Is Pemphigus foliaceus an autoimmune disease caused by cross-targeting? Do 2 infections trigger disease?

Cross-targeting:  the layering of 2 different infections on one target causing autoimmune disease.  A viral infection marking the inside. A larger infection marking the outside.

Does Pemphigus foliaceus have 2 associated infections?

Herpes virus and Pemphigus foliaceus
http://www.ncbi.nlm.nih.gov/pubmed/19822095
http://www.ncbi.nlm.nih.gov/pubmed/21038546
http://www.ncbi.nlm.nih.gov/pubmed/10606848
http://www.ncbi.nlm.nih.gov/pubmed/21537760


Mycobacterias and  Pemphigus foliaceus
(psoriasis might be mycobacteria caused)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276776
leprosy and Pemphigus
http://www.ncbi.nlm.nih.gov/pubmed/1897831

Mycobacterium chelonae?
http://www.ncbi.nlm.nih.gov/pubmed/16405612

Autoimmune cross-reactivity versus cross-targeting: what is the difference?

Autoimmune cross-reactivity versus cross-targeting: what is the difference?

Think of antibodies as flags the immune system marks an infection with. The antibody flags are only suppose to stick/bind to a sequence of the infection.

Cross reactivity is when an antibody binds not just the antigen(sequence) of the infection but an antigen of self because the protein is either the same or similar enough.  Our own body has accidentally become labeled with infection flags.

Even with the mislabeling our body's immune system is usually intelligent enough not to attack self.

This is where cross targeting comes in.  Cross targeting is when 2 infections have made the immune system focus on one organ.  Antibodies have mislabeled or both infections infect the target.  For the immune system to attack self and turn into autoimmune disease it is my theory that a viral infection has to mark it for t-cells and an outer infection for B-cells has to mark it. 

For example:  Anti-insulin from E.coli could mark the outside of the pancreas through cross reactivity.  Then the person develops the flu which replicates in our pancreas....the virus marking the inside of the pancreas cells.

The layering of infections causes cross-targeting of the immune system to attack from 2 levels and results in type one diabetes where our immune system would attack our pancreas.

Does this make sense?
I hope I am getting better at explaining this.
Angela Biggs

Masticatory Muscle Myositis in dogs similar to muscle issues in children with ulcerative colitis &hip pain or the adult polimyositis?

This page is still under construction and I am unclear what we are looking yet.  I will post my reasons for these posts in the future.

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. A virus marks the inside of the tissue while an outer infection marks the outside...a bacteria or a fungus.

Masticatory muscles myositis and Myasthenia gravis
 http://www.ncbi.nlm.nih.gov/pubmed/12839242
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC340171/


c. diff and dogs
http://www.ncbi.nlm.nih.gov/pubmed/12683608


autoimmune disease of the jaw muscles of german shepards similar to the eye muscles in golden retrievers

target of autoantibodies
http://www.ncbi.nlm.nih.gov/pubmed/17878394

Graves and muscle issues in a child is this similar?
http://www.ncbi.nlm.nih.gov/pubmed/18769095
Hip pain due to muscle atrophy in a ulcerative colitis patient....is this C.diff or c. sordelli?
http://www.ncbi.nlm.nih.gov/pubmed/21453889
muscle wasting in children with IBS
http://www.ncbi.nlm.nih.gov/pubmed/19637389

 like polimyositis in adults?
ulcerative colitis and polimyositis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1374324

Gluten and Schizophrenia? T.gondii's pvm is thread-like and gluten sensitive? or is the gluten sensitive group the tumor/mycobacteria group?

Newer posts have decided that morphology does not connect to gluten and casein. Rather what all these infections have in common is the ability to cross barriers: the intestine and the Blood brain barrier. 
http://angelabiggs.blogspot.com/2015/03/infections-that-break-tight-junction.html

Several autoimmune diseases have gluten and casein sensitivities.  This could be due to morphology shifting. For fungus that means yeast to mold. For bacteria:  rod to string like lengths.

Schizophrenia and t.gondii
http://www.ncbi.nlm.nih.gov/pubmed/24413543

T. gondi has the LON enzyme http://www.uniprot.org/uniprot/B6K9X1
I didn't find t. gondi to have morphology switching so I do not know what we are looking at.

Schizophrenia has the gluten sensitivity: http://www.ncbi.nlm.nih.gov/pubmed/22446142
So something is happening:

T. gondii morphology may not be altered by LON rather the ability of it and other parasites to invade cells. Here is a paper talking about serine proteases and cystene proteases inhibition preventing cell invasion: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1797762
http://aac.asm.org/content/43/6/1358.full 

What I am considering is the PVM, parasitiophorous vauole membrane, is a threadlike extension that T.gondii creates during infection. Could this thread like system be sensitive to gluten and casein like the mold form of a fungus?  Is the LON enzyme involved here?

