for 1 to 3+ months if tolerated
PIROPLASMS (Babesia species)
• Many different species found in ticks (13+). Can test for only B. microti and B. duncani
• B. duncani more difficult to treat than B. microti
• Diagnostic tests insensitive
• Chronic persistent infection documented
• Infection is immunosuppressive
• Renders Lyme more severe and more difficult to treat, with worse symptoms and more organ damage

BABESIOSIS- ACUTE AND CHRONIC INFECTIONS
• Acute-
– Abrupt onset of symptoms; no rash
– Spectrum of mild to severe presentations
– Can be fatal!
• Chronic-
– Symptoms blend with those of Lyme and diagnosis often missed

BABESIA TESTING
• Standard smears useful only for acute infections !
– Smears universally negative after two weeks
• Enhanced smears-
– Buffy coat
– Prolonged scanning, with digital photography
• Fluorescent in-situ hybridization assay
– Fluorescent-linked RNA probe
– Increases sensitivity 100-fold over conventional Giemsa-stained smears
• PCR and serology
• All methods are of low yield, but may not overlap! Therefore, recommend use all available tests

DIAGNOSING ACUTE BABESIOSIS
• Acute onset of symptoms
– Sweats, high fever, chills, headache, dark urine, acute hemolytic anemia, severe illness
• Blood smear usually reliable
• Serologic tests may convert within one week, but not always reliable
• Rule out other acute infections

DIAGNOSING CHRONIC BABESIOSIS
• Acute onset of initial illness
• Incomplete response to Lyme treatments
• **Symptoms more severe than expected with Lyme alone**
• Also:
– Marked night sweats which may cycle every several days
– Air hunger, cough
– Severe persistent headaches
– Unrelenting fatigue
– Off balance- “tippy”, not vertigo
• ANY positive test in proper clinical setting

TREATING BABESIOSIS
• Is a parasite, so is treated differently than Lyme, but can be treated concurrently while on Lyme medications
• Mepron (atovaquone) 5+ cc bid, plus azithromycin 600 mg daily for 4 to 6 months minimum, but higher doses may be needed, especially with B. duncani
• Oral clindamycin + quinine rarely used as first line
• Malarone (atovaquone + proguanil), 6+ tabs daily
• Added sulfur (Bactrim DS), 2 to 4 daily
• Added metronidazole (Flagyl), 750 to 1500 mg/d
• Always add artemesia or artemesenin but must be given in cycles- 2-3 weeks on, and 1-2 weeks off
• No Co-Q 10
• In extremely difficult cases, IV clindamycin may be helpful

EHRLICHIOSIS AND ANAPLASMOSIS
• Less common than the other tick-borne infections
• Acute and chronic forms
• Acute- rarely, causes a spotted rash
– Abrupt onset, high fever, muscle pain, headache, low WBC count, elevated liver enzymes
• Chronic-
– Headaches and muscle soreness
– Persistent leucopenia
– Test with serology, PCR or smear
• Treat with doxycycline for 2 to 4 weeks
• Fluoroquinolones and rifampin MAY be (poor) alternatives

MYCOPLASMA
• “Chronic fatigue” germ
• Not clear its origin or source
• More often seen in the immunosuppressed
• Test with serial PCRs (still insensitive)
• Treat with doxycycline and/or a fluoroquinolone, and add hydroxychloroquine (Plaquenil)
• Erythromycins & rifampin, with added hydroxychloroquine OK but less effective
• Treat for three years?
• Restoring better immune function is probably the best approach

OTHER CO-INFECTIONS
Especially in the chronic Lyme and immunosuppressed patients
• Viruses: TBE, West Nile, HHV-6, CMV, other herpes, bornavirus
• Chlamydia, Yeasts, Q-fever?, XMRV?, Others?

