Multiple Sclerosis Lyme Pathology Research Fund

General or non-medical topics with information and discussion related to Lyme disease and other tick-borne diseases.
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inmacdonald
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Multiple Sclerosis Lyme Pathology Research Fund

Post by inmacdonald » Mon 30 Dec 2013 15:01

A new foundation devoted to Multiple Sclerosis and Lyme and borreliosiis Human Nervous system diseases
has been established.[/size][/b]
Goal: to Prove from Pathology Study of Multiple Sclerosis Autopsy Brain tissues with DNA probes
which specifically bind unique DNa of Borrelia spirochetes, that the demyelination disease
of Multiple Sclerosis is CAUSED by borrelia spirochetal infections.
Foundation support: Tax exempt contibutions are gladly received in ANY amount
and all donated monies are distributed to Pathologists and researchers with Microscopes
with an interest in Multiple Sclerosis.
Methods: DNA probes specific for binding to DNA of Borrelia and excluding all other DNa
will be used in creating microscopic slides for Study and for photography to document
the presence of Borrelia spirochetes in Multiple Scleosis brain tissue. Spinal cord tissue
is also being recruited for study.
Scope of research colaboration: DNa probes and a research protocol along with positive an negative
borrelia spirochete control DNA will be disributed free of charge to qualifyiing investigators.
Historical background for the connection of Multiple Sclerosis with Chronic Spirochetal Infection of
the human nervous system: A detailed bibliography (13 pages of published references from the
National Library of Medicine ; "Multiple Sclerosis, borrelia, spirochetes" is posted on the
foundation website;
Already published images of borrelia brain and spinal fluid infections and Multiple sclerosis:
{ select images }
---
NCMC Multiple sclerosis autopsy brain with Warthin starry spiirochete Annottated with Arrows.jpg
MacDonald AB year 1986 borrelia spirochete in Multiple Sclerosis Autopsy Plaque
NCMC Multiple sclerosis autopsy brain with Warthin starry spiirochete Annottated with Arrows.jpg (269.66 KiB) Viewed 6205 times
--
Cystic spirochete from MS brain europe.jpg
Cystic borrelia in brain in multiple sclerosis plaque
Cystic spirochete from MS brain europe.jpg (112.42 KiB) Viewed 6205 times
____
Multiple Sclerosis Plaques show spirochetes with bulboslities.jpg
European study of Multiple Sclerosis showing Spirochetes in MS plaques
Multiple Sclerosis Plaques show spirochetes with bulboslities.jpg (106.86 KiB) Viewed 6205 times
___
Address for Donors:


The Dr Paul H. Duray MD Fellowship Foundation Endowment
Care of:
Alan B.MacDonald MD , FCAP,FASCP
8427 Benelli court
Naples, Florida, 34114, USA
Telephone 1-239-592-4353

___Foundation website:
http://www.lyme-ms-pathology.com/

Source of Study materials for the Multiple Sclerosis Lyme borrelia project:
Harvard University Brain Bank, Belmont , Mass. USA

-----
All donations will be distributed directly to Investigators as approved by the Foundation Board.
There are No OVERHEAD costs for this Research Foundation.
There are No Fundraising Costs for this Foundation
100% of Dollars contributed goes directly to Research overseen by Senior Borrelia researchers
and conducted by young pathologists and graduate students .
All participating laboratories Participate voluntarily.
Members of the Foundation Board of Directors - Serve pro bono
All donations will be tax deductible : the Foundation is a 503c entity.

Respectfully submitted,
Alan B.MacDonald MD
December 30, 2013
Last edited by inmacdonald on Wed 1 Jan 2014 1:48, edited 2 times in total.

Joanne60
Posts: 110
Joined: Mon 13 Feb 2012 15:49
Location: Guildford Surrey UK

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by Joanne60 » Tue 31 Dec 2013 10:23

Dr MacDonald

Excellent.

Please let us know when you have set up a facility for on line contributions so that those of us not in US can more easily contribute.