The PVM appears to be the specialized invasion tool
http://www.ncbi.nlm.nih.gov/pubmed/18512349

LON is casein sensitive (and I believe with the similar amino acid sequence gluten sensitive too).  This could explain the gluten sensitive of schizophrenia.  The parasite is inhibited by gluten...and may react.


T.gondii appears to cross the blood brain barrier.
http://www.ncbi.nlm.nih.gov/pubmed/13678858

Lets consider that maybe it doesn't cross the BBB.  what if it is only when the antibodies get across the BBB when a mycobacteria or strep creates a hole? but then...if you read on...i had previously found that gluten sensitive occur after mice were infected with t. gondi.  If only t.gondi was dimorphic...then this would make sense to me.

By antibodies i am referring to my earlier post of pan/apple domains and receptors. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030169 

THE OTHER POSSIBILITY:
There exists more then one type of schizophernia. The Ovarian teratoma tumor form generates NMDA receptor antibodies just like t.gondii but the tumor's antibodies can't cross the BBB (blood brain barrier) unless another infection which is gluten and casein sensitive does.

So autoimmune schizophrenia has these possibilities:
t.gondii followed by a virus like herpes virus 8
or
tumor with BBB crossing-infection then the herpes virus
This could be why all cases are not gluten casein sensitive. The most likely infection would be mycobacterias because some schizophrenia has been associated with MS and psoriasis...which i have linked to mycobacterias!
http://asdresearchinitiative.wordpress.com/2014/02/22/schizophrenia-greater-risk-of-other-autoimmune-diseases/

Mycobacterias are gluten and casein sensitive. Changing morphology with them. 

Previous thoughts on Schizophrenia:
Here are the references and thoughts I have on Schizophrenia.

First schizophrenia can be autoimmune in that antibodies generated against the NMDA receptor of the brain can cause Hallucinations

ref: Antibody mediated encephalitis: a treatable cause of schizophrenia
British Journal of Psychiatry 2012
200:92-94

The bacteria infection T. gondii can be linked to the NMDA receptor through pan/apple domains.

 T. gonii has pan/apple on it. 

ref: A novel pan/apple domain containing protein for Toxoplasma gondii: characterization and receptor indentification 
PLoS

Schizophrenia has T. gondi antibodies

ref: Antibodies to Toxoplasma gondii in patients with Schizophrenia.
schizophrenia bulletin vol 33 no 3 pp 729-736

In our body when blood clots are degraded, plasminogen which has the PAN sequence in  it, is activated by tPA (tissue plasminogen activator)

t-PA binds not just plasminogen but the NMDA receptor.   Does this mean the NMDA receptor has a PAN/apple domain?

ref: t-PA is a new ligand of NMDA receptor
JBC papers Sept 23. 2004

If antibodies develop against T.gondii included the pan/apple domain does this mean the antibodies might also bind the NMDA receptor? 

Now I can apply my autoimmune hypothesis to it.  A dimorphic infection triggers an autoantibody precursor stage which then progresses into the the disease following a viral infection cross targeting event.

The strain ME49 of T.gondi contains more then one morphology. Both spherical vesicles and tubular elements are found.

The change in morphology might be just like e.coli using LON.  T.gondii appears to trigger a gluten response....but perhaps in this case gluten is inhibiting the "root like" PVM?

ref: Anti-gluten immune response following toxoplasma gondii infection in mice.
PLo S Nov 29 2012 , 7 (11)e50991

Schizophrenia has been associated with gluten and casein

ref. The gluten connection: the association between schizophrenia and celiac disease.
Acta Psychiatr Scand 2006 Feb: 113(2): 82-90

ref: Specific IgA antibody increases in Schizophrenia
1995 society of biological psychiatry 

So we have the bacteria creating the antibodies where the immune system is looking at the neuron's receptor but then we need the cross-targeting virus. The virus would infect the inside of the neurons bearing these receptors thus causing the immune system to have verification of the neuron as a target.  Cross targeting would push one into attacking one's self....making schizophrenia an autoimmune disease. 

Retroviruses were linked to schizophrenia patients in 2001in Germany.  An example of a retroviruses is the Borna virus...a virus which infects the central nervous system.

OR a herpes which infects nerves could be involved.  Herpes virus 8 and 2 are suspects. Could the this virus trigger the cross targeting? The t.gondii antibodies marking the outside of the neuron and the herpesvirus 8 marking the inside of the neurons?

herpes 2
http://www.ncbi.nlm.nih.gov/pubmed/15319094
herpes 8
http://www.ncbi.nlm.nih.gov/pubmed/24560611

Only after cross-targeting would the autoimmune form of schizophrenia develop...but this is a hypothesis and this is just something to consider. It is not proven.

