LYME AND MS HAVING THE SAME ETIOLOGY – Kathy Cavert

LYME AND MS HAVING THE SAME ETIOLOGY

From: jwissmille [at] aol [dot] com (JWissmille)
Newsgroups: sci.med.diseases.lyme
Subject: MS or Lyme from the archives
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Date: 30 Jun 1999 19:44:26 GMT
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Xref: news.gmd.de sci.med.diseases.lyme:50155 from the archives–excellent info.
Subject:
MS/Lyme literature
Date:
Wed, 08 Oct 1997 12:55:25 -0500
From:
John Haynes
Newsgroups:
sci.med.diseases.lyme

JOURNAL REFERENCES

compiled by
Kathy Cavert

html-edited by Joachim Gruber
Due to several reqeusts for posting and hundreds of snail mail requests around the country, I am posting the listing of research I have accummulated on the net so that more people will have access to information re: Lyme and MS having the same etiology perhaps and providing hands-on info for those whose interest lies in thise area so that they may access this list for future use. I accummulated this list in 1992 and so there are many more that follow I am sure. Feel free to make addendums

This should give one a good start anyway.

This has been sent to the National MS Society in NY and they have discredited its profound implications as being not worthy of bacteriologic research into the etiology of Lyme disease which I found to be a very sad commentary on the mindset of their organization.

Note: These articles do not all insist that Lyme and MS are the same but keep in mind that MS means “multiple sclerosis”. Multiple sclerosis simply put means “many lesions”. It is simply a DESCRIPTIVE NAME of a disease which causes the nerves

to lose their myelin sheath and in particular
to show lesions on the brain on MRI which Lyme does as well.
My readings and research have indicated that the brain lesions, the spinal fluid findings and the actual clinical manifestations of Lyme and MS cannot be distiguished one from the other, perhaps simply due to a strain variance of Lyme.
We know that Lyme causes an immunologic dysfunction including a component of autoimmune activity possibly causing this neuro-damage in the form of MS activity.

The bottom line -and most disturbing thing- to me is that the MS society refuses to put out money for intensive research even after Dr. Vincent Marshall’s exhaustive research from the 80’s showing spirochetes on the axons of nerves of MS patient autopsies in Europe. When viruses became popular, they threw the baby out with the bathwater and now research funding is geared toward viruses and immunologic work; bacterial taking a second seat. The worst of all, there is no etiology to MS or other autoimmune diseases and there seems to be clinical response of polymyalgia rheumatica, MS, polymyositis, rheumatoid disease, Alzheimers, ADD, chronic fatigue syndrome, fibromyalgia and other diseases such as lupus (we see them feeling better) when given antibiotic therapy. This is most frightening when the antibiotic therapy is taken away from them by their rheumatologists and ignored by their internists. The very key that may unlock the door to these illnesses and the publications that implicated ALS and other life-threatening diseases are being ignored as having an infectious underpinning.

Personally, I find this inexcusable and find antibiotic over 3 months IV to be much less damaging than methotrexate, Cytoxin, prednisone high dose etc. over the long haul for these patients.

Please do attach my name when using this listing, as I want to maintain the research rights to this time-taking work. Thanks to everyone for your interest and support through the years.

When looking up some of these journal articles, one will have to use a medical school or sophisticated library which contains most journals so that they can more easily access them in one trip.

For those pondering the MS diagnosis, perhaps this will make a better case for the parallel between the two diseases. Rarely do we pick up an article on neurologic Lyme (neuroborreliosis) in which we do not see demyelinating syndrome as part of the disucssion (brain lesions).

Also remember that syphilis caused demyelination and we are but a cousin to this dreaded infection.

The one thing good that did come of this research was the posting of the MS Society of Lyme on their web page as being a demyelinating disease.

This post is also intended for ALS patients and perhaps even Guillain-Barre patients as well.

1. MRI Reveals Pathology in Neuro Lyme Disease. “Diagnostic Imaging-MRI Insights”.

2. “Biopsy-confirmed CNS Lyme Disease: MR Appearance at l.5T” American Journal of Neuroradiology-11:482-484.

3. Allen Steere, MD. et al. “The Long Term Course of Lyme Arthritis in Children” The New England Journal of Medicine. Vo. 325No. 4, Jly 18, 1991.

