ALZHEIMER'S DISEASE - A NEUROSPIROCHETOSIS

Alzheimer's disease - a neurospirochetosis. Analysis of the evidence following Koch's and Hill's criteria.

Judith Miklossy

• Correspondence: Judith Miklossy judithmiklossy@bluewin.ch

Journal of Neuroinflammation 2011, 8:90 doi:10.1186/1742-2094-8-90

Published: 4 August 2011

Abstract (provisional)

It is established that chronic spirochetal infection can cause slowly progressive dementia, brain atrophy and amyloid deposition in late neurosyphilis. Recently it has been suggested that various types of spirochetes, in an analogous way to Treponema pallidum, could cause dementia and may be involved in the pathogenesis of Alzheimer's disease (AD). Here, we review all data available in the literature on the detection of spirochetes in AD and critically analyze the association and causal relationship between spirochetes and AD following established criteria of Koch and Hill. The results show a statistically significant association between spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral techniques recognizing all types of spirochetes were used, or the highly prevalent periodontal pathogen Treponemas were analyzed, spirochetes were observed in the brain in more than 90% of AD cases. Borrelia burgdorferi was detected in the brain in 25.3% of AD cases analyzed and was 13 times more frequent in AD compared to controls. Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum, T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi were detected using species specific PCR and antibodies. Importantly, co-infection with several spirochetes occurs in AD. The pathological and biological hallmarks of AD were reproduced in vitro. The analysis of reviewed data following Koch's and Hill's postulates shows a probable causal relationship between neurospirochetosis and AD. Persisting inflammation and amyloid deposition initiated and sustained by chronic spirochetal infection form together with the various hypotheses suggested to play a role in the pathogenesis of AD a comprehensive entity. As suggested by Hill, once the probability of a causal relationship is established prompt action is needed. Support and attention should be given to this field of AD research. Spirochetal infection occurs years or decades before the manifestation of dementia. As adequate antibiotic and anti-inflammatory therapies are available, as in syphilis, one might prevent and eradicate dementia.

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It is good to see further research by Judith Miklossy to visit her website click here and to read the full paper click here

I have posted about Alzheimer's before here of course those of us who have been following the information about Lyme disease are already aware of the work of Alan Mac Donald interviewed in Under Our Skin Documentary visit their website here or watch a Turn The Corner Foundation U Tube where Alan Mac Donald was interviewed. here

MISTS AND MYTHS SWIRL AROUND INVERNESS

Letter to the ME/CFS/FM community in response to comments under the heading "Lyme disease - let’s dispel the myths", by Dr D. Ho-Yen, October 2006 ME Essential, published by the ME Association, UK.

Mists and Myths swirl around Inverness
By Annie Drummond

Scotland is a land of mists, mountains, and malicious ticks. Sorry Scotland, I love your beautiful country and your hospitable, friendly people, but it is where I was bitten by a tick which gave me Lyme disease (also known as borreliosis.)
Several researchers have found that many patients diagnosed with myalgic encephalomyelitis (ME), Chronic Fatigue Syndrome (CFS), Fibromyalgia (FM) (1,2,3) and Multiple Sclerosis (4,5,6,7) have borreliosis, as do a certain proportion of psychiatric patients (8,9,10).

Scotland has its very own Lyme diagnostic laboratory at Raigmore Hospital in Inverness, while the rest of the British Isles relies on one reference laboratory at Southampton in England. At Raigmore, Dr D. Ho-Yen is the chief microbiologist and has been interested in ME for many years. In fact, he published the first "How to treat ME" book in 1985. He maintains that only a small minority of ME/CFS patients could have Lyme disease as the cause of their illness (11). But is he right?

Lyme disease was brought to worldwide attention in 1975, but its history goes back further (12). However, Ho-Yen in 2006 still feels that he must call Lyme an "emerging disease". Perhaps the pandemic levels (13) that have now been reached have allowed the illness to "emerge" from the cloak of silence that has covered the spread of the disease in the UK. Yet as far back as 1989, i.e. over 17 years ago, the World Health Organisation was aware that the whole of the British Isles, plus Scandinavia, Germany, Austria, half of France, California, areas South of the Great Lakes, and other areas, were endemic for Lyme disease (14).

Ho-Yen has recently admitted that his laboratory missed 33% of Lyme cases (15). He retested old serum samples for the year 2003 to 2004, using different methods of interpretation, and found that previous negative tests were becoming equivocal or strongly positive. One is left to speculate how many suspected victims over the last 30 years have been retested, if any, using these new criteria, and how many patients have been recalled for further investigation. It is admirable that Ho-Yen has published these results, but they sit uncomfortably with his latest pronouncements on the ME/Lyme question.