Schizophrenia, infections, and autoimmune disease genetic predisposition (evidence schizophrenia is autoimmune like celiac disease and autism?)
http://www.ncbi.nlm.nih.gov/pubmed/24557043
http://www.ncbi.nlm.nih.gov/pubmed/22193673
http://www.ncbi.nlm.nih.gov/pubmed/16513876

Polyarteritis Nodosa and autoimmune cross-targeting? Linked with autoimmune liver disease?

 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. A virus marks the inside of the liver while an infections marks the outside.....in this case instead of at the liver it occurs in the blood vessels....maybe starting near the liver?


Polyarteritis nodosa is known to have active Hepatitis B
http://www.ncbi.nlm.nih.gov/pubmed/20605819 
http://www.ncbi.nlm.nih.gov/pubmed/11059878

 Polyarteritis nodosa could be caused by cross-targeting involving e.coli because I have previous linked the dimorphic e.coli of bladder infections to autoimmune hepatitis and celiac disease.

Polyarteritis nodosa connected to bladder infections and autoimmune hepatitis.
http://www.ncbi.nlm.nih.gov/pubmed/21119556
but the infection would have to get to the arteries or make antibodies against them.  

Mycoplasmas infecting most organs over time.  This would mean that polyarteritis may more commonly be linked with lupus?
http://www.ncbi.nlm.nih.gov/pubmed/21763578
http://lup.sagepub.com/content/4/6/494.abstract

Because mycoplasmas and e.coli infect the bloodstream...it makes sense how this once started could occur all over. 

Stiffman's syndrome and 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. A virus marks the inside of the kidney while an infections marks the outside.


antibodies to GAD precursor to GABA (nerves are the focus of the cross-targeting)
http://europepmc.org/articles/PMC1753919/pdf/v061p00939.pdf
causes lower back pain 

mycoplasmas and nerves (they can infect them)
http://www.ncbi.nlm.nih.gov/pubmed/16914976
http://www.ncbi.nlm.nih.gov/pubmed/3100660

Lupus and stiffman  (lupus, type 1 diabetes and graves i have previously connected with mycoplasmas)
http://lup.sagepub.com/content/13/3/215.extract
http://onlinelibrary.wiley.com/doi/10.1002/mds.22942/abstract
http://www.ncbi.nlm.nih.gov/pubmed/20537445

Type 1 diabetes and stiffman
http://www.ncbi.nlm.nih.gov/pubmed/10460456
http://www.ncbi.nlm.nih.gov/pubmed/19828214

Graves and stiffman
http://www.ncbi.nlm.nih.gov/pubmed/17712846
http://www.medscape.com/viewarticle/508849_2

Herpes  B and stiffman (rare herpes virus)
http://www.ncbi.nlm.nih.gov/pubmed/15999237
Monkeys as pets risk
http://www.ncbi.nlm.nih.gov/pubmed/9452406

Herpes vaccine and stiffman (genital herpes)
http://patientsville.com/vaccines/hpv4/stiff-man-syndrome-hpv-gardasil-2009.htm

mycoplasmas infect the nerve and then the herpes exposure causes cross-targeting on nerves by the immune system?

This page is still under construction and  may change.

Berger's disease and cross-targeting autoimmunity (NOT Buerger's)

Berger's disease is an autoimmune disease of the Kidney

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. A virus marks the inside of the kidney while an infection marks the outside.

Tonsillitis
http://www.ncbi.nlm.nih.gov/pubmed/16566197

Viruses of the Tonsils that have respiratory infections
RSV Respiratory Syncytial Infection  therefore the most likely culprit

RSV of the Kidney (the virus replicates in the kidney not just the tonsils & lungs) The kidney is the cross-target focus.
http://link.springer.com/article/10.1007%2FBF00862085 

duration of RSV virus secretion (IgM and IgA...IgA lasts around 30 days)
http://www.ncbi.nlm.nih.gov/pubmed/9406652
http://www.ncbi.nlm.nih.gov/pubmed/10830453

boys more likely to have RSV detected
http://www.ncbi.nlm.nih.gov/pubmed/15198187
Note that males are more likely to have Berger's then females.

These diseases are connected: Henoch-Schönlein purpura and Berger
http://www.ncbi.nlm.nih.gov/pubmed/10392263  the emphasis is on IgA antibody levels


Now Looking for the non viral infection:

infections possible...
http://www.ncbi.nlm.nih.gov/pubmed/10392263
Bowel angina...might connect bladder infection e.coli and celiac
Arthritis would connect mycoplasmas

NOTE that the either mycoplasmas or e.coli could be the culprit for cross-targeting with the RSV virus at the kidney.