4. Stephen L. Schechter, MD. “Lyme Disease Associated with Optic Neuropathy” The American Journal of Medicine. July 1986. v. 81, 143-145

5. H. Kohler, Dept. Clinical Neurology and Neurophysiology, University of Freiburg, West Germany. “Letter to the Editor”. Borrelia encephalomyelitis.” The Lancet. July 5, 1986, p35.

6. “Kyke Award: GD-DTPA-Enhanced MR Imaging of Experimental Bacterial Meningitis: Evaluation and Comparison with CT. American Journal of Neuroradiology. 9:1045-1050; Nov./Dec. 1988.

7. Derek Gay et al. “Multiple Sclerosis Associated with Sinusitis: Case-controlled study in General Practive. [Ed. note: Recent research in showing 99% Lyme patients have active sinusitis as presenting symptoms which often go undetected {unpublished results from personal research on symptomatology}]. The Lancet. Saturday 12 April 1986. 815-819.

8. Eric L. Logigian, MD; Allen Steere, MS et al. “Chronic Neurologic Manifestations of Lyme Disease. “The New England Journal of Medicine” 323:21;1438-1444, 1990.

9. Derek Gay , “Hypothesis” Is Mutiple Sclerosis caused by an Oral Spirochete? The Lancet. July 12. 1986. pp. 75-77.

10. Fernandez et al. “Lyme Disease of the CNS: MR Imaging: Findings in 14 cases. American Journal of Neuroradiology. 11; May/Jyne, 1990.

11. John Halpersin, MD et al. “Immunologic Reactivity Against Borrelia burgdorferi In Patients with Motor Neuron Disease.” Archives of Neurology 47:586-594. May 1990.

12. Will Kohlhepp. et al. “Extrapyramidal Features in Central Lyme Borreliosis.” European Neurology. 29:150-155, 1989.

13. Joh J. Halpersin, MD “Lyme Neuroborreliosis.” Laborabory Medicine. 21:5; May 1990.

14. Louis Reik, Jr., MD et al. “Demyelinating Encephalopathy in Lyme Disease. Neurology. 46:790-795, July, 1989.

16. Presentation to Rocky Mountain Lab by Kenneth Liegner, MD from Armonk, New York, re: growing evidence for link between Lyme and MS. Missoulian Newspaper. Wed August 15, 1990. Gred Lakes. Hamilton, Montana, Rocky Mountain Lab; NIH facility where Dr. Willy Burgdorfer discovered the spirochetal etiology of Lyme disease.

17. R. Ackerman, E. Gollmer and B. Rehse-Kupper. “Progressive Borrelial Encephalomyelitis”: The Chronic Neurologic Manifestations of Erythema Chronicum Migrans (ECM) Disease.” Lyme Times Newsletter. April, 1993, p. 48 Phyllis Mervine, Editor. Reprint of German publication called Deutsche Medizinische Wochenschrift 110. 1995. Translated by Ron Ferris, Calgary, Alberta, Canada. Reprinted with persmission. English title, “Untreated neuroborreliosis progresses over years to cause serious MS-like encephalomyelitis.”

18. J.H.J. Wokke, MD:,.van Gign, MD; A. Elderson, MD; and G. Stanek, MD. “Chronic Forms of Borrelia burgdorferi infection of the nervous system,” Neurology 37:1031-1034: 1987.

19. Michael B. chancellor, MD; David E. McGinnis. Patrick J. Shenot, MS et al. Dept. Urology, Jefferson Medical College. Thomas Jefferson University, PA 19107. “lette” The Lancet. Vol 339: May 16, 1992 p.1237-1238.

20. Keffreu A. Nelson, MD; Mitchel, D. Wolf, MD; William T.c. Yuh, MD et al. “Cranial nerve involvement with Lyme borreliosis demonstrated by magnetic resonance imaging”. Neurology. 42:671-673. March 1992.

21. P.K. Coyle,MD;Z.Deng, MS; S.E. Schutzer, MD; A.L. Gelman,MD et al. “Detection of Borrelia buergdoferi antigens in cerebrospinal fluid.” Neurology. 43:1093-1097, 1993.

22. Saul Rosen, PhD, MD, Section Editor. “Current Perspectives on Lyme Borreliosis”. Journal American medical Association. 276;10, March 11, 1992. “Gran Rounds at the Clinical Center of the National Institute of Health.”.

23 Ackerman, R,MD; Rehse-Kupper, B. MD, “Chronic Neurologic manifestations of erythema chronicum migrans borreliosis”. Annals NY Academy of Science. 539-16-23.

