Autoimmune Basal Ganglia from 2 infections in: PANDAS, OCD, Tourettes, narcolepsy, & Encephlaitis Lethargica. Cross-targeting autoimmunity

 Hypothesis: The cross-targeting of infections at the same tissue causes autoimmune disease.  One infection marks the outside while another marks the inside...only then does the immune system become confused and attack

Please see newer post: http://angelabiggs.blogspot.com/2015/02/over-view-of-brain-autoimmunity.html

I started to post how my cross-targeting theory applies to PANDAS, Tourettes, OCD and narcolepsy...and then I remembered Encephalitis Lethargica.

Before I start posting suspects and demonstrating the cross-targeting on the Basal Ganglia that I suspect I need to respectfully identify Dr. Andrew Church who works on Encephalitis Lethargia.

Everyone remembers the 1990 Awakenings movie with Robin Williams as Dr. Oliver who in 1918 dealt with an cluster of encephalitis lethargia patients.  In 1993 Dr. Andrew Church found himself with another Encephalitis cluster and he discovered that 2 infections were there not just the flu. Dr. Andrew discovered that a high number of his patients had a rare form of strep called Diplococcus along with the spanish flu.  He has spent a life time trying to piece together this disease.

In 2011 Dr. Andrew came out with this paper proving Encelpalitis lethargia was an autoimmune disease with antibodies directed at the Basal Ganglia. http://brain.oxfordjournals.org/content/127/1/21.full.pdf

Here today I am looking at the autoimmune diseases that cross-target on the Basal Ganglia. In this case the severity of the disease may depend on what mix you had causing the cross-targeting.  My theory supports and validates his research.

Other Basal ganglia autoimmune diseases: http://qjmed.oxfordjournals.org/content/96/3/183.full

The NY cluster of LeRoy High PANDAS cluster.  Dr. Trifiletti has also found 2 infections involved with this autoimmune disease which targets the Basal Ganglia.  He has found Streptococcus pyogenes in 5 of the 8 girls and Mycoplasma pneumonia in 7 of the 8.

Parents of PANDA children have discovered their kids can relapse even after antibiotic recovery when their children receive a flu shot.  I believe this is because the flu shot generates antibodies against the Basal Ganglia.

In England a cluster of children developed Narcolepsy which is a disorder of the basal ganglia after receiving a swine flu shot.  The question is did they have another infection's antibodies there too? What infection broke the brain's blood barrier?
Update 6/29 History of strep was found in Narcolepsy patients
http://med.stanford.edu/psychiatry/narcolepsy/articles/ResponseToMarcusH1n1.pdf  
Antibodies for strep found in narcolepsy patients
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2717204/pdf/aasm.32.8.979.pdf

Tourettes has been associated not just with strep but with borrellia burgdorferi (lyme disease). Although  I am about to show a connection with Lyme I think there exists a genetic disposition where only strep is required to develop the autoimmune reaction but this would be the kind of Tourettes that runs in families. (Rheumatic fever which is also an autoimmune reaction to strep has a genetic component and runs in my family....strep alone causes the autoimmune response of the joints etc)
Lyme and Tourettes:
http://www.ncbi.nlm.nih.gov/pubmed/15590039 
http://www.tourette-gesellschaft.de/download/bts_lymedisease_muelleretal.pdf
http://www.ncbi.nlm.nih.gov/pubmed/9482302

Tourettes and lyme (this link added 2016)
http://abcnews.go.com/Health/girl-tics-bucks-doctors-blames-lyme-disease/story?id=19128125
 
My cross-targeting hypothesis is supported when one looks at the Basal Ganglia related autoimmune diseases.  In order for autoimmune disease to develop 2 infections typically exist both causing the immune system to target the same thing.