Certainly in the fund raising for Dr Jones and Dr Sapi even small contributions from very many people made a difference.

Best wishes and thank you

Joanne

hv808ct
Posts: 256
Joined: Wed 30 Jul 2008 4:11

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by hv808ct » Wed 1 Jan 2014 20:53

From: http://www.aldf.com

Are the signs and symptoms of Lyme disease identical to those of multiple sclerosis (MS)?

Rarely, and mostly in European patients, does Lyme disease cause inflammation in the central nervous system (CNS), i.e., the brain and/or spinal cord. Although the few patients with such clinical problems were described in the 1980s, this appears to be an even rarer event today, since patients are usually diagnosed and treated for Lyme disease, well before there is significant involvement of the CNS.

When CNS involvement does occur, typical changes are noted on brain MRI scans; unfortunately, early descriptions of these findings led to several misconceptions. Non-specific abnormalities are seen frequently in brain MRI scans of otherwise healthy individuals, particularly those with high blood pressure, diabetes, migraine or even those who simply are over the age of 50. When such changes are seen, it has become commonplace for radiologists to suggest they might be due to Lyme disease, even though this is probably the least likely explanation.

It is important to note that the real brain and spinal cord abnormalities that rarely occur in CNS Lyme disease look much like those of any other form of brain inflammation, and can be confused with changes seen in multiple sclerosis (MS). Although the location of these abnormalities can differ somewhat between Lyme and MS, this is not always helpful. However, there are two characteristic features that can help one differentiate between MS and CNS Lyme disease. Typically, MS is a disease with relapses and remissions occurring over the course of years; such a pattern is not typical of CNS Lyme disease. More helpful, though, are observations noted upon examination of the cerebrospinal fluid. In both MS and CNS Lyme, the spinal fluid shows inflammatory changes that include locally elevated concentrations of white blood cells, protein and antibodies; such changes were not noted in a large clinical study of patients with persistent symptoms and a history of Lyme disease (1). As with many other infections, when there is locally elevated antibody concentration in the spinal fluid because of an infection, the locally concentrated antibodies can readily be shown to be specific for the infecting organism, i.e., Borrelia burgdorferi, in the case of Lyme disease. Although this measure of local production of anti-borrelial antibody may not be elevated in all cases of CNS Lyme disease, it should be elevated in any patient in whom there is an overall increase in spinal fluid antibodies, a finding that is universal in MS. This, coupled with the clinical aspects of the patients illness, allows straightforward differentiation between these two disorders.

References:

1. Klempner, M., Hu, L., Evans, J. et al. Two controlled trials of antibiotic treatment in patients with persistent symptoms and a history of Lyme disease. N. Eng. J. Med. 345: 85-92, 2001.

X-member
Posts: 8203
Joined: Mon 30 Jul 2007 18:18

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by X-member » Wed 1 Jan 2014 21:59

hv808ct wrote (or was it a quote?):
Rarely, and mostly in European patients, does Lyme disease cause inflammation in the central nervous system (CNS), i.e., the brain and/or spinal cord.
About 1/6 of the Swedish Lyme cases have neuroborreliosis when diagnosed and about 5% af those have late neuroborreliosis when diagnosed.

References:

1: EFNS guidelines on the diagnosis and management of European Lyme neuroborreliosis

http://www.efns.org/fileadmin/user_uplo ... liosis.pdf


2: Allmän neurologi och multipel skleros

http://www.lakemedelsboken.se/r1_neu_al ... 3fm10.html

Edit to add:

hv808ct also wrote (or was is a quote?):
Although the few patients with such clinical problems were described in the 1980s, this appears to be an even rarer event today, since patients are usually diagnosed and treated for Lyme disease, well before there is significant involvement of the CNS.
Do you really think that is true?


Ps! This is an European Lyme forum. Ds.
Last edited by X-member on Wed 1 Jan 2014 22:41, edited 1 time in total.