Gluten (e.coli/celiac)
http://www.ncbi.nlm.nih.gov/pubmed/12046028
http://www.ncbi.nlm.nih.gov/pubmed/1582590
http://www.ncbi.nlm.nih.gov/pubmed/3113643


Antiphospholipids and the kidney (mycoplasmas/lupus)
http://www.uptodate.com/contents/antiphospholipid-syndrome-and-the-kidney
http://www.uptodate.com/contents/antiphospholipid-syndrome-and-the-kidney/abstract/2

churg-strauss and 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.

Churg-strauss syndrome: nasal polyps, asthma, rhinitis

staph or aspergillus?

Churg-strauss and rheumatoid
http://www.ncbi.nlm.nih.gov/pubmed/12589235...rheumatoid factor was there and staph was too

Note that in the past  had made associations of Aspergillus with Churg-strauss:
http://angelabiggs.blogspot.com/2013/04/churg-strauss-autoimmune-vasculitis.html

Churg-stauss and hepatitis B
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845776/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752586/
http://www.ncbi.nlm.nih.gov/pubmed/11791655

interesting especially after my other posts:
http://www.ncbi.nlm.nih.gov/pubmed/11361200

Takayasu: mycobacteria & hepatitis B
Churg-stauss: aspergillus & hepatitis B

Also keep in mind that I have connected Hashimoto's thyroid to fungal infections which means that Churg-strauss should have connections to Hashimoto's.

If the walls of the blood vessel become surface infected by staph or mycobacteria and then the cells themselves become infected with  a virus I believe autoimmune cross-targeting can occur.

The infections can be different in triggering the autoimmune cross-targeting....because it is the target that is significant. 

CPPD with high cholesterol, and mycobacteria or is it gout, staph, and septic arthritis? 2 types?

 Is Gout is connected to mycoplasmas but  CPPD is connected to mycobacterias?

http://www.rheumatology.org/I-Am-A/Patient-Caregiver/Diseases-Conditions/Calcium-Pyrophosphate-Deposition-CPPD

 metabolic syndrome,
http://rheumatology.oxfordjournals.org/content/48/suppl_2/ii2.full 
(i have type 2 diabetes connected to mycobacteria )

psoriasis,
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2426549/
http://archderm.jamanetwork.com/article.aspx?articleid=543012
(note that I have connected psoriasis to mycobacteria on other blog posts and that psoriasis is gluten sensitive)

asthma,
http://www.nejm.org/doi/pdf/10.1056/NEJM185903100600602

Gout and crohn's? is this really CPPD?
not high numbers: http://www.ehealthme.com/cs/crohn%27s+disease/gout
http://www.gout-pal.com/gout-pal-forum/please-help-my-gout/gout-and-crohns-disease/
so maybe this is also genetic susceptibility on top of the mycobacteria or not real?  or it is a mycobacteria related to psoriasis but not crohn's...the type of mycobacteria?

Testimonials of gout and gluten:
http://health.usnews.com/health-news/family-health/pain/articles/2009/02/27/gout-quiz-how-much-do-you-know-about-gouty-arthritis/comments (not celiac disease but gluten sensitive..causes the mycobacteria to morphology switch like I think e.coli can in celiac disease?)


mycobacteria grows on uric acid
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC217648/
http://www.faculty.biol.vt.edu/falkinham/Articles/JB36.pdf

Maybe in these genetically susceptible people their response to a mycobacteria eating their uric acid is to increase the amount of uric acid they make?  No feedback loop occurring so their bodies ramp up production?  (the Hyperuricaemia seen in the first reference)

Gout and high cholesterol
http://www.livestrong.com/article/490117-what-is-the-relation-between-high-levels-of-cholesterol-uric-acid

Cholesterol and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/19634704
http://www.ncbi.nlm.nih.gov/pubmed/18334639
 http://www.ncbi.nlm.nih.gov/pubmed/18505807

 cholesterol as part of the immune system
http://onlinelibrary.wiley.com/doi/10.1111/j.1348-0421.2009.00203.x/full

Note that green tea inhibits the growth of mycobacteria
http://www.sciencedirect.com/science/article/pii/S1357272505003778

Green tea could help the symptoms of gout (by inhibiting the growth?)
http://goutandyou.com/gout-and-green-tea/

Are there 2 types of gout? the uric acid type that green tea might help versus the calcium phosphate type that cherries would help?  Mycobacteria versus mycoplasma type? which group do cherries help?