The ME charities, Action for ME, the ME Association and the TYMES Trust, have relied on Ho-Yen to inform the ME community on the relationship between Lyme and ME in the October and November 2006 issues of their recent magazines. Many scientists and commentators, while not disputing his personal findings and his integrity, would wish to respond to some of the statements he has made in these articles.

There are 6 so-called "myths" that Ho-Yen identifies as current in the Lyme world; each one will be discussed in the light of knowledge available. A very different picture from the one he paints will emerge.

Myth 1: The Internet has the best information on Lyme disease. Verdict: True. This is not a myth. The Internet is the source of millions of archived peer-reviewed scientific reports. We all use the Internet; most of us would be lost without it. The data is more accessible and available to be used more readily; researchers no longer have to physically retrieve dusty documents from medical or university libraries.

To be fair there is a lot of rubbish on the World Wide Web, but it is the easiest place to look for the very latest research. Ho-Yen suggests that it is almost impossible to discern the rubbish from the good material, and at first it can be difficult. However, a recent peer-reviewed paper from 2005, authored by several of the most experienced doctors and scientists working in the Lyme field (16), gives a very useful overview of the data available on the Internet and how this relates to their clinical experience.

Myth 2: Doctors are ignorant of Lyme disease.
Verdict: True. This is not a myth and is definitely true in Britain. Please ask your GPs, whether rural or urban [(Richmond Park, as well as other London parks, has been found to harbour Lyme-carrying ticks (17)] if they have heard of Lyme, or of borreliosis, or of the latest infection rates being reported in Europe?

Most doctors, and members of the public too, think of it as an American disease, (that is, if they have heard of it at all!). But the increasing number of cases across Europe is a cause of concern. For example, in Holland (18), the incidence of the "bull’s eye" rash, Erythema Migrans, (EM), which is pathognomic for Lyme disease, was estimated at 39 per hundred thousand in 1994, which doubled to 74 per 100,000 in 2001, and tripled to 103 per 100,000 in 2005. In southern Sweden (19), the mean annual incidence rate in 2005 was 464 cases of EM per 100,000 inhabitants. The incidence was significantly higher in women than in men, 505 and 423 cases per 100,000 respectively.

These are epidemic rates of infection. Britain’s approximate incidence figures, quoted from the Health Protection Agency (20) are no greater than 1.1 per 100,000. It is difficult to rationalise figures that are 2 orders of magnitude lower than those in Holland for example. The island status of the UK will not have protected it from migratory birds, which are well-documented carriers of Lyme-infected ticks (21,22,23,24). It is also not necessarily true that rural doctors are aware of Lyme disease. There have been several cases in my own rural area of the so-called "well recognised" EM rash being labelled as ringworm and others have been told that they were suffering from shingles or allergies. How many GPs will recognise the condition Acrodermatitis Chronica Atrophicans (25), which is a skin disease associated with Lyme?

Ho-Yen has stated himself that the number of cases in Scotland
is underestimated by as much as a factor of 1 in 10. The point is
• if Lyme is continually labelled as one of "those obscure foreign diseases" doctors will not even bother to test for it. The head of the UK’s Lyme reference lab continues to inform the medical world that the disease is rare in Britain (26) and that positive tests are to be ignored in non-endemic areas.
With the exception of Scotland, Lyme is yet to be made a notifiable disease in Britain. Currently the Health Protection Agency (HPA) website (20) gives the estimated incidence as 1000 to 2000 additional cases per year. This is to be added to the figure for the lab reports for the year, which was 585 cases in England and Wales. The true incidence is unknown.
If the laboratories testing for Lyme are not aware of the many reasons for negative antibody tests in the presence of the disease, and do not inform consultants that the patient could still have Lyme, despite the serology being negative, then the situation is perpetuated.

Myth 3: Most ME is Lyme disease.
Verdict: Open. But it is likely to be true for a high proportion of ME/CFS/FM cases, and not a myth at all, according to many Lyme specialists (27,28,29). Most open-minded people agree that not all cases of ME/CFS/FM would be due to Lyme but there are now thousands of people with these conditions who are finding out that they have Lyme borreliosis or other tick-borne infections.
Recent research in the UK points to the fact that biochemical and immunological markers are very similar in Lyme and ME. In a presentation to the Edinburgh ME group in September 2005, Professor John Gow of Glasgow University stated that gene expression regulation in those with ME is identical to that seen in Lyme patients.