24. Matuschka, Fr. and Spielman, A. The emergence of Lyme disease in a changing encironment in North American and Central Europe”. Experimental and Applied Acarology. 2: 1986; 1337-1353.

25. JJ Halpersin, MD; Raymond Dattwyler, MD et al. “Lyme Disease: Cause of a Treatable Peripheral Neuropathy.” Neurology. 37; No 11; 1700-06; 1987.

26. Belman, A.L.; Coyle, Patricia K.; Nachman, S. and Roche, C. “Brain MRI abnormalities in children infected by Borrelia burgdorferi.” Neurology. 41 (Suppl 1) Item 73 P: March 1991.

27. Vincent Marshal, DVM, “Multiple Sclerosis is a chronic central nervous system infection by a spirochetal agent.” Medical Hypothesis. 25:89-92, 1988.

28 A. Kirk E. winward, MD; J. Lawton Smith, MD et al. “Ocular Lyme Borreliosis.” [ Ed. note: eye diseases found in MS patients called “pars planitis” and uveitis, scotomas, disk edema, optic neuritis and neuropathy, blurred vision etc. are implicated in this article as Lyme disease eye phenomenon as well]. “A similar association with pars planitis has been reported in multiple sclerosis [18] Because a demyelinating syndrome nearly indistinguishable from multiple sclerosis may also occur in Lyme disease, it is possible that Lyme borreliosis, pars planitis, and demyelinating disease may, in some cases, share a common pathogenic mechanism.” p. 656. American Journal of Ophthalmology 108:651-657, 1989.

30. A. Berger, B.C., and Leopold, I.H. “The incidence of uveitis in mutiple sclerosis.” American Journal of Ophthalmology. 62-540., 1966.

31.DuPuis, MJ , Multiple neurologic manifestations of Borrelia burgdorferi infection , Reviews in Neurology (Paris), 1988;144(12):765-775. [Article in French, English abstract available on Medline]
Exerpt: The central nervous system involvement is characterised by slowly progressive or fluctuating course during month or years,

ataxic or spastic gait disorder,
bladder disturbances,
cranial nerve sydrunction including
optic atrophy and
hypoacusia,
dysarthria,
focal and diffuse encephalopathy.
This chronic central nervous system disease can mimic multiple sclerosis psychic disorders or subacute presentile dementia. It is often associated with
pelocytosis,
abnormal EEG and
evoked potentials,
sometimes multifocal and mainly periventricular white matter lesions visualized by CT or MRI……
Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parencymetous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator…and can cause

acute transverse myelitis,
severe encephalitis,
myositis,
chronic neuropathy…
recurrent strokes…
meningoradiculitis…
lyphocytic meningitis with an acute or even relapsing course,
apparently idiopathic facial palsy,
neuritis of other cranial nerves,
polyneuritis cranialis,
Argyll-Robertson sign and so on.
32. Baig S., Osson T, Hojeberg G, Link H., Dept. of Neurology, Karolinska Institute, Hugginge Unversity Hospital, Stockholm, Sweden, Cells secreting antibodies to myelin basic protein in cerebrospinal fluid of patients with Lyme neuroborreliosis. Neurology 1991; April, 41(4):581-587.
33. Lyme borreliosis neuropathy. A Case report Am J. Phys. Medicine and Rehabilitation, 1996 Jul;75(4):314-316.

34. Coyle, PK, Dept. of Neurology, School of Medicine, State University of New York, Stony Brook, Neurologic complications of Lyme disease. Rheumatologic Discussion Clinical North American, 1993, Nov;19(4)993-1009.

______________________

” In 84% of multiple sclerosis patients we were able to demonstrate intrathecal antibody production against measles, rubella or mumps virus…………”
(This quote is from the first of the following abstracts.
I find it interesting because these three viruses are also included in one shot for vaccinations. What are these antibodies doing in the spinal fluid and being used as a marker for MS?
Does anyone know?
Georgia)

Heller J, Holzer G, Schimrigk K. Immunological differentiation between neuroborreliosis and multiple sclerosis. J Neurol. 1990 Dec;237(8):465-70.
Heller J, Holzer G, Schimrigk K. [ELISA for specifying oligoclonal bands of isoelectric focusing of cerebrospinal fluid in patients with neuroborreliosis and multiple sclerosis], Nervenarzt. 1990 Apr;61(4):248-9. German.