When gout is connected to RA then cherries and peaches seem to remedy it.
http://www.webmd.com/arthritis/news/20101110/cherries-may-cut-risk-of-gout-flare-ups

RA I have connected to mycoplasmas.
http://angelabiggs.blogspot.com/2013/04/lupus-and-ra-leukemia-and-mycoplasmas.html

Peaches, nectarines, and cherries are constantly battling mycoplasmas. 
http://ohioline.osu.edu/hyg-fact/3000/pdf/HYG_3206_08.pdf

cherries do seem to lower uric acid
http://www.ncbi.nlm.nih.gov/pubmed/12771324

is this gout verse CPPD connection correct?

staph can move in with fungal or mycoplasma biofilms

 Is gout, uric acid, connected to staph infections?
septic arthritis and gout have connections
http://rheumatology.oxfordjournals.org/content/42/9/1062.long

eczema has been found to have high uric acid concentrations
http://archinte.jamanetwork.com/article.aspx?articleid=534273

Takayasus caused by autoimmune cross-targeting?

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.


Takayasu and lupus?are these actually Kawasaki patients?
http://www.ncbi.nlm.nih.gov/pubmed/1351317
http://link.springer.com/article/10.1007%2Fs00296-009-1133-y#page-1
http://www.ncbi.nlm.nih.gov/pubmed/10380843
http://www.ncbi.nlm.nih.gov/pubmed/14986087

Takayasu's and mycobacteria
TA and tuberculosis are chronic granulomatous diseases
http://www.ncbi.nlm.nih.gov/pubmed/8839810
http://www.ncbi.nlm.nih.gov/pubmed/10371844 

type 2 diabetes patients with Takayasu (therefore the virus cannot be common)
http://www.ehealthme.com/cs/type+2+diabetes+mellitus/takayasu%27s+arteritis

confusing review (more common in women...dimorphic supports mycobacteria)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3232509/

crohn's and Takayasu (strong association implicates mycobacteria)
http://www.ncbi.nlm.nih.gov/pubmed/12746644
http://www.ncbi.nlm.nih.gov/pubmed/11907362
http://www.ncbi.nlm.nih.gov/pubmed/33869
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722706/
http://practicalgastro.com/pdf/March09/JudahArticle.pdf
http://www.jmedicalcasereports.com/content/2/1/87

The BCG vaccine? (mycobacteria vaccine)
http://www.ncbi.nlm.nih.gov/pubmed/7901414 (erythema nodosum induced too?)
http://www.ncbi.nlm.nih.gov/pubmed/8569543


erythema nodosum and mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/23650522

looking for virus now: maybe this is not autoimmune?

the genetic susceptibility  found for Takayasu involve the t-cell mail box the HLA?
http://www.news-medical.net/news/20130730/Researchers-uncover-genetics-behind-what-makes-some-people-susceptible-to-Takayasu-arteritis.aspx      That would indicate a virus because HLA tells the t-cell what is inside...if a virus infects a piece would end up in the mailbox...huh.

found it!  Hepatitis B and Takayasu
http://www.ncbi.nlm.nih.gov/pubmed/11361200
http://www.ncbi.nlm.nih.gov/pubmed/7901414

Kawasaki is it autoimmune Cross-targeting triggered? Bcells infected by mycoplasmas?

 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.

Kawasaki is autoimmune:
http://link.springer.com/article/10.1007%2Fs00296-013-2770-8

Mycoplasma pneumonia and kawasaki
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1511717/
http://www.ncbi.nlm.nih.gov/pubmed/21042274
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3120998/
http://www.hindawi.com/crim/medicine/2011/606920/
http://onlinelibrary.wiley.com/doi/10.1111/j.1651-2227.2001.tb00810.x/abstract

Lupus and Kawasaki (lupus could be red blood cells infected by mycoplasmas see earlier posts)
http://www.ncbi.nlm.nih.gov/pubmed/22868216
http://www.ncbi.nlm.nih.gov/pubmed/3379628
http://treato.com/Kawasaki+Disease,Lupus/?a=s

The infection of Bcell lines by mycoplasmas (Lymph nodes are the hubs for Bcells)
http://www.ncbi.nlm.nih.gov/pubmed/16054780

Kawasaki and hepatitis B
http://www.ncbi.nlm.nih.gov/pubmed/14677029
http://www.ncbi.nlm.nih.gov/pubmed/14521027
http://cpj.sagepub.com/content/early/2015/01/29/0009922815569206

Kawasaki and other polyomaviruses
http://www.ncbi.nlm.nih.gov/pubmed/9622713

EBV virus (mono) and Kawasaki
http://jid.oxfordjournals.org/content/162/5/1215.extract
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC499744/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2687726/
http://www.ncbi.nlm.nih.gov/pubmed/7871990
http://pediatrics.aappublications.org/content/73/3/413 

I am considering a separate Kawasaki with Yersinia.....to be continued.  This would have reactive arthritis, graves based thyroiditis (the enlarged thyroid), and  mesenteric lymphadenitis.