In contrast to Ho-Yen’s assertion that the EM rash of Lyme is an easily recognised indicator, half of those bitten do not show the rash and those that do may have atypical presentations (30,31). Seventy percent of Lyme patients who responded to a poll by the Internet group EuroLyme stated that they were previously diagnosed with ME/CFS. The UK government has stated that Lyme can cause Chronic Fatigue Syndrome, but has not broadcast this statement as an important issue. While there is a heated dispute between specialists who believe that Lyme infection is easily cured by a short course of antibiotics and those who say it persists, nevertheless, both sides agree that the "post Lyme syndrome" often presents as fibromyalgia and chronic fatigue syndrome. However, many studies have shown that there is persisting infection, and that this is treatable (32,33,34,35).

Late Lyme is also hard to distinguish from many other diseases, and is more often under-diagnosed than over -diagnosed (36,37,38,39). Most importantly, although Ho-Yen has listed cardiac, joint and skin manifestations of Lyme, he has omitted to mention the devastating neurological symptoms manifest both in ME/CFS/FM and Lyme (40), unless he is implying that the term "fatigue state" encompasses all of the central and peripheral nervous system deficits that may occur in neuroborreliosis, (e.g. encephalopathy, facial paralysis, vertigo, light and sound sensitivity, tinnitus, meningitis). Ho-Yen fails to state the source of his belief that only 10% of late Lyme patients show this "fatigue state". Most people with late Lyme are crippled by a "fatigue state", as are most people with ME/CFS/FM.

Ho-Yen contends that only 5% of Scottish ME patients studied by him had Lyme. However, he does not state which criteria were used for diagnosing Lyme (as mentioned earlier, blood tests cannot be relied upon to rule out Lyme.) Neither does he mention the length of time of follow up of these patients, despite the fact that Lyme, like ME, is known to be a relapsing-remitting disease (41).

Myth 4: Antibiotics can cure Lyme disease.
Verdict: True. This is not a myth. Antibiotics and other drugs in combination or in series can cure many cases of Lyme disease. The treatment needs to be under the supervision of an experienced Lyme specialist and sometimes must be carried out for months or even years.
According to Ho-Yen "the very need for such prolonged treatment with antibiotics suggests that the success rate is not good". Applying his criteria we would refuse to treat TB patients and leave them to their misery. The longer that Lyme disease remains untreated or under-treated, the worse the potential for permanent damage. In some cases, antibiotics may merely lessen the progress of the disease. However Lyme patients across the world who can access appropriate medical care may recover their health or at least have partial remission. (42).

Ho-Yen states "Indeed, it is difficult to separate the natural improvement that occurs with chronic disease from the effects of antibiotic treatment". His solution is to treat ME/CFS as if it were a viral illness, but this is not appropriate knowing the bacterial causation of Lyme. Viruses and bacteria are quite different biologically, needing completely different treatment approaches.

Myth 5: All laboratories produce dependable results. Verdict: False. This is perhaps the only myth on which we have a point of agreement: if all laboratory tests were reliable, Ho-Yen would not have published his 2005 paper, saying that his lab had had to reinterpret a third of its own tests.
Two comprehensive reviews of the accuracy of standard tests for Lyme, in Europe (43) and the US (44), showed that the same sample of blood could test positive or negative depending on which lab it was sent to, or even if tested again in the same lab. Worse still for those with suspected Borrelia infections, the Polish National Institute of Health has reported that patients with low or negative antibody levels have tested positive using other more sensitive techniques. Specific DNA capture and culturing showed that there were live bacteria in their body fluids (45) indicating that those with negative blood tests could be even more ill than those who have circulating antibodies. The problem of co-infections with other organisms is another complicating factor.

In 2003 Dr Lowes, head of microbiology at Southampton, where the Lyme reference laboratory is housed, promised that an internal audit would be conducted into the lab’s operations. He made that promise following complaints that inaccurate testing and interpretation procedures were being carried out at the Lyme lab. The results of that audit have never been made public to this day.

We agree with Ho-Yen that commercial motives could compromise the quality of lab diagnostics. However, nowhere is this more reflected than in the vested interests of the Lyme committee of the Infectious Disease Society of America (IDSA), which as mentioned below, is currently the subject of an anti trust investigation by the Attorney General in Connecticut, where there is one of the highest rates of Lyme infection in the world.

Dr Susan O’Connell, the head of the UK’S Lyme Reference Laboratory, was a consultant to that committee, and both she and the Department of Health promote its viewpoint as a model for diagnostic and treatment policy in this country. Ho-Yen’s recent article demonstrated that he too has adopted much of that view.