SORTING IT ALL OUT !
• LYME-
– Multisystem, 4-week cycles, afternoon fevers, no sweats, gradual onset of illness

• BARTONELLA-
– CNS out of proportion to skeletal
– CNS irritability, GI, Sore soles, sub Q nodules, AM fevers, light sweats, gradual onset of illness

• BABESIA-
– Sweats, fatigue, global headaches, air hunger, cough, hypercoaguable, cycles every few days, rapid onset, very severe Lyme symptoms

• EHRLICHIA-
– Headaches (knife-like), muscles, low WBC, elevated liver function tests, rapid onset

• MYCOPLASMA-
– Fatigue, poor exercise tolerance, slow or minimal response to antibiotics, lots of neuropathy

TREATMENT
More Than Antibiotics!
• Enforced rest, No caffeine, No alcohol, No smoking at all, Low carb, high quality protein diet
• Daily vitamins and other nutritional support, Maintain hydration, Exercise program, Never any steroids!

CLINICAL MEDICINE IN THE 21ST CENTURY: LYME DENIALISM
• If the test does not show it, it does not exist
• If organized medicine did not discover it, it does not exist
• New illnesses become real only after years or decades of clinical trials
• But– will not perform clinical trials on something that does not exist!

WHAT MUST BE DONE
• EDUCATION: Become your own advocate
• AWARENESS: Keep up with not only the latest medical news, but also the political developments
• ADVOCACY: “We will not go away”; Support those who support you
• NEVER GIVE UP
RESOURCES
www.ILADS.org
www.lymediseaseassociation.org
www.mentalhealthandillness.com

Thursday, 19 August 2010

XMRV - HGRV

Hello all from Dr. B.
[Dr. Burrascano is a leading authority on tick-borne diseases, particularly Lyme disease.]

I just returned from the first official scientific symposium of the Whittemore-Peterson Institute on the topic of XMRV.

We formed a working group to be in constant touch and we plan to meet regularly because advances are coming so rapidly.

Big news that everyone should know and adopt is that we have proposed a name change for the virus.

This virus is a human, not mouse virus, and it is the first and so far only gamma-retrovirus known to infect people.

Also, it is clearly not an "endogenous" retrovirus (one that is present in all genomes due to ancient infection). Because of all of this, and because of the desire to begin on the right track:

• The new name of the virus is HGRV - Human Gamma Retro Virus.•

The illness caused by this infection is named HGRAD- Human Gamma Retrovirus Associated Disease.

We plan to announce this at the upcoming NIH retroviral conference this September.

Definitely stay tuned - the volume of new and important information about this virus and its disease associations is increasing rapidly and in my opinion should be a concern to every patient with chronic neuro-immune diseases, including those with chronic Lyme.

Joseph J. Burrascano Jr. M.D.Water Mill, NY, USA
_______________________________________
The above was posted on Eurolyme this evening but on checking through Twitter I also found it On Pro Health here

I had been meaning to post with news of XMRV as the Internet has been humming these last few days.

blog My Life as I stand up 2ME posted the TV program with Annette and Andrea Whitmore see here

and further news on Phoenix rising from Judith Mikovits here

SAD LOSS TO THE LYME COMMUNITY

Dr. Teresa "Terri" Royer MacKnight, 57, passed away on Sunday, Aug. 15, 2010, peacefully at her home in Andover.

Dr. MacKnight practiced medicine in Hollywood, Fla., Seattle, Wash., Negley, Ohio, and Beaver, Pa., before moving to Maine in 1990. She practiced medicine in Rumford until being disabled by Neurologic Lyme Disease. She was one of the founders of the International Lyme and Associated Disease Society and the society's first president in 1999. As a lecturer and author, she strived to help the medical community and the public to recognize, treat and prevent Lyme Disease. Her desire to help others also took her to Barrow, Ala.; American Samoa and into rural areas where she was able to help those without access to medical care.

Read the whole article here

Wednesday, 18 August 2010

MORPHEA - SCLERODERMA - LYME DISEASE- BORRELIA

I was recently asked if Morphea could be a symptom of Lyme Disease.