Encephalitis lethargia: strep and spanish flu virus (H1N1 subtype not seen right now)
Tourettes: strep/ lyme's Borrellia and herpes ?
PANDAS/OCD: strep / mycobacteria and swine flu (common H1N1?)
Parkinson's: mycobacteria and avian flu virus
Cataplexy : strep and swine flu


Looking at this list Strep stands out.  Strep definitely can get through or weaken the Blood Brain Barrier. http://blog.lib.umn.edu/nich0185/myblog/2011/10/the-blood-brain-barrier-and-ocd.html
http://nizetlab.ucsd.edu/publications/iaga-jci.pdf

The borriella of lyme disease drills a hole for itself through the barrier.
http://www.ncbi.nlm.nih.gov/pubmed/22355605

Mycobacteria weave their way through the barrier.
http://www.ncbi.nlm.nih.gov/pubmed/16586367

Once the protective barrier of the brain is down the antibodies seep through.  All of these infections focus the immune system on the Basal Ganglia as a target but the mix you have could determine which disease you have?

Herpes and Tourettes references:
http://www.ncbi.nlm.nih.gov/pubmed/?term=herpes+virus+tourettes 
http://www.ncbi.nlm.nih.gov/pubmed/3195682
http://www.autism.com/ari/newsletter/112/page2.pdf
http://www.ncbi.nlm.nih.gov/pubmed/18378549   (basal ganglia,herpes and movement)

Note that there are multiple types of swine flu and the CDC needs to start tracking which flu is associated with which autoimmune disease. (which swine flu etc since there are different ones)

The idea is: the outside of the nerves are targeted by the first infection then the virus causes the targeting of the inside of the nerve....the cross targeting causes the autoimmune disease.

*this page is under construction and more references and OCD will be discussed soon.

Tics/OCD and strep
http://www.ncbi.nlm.nih.gov/pubmed/11466169
http://www.ncbi.nlm.nih.gov/pubmed/15241433

low levels of histamine, histamine gene, and genetic tourettes
http://www.scientificamerican.com/article/treating-tourettes/



Angela Biggs

Is Chronic Fatigue (myalic encephalomyelitis ) an autoimmune disease?

Hypothesis: An infection first produces an antibody response towards self  but autoimmunity does not develop until a virus infects the target too and causes cross-targeting.  The immune system is attacking self because 2 different infections push the system over the edge and only then does autoimmune disease develop.

In Chronic Fatigue the antibodies are directed toward serotonin and the 5-ht neurons.
http://www.ncbi.nlm.nih.gov/pubmed/23664637

The Borna disease virus is known to infect these neurons in animals which typically results in an induced up regulation of serotonin. I suspect this virus.

 Just found references showing BDV in patients:
http://www.ncbi.nlm.nih.gov/pubmed/9396313
http://www.ncbi.nlm.nih.gov/pubmed/10529109
http://www.ncbi.nlm.nih.gov/pubmed/8839433
http://www.hirou.jp/english/pdf/ikuta.pdf
https://scholars.duke.edu/display/pub703748

As for the initial infection: RA tends to overlap chronic fatigue.  My suspect for that is Mycoplasmas which could also infect nerves and it has been found in some Chronic fatigue patients.
http://www.ncbi.nlm.nih.gov/pubmed/12879275
http://www.ncbi.nlm.nih.gov/pubmed/10691196
http://onlinelibrary.wiley.com/doi/10.1111/j.1574-695X.2002.tb00626.x/abstract
http://www.cfids-cab.org/cfs-inform/Mycoplasma/endresen03.pdf

What could be happening here: the mycoplasmas infect the 5-HT neurons first generating the antibodies to develop then if the person is unlucky enough to then catch the Borna virus which infects these nerves....cross-targeting triggers the autoimmune disease.

Too early to say that this is happening because not enough research has been done. However based on the immune suppression drugs given to patients Chronic Fatigue syndrome does appear to be autoimmune.
http://discovermagazine.com/2013/may/01-are-b-cells-to-blame-for-chronic-fatigue-syndrome#.Ub_AzpwQMs3

Addison's Disease : is it a 3 stage autoimmune disorder?

The autoimmune hypothesis typically is 2 stages:  an infection creates the build up of antibodies through morphology switching  followed by a viral infection which causes cross-targeting triggering the autoimmune disease.

This particular autoimmune disease requires more then the genetic susceptibility to infection followed by cross targeting.  It is known to have the recessive gene AIRE associated with it.  AIRE is an "Auto-Immune-REgulator" gene.

This makes some sense because Addison's disease is not common but the culprits Candida and Hepatitis I am considering are rather common.