Myth 6: There is misleading expert comment
Verdict: True. This is definitely not a myth. As alluded to earlier, in November 2006, Connecticut Attorney General Richard Blumenthal ordered a Civil Investigative Demand under the anti-trust laws concerning the recently published guidelines produced by the Lyme committee of the IDSA. This group of 14 scientists have been the most vociferous in stating that Lyme disease is never chronic and that treatment, beyond a few weeks of antibiotics, is not indicated. (46).

In a press interview (47) Blumenthal voiced his fear that the guidelines were being used by the powerful US insurance industry to deny health coverage to Lyme patients. In addition to the close ties with the insurance industry held by some members of the committee, a number of them have significant conflicts of interest due to their involvement with companies producing Lyme vaccines or test-kits.

Two of the members, Gary Wormser, lead author of the guidelines, and Allen Steere, admit to receiving money from the multi-national Baxter corporation, which is currently developing a vaccine for the European market. A restrictive approach to Lyme diagnosis serves the interests of vaccine manufacturers as it can cover vaccine failure. It is also difficult to conduct clinical testing of vaccines without using antibody tests to rule out the disease. However, all the evidence indicates that the tests are not sensitive enough to be used in this way. The end losers are the patients.
Clinicians associated with the International Lyme and Associated Diseases Society (ILADS) oppose the IDSA, and treat thousands of patients in the US and across the world with long-term antibiotics if necessary (48).

How many Infectious Disease experts in the UK know about the many reasons (49) why both chronic and early Lyme disease can show no antibodies in blood tests (seronegative)? Why does the Health Protection Agency’s Lyme Reference Laboratory inform doctors that a negative ELISA test rules out Lyme in all but the earliest stages, when there is documented evidence (50) that this is not the case?

Conclusion
A combination of the facts above, and the lack of openness surrounding the topic of Lyme borreliosis, has left many thousands of Lyme patients undiagnosed and untreated.

There are many people who suffer for long periods of time, decades in some cases, who have never been tested for Lyme or who have had negative tests. Years later, they find that the antibodies can be seen in their blood or that other more precise tests reveal the DNA of borrelia in their bodies.

A Lyme diagnosis means virtually nothing here in Britain since there are very few doctors who know how to proceed. The persistence of borrelia infections (51,52) means that antibiotic therapy must be extended in order to reduce the bacteria to a low enough level for the immune system to take over.

There is also the problem of co infections, with growing evidence that many Lyme patients may be infected with anaplasma, babesia, bartonella and mycoplasma species (53,54,55,56).

If the patient has been ill for years, thousands of generations of bacteria will have multiplied and spread throughout the body. They may then lie dormant until the immune system is challenged by other events - perhaps by toxicological insult from organophosphates and other poisonous chemicals in the environment, or by catastrophic life events such as automobile accidents etc.

In other patients, the bacteria may rampage continuously and may cause ME/CFS/FM, heart disease, arthritis, MS, ALS, thyroid disease, and visual defects. They may endure pain and vertigo and brain fog, arthralgia and arthritis, endocrine problems, endometriosis, irritable bowel and bladder disease, skin rashes, rapid heart beats, heart failure, hearing loss, seizures, temporary or permanent paralysis, muscle spasms, tendonitis, memory loss and panic attacks. There is even some evidence to suggest that borrelia infection may lead to bipolar disorder, schizophrenia and Alzheimer’s disease (6, 57,58).

On and on the list goes, making many doctors certain that it is an impossible mixture of symptoms to have and therefore must be all in the patient’s mind. Victims of Lyme disease, like those with ME/CFS/FM, have consequently been called over-emotional yuppies with personality problems, stressed-out under-achievers, or over-anxious and depressed individuals.

Now Ho-Yen has exacerbated this situation by accusing British Lyme patients of hysteria. Lyme victims are hysterical, and demand antibiotics. They are hysterical, and say they know more than doctors. Worse still, people with ME/CFS/FM are catching the hysteria, and phoning him up in hundreds to ask if they have Lyme.

Patients with ME/CFS/FM are advised to beware of this hysterical label and to remember how the two hundred or so nurses, doctors and patients in the Royal Free Hospital came down with a nasty epidemic of so-called "hysteria" in 1955. Many of them never recovered from the disease, and never recovered from the stigma attached to that label.

Over the last 30 years Lyme patients have received the same sort of treatment as people with ME/CFS/FM, - ridicule, contempt, disbelief, denial of investigations and treatment, and the ignominy of a psychosomatic label.

Unfortunately, over the last 20 years, there has been a concerted effort by a small but very influential group of psychiatrists to inundate both the scientific literature and the ordinary press with tales of "psychosocial" causes of ME/CFS/FM (59).