A Google search found some interesting results which I post below. I draw attention to Eisendles findings. He uses Focus-floating microscopy and finds this more reliable than PCR. I heard Eisendle present at the Lyme Disease Action 2008 conference, very impressive.

I have to wonder how many patients are PCR tested negative for Borrelia when indeed they actually still have an active infection?

so in no order but all very interesting:-

http://www.thedoctorsdoctor.com/diseases/scleroderma_morphea.htm#ddx
Scleroderma-Morphea

Background
Scleroderma means hard skin. It exists in two clinical variants. The localized form is commonly referred to as morphea. The systemic form is usually referred to as systemic scleroderma. Morphea is a disease of skin the underlying connective tissue. Several variants have been described, as discussed below. Systemic scleroderma may affect multiple organ systems and is usually classified under autoimmune diseases. Occasionally, morphea and scleroderma may occur in the same patient. In these cases, morphea arises first followed by a milder and nonprogressive form of systemic scleroderma.

LYME DISEASE/BORRELIA INFECTION

J Am Acad Dermatol. 2009 Feb;60(2):248-55. Abstract quote
"Borrelia-associated early-onset morphea": a particular type of scleroderma in childhood and adolescence with high titer antinuclear antibodies? Results of a cohort analysis and presentation of three cases.
Prinz JC, Kutasi Z, Weisenseel P, Pótó L, Battyáni Z, Ruzicka T.
Department of Dermatology, University of Munich, Munich, Germany.
BACKGROUND: Morphea is an inflammatory autoimmune skin sclerosis of unknown etiology. A causative role of Borrelia burgdorferi infection has been controversially discussed, but no conclusive solution has yet been achieved. OBJECTIVE: Intrigued by 3 young patients with severe Borrelia-associated morphea and high-titer antinuclear antibodies, we retrospectively examined the relationship between Borrelia exposure, serologic autoimmune phenomena and age at disease onset in morphea patients. METHODS: In 90 morphea patients the presence of Borrelia-specific serum antibodies was correlated to the age at disease onset and the presence and titers of antinuclear antibodies. Patients with active Borrelia infection or high-titer antinuclear antibodies due to systemic sclerosis or lupus erythematosus served as controls. RESULTS: We observed a statistically highly significant association between morphea, serologic evidence of Borrelia infection, and high-titer antinuclear antibodies when disease onset was in childhood or adolescence. LIMITATIONS: Because pathogenic Borrelia species may vary in different geographic regions the relevance of Borrelia infection in morphea induction may show regional variations. CONCLUSION: B burgdorferi infection may be relevant for the induction of a distinct autoimmune type of scleroderma; it may be called "Borrelia-associated early onset morphea" and is characterized by the combination of disease onset at younger age, infection with B burgdorferi, and evident autoimmune phenomena as reflected by high-titer antinuclear antibodies. As exemplified by the case reports, it may take a particularly severe course and require treatment of both infection and skin inflammation.

http://www.canlyme.com/morphea08.html

http://www.canlyme.com/gestational_lyme_cardiac_gi_tract.html

Morphea and Lyme Disease: Are They Related?
Morphea is a rare and untreatable dermatologic condition characterized by thickening and induration of the skin from excess collagen deposition. There are at least 5 forms of the disease: localized, generalized, guttate, linear, and coup de sabre (an indentation that can extend to and damage the underlying muscle and bone). The cause is generally not known, but as with any idiopathic condition, proposed etiologies abound, including radiation damage, autoimmunity, infection, vaccination, trauma, and genetic predisposition. One of the leading infectious disease candidates in the pathogenesis of morphea is B burgdorferi, although this association is a subject of controversy.[1] A number of European studies have found a correlation, while most US studies, including a frequently cited study from the Mayo Clinic,[2] have found no evidence of B burgdorferi in morphea lesions.
Andrew G. Franks, Jr, MD,[3] of New York University School of Medicine (NYU), believes there is a connection between the 2 diseases. For instance, it can be difficult to differentiate between EM and certain morphea lesions, especially if the EM lesion is not the typical bull's-eye with central clearing. The differential diagnosis for EM-like lesions is varied and can include spider bites, herpes simplex or zoster, cellulitis, fungus or tinea, granuloma annulare, drug eruption, erythema multiforme, and subacute lupus erythematosus. In many cases, it can be difficult to culture B burgdorferi from EM lesions.