Further Reading on neuroborreliosis/MS

Lawrence C, Lipton RB, Lowy FD, Coyle PK, Seronegative chronic relapsing neuroborreliosis. Eur Neurol 995;35(2):113-7.
Garcia-Monco JC, Seidman RJ, Benach JL, Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides.Infect Immun 1995 Oct;63(10):4130-7 (Full text)
Mattman L, Spirochaeta Myelophthora in Multiple Sclerosis, in: Cell Wall Deficient Forms: Stealth Pathogens, 2nd Edition, CRC Press, Boca Raton, Boston, London, New York, Washington D.C., 1993
Martin Roland, Cellular Immunology Section, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, Research Interests:
“In treatment trials as well as in longitudinal studies of disease activity in MS patients immunologic disease markers

-measured by
ELISA,
quantitative PCR,
cDNA microarrays,
T cell frequencies and specificity-
are correlated with
the clinical course and
disease activity as assessed by MRI.”
Dr. Martin’s laboratory investigates the cellular immune system in multiple sclerosis and chronic Lyme disease and, together with Henry McFarland, develops novel treatment modalities for MS.”

Example:.
In the case of a
a history of Lyme disease and
a neurological picture compatible with atypical multiple sclerosis, that seems to improve with intravenous antibiotics and relapse when antibiotics.have been discontinued
it seems a probably safe option to use of both,
i.v. antibiotics directed against Lyme and simultaneously
copaxone to reduce autoimmune damage.
Background of this is the lack of diagnostic tests that actually verify an active infection, i.e. the persistence and reproduction of a B. burgdorferi population (personal communication from Roland Martin).
Martin R, Gran B, Zhao Y, Markovic-Plese S, Bielekova B, Marques A, Sung MH, Hemmer B, Simon R, McFarland HF, Pinilla C., Molecular mimicry and antigen-specific T cell responses in multiple sclerosis and chronic CNS Lyme disease, J Autoimmun 2001 May;16(3):187-92
Immunology Division, Department of Pathology, University of Cambridge: “The implications of this are
that the continuous stimulation of T cells is required to maintain the inflammatory process and
that TNFalpha plays a key role in that process.
The currently accepted view is that whatever initiates the disease, once joint damage is established it is a self-perpetuating process in which
auto-antigens released as a result of the damage
stimulate T cells
which recruit and activate macrophages
which lead in turn to further damage, the maintenance of inflammation – via vascular endothelial activation – and the perpetuation of the proliferation and cytokine secretion of local TH1 cells.
Presumptively the key cytokines are
TNFalpha and IL-12 released by macrophages and
IFNgamma from T cells.”
(https://www.path.cam.ac.uk/immuno/part1/lec13/lec13_97.html)
Activity of Copaxone:
Li QQ, Burt DR, Bever CT., Glatiramer acetate inhibition of tumor necrosis factor-alpha-induced RANTES expression and release from U-25 MG human astrocytic cells. J Neurochem. 2001 Jun;77(5):1208-17.

Antimyelin antibodies in Lyme

Epidemiol Mikrobiol Imunol 2002 Apr;51(2):60-5

[Article in Czech]

Ryskova O, Vyslouzil L, Honegr K, Lesna J, Horacek J, Skrabkova Z.

Ustav klinicke mikrobiologie, UK Praha, LF Hradec Kralove. ryskovao [at] lfhk [dot] cuni [dot] cz
The method of enzyme immunoassay (ELISA) was used for detection of antibodies against the basic protein myelin (antimyelin antibodies) for a group of serum samples (n 36) with positive anti-borrelia immunoglobulins IgG and IgM (ELISA-Borrelia afzelii) and their immune complexes (ELISA-PEG).

Antimyelin antibodies (ELISA-Doxa Kit-Myelin Basic Protein Antibodies) were assessed in 31% (n 11) of examined serum samples of patients with the working diagnosis of Lyme borreliosis.
Statistical analysis (p 0.07) confirmed a more frequent incidence of antimyelin antibodies in younger female subjects (age 31 years) as compared with a group of sera (n 25) where the authors did not record the formation of immunoglobulins against the basic myelin protein (age 51 years).
Neither the value of titres nor the frequency of detected anti-borrelia IgG and IgM and immune complexes differed significantly in the two groups.
From the assembled results ensues that in the course of Lyme borreliosis, in chronic affection of organs an autoimmune reaction may develop where the basic myelin protein is damaged (demyelinizatio) and subsequently antimyelin antibodies are formed.
PMID: 11987581 [PubMed – in process]

version: August 28, 2002
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