We are all being confused by myths, according to Ho-Yen, but is it possible that he has himself been myth-taken? His suggestions that "fatigue" is only shown by the minority of Lyme patients; that antibody tests can rule out the disease; and that chronic Lyme responds to palliative rather than antimicrobial therapy, are all unproven. They are especially unhelpful in the present situation.

Now the common sense of decent people and the integrity and honesty of certain doctors and scientists, such as Kenneth Liegner (60), will unearth the truth about the causes of ME/CFS/FM. These may be multiple. However, in every case, patients are entitled to full information about their diagnosis and prognosis.

Ho-Yen concludes with "In the end, it is a matter of what makes you better" and urges patients to take responsibility for their own illness. We contend that ME/CFS/FM patients struggle heroically to cope with their condition and are forced to take responsibility for their illness every day. Patients will never get better until there is clarity (61) over the issues surrounding Lyme, ME/CFS/FM and other chronic infections.

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(56.) Nasralla, M., Haier, J. Nicolson, G.L. Multiple mycoplasma infections detected in blood of patients with CFS and/or Fibromyalgia. Eur J Clin Microbiol Infect Dis. 1999; 18: 859 - 65
(57.) MacDonald, A.B., Miranda, J.M. Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987; 18(7): 759 - 61
(58.) Miklossy, J., Khalili, K., Gern, L., Ericson, R.L., Darekar, P.,
Borrelia burgdorferi persists in chronic Lyme neuroborreliosis
and may be associated with Alzheimer disease. J Alzheimers
Dis. 2004; 6(6): 639 – 49
(59.) Document prepared for the Countess of Mar by Malcolm Hooper, Emeritus Professor of Medicinal Chemistry, University of Sunderland UK, in collaboration with members of the ME community. The mental health movement: persecution of patients? A consideration of the role of Professor Simon Wessely and other members of the "Wessely school" in the perception of myalgic encephalomyelitis (ME) in the UK. Background briefing for the House of Commons Select Committee. December 2003.
(60.) Kenneth B. Liegner, M.D., P.C. Remarks before the NYS Assembly Committee, chaired by Richard Gottfried. Albany, 2001, November 27th.
(61.) Stricker, R.B., Lautin, A. The Lyme Wars: time to listen. Expert Opin Investig Drugs 2003; 12(10).

_________________________

Not a lot has changed in how patients are left undiagnosed and undertreated since this was written although there has been considerable research published that supports ILADS views. This is still ignored by our so called experts as they continue to put their personal spin when they publish papers that illustrate their view rather than a comprehensive view of all the research.

NEW ME/CFS AND LYME DISEASE RESEARCH

New research has just been published, highly significant for those with Chronic Lyme disease and ME/CFS.

Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome

Can be accessed through Plos One click here


Abstract Top

Background
Neurologic Post Treatment Lyme disease (nPTLS) and Chronic Fatigue (CFS) are syndromes of unknown etiology. They share features of fatigue and cognitive dysfunction, making it difficult to differentiate them. Unresolved is whether nPTLS is a subset of CFS.

Methods and Principal Findings

Pooled cerebrospinal fluid (CSF) samples from nPTLS patients, CFS patients, and healthy volunteers were comprehensively analyzed using high-resolution mass spectrometry (MS), coupled with immunoaffinity depletion methods to reduce protein-masking by abundant proteins. Individual patient and healthy control CSF samples were analyzed directly employing a MS-based label-free quantitative proteomics approach. We found that both groups, and individuals within the groups, could be distinguished from each other and normals based on their specific CSF proteins (p<0.01). CFS (n = 43) had 2,783 non-redundant proteins, nPTLS (n = 25) contained 2,768 proteins, and healthy normals had 2,630 proteins. Preliminary pathway analysis demonstrated that the data could be useful for hypothesis generation on the pathogenetic mechanisms underlying these two related syndromes.

Conclusions

nPTLS and CFS have distinguishing CSF protein complements. Each condition has a number of CSF proteins that can be useful in providing candidates for future validation studies and insights on the respective mechanisms of pathogenesis. Distinguishing nPTLS and CFS permits more focused study of each condition, and can lead to novel diagnostics and therapeutic interventions.

TIME TO EDUCATE OUR NHS CONSULTANTS

I don't generally post personal stories of patients with Lyme disease but this one particularly touched me.

With permission I am only going to post a small section of it but do go to the full details here

Apart from highlighting patients' struggle with the disease and getting a diagnosis for their multi system problems it so highlights the crass comments our 'esteemed' medical professionals come out with, it is time they were taken to task over their behaviour and held to account for their comments to patients when clearly they are not informed of the complexities of Tick borne illness. Lyme Disease and the many co infections that can also affect us.