http://www.nature.com/jid/journal/v100/n5/abs/5611650a.html

Further Evidence for Borrelia burgdorferi Infection in Morphea and Lichen Sclerosus et Atrophicus Confirmed by DNA Amplification
Christoph Schempp1, Hubertus Bocklage2, Robert Lange2, Hans W Kölmel2, Constantin E Orfanos1 and Harald Gollnick1
Abstract
We present further evidence in support of the notion that Borrelia burgdorferi is possibly involved in the pathogenesis of morphea and lichen sclerosus et atrophicus (LSA). Running a nested polymerase chain reaction (PCR) with a primer set specific for the flagellin gene of B. burgdorferi enabled us to demonstrate the presence of Borrelia DNA in skin biopsies of patients with morphea (nine of nine) of LSA (six of six). Biopsy specimens obtained from patients with erythema chronicum migrans (two patients, four of four samples) and acrodermatitis chronica atrophicans (one patient, one of one sample) also showed positive PCR results. By contrast, there was no amplification of Borrelia DNA in control biopsies either from patients with chronic eczema (three of three) or psoriasis (two of two) or from normal skin (three of three). Antibodies directed against B. burgdorferi were only detected in the serum of patients with erythema chronicum migrans (two of two) and acrodermatitis chronica atrophicans (one of one) but were not present in cases of morphea (five of five), LSA (three of three), or in control subjects (three of three). These data suggest that B. burgdorferi may play a role in the pathogenesis of both morphea and LSA. Furthermore, we conclude that PCR analysis provides an important diagnostic tool, even in seronegative Borrelia infections.
http://www.ncbi.nlm.nih.gov/pubmed/17941947

Morphoea: a manifestation of infection with Borrelia species?
Eisendle K, Grabner T, Zelger B.
Department of Dermatology and Venereology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. klaus.eisendle@uki.ac.at
Abstract
BACKGROUND: Morphoea or localized scleroderma is a cutaneous inflammatory disease with still unknown aetiology. Borrelia burgdorferi as causative agent has been discussed controversially. OBJECTIVES: To assess the evidence for infection with B. burgdorferi in patients with morphoea by focus-floating microscopy (FFM). METHODS: Using standard histological equipment, tissue sections stained with a polyclonal B. burgdorferi antibody were simultaneously scanned through in two planes: horizontally as in routine cytology, and vertically by focusing through the thickness of the section, i.e. FFM. Part of the material was also investigated with a Borrelia-specific polymerase chain reaction (PCR). RESULTS: One hundred and twenty-two cases of morphoea and 68 controls (58 negative and 10 positive by PCR) were investigated for the presence of Borrelia within tissue specimens. Using FFM Borrelia was detected in 84 cases (68.9%) of morphoea and in all positive controls, but was absent in all negative controls. Borrelia was significantly more frequent in early inflammatory-rich (75%) than late inflammatory-poor (53%) cases (P = 0.018). What seemed to be vital microorganisms were mostly found close to the active border, while degenerated forms were more common in fibrosclerotic parts. The presence of B lymphocytes determined by CD20 staining proved to be a good positive predictor of the microorganism (correlation 0.85, P < 0.001). Borrelia-specific DNA was detected in only one of 30 cases of morphoea analysed by PCR. CONCLUSIONS: FFM is a reliable and highly sensitive method to detect Borrelia in tissue sections. The frequent detection of this microorganism in morphoea points to a specific involvement of B. burgdorferi or other similar strains in the development of or as a trigger of this disease.
PMID: 17941947 [PubMed - indexed for MEDLINE]