X-member
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Joined: Mon 30 Jul 2007 18:18

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by X-member » Wed 1 Jan 2014 22:31

hv808ct wrote (or was it a quote?):
As with many other infections, when there is locally elevated antibody concentration in the spinal fluid because of an infection, the locally concentrated antibodies can readily be shown to be specific for the infecting organism, i.e., Borrelia burgdorferi, in the case of Lyme disease.
From the link below:
We were able to demonstrate intrathecal borrelial antibody production in only 14 (42%) of 33 patients, including 13 (59%) of 23 from the B. garinii group and 1 (10%) of 10 from the B. afzelii group.
References:

1: Comparison of Findings for Patients with Borrelia garinii and Borrelia afzelii Isolated from Cerebrospinal Fluid

http://cid.oxfordjournals.org/content/43/6/704.long

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inmacdonald
Posts: 977
Joined: Fri 13 Jan 2012 22:32

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by inmacdonald » Thu 2 Jan 2014 13:26

NCMC Multiple sclerosis autopsy brain with Warthin starry spiirochete Annottated with Arrows.jpg
A borrelia spirochete in a human MS plaque from Long Island NY 1986
NCMC Multiple sclerosis autopsy brain with Warthin starry spiirochete Annottated with Arrows.jpg (269.66 KiB) Viewed 5904 times





For More spirochetes in Autopsy MS human brain tissues, visit

http://www.lyme-ms-pathology.com


Alan B. MacDonald MD FCAP FACP
January 2 2014

admin
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Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by admin » Thu 14 Apr 2016 0:59

Topic moved from Published Studies to General Topics.

A question for inmacdonald:

What is the current status of the Duray Research Fund/Foundation?

A LNE reader notified me that the URL to which you link twice, lyme-ms-pathology.com, now leads to a Japanese language website with information about certain drugs. So, could you update or remove the links?

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inmacdonald
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Joined: Fri 13 Jan 2012 22:32

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by inmacdonald » Tue 3 May 2016 16:13

MULTIPLE SCLEROSIS RESEARCH at the Dr. Paul H Duray Research Fellowship Endowment, Inc.
an not for profit IRS Tax Exempt (501c3b) Medical Charity
[SEE Bullet Point Discoveries 1. and 2 and 3 below]

Address for those who wish to donate by Check to the Duray Foundation:

Dr. Paul H Duray Research Fellowship Endowment, Inc.
8427 Benelli Court
Naples, Florida 34114-2754, USA


Recent Research Discoveries related to Multiple Sclerosis:

1. Spinal fluid from a single Multiple Sclerosis patient ( Resident of Oslo, Norway)
Borrelia Miyamotoi present in Cerebrospinal fluid by FISH DNa probe Analysis
Burgdorferi family [ (sl) burgdorferi ] borrelia present in Cerebrospinal fluid by FISH DNa Probe analysis - Molecular Beacon Probe for ORF bbo 0740

Note: Detail of the Species of Borrelia included in the DNa probe Coverage of
Gene equivalents ( open reading frames "ORF" ) is described in detail on the Duray Foundation Website.
------- From the Duray Foundation website---------------

"Lyme Serology: DNA Probes Reveal a Phalanx of False Negatives

It is widely agreed that Lyme Borreliosis serology can be falsely negative in the first few weeks after a tick-bite. Yet the phenomenon of late-stage false negatives has flown largely under the radar. The oft-repeated mantra that the CDC-recommended two-tier protocol easily detects all stages of Lyme after the immediate post-tickbite period is proving itself, more and more, to be a hollow incantation.

For those patients in whom chronic Borrelia infection remains undetected, the consequences can be dire. Outcomes ranging from chronic pain and disability to total incapacitation and death have been recorded.

At the Dr. Paul Duray Research Fellowship Endowment, the renowned Lyme pathologist Alan B. Macdonald MD, FCAP is seeking to change all that. He has been researching the phenomenon of antibody-negative, yet DNA-positive Borreliosis, utilizing the FISH (Fluorescence In Situ DNA Hybridization) technique with highly specific "molecular beacon" DNA probes which he has developed for this purpose.