***************************************************************************** the ----establishment had so badly let me down and basically left me for dead at 36 years old !!

I went to London to the Infectious Disease clinic and the journey itself was hard as I am so poorly.

We were seen and told from the offset that, "we were there to listen to his opinion and that we would not be discussing Lyme until we had heard what he had to say" and i felt like a naughty schoolgirl that had been pulled up in front of the headmaster and was really tired of being treated so awfully when I was sick .

He asked about where I had traveled to tropically and then in Europe and then in the UK.... I reeled of the list of many places as I had travelled to all of these in my youth through bar work.

He then said "well you haven't been anywhere that is tick endemic and so its not Lyme" ..I, this time, had no patience to argue ,as the last time had taught me I was banging my head up a brick wall so I just sat there and silently disagreed with him in my head.

So he preceded to examine me which was very different to the previous 20 or so examinations I'd had by other doctors...and consisted of my lymph glands down my body and my spleen....he had said he would check my eyes as I was wearing the sunglasses but after he had done his tests he told me to go back and sit down and did not again look at toenails,rash or the eyes .

My husband then played him the video footage of me and my attack ...he watched about 10 seconds of it and said" that's enough "and then showed him the positive test results and he asked ..".who done these..."my husband replied "Igenex" and he said "well i can get a positive result for any test I want if I send it to the right place "and then told me that the "Americans are all mental and blame every symptom they have on Lyme" ....he said "don't get fixated with Lyme "...

to which I replied "I'm not fixated ..its just I have every symptom ..even definitive ones of Lyme ..positive test results that are non biased .. and the most important thing is ...if its not then what is it ??..

because I have seen nearly 20 doctors now ...who either tell me they don't know.. or we can tell you what its not ...or its a headache.... or a stiff neck ... or I may never get a diagnosis for this...or the last doctor who had the cheek to tell me there was NOTHING wrong with me...or its all in your head ....so believe me, I'm not fixated, I just haven't even been given anything else that it realistically could be ...and the fact that this is capable of evading normal routine tests, which is what's happened with me is surely proof enough to give antibiotic treatment a go

""He then said that, as this is an infectious disease clinic then he was going to run 3 tests of diseases that are of African nature..... and although the timing is out as to when I should have got ill with these after my return from Africa..... and the chances of me having them are next to none... he needed to rule them out anyway ....

to which I agreed ,but wondered why this wasn't checked for in the hospital on my admission on that first night ..as they were made fully aware of the fact we had not long returned from a tropical country and they did tell my husband that all possibilities had been checked for ...

Then we had the punchline delivered to us..in a very sinister way indeed ... considering he had just told me that if he wanted to ,then he could get a positive result for any test if he sent it to the right place.

..one of the tests that he was running was for an African borne disease that's VERY ,VERY RARE.. but the only treatment for it is to pump arsenic into your blood ..which results in 3 out of 5 death rate anyway...

I couldn't believe it ...one of the possible options that he'd managed to come up with rather than even acknowledging there is even a slight chance that it might be Lyme was of a rare disease that you had hardly any chance of surviving from the treatment..

.and it had sounded more like a threat ...

and I wondered why he had no worries about putting arsenic into me but I was having such a tough time getting antibiotics ..

I had also, before I'd found Lyme gone through, like I said every disease going ..and had studied African diseases especially hard, as we had spent a lot of time in Africa in the last two years and the symptoms and timing didn't match any of the diseases. .

So I'd agreed to his tests (or death sentence )that he had given me... and then I continued talking about Lyme .

This is when I believe ...he used the sentence that it had taken the doctors all these months to come up with ...of how to get around this situation, without actually telling me they would not treat me long term.

He said I am going to put you on a course of doxycycline for 3 weeks..if you get better then it was Lyme and you are cured...if not then it wasn't Lyme.

Here's how this interprets ...3 weeks course of doxycycline does treat and cure Lyme disease if caught in the early stages ..ie after the bite of an infected tick ..or the trademark rash being present ...after that if left untreated it grows in your body and will eventually turn into stage 2 which is harder to treat... and if still not detected it will go to stage 3 ...when it crosses the blood borne barrier and enters the brain and internal organs and this is where I am at and is extremely difficult to treat

and the NHS are not willing to invest the time or money to see if long term IV antibiotics make a difference...even though it has been proved by real people suffering with the disease at late stage... who have had to raise money and sell there homes .beg and borrow to find theirself a LLMD (Lyme Literate Medical Doctor) who specialises in the treatment of Lyme and its co infections and understands the complexity of the disease and of the treatment plan ,for life .