http://www.lymeinfo.net/medical/LDSymptoms.pdf
Enter Scleroderma in the search box

http://www.ncbi.nlm.nih.gov/pubmed/15649200

Eur Acad Dermatol Venereol. 2005 Jan;19(1):93-6.
Acute exacerbation of systemic scleroderma in Borrelia burgdorferi infection.
Wackernagel A, Bergmann AR, Aberer E.
Department of Dermatology, Medical University, Graz, Auenbruggerplatz 8, A-8036 Graz, Austria.
Abstract
In recent years a possible aetiological connection between skin sclerosis and an infection with Borrelia burgdorferi has been discussed, but this association has not yet been reported for systemic scleroderma. Several treatment modalities are suggested for systemic scleroderma, but no treatment has yet been found to alter the overall course of the disease. This report describes a 61-year-old woman with Raynaud's phenomenon, nail-fold changes and circulating anticentromere antibodies, who showed an abrupt onset of erythemas and doughy swellings involving the face and upper trunk, followed by thickening and induration of the skin mimicking diffuse systemic scleroderma. Laboratory tests including enzyme-linked immunosorbent assay (ELISA), immunoblot and urine polymerase chain reaction (PCR) showed an infection with B. burgdorferi sensu lato that was successfully treated with intravenous ceftriaxone, an antibiotic recommended for Lyme borreliosis. Fourteen days after the end of treatment the skin was no longer stiff and indurated and had returned to its normal predisease state. This case suggests that Lyme disease should be considered in atypical cases of skin sclerosis in patients predisposed to the development of systemic scleroderma.
PMID: 15649200 [PubMed - indexed for MEDLINE]

Tuesday, 17 August 2010

AWARENESS IN THE MEDIA

An excellent article where the Daily Mail raises awareness of Lyme disease read here

Stella Huyshe-Shires, chair of the charity Lyme Disease Action: 'The risk of Lyme disease - which can cause fever and dizziness, bladder problems and fatigue - is increasing everywhere in the world. The bacteria which causes this awful disease is carried in ticks - in their saliva. 'So I travel with a tick remover - a small hooked device that works by gently lifting and twisting the tick out of the skin without pressure.' (Tick remover, £4.99, lymediseaseaction.org.uk)

My response
All excellent advice.
Stella I wish I had read your advice years ago.

I did not know that Lyme Disease could be caught in the UK I had thought it unique to USA. It took 5 doctors and 3 rheumatologists 4 years to diagnose me.

I had been diagnosed with Fibromyalgia, ME/CFS, Arthritis, Musculo Skeletal Disease, Polymyalgia Rheumatica as my symptoms deteriorated and then a chance course of antibiotics led GP to suspect Lyme Disease.

Following ILADS guidelines on long term antibiotics I have my health and my life back.

Where is the awareness?

When my MP Anne Milton wrote to ask HPA that question a couple of years ago the reply came back that they had updated their website!! What use is that if there is no public awareness.

Where I live in Guildford I am in touch with 23 people diagnosed with Chronic Lyme disease the latest case like me was diagnosed with PMR and then Parkinson's last Christmas he has now tested positive for Lyme Disease and already responding to antibiotics.

A terrible quote from the IrishTimes can be seen here

'Thanks to all of you who responded to the column on ticks and Lyme disease some weeks back. One reader told me of an effective way to remove ticks from the skin, courtesy of her father who survived the trenches of the first World War. Light a match and blow it out. Apply the still hot head of the match to the protruding tick, which will promptly withdraw its head from under the skin'.

My response by e mail to the newspaper.

I take great exception to the flippant and misleading comment in your recent article. You do your public a gross mis service with this comment. Your original article was reasonably written and you did quote ' Dr Paul McKeown, of the Health Protection Surveillance Centre. “The entire tick, including any mouthparts which might break off, should be removed with a tweezers by gripping it close to the skin.' which is currently the correct advice following over 19000 research articles on Borrelia infection clearly not known by the soldiers in the trenches during the first World War.