Note that I think it is the target that is more relevant then the infection...both Yersinia and mycoplasmas can cause the disease...with EBV.

cogan's syndrome and autoimmune cross-targeting

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.

cogan's syndrome is autoimmune
http://www.ncbi.nlm.nih.gov/pubmed/22846458

 Chlamydia pneuoniae appears in the case history of several Cogan's syndrome patients.
http://www.ncbi.nlm.nih.gov/pubmed/15904966

Looking for the virus culprit now.  Considering the pinkeye connection.

Pinkeye and conjuctivitis
http://www.ncbi.nlm.nih.gov/pubmed/17457917

Looking at Coxsackie B and the ear
Coxsackie B has been implicated in tinnitus
http://www.ncbi.nlm.nih.gov/pubmed/17984924

Board under construction. 

Dermatitis Herpetiformis, Celiac, and E.coli ...caused by cross-targeting autoimmunity?

Autoimmune Hypothesis:
Cross-targeting of the immune system by a viral infection marking the inside of a host cell and second infection marking the outside of the host cell causes autoimmune disease where the organ is attacked.  In the case of Celiac disease: Antibodies against e.coli mark the outside of the intestine then an intestinal virus (mono or hepatitis) infection marks the inside of the intestinal cells.

If celiac disease is e.coli then what about Dermatitis Herpetitformis?

Dermatitis Herpetiformis has been correlated with Celiac.  25% of patients with Celiac disease have  HD.
http://celiac.nih.gov/Dermatitis.aspx

D. herpitiformis and  thesmall intestine's bacteria
http://www.ncbi.nlm.nih.gov/pubmed/4210511

E.coli causes small intestine infections
http://www.pathologyoutlines.com/topic/smallbowelEcoli.html

 The e.coli of bladder infections is the same e.coli of skin infections
http://jcm.asm.org/content/47/6/1811

 Bladder Infections and celiac disease in children
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1511510/

Celiac viral infections: hepatitis and adenoviruses (mono)
http://www.sciencedirect.com/science/article/pii/S1568997208002012
http://www.ncbi.nlm.nih.gov/pubmed/25212692
http://www.ncbi.nlm.nih.gov/pubmed/15492610
http://www.ncbi.nlm.nih.gov/pubmed/23982094

Celiac disease found in hepatitis patients
http://www.ncbi.nlm.nih.gov/pubmed/15645466

This page is still under construction...See previous post of mine: Celiac disease as an autoimmune disease where e.coli is connected to gluten through dimorphic switching.

http://www.blogger.com/blogger.g?blogID=2399123431411408462#editor/target=post;postID=5260289305288915498;onPublishedMenu=posts;onClosedMenu=posts;postNum=44;src=postname

Pick's disease, ALS. and microscopic colits

Autoimmune Cross-targeting hypothesis: that 2 infections exist on a target triggering the autoimmunity.  One viral infection marks the inside while another infections marks the outside.

Link to newer review post
http://angelabiggs.blogspot.com/2015/02/over-view-of-brain-autoimmunity.html

Pick's disease and ALS
http://www.ncbi.nlm.nih.gov/pubmed/3322801
http://www.ncbi.nlm.nih.gov/pubmed/21369423
http://www.ncbi.nlm.nih.gov/pubmed/8410013
http://www.ncbi.nlm.nih.gov/pubmed/15068178

Tau with ALS
http://www.neurology.org/content/66/11/1770.abstract

AlS associated protein found in Pick's
http://www.ncbi.nlm.nih.gov/pubmed/23888880

  Can infections of the feet explain the sport association of ALS? Lou Gehrig's disease
 Trichophyton is the most common skin fungus and causes athletes foot.
http://www.ncbi.nlm.nih.gov/pubmed/18578874

 Trichophyton has a wood rot variety.  This could be found in rotting beaver dams....which might explain the ALS clusters around lakes in north America.
http://link.springer.com/article/10.3839%2Fjksabc.2010.026#page-1

I keep wondering if trichophyton is a type of blastomyces....able to cross the blood brain barrier. http://www.ncbi.nlm.nih.gov/pubmed/9703159
or does it need help? obviously people can have ALS and not pick's....does it require strep or a mycobacteria to make the path to the brain?

The intestinal condition of colitis fits with the other fungal infections (Candida and Saccharomyces) causing colitis which is why I am looking for a fungus in ALS.  I am considering hemorrhoids but i have no evidence.

In addition to not being gluten and casein sensitive it must not have the insulin-like factor.
ALS does not have diabetes associated with it. (candida causing microscopic colitis does have type 1 associated with it) This is another way to determine  that the other fungal infections do not cause ALS even if they all look like microscopic colitis.
 Pick's disease involves Tau proteins in the frontotemporal lobe. This is very different from the parkinson's and alzheimer's which may have connections to mycobacterias.