This is the aim of this appeal... I need to find myself a LLMD who will treat me and this will be outside the NHS and possibly outside the UK ...

Thankyou for reading my story ..please educate yourself and your family and friends on Lyme....... because if I can stop this happening to someone else it will do some good ...please if you are on facebook join the group that was my daughters idea and my husband set up ...called Would you pay a £1 to help save my mummy's life?..pass it on to your friends and ask them to pass it on and so on ...the more people that join ..the more awareness there is and it also gives my little girl some hope and makes us not feel not so totally alone in this situation http://www.facebook.com/profile.php?id=1109650270&ref=search#!/group.php?gid=134675306560444&ref=mf thankyou so much if you would like to donate click on the link below or if you would like to send a cheque ..please make payable to ...The Sonia Smith Appeal Fund 29 St Johns Rd
Bletchley
Milton Keynes
MK3 5DU
England
or for further queries contact soniasmithappeal@aol.com

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

Initially Sonia was admitted to hospital with a suspected Brain Tumour or stroke but when tests showed nothing she was dismissed with 'It's all in your head' despite symptoms of paralysis, Bells Palsy, verbal stuttering and difficulties speaking, light and sound sensitivity to mention just a few of her symptoms.

As most of us find with Lyme Disease here in the UK like elsewhere in the World getting diagnosis even with positive Igenex tests is no guarantee that NHS will treat with antibiotics. Quite remarkable that this ID specialist would consider IV arsenic for some rare African Disease and yet simple antibiotics even oral antibiotics have significantly improved the lives of many patients with a clinical diagnosis of Lyme Disease let alone a serological diagnosis.

All these consultants in denial should listen to the recent presentations at the Institute of Medicine Workshop showing how complex all these tick borne diseases are to test for let alone to treat. Click here

AUTISM SPECTRUM AND INFECTION

Dr. Jones speaks on the Lyme Autism Connection at the recent LIA (Lyme Induced Autism) Foundation conference in April, 2008. Full DVD set is available from http://www.lymebook.com/autism

I have previously posted about Dr Jones further links found here here here or by putting Dr Jones in the search in my right hand column

Also other interesting videos from Dr Bhakta can be seen here

Dr Bransfield published about The association between tick-borne infections, Lyme borreliosis and autism spectrum disorders here

'Chronic infectious diseases, including tick-borne infections such as Borrelia burgdorferi may have direct effects, promote other infections and create a weakened, sensitized and immunologically vulnerable state during fetal development and infancy leading to increased vulnerability for developing autism spectrum disorders.

A dysfunctional synergism with other predisposing and contributing factors may contribute to autism spectrum disorders by provoking innate and adaptive immune reactions to cause and perpetuate effects in susceptible individuals that result in inflammation, molecular mimicry, kynurenine pathway changes, increased quinolinic acid and decreased serotonin, oxidative stress, mitochondrial dysfunction and excitotoxicity that impair the development of the amygdala and other neural structures and neural networks resulting in a partial Klüver-Bucy Syndrome and other deficits resulting in autism spectrum disorders and/or exacerbating autism spectrum disorders from other causes throughout life.

Support for this hypothesis includes multiple cases of mothers with Lyme disease and children with autism spectrum disorders; fetal neurological abnormalities associated with tick-borne diseases; similarities between tick-borne diseases and autism spectrum disorder regarding symptoms, pathophysiology, immune reactivity, temporal lobe pathology, and brain imaging data; positive reactivity in several studies with autistic spectrum disorder patients for Borrelia burgdorferi (22%, 26% and 20-30%) and 58% for mycoplasma; similar geographic distribution and improvement in autistic symptoms from antibiotic treatment.

It is imperative to research these and all possible causes of autism spectrum disorders in order to prevent every preventable case and treat every treatable case until this disease has been eliminated from humanity.'

NEED FOR MORE STUDIES

Brian Fallon, M.D., M.P.H.
Director of the Center for Neuroinflammatory Disorders and Biobehavioral Medicine
Director of the Lyme and Tick-Borne Diseases Research Center
Columbia University Medical Center


Summary from Brian Fallon's talk at the IOM: here 13 mins in

A European study showed 50% Neuro Lyme pateints had persistent symptoms after 3 years compared to 16% of EM patients

Lyme does not have the same trigger points as Fibromyalgia patients

When requesting patient criteria for chronic Lyme it is pointless asking for only those with IgG positive WB as many would not match the criteria

Need more studies outside the use of antibiotics to track improvements (ie a whole management look at Lyme in line with other conditions)

Talks about doctors calling patients with symptoms after 4 weeks treatment as having a somatic disorder - says this can be down to lack of knowledge, the belief that 2-4 weeks is sufficient, lack of recognition of the chronic form of disease or just plain hostility towards the patient

Talked about various studies that showed that fatigue & pain was helped by IV treatment. Criticised a study (Krupps) that claimed that cognitive function was not improved when people were recruited for fatigue & not cognitive related issues, so he reasoned that if the subjects had little cognitive problems to start with then there's no surprise if they didn't improve anymore than the control group

What do we know about non antibiotic treatment therapies? We know nothing there has not been one study and that is absurd these patients are suffering so much and we don’t have a single study except for a few antimicrobial but nothing outside of the realm of antibiotics.