By shocking the tick in any way either by heat, Vaseline, or grabbing the tick, risks the tick regurgitating it's stomach contents into you, if it is infected.

As well as Borrelia there are many other infections a tick can carry including Bartonella, Babesia, Ehrlichia, Anaplasma, Mycoplasma and others most of which can cause serious health problems alongside a Borrelia infection although rarely tested for in the chronically sick patient by our Health Authorities.

You have barely scratched the surface of the problems for patients who contract these tick borne diseases, please write something to contradict your latest error of judgment at the very least.

I am in touch with a number of patients from Ireland with Chronic ill health following a tick bite some travel to USA to see World experts in this field.

This is a link to a blog I follow which is trying to get the Health Authorities to take note of the problems http://ticktalkireland.files.wordpress.com/2010/08/stats-analysis-lyme-ireland.pdfhttp://ticktalkireland.files.wordpress.com/2010/08/stats-analysis-lyme-ireland.pdf

I was sent this link from a Canadian Lyme patient who was infected in Ireland
http://www.ncbi.nlm.nih.gov/pubmed/9360424
'Data of Lyme disease seroprevalence has been established in European patients or at-risk populations and in blood donors or control subjects'. 'The range of antibodies to B. burgdorferi in blood donors or control subjects shows the highest spikes in Ireland 15%'

This is also mentioned on Tick talk Ireland.

I have long been critical of our Media in the UK for their lack of wanting to get involved in the controversy surrounding diagnosis, blood tests and treating of Lyme Disease, but I can not forgive them their lack of at least wanting to raise awareness amongst the general public, I was pleasantly surprised at your original article but hope you do something to rectify your latest misleading quote.

I live in Guildford Surrey and have suffered from Lyme disease since 2003 it took 5 doctors and 3 rheumatologists 4 years to diagnose me. My GP suspected Lyme Disease after a chance course of antibiotics improved my symptoms although I had attended surgery at times of bites, bulls eye rashes summer flu' and migrating arthralgias.

As my symptoms deteriorated I was diagnosed with Fibromyalgia, ME/CFS, Arthritis, Muscle Weakness, Musculo Skeletal Disease, Polymyalgia Rheumatica and finally Lyme Disease. I was retired early from the Civil Service on Ill health grounds, at my worst I had difficulty standing and walking across a room and could not walk up or down stairs properly for 3 1/2 years now after long term antibiotics following alternative guidelines by International Lyme and Associated Diseases society rather than the restrictive HPA/IDSA guidelines I am recovered, I have no pain, no disability and can garden and cycle again.

My experience is like so many others whose doctors fail to catch this awful disease at the time of the tick bite when it is so easily treated although on a longer and higher course of antibiotics than NHS would give, as several patients have found to their cost. My local surgery is now treating a number of patients in the early stages of tick bite but also several others whose illness has become chronic like mine.

I now know of 23 patients in the Guildford area with Chronic Lyme Disease the latest case like me was diagnosed with PMR and then Parkinson's last Christmas he has now tested positive for Lyme Disease and on antibiotics his symptoms are improving.

There is so much more that our media could do to help raise awareness of this emerging disease but also bring into the open the controversy that surrounds this illness the best place to start your education would be by reading some of the information on www.lymediseaseaction.org.uk website

There are an increasing number of doctors and consultants now in the UK supporting ILADS way of treating, some because they or their family member have become infected and they have had to travel to the USA to see the expert Lyme Doctors.

'Of course, you can never replace the value of talking with patients.' It is the listening to patients that our doctors have lost the art of.

My greatest concern is for the children who are the most vulnerable and the hardest to get adequate treatment for, if you read some of the e mails I have had from parents of children with Chronic Lyme Disease it would break your heart.
------------------------------------------------
So much more needs to be done and the media could do so much more to raise public awareness and save countless people from this awful disease.