This method, Dr MacDonald explains, has enabled "the identification of a large number of seronegative chronic borrelia infections caused by Borrelia species in the overall greater family of burgdorferi borrelia (sl) strains...whose DNA differs significantly from the B31 strain to justify the assignment of a separate species and sub-species name.

"These sub-strains are endowed with proteins that do not cross react with B31 proteins in ELISA and Western Blot test kits."

B31 is the prototype Borrelia burgdorferi strain on which the current CDC-recommended protocol is based. Yet B31, a lab strain cloned from a single tick-derived Borrelia cell, has never been detected in a human and can differ significantly from "wild-type" strains. Dr. MacDonald stresses the importance of the VBNC's - the "viable but uncultivable" strains that are circulating in the environment and which may be causing undetected disease. Once upon a time, he reminds us, all the named strains known today were "VBNCs".

The molecular beacon DNA probes utilized by the Duray foundation researchers are extremely unlikely to throw up false positives, as they require a 100% nucleotide match before they will release their telltale fluorescent signal.

Dr. MacDonald has named the following Bb sensu lato strains as some of those detectable using his probes:

1. Burgdorferi: (sub-strains : CA283, N40, JD1, ZS7)
2. Afzelii (sub strains : K78, Tom3107, HLJ01, Pko)
3. Valaisiana (sub-strain: Tom4006)
4. Garinii (sub-strains: PBi, BgVir, SZ)
5. Bissetti (DN127)"

This list includes strains detected in Europe and Asia.
The DNA probe is derived from ORF bb0 0740, which codes for the Inner cell membrane of many borrelia species.

A separate yet equally significant issue is the dismal performance of current antibody tests in patients infected with Borrelia strains which are outside of the Bb sensu lato group altogether
.
----------------------------
-------------------------------Multiple Sclerosis as a Neuroparasitic (Neural Larval Migrans equivalent) Disease


2. Identification of Parasitic Eggs, Larvae, and Adult worms in Cerebrospinal Fluid from 10 multiple Sclerosis
patients : ( Autopsy documented cases from the Rocky Mountain Multiple Sclerosis Brain Bank, Boulder Colorado)

Darkfield examination of 10 Spinal fluids from 10 Multiple Sclerosis patients reveals that multispecies parasites
presumptively nematode parasites are present in Cerebrospinal fluids.
Darkfield Microscopy of Cerebrospinal fluid has never before been performed in Multiple Sclerosis.