Why are there persistent symptoms?

it could be
Persistent infection
reinfection from a further tick bite
re activation of latent dormant infection
Physiologically active but post infectious spirochetes
Widely distributed effects post infectious phenomena
hypothyroidism
Neuro transmitter changes
Why might it be labeled as a somatic illness, because of the limitations of the physician believing that two to four weeks of antibiotics is always curative. Assuming any symptoms after antibiotic treatment are due to other causes.
Or a lack of recognition that post infectious symptoms can go on for years where you can have chronic fatigue cognitive symptoms and pain
Or could be that there is hostility to chronic illness because some physicians can’t deal with that.


He believes that the NIH to set up a specific sub-committee solely to look at chronic Lyme infection...

HOW TO PREVENT HEALTH CARE COSTS

'Dementia and stroke as a consequence of Treponema and Borrelia infections also occur in the tertiary or late stages of these spirochetal diseases.

In meningovascular neurosyphilis and neuroborreliosis the leptomeninges and leptomeningeal arteries are involved leading to Heubner's arteritis and arterial thrombosis with secondary cerebral infarct (indirect parenchymal involvement). When Treponema or Borrelia spirochetes invade the nervous tissue (direct parenchymal involvement) there is a meningo-encephalitis or encephalitis. With respect to the direct parenchymal involvement, which corresponds to a meningoencephalitis, two different forms are distinguished. In the infiltrative form there is a severe lymphoplasmacytic infiltration and in the atrophic form, a poor or absent lymphoplasmacytic infiltration, but severe microgliosis, neuronal loss and cortical atrophy are present. The pathology of both, the infiltrative and atrophic forms were clinically and pathologically documented in both neurosyphilis and Lyme neuroborreliosis.

The cases with chronic or late Lyme neuroborreliosis, illustrated in the chapter, were published in per reviewed, internationally recognized medical journals. Some of them more than 15 years ago. Chronic or late Lyme neuroborreliosis was confirmed by clinical, pathological and serological examinations and the spirochetes, their antigens or their genes were detected in the tertiary lesions of the brain. Improvement of late or chronic neurosyphilis and neuroborreliosis following antibiotic treatment was repeatedly reported both in syphilis and Lyme disease, however the treatment of late or chronic cases are more difficult. Syphilis was virtually eradicated by the use of Penicillin, indicating that we can also eradicate Lyme disease.


Newer approaches to the treatment of Lyme disease should take into account the frequent co-infection with other pathogens and the need for a more prolonged combination therapy, as it is the case in the treatment of tuberculosis. Even in the doubt of tuberculosis the treatment of the patients with "tritherapy" is necessary for 6 months. It should be an example for the future treatment of Lyme disease. Such treatment, in analogy to tuberculosis and syphilis will substantially prevent extensive healthcare costs in the future.'

************************************************************
The above was posted on Judith Miklossy's website here

I have long since been a fan of the outstanding work Judith Miklossy has done in the field of Lyme Disease but also in Alzheimer's and it was a privilege to meet her in 2009 at the Lyme Disease Action conference.

Those of us unfortunate enough to get Lyme Disease who are lucky enough to get diagnosed and find a good knowledgeable Lyme Doctor who is able to tailor treatments to suite us are testament to Miklossy's recommendation about treatments.

Sadly there are many thousands more who go undiagnosed and untreated because not enough attention is being paid to this formidable disease.

I was browsing through an earlier post I did on the UK figures for Lyme Disease 2009 here

1467 in the UK

but according to Dr Ho Yen HPA Scotland ten times the figure of serologically positive tested cases is more likely.

14670 likely Lyme Disease cases in the UK in 2009

As many of us have been sick several years even on the conservative side say 5 years mean that is still an incredibly high number of 73000 people here in the UK many of whom will be unable to work full time due to their illness.

Just imagine how much our Government could save if only there was more awareness and early adequate treatment as well as appropriate treatment for late stages of Lyme Disease.

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.