Monday, 16 August 2010

TRAGIC DEATH CAUSED BY UNDIAGNOSED LYME BORRELIOSIS

This is a truly tragic case of a little boy with Lyme Disease whose doctors failed to diagnose him and then he died. This was not a case of Acute Lyme Disease the boy had been ill three years and so was suffering with Chronic Lyme Disease.

My heart goes out to the Linus' family and thank them for their efforts to ensure no other family will lose a child so un necessarily with a treatable illness such as Lyme Disease.


Below is a translation from the Swedish newspaper original can be found here

Top Photo caption: Linus parents, Lennart and Jeanette Wallberg, report the doctors who missed their son's illness. "We are doing everything that others will not be part of the same thing."

Boy's photo caption:Linus Wallberg fought against his illness a long time - eventually he died, aged 15, of Lyme.

Main body:For several years fought Linus Wallberg, 15, to their pain. Last spring, he died of neurological Lyme disease at home in the family's couch. Now they report three family physicians to Health and Medical Treatment.- I have no confidence in care longer. We are doing everything that others will not be part of the same thing, "says Lennart dad.Linus Wallberg had been sick more than three years.

On several occasions he had been given emergency leave to the emergency department in Nyköping with all-over body pain, severe nausea, and vomiting. But when the family rushed to the hospital were sent home again, Linus usually diagnosed with stomachflu or influenza.- "We believed in what the doctors said. Nobody wants to believe that your child is seriously ill, "said Linus' Mom Jeanette Wallberg.

Doctors dismissed the fears
One of the doctors gave Linus a diagnosis of asthma stomach [needclarification on dx] and said that his pain would disappear by itself overtime. And when Jeanette told the doctor that she was worried that she would one day find her son dead the doctor laughed and dismissed her concerns.

But Linus was seriously ill. Early on the morning of February 17 last year,when Dad would get Lennart Linus, he found him dead in the family's couch.

Autopsy report showed that Linus had died from complications of neuro-Lyme.

- To my knowledge, none of any doctors with Linus tested him for Lyme. Had they taken the spinal cord samples, and gave him antibiotics Linus, he would have lived today. But it felt like they did not take us seriously, "says Jeanette.

Important to the case investigated Linus' parents have now sent three doctors to the health care committee and Responsibility. One of them is Chief Diana Born Welff Stein, who is medical director of children's hospital in Nyköping.- It has stood in the records and they saw symptoms Linus and did not automatically suspect neurological Lyme disease, otherwise they would have investigated and dealt with Linus. But this is a very difficult diagnosis to make, "she says.

Have you failed in the treatment of Linus?- Yes of course I just had to say when a child dies from a treatable disease. I can understand that the family chooses to report and it is important that the case be investigated, "said Diana Stein Born Welff.

But it is of little comfort to Linus family.- They did not believe us. We will never get over this, but if notification helps other parents to avoid going through the same thing [so there is always something], "says Jeanette Wallberg.

Grey box:Facts - Borrelia Less than one in ten people who suffer from Lyme borreliosis may have neurotoxicity. Usually noticeable symptoms show between one to two months after the tick bite, but time may vary from just a few weeks up to six months.
Usually it begins as a skin infection, many notice no change in skin before they get symptoms from the nervous system. Neuro-borreliosis is common among children than adults.(Source: www.1177.se)

two other articles were here and here

Sadly doctors not taking patients seriously when they complain of the symptoms of Lyme Disease is all too common as the several thousand patients who subscribe to Eurolyme will testify to.

Sunday, 15 August 2010

TICKBITE-LYME DISEASE-MOTOR NEURONS, PARKINSON'S, MULTIPLE SCLEROSIS



a2zmedia 23 August 2009
This video clip was put together to demonstrate to Norwegian broadcasters what problem Lyme Disease is and how it can affect your life if not treated. For more information about our project, please go to http://www.lymefilm.com/


Below is a translation from a newspaper article on Eivind's struggles not just with Borreliosis but with his medical Authorities.