This discovery of the First Case in the world literature of Nematodiasis of the Cerebrospinal fluid from human Multiple Sclerosis patients by MacDonald, {F1000 Research Jan 2016){ MacDonald A. Nematode filarial Worms in cerebrospinal fluid of a Multiple Sclerosis patient at autopsy [v1; not peer reviewed]. F1000Research 2016, 5:79 (poster),
(doi: 10.7490/f1000research.1111264.1)
reproduces the Veterinary Medical published studies of Innes and Shoho [ British Medical Journal,1952,vol 366 ,pp 366-368] citing the discovery by Griffith Evans in year 1880 of .."A trypanosome caused Surra of horses in India" ,extensive Japanese research linking Epizootic Neuroparalysis ( epizootic cerebrospinal nematodiasis ) in domestic animals and[ Tanaka et al, 1945, ".. in a pathological study of the brains of 100 old horses, found lesions with and without parasites in nine animals in which no clinically apparent signs were seen during life.."
{ Japan J. Vet Sci., 1945,7:117)
Innes and Shoho further comment that " The essential pathological process is that of a focal encephalomyelomalacia, which in many cases proceeds within a few days to liquefaction and cavitation." ..." The process is an acute malacia in a restricted track followed by secondary degeneration of nerve-fibre tracts, and by the gigantic swellings of axis cylinders (Wallerian Degeneration) in, around, above and below the malacia are a predominant feature. the findings are unmistakably diagnostic, and are consistent with our concept that the process is simply a mechanical traumatic effect of a wandering worm -now proven experimentally."
"It was proven by Japanese workers that the animal neuro-paralysis in Korea and Japan was caused by young worms (Setaria digitata). this finding was based on the association of worms with lesions, and later by experimental production of the disease in sheep, goats, and horses. the aetiological concept was first suggested by Fujita and amplified and proven experimentally by Niimi and Kimura ( 1939-43) and 28 others. A full account is available in a five-volume Report of a Special Commission (1939-43), but unfortunately an English translation is not available. Our other papers summarize all these studies, while in the caprine paralysis of Ceylon, McGaughey (- at our institution- subsequently demonstrated the causal Setaria. The name given now is appropriate - namely epizootic cerebrospinal nematodiasis - for it is better that the original Japanese label of Setariasis, and we think )"other filarial or immature nematodes might be involved in the production of the same pathology in the same or different species. The natural host of Setaria digitata cattle, in which the adults reside in the abdominal cavity and without an visible pathological effect, and in which the species microfilaria finally enter the blood. In the Orient the vectors of the worm are mosquitoes.."
"Beautyman and Woolf discuss this with particular reference to the classical work of Yokogawa (1923) on ascaris and therefor emphasis is laid on intravascular paths. It is generally accepted that ascarids, after hatching of the eggs in the intestines, go on a tour to the lungs and that some larva may wander in the general circulation and reach the nervous system of the eyes. Yokogawa's original experimental findings, in which 10 out of 14 mice (given a large number of ascarid eggs) showed haemorrhages of the cerebrum due to migrating larvae, were also interpreted to mean that the route was via the circulation. We wonder why a direct pathway cannot be considered to account fo all such cases. In cerebrospinal nematodiasis it can hardly be questioned that the direct tissue path is the one taken by Setaria, to the malacic lesion is not embolic in nature but mechanically traumatic. We might draw attention to some obscure work by von Brand and Culliman (1943), who showed that stongyloid larvae of fish, when transplanted into unnatural hosts ( rats and chickens), invaded the nervous system and paralyzed and killed the latter.. These larvae took the direct route, for one could trace the histological path through the connective tissue and muscle tissue, and vertebral joints to the cord, revealed by granulomatous eosinophilic tissue reaction.. The problem of what parasites do in unnatural , as compared with natural , hosts might be the crux of many problem. The thesis that the nervous system ( and eye perhaps) may be a strange anatomical site of attraction in unnatural hosts receives further support from Tiner (1951), who reported 100% mortality in white mice from damaged to the brain, following infection by ascarids derived from raccoons."
...
"Possibility of an Analogous Cerebrospinal Nematodiasis of Animals Occurring in Man .."
"This has been covered fully in another paper (Innes and Sohoo,1952) ...Such a disorder could evade both accurate clinical and pathologic detection - in fact, if patients lived diagnosis might be impossible."
"...draw attention to reports of eosinophilic meningitis with focal malacia- with clinical acute paralytic signs ( or those of transverse myelopathy) and a complete absence of evidence indicative of a cause (virus, bacteria, or any other - but helminths never considered.) It is even conceivable that some cases of reputed disseminated sclerosis, with prominent spinal signs, which do not progress after a primary paralytic attack, could be of this nature."

{MacDonald Comment: Cavitation of the Spinal cord is Syringomyelia - Cases of Syringomyelia are now
being requested for pathological examination for parasitic worms by the Duray Foundation researchers)

------------------------------------------------------------------------
--------------------------------------
Pathogen ]Borrelia) Inside of a Pathogen ( Parasite Worm )

3. Identification of Borrelia spirochetal DNa INSIDE of Parasitic Worms infesting human Cerebrospinal fluid in Multiple Sclerosis.

FISH studies of Adult worms produced images of Borrelia family (sl) DNA inside of Adult worms in
Multiple Sclerosis Spinal Fluids.

This observation of a Pathogen Inside of a Second Pathogen ( Trojan Horse Model) recapitulates the discovery of Wolbachia species microbes residing INSIDE of the Parasitic worms which cause River Blindness.
It is now believed that the Wolbachia spp. microbes add to the pathogenic effect of the worm parasites, which in aggregate cause River Blindness in underdeveloped nations.