Stage one infection Candida
 (some have AIRE gene also)
http://www.ncbi.nlm.nih.gov/pubmed/23000069 
http://www.ncbi.nlm.nih.gov/pubmed/17891543
http://www.ncbi.nlm.nih.gov/pubmed/11978574

Stage two infection Hepatitis
Hepatitis C
http://www.ncbi.nlm.nih.gov/pubmed/22839422
Hepatitis B
http://www.ncbi.nlm.nih.gov/pubmed/22346436

Stage 3  The autoimmune chases the virus to more organs

Hepatitis can spread to multiple organs. Perhaps in Addison's disease the autoimmune trigger started somewhere else, cross-targeting at the pancreas for example causing Type 1 diabetes.  The AIRE gene however makes cross-targeting unnecessary at the later targets....for the adrenal glands all you would need would be the virus.  If this is true then Addison's is never the first autoimmune disease to develop rather it is an echo...of another.  Possible?  

Addison's disease HLA-B8 HLA-DR3
https://www.ncbi.nlm.nih.gov/pubmed/25040682

Salt , autoimmune disease, and viruses

If we say that Cross-targeting must occur for Autoimmune disease to attack then how does salt fit in?


Cross-targeting is where the immune system attacks from Bcells looking for a visable infection like bacteria, fungus or mycoplasma and from a Tcell viral infection inside of cells. Two modes of attack focused on the same target.

Maybe salt increases the likelihood that cells are virus infected in the first place and attacked.   

Salt increases autoimmune disease:
http://www.huffingtonpost.com/2013/03/06/salt-autoimmune-disease-sodium-multiple-sclerosis-diabetes_n_2821200.html

Salt increases the amount of viruses absorbed by cells
http://www.jimmunol.org/content/61/1/65.abstract

Salt effects the immune system's tcells
http://www.ncbi.nlm.nih.gov/pubmed/23467095

Note that while Bcells are suppose to flag targets that are visible with antibodies Tcells go to HLA mailboxes expressed on all cells and check what is inside cells thus Tcells are responsible for finding viruses. 

Does salt increase the activation of HERVs? the old viruses that are are dormant merely buy favoring more virus infections? Further does salt increase the likelihood that t-cells would attack a herv activated cell?

I am just trying to fit this new piece of the puzzle into my current Hypothesis.

Still's disease (Juvenile arthritis ) is it autoimmune cross-targeting?

Autoimmune Hypothesis: An infection builds up antibodies in the early stages then a viral infection causes cross targeting triggering the autoimmune disease.

Page under construction still

Staph pyogenes and Still's disease
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1888950/?page=1


Septic Arthritis and still's disease mixed up?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3341832/

Epstein Barr and cytomegalovirus infecting synovium tissue
http://www.ncbi.nlm.nih.gov/pubmed/15044921

Epstein Barr and Still's disease
http://www.ncbi.nlm.nih.gov/pubmed/23166163
http://www.ncbi.nlm.nih.gov/pubmed/22370999
http://www.ncbi.nlm.nih.gov/pubmed/9855218 

Does the cross targeting occur on the synovium tissue of the joint?

Idiopathic Juvenile arthritis and Epstein Barr
http://www.ncbi.nlm.nih.gov/pubmed/19093474
http://www.ncbi.nlm.nih.gov/pubmed/9855218
http://www.ncbi.nlm.nih.gov/pubmed/22057635
http://www.ncbi.nlm.nih.gov/pubmed/22589331

Juvenile arthritis and Staph
http://www.ncbi.nlm.nih.gov/pubmed/834493
http://www.ncbi.nlm.nih.gov/pubmed/19579150

I have associated eczema with staph...so i need to look and see if there is an overlap with eczema and Juvenile arthritis.

Microscopic and Lymphocytic colitis are they fungal?

Autoimmune Hypothesis: a dimorphic infection produces antibodies until a secondary viral infection produces antibodies that cross-target thus triggering the autoimmune disease.

collagenous colitis and lympocytoic are different forms of IBS microscopic colitis
 Lymphocytic colitis tends to be the non bloody diarrhea form.