Here is a case where the person had an ALS diagnosis but it wasn't and gluten free solved it. http://www.youtube.com/watch?v=Wliz6Gbg4fE

 Prediction of ALS associated with Hashimoto's thyroid....looking for references now
only personal posts right now http://treato.com/ALS,Hashimoto%27s+Disease/?a=s 

reference als and hashimoto's
http://users.otenet.gr/~dkount/oldpage/8-1.htm

Alzheimer's, parkinson's,Tourettes: How do they overlap?

Alzheimer's I have been viewing as a mitochondrial disease where the nerve gets stuck in growth mode attempting to call mitochondria down the nerves axon.  Mothers of down syndrome children tend to get the early form of Alzheimer's disease. Down syndrome is caused by malfunctioning mitochondria not making enough ATP for dividing the chromosomes correctly.  Without decent ATP levels the mitochondria do not move correctly.

The herpes virus (cold sore) has recently been discovered to cause mitochondrial dysfunction.  The mitochondria do not move where they are suppose to. In 2011 the herpes virus was associated with Alzheimer's disease.  Infecting the neurons in question.
ref
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1796774/
http://www.sciencedaily.com/releases/2011/04/110404122203.htm

So the question is: How did the virus get past the blood brain barrier?  Everyone with cold sore herpes does not have dementia.

Type 2 diabetes has been associated with Alzheimer's disease.  I have postulated that some type 2 diabetes maybe caused by mycobacterias. So perhaps a mycobacteria has broken the blood brain barrier.  Something must be involved in breaking the BBB like strep or t.gondi or a mycobacteria in order for the herpes virus to get into the brain.

Mycobacteria has been debated: http://www.ncbi.nlm.nih.gov/pubmed/10426143

Parkinson's I have associated with mycobacteria and avian flu/flaviviruses possibly causing an autoimmune disease by cross-targeting.  Do Parkinson's patients who develop Alzheimer's have the herpes virus on top? The mycobacteria breaking the BBB allowing both viruses to sneak through a hole for both diseases?

Tourettes I was considering strep followed by a herpes virus. I am reconsidering now.  Do all Tourettes patients develop Alzheimer's ? Strep breaks the blood barrier. This does not make sense because Tourettes patients tend to have enhanced memory skills.  Is alzheimer's only caused by mycobacteria because strep rarely is infecting a patient long enough to allow herpes across and when it does tourettes results instead?

reference of Strep in brains cells and autoimmunity to brain cells in Tourettes or is this Pandas?
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1174655/  

reference of herpes and Tourettes
http://www.ncbi.nlm.nih.gov/pubmed/3195682

Must mycobacteria be involve with the herpes virus for Alzheimer's to develop? Tourettes with just strep and herpes infections will only have the autoimmune triggered tics? Or is tourettes so genetic that it only needs strep?  you would think the herpes could cross over and do damage causing Alzheimer's which we do not see.....Tourettes patients tend to have brilliant memories. 

2015 update Tourettes is Genetic while pandas which is tourettes like is autoimmune? http://angelabiggs.blogspot.com/2015/02/over-view-of-brain-autoimmunity.html

Cross-targeting means:
 A first infection marks a target with antibodies on the outside and then a virus marks the inside of a target to the immune system. Hypothesis is that cross-targeting triggers autoimmune disease.

I believe that Alzheimer's is not an autoimmune disease rather a mitochondria dysfunction while parkinson's and Pandas are autoimmune. Maybe?

Could this overlap of infectious culprits explain some of the  overlap we see in some patients with Alzheimer's disease? Could herpes be destroying the mitochondria of some elderly causing some cases of Alzheimer's but the patients can later develop parkinson's because it was a mycobacteria the opened the blood brain barrier?   This means there is no order to Parkinson's or Alzheimer's concerning mycobacteria. one could even get parkinson's first?

Where syn and amyloid plaques appear together mycobacteria exists? With Parkinson's as an autoimmune disease of cross-targeting between a mycobacteria and avian flu/west nile? Can we get syn build up before the autoimmunity? before the parkinson's even if just mycobacteria is there?

Do mothers of down syndrome children have the amyloid plaques? When are the plaques not there? Are they a sign the mitochondria can't move and all Alzheimer patients will have some? But the dementia is really the inability of the mitochondria to move? Obviously their mitochondria has malfunction and herpes did not have to be involved.  Again Alzheimer's would be a mitochondria moving disease.

Can the t.gondi of schizophrenia allow the herpes virus across? Notice a theme of larger infections creating the holes allowing viruses to slip through.