Images of Parasites identified by Dark Field Microscopy of Multiple Sclerosis Cerebrospinal fluid ( 10 MS patients)
are presented in the Posts below, and may be downloaded from the F1000 Research Site.

Comment: In the United Kingdom, an NHS funded study of the intentional induction of Nematode infections in more than 70 multiple sclerosis patients was completed. This Study was predicated on the notion that a parasitic infection ( malaria or nematode) might, by the induction of a host immune response, counteract the "Autoimmune (sic)" events in Central Nervous system tissue in Multiple Sclerosis.
Readers can draw their own conclusions .


Respectfully submitted,

Alan B. MacDonald, MD, Fellow, College of American Pathologists
May 3,2016

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inmacdonald
Posts: 977
Joined: Fri 13 Jan 2012 22:32

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by inmacdonald » Tue 3 May 2016 16:49

Multiple Sclerosis Cerebrospinal Fluid

Parasitic Worms:
MS CSF Worm  277  with Grid Ribogreen.jpg
MS CSF Worm 277 with Grid Ribogreen.jpg (35.49 KiB) Viewed 3772 times
MS  CSF Tangle of worms 277 Ribogreen.jpg
MS CSF Tangle of worms 277 Ribogreen.jpg (64.45 KiB) Viewed 3772 times
Respectfully submitted,

Alan B. MacDonald, MD, Fellow, College of American Pathologists
May 3, 2016

User avatar
inmacdonald
Posts: 977
Joined: Fri 13 Jan 2012 22:32

Re: Multiple Sclerosis Lyme Pathology Research Fund

Post by inmacdonald » Tue 3 May 2016 19:10

Miyamotoi borrelia and Burgdorferi borrelia (sl family)
in Cerebrospinal fluid from Multiple Sclerosis patient , Adult Male, from Oslo Norway;

FISH detection of Borrelia species ( two Borrelia species simultaneously present in
Multiple Sclerosis Cerebrospinal Fluid {CSF})

FISH = Fluorescence In Situ DNA Hybridization - DEFINITIONS
DNA probes : Burgdorferi ( sl family of European and North American Borrelia species) -Probe 740
which uniquely hybridizes to DNA of the Gene for the inner cell membrane locus
bbo 0740. (green color probe- visible only if DNA probe finds its target DNA - Specific and unique-

Miyamotoi borrelia - Gene locus for glpQ ; ( yellow color probe - specific and unique)
glpQ is present in Relapsing Fever Group borrelia [ including Miyamotoi ],
and glpQ is never present in Burgdorferi (sl) group of borrelia
Miyamotoi Borrelia - Gene locus for Flagellin B ( miyamotoi FlaB -Red color probe is
unique and specific)
Validation: All of the above DNa probes are validated in Peer Reviewer's laboratories
and all demonstrate specificites ( unique) for the intended DNa Targets

Link to PDF file - Case Study - Patient Name redacted for HIPPA compliance/confidentiality
of patient and referring Physician.
Image below- Three colors - Borrelia Spirochetes in CSF from Multiple Sclerosis patient

Norwegian MS CSF Burgdorferi sl and Miyamotoi.jpg
Norwegian MS CSF Burgdorferi sl and Miyamotoi.jpg (58.54 KiB) Viewed 3719 times
----------------------------------------------------------------------
Reference : Cerebrospinal fluid Miyamotoi borrelia in Meningoencephalitis Patient Case Study:
--
Meningoencephalitis from Borrelia miyamotoi in an immunocompromised patient.,Gugliotta JL, Goethert HK, Berardi VP, Telford SR 3rd.,N Engl J Med. 2013 Jan 17;368(3):240-5. doi: 10.1056/NEJMoa1209039.
PMID: 23323900 Free PMC Article
-----------------------------------------------------------------------

Respectfully Submitted:

Alan B. MacDonald, MD, Fellow, College of American Pathologists
May 3,2016

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