Microscopic divided into Collagenous and Lymphocytic
http://www.ncbi.nlm.nih.gov/pubmed/2912870

Collagenous microscopic colitis is associated with anti-saccharomyces antibodies
http://www.ncbi.nlm.nih.gov/pubmed/?term=collagenous+colitis+saccharomyces
http://onlinelibrary.wiley.com/doi/10.1111/j.1440-1746.2005.04027.x/abstract

IBS and candida
http://www.ncbi.nlm.nih.gov/pubmed/20885347

Lymphocytic colitis is associated with Candida
http://www.ncbi.nlm.nih.gov/pubmed/23314667

 Lymphocytes actually bind the candida
http://www.ncbi.nlm.nih.gov/pubmed/11796578
http://www.ncbi.nlm.nih.gov/pubmed/8660804

Microscopic colitis affects women more often then men
http://www.ncbi.nlm.nih.gov/pubmed/20878755

Fungal infections change morphology with estrogen. It is possible that these fungal infections generate the antibodies as they peek-a-boo between mold and yeast forms. Since soy is a natural estrogen a patient may be sensitive to soy.  (E.coli which I have connected to Celiac disease is not a fungal infection and is probably not estrogen or soy sensitive.)

Another difference between celiac disease and IBS maybe the gas produced after sugar intake.  Fungal infections feed on sugar and produce gas.

 ( E.coli would not do this thus true celiac disease does not have the bloating after sugar intake rather e.coli turns the sugar into a slime which is seen as mucus in the diarrhea however....c.diff or c.sordelli does make gas)

Remember this is a hypothesis blog. This has not been proven but I am suggesting how things could be occurring.  

If the infections are playing peek-a-boo...and tons of antibodies are being generated what then pushes the immune system into attack, into what we truly call an autoimmune disease I believe requires an virus.

The Viral cross-targeting the intestine seems likely to be the rotavirus or norovirus or cytomegalovirus
http://www.ncbi.nlm.nih.gov/pubmed/17249458

Is IBS merely fungal infections? For the damage to the intestine to occur does the virus have to be there? Is it really an autoimmune disease or just inflammation looking for the virus?

I hope my thoughts help someone out there figure out their disease.
Angela Biggs

UPDATED Feb 25 2016: Gluten sensitivity means you have an infection that crosses barriers : intestinal or blood brain barrier

Is Ulcerative Colitis a c.sordellii infection?

Autoimmune Hypothesis: an infection like C. difficile first builds up antibodies then a virus cross-targets the same focus triggering the autoimmune disease.

(this page is still being worked on)

 c.diff and ulcerative colits
http://www.ncbi.nlm.nih.gov/pubmed/12974208

anti-lactoferrin antibodies in ulcerative colitis
http://www.ncbi.nlm.nih.gov/pubmed/8432453
http://www.ncbi.nlm.nih.gov/pubmed/19758145

Lactoferrin is an antimicrobial protein of our innate immune system. It is found in mucus. The intestine is considered a mucosal membrane. Perhaps the cross-targeting focus is the intestine.

Lactoferrin extremely high amounts and C. diff
http://www.ncbi.nlm.nih.gov/pubmed/23135940
http://www.ncbi.nlm.nih.gov/pubmed/20439046

Epstein-barr virus (mononucleosis)  and Ulcerative colitis
www.annalsgastro.gr/index.php/annalsgastro/article/view/799/593
http://www.ncbi.nlm.nih.gov/pubmed/23574759
http://www.ncbi.nlm.nih.gov/pubmed/2103
this virus can infect the intestine

 My hypothesis is : The c.diff does not alone cause the ulcerative colitis or the epstein-barr virus independently. The cross-targeting of the 2 together that sets off the immune system.

 Other thoughts and questions:

 The ulcerative colitis herbal remedy is said to be chamomile.
People with ulcerative colits  might have daisy flower family allergies. Any one have evidence of this? further some latex is made from dandelions which could cause some people to develop a latex allergy.

Since ulcerative colits is said to be milk and egg sensitive I have been looking to see if the yellow diarrhea is connected to c.diff pigment similar to the staph pigment when plated on egg.  anyone know the answer?

Even more interesting 8/30 thoughts from a newer post:

My thoughts....c.diff may not really be the culprit. C. sordellii which is closely related makes urease like H. Pylori.  H. pylori we know causes ulcers.


Hopeful,
Angela Biggs