The original article and further video can be seen here

Lived at ten years of death sentence after the tick bite
The state says Eivind Markhus (45) has the deadly disease ALS. Although he is convinced that a tick bite have linked him to the wheelchair.
ASLE HANSEN -->

Living in a wheelchair: Eivind Markhus (45) was formerly an active player on Strømsgodset A-team. This video reportage made a few weeks before the trial in summer 2007. Video: Anja Nygren Lohne
Borreliosis Lyme
The most common tick-borne disease is Lyme borreliosis. It is caused by a bacterium. The disease should be treated with antibiotics. There is no vaccine against borreliosis. • So far this year is 59 Norwegians diagnosed with severe Lyme borreliosis. • In 2007, 328 people registered with complicated borelliasykdom, in 2008 346 persons and 273 persons in 2009. • Most cases of this tick disease occurs in coastal areas on both sides of the outer Oslofjord, Telemark and Agder counties. Kilde: MSIS og Folkehelseinstituttet Source: MSIS and Public Health
annonse


Communicate via PC: The disease has weakened speech and Eivind Markhus communicate better through e-mail.



In the summer of 2007 lost Eivind Markhus compensation case he had filed against the state by Pasientskade Committee in Oslo District Court. The court did not agree that a failure treated neuro-borreliosis after tick bites have linked him to the wheelchair. Now the 45-year-old ready for the rematch in the Borgarting Court of Appeal, the appeal is scheduled in late June 2011. - Now, health-Norway to accept that I have Borrelia and ALS, "says Markhus the way he does best, via e-mail.


Former football player Within a few years the 45-year-old from a well-trained athlete, who played 13 First Division appearances for Strømsgodset in 1987, to be completely paralyzed and completely dependent on the wheelchair. Norwegian doctors have given him a diagnosis of ALS (amyotrophic lateral sclerosis), a nerve disease with fatal outcome. Foreign experts believe he has an active Borrelia infection in the body that mimic ALS. Eivind Markhus think he would have had a different health situation today if the Norwegian doctors earlier had put him on høydosebehandling with antibiotics for a long time.
Denied compensation Director Rose-Marie Christiansen in Pasientskade Committee say they maintain their argument from the court process where the board argued that it is "unlikely that the patient's disease, ALS is caused by borreliosis. If the disease still be triggered by tick bacterium, said Pasientskade Committee that the hospital acted properly regardless of the basis of available knowledge at that time. Eivind Markhus was given three, four years left to live in 2001, but has made the death sentence to shame. He lives now in the tenth year of his ALS diagnosis, without the need for breathing assistance, which is very unusual. Markhus am sure that antibiotic treatment he got against neuro borreliosis in the USA in 2003 slowed the disease and saved his life. He is optimistic ahead of the appeal, referring to an article in the Journal of the Norwegian Medical Association in May 2008 where it is established that Borrelia in rare cases can cause an "illness resembling amyotrophic lateral sclerosis. - When the experts of the Respondent now admits that Borrelia can mimic ALS, and even wrote a fagartikkel about it, I stated. This did not believe these experts last time when I said this, " From 2000 until today, the Norwegian Patients (NPE) received 28 cases concerning delayed or incorrect treatment of Borrelia / borreliosis. . It is only given under the two cases, while 26 cases are rejected.

ALS is referred to as Motor Neurons in the UK.

I have posted before about Dr Martz incredible story recovering from ALS or Motor Neurons diagnosed by John Hopkins Neurologist but found to be caused by Borrelia, Lyme disease. His presentations at the 2010 London ILADS conference were amazing as were his findings from the clinic he opened where he treated patients with Multiple Sclerosis, ALS/Motor Neurons and Parkinson's. Soon to be available on DVD. For earlier posts on Dr Martz put Dr Martz into the search box in the right hand column or click here

With my experience and knowing about Dr Martz findings I was able to encourage a local man who had been diagnosed with Polymyalgia Rheumatica like myself and then later Parkinson's, to see a specialist in tick borne diseases. He has now been diagnosed with Lyme Disease -already he is responding well to antibiotics.