I will research this and post references soon. This page is still under construction. (it is a tad confusing at the moment )

Other things that need to be tied in: the diacetyl link to Alzheimer's disease.  Used as the artificial butter in popcorn and margarine it is also the undesirable butterscotch taste in beer.  The mitochondria of S. cerevisiae make diacetyl during the early stages of fermentation.  My suspicion is that since it comes from a mitochondria....it will interfere in high levels with the function of mitochondria in some kind of negative feedback loop.  Thus the popcorn and alcohol dementia are caused by malfunction mitochondrias not moving?  I really hope this is not true. I can't give up my quality beer or wine....honestly i might choose some mental loss later. Or at least hope that it is really just when overdoses and drinking in moderation is fine....we can hope.  My bet is that extremely high doses are required. That or i have to switch to Red Wine.

diacetyl in popcorn and Alzheimer's
http://www.cbsnews.com/8301-504763_162-57489905-10391704/diacetyl-chemical-in-artificial-butter-popcorn-linked-to-alzheimers-plaque-build-up/

So what might be true...herpes with mycobacteria cause mitochondria dysfunction but alone they may not? Or is it that Tourettes is only a genetic attack on the basal ganglia once strep has broken the barrier regardless of herpes....and herpes only makes things worse later for the Tourettes patient.  And herpes just needs to cross the blood brain barrier (a hole made by any of the infections that can ) in order to cause the mitochondria to malfunction.....maybe?

Schizophrenia which could be an autoimmune attack caused by t.gondi breaking the blood brain barrier has had issues with dementia. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1737362
Could these be the patients with the herpes (cold sore) viruses?

update herpes and schizophrenia
http://www.ncbi.nlm.nih.gov/pubmed/15319094

Anyone else have thoughts on this?  Is this possible?

alpha-synuclein and parkinson's

If...and that is a huge if...parkinson's has mycobacterias as part of the causation then how do we end up with alpha-synuclein plaques?

(Parkinson's could be cross-targeting of mycobaterias and avian flu)
 http://angelabiggs.blogspot.com/2013/06/autoimmune-basal-ganglia-from-2.html

We know that Mycobacterias use/eat glutamate and it is routinely used as a component of growth plates.

What if....syn which is involved with the vesicles and secretions of Glutamate by neurons is precipitating in parkinson's disease thus forming the signature synuclein plaques because the demand for glutamate  has increased? more transport vesicles moving the glutamate....extra synuclein proteins...neurons  stuck in secretion mode.

Alpha-synuclein is increased in Parkinson's verse Alzheimer's
http://www.ncbi.nlm.nih.gov/pubmed/23362176 

Over expression of synuclein in mice looks like Parkinson's
http://www.sciencedaily.com/releases/2013/06/130607160329.htm

The amount of glutamate does appear to be increased in Parkinson's disease patients. 
http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030918

They say that Rifampicin which is a antibiotic against mycobacterias interferes with synuclein  expression by interfering with the synthesis of RNA.....it could be helping parkinson's patients more then we realize.....if mycobacterias are instigators of the disease itself.

This could be too far fetched to be real.....but if mycobacterias are in the brain are they attached to the neurons? is it the immune system attacking the nerves?

 Alcoholics have increased synuclein and they do not have parkinson's but can have parkinson's like symptoms. Alcohol causes an increase in GABA release and a decrease of glutamate.  which means the issue is not so much glutamate but synuclein...which is part of the release vesicle.  
 http://www.ncbi.nlm.nih.gov/pubmed/15897720

(glutamate is the green light stimulation transmitter while the GABA is the red light calming nerves)

Not all alcoholics have parkinson's features. Not all mycobacteria infected people have parkinson's....so it still comes down to our own immune system cross-targeting.

The avian flu under suspicion as a Parkinson's trigger increases the expression of synuclein.  Proving that the virus was in the neurons involved.  http://www.ncbi.nlm.nih.gov/pubmed/23851655 

Imagine the outside of the brain cell clutched by a mycobacteria and the inside infected by the flu...even after the infections are gone the immune system has cross-targeted the nerves..the ones with extra synuclein.

Is parkinson's a state where the immune system  does not stop with the infection but continues because of the autoimmune cross-targeting...stuck in a state of inflammation?

immune myelitis after hepatitis B vaccine

The hypothesis up until now has been that autoimmune attack is triggered by the cross-targeting of an infection like a bacteria/fungus then a viral infection.

Anti-insulin marking the pancreas then the flu virus infecting and replicating there causing the immune system to attack the pancreas and causing type 1 diabetes (just one example)

It is baffling then to read that after a hepatitis B vaccine that some kids develop myelitis which is a swelling of the spinal cord.

Hepatitis B is an infection of genital secretions, the blood, the bloods filter the liver....liquid based cells.  How does it cause antibodies to the central nervous system?

The only cross over I can fathom is one between Herpes HSV-2 and Hepatitis B as sexually transmitted diseases of the genitals. Here the location is the same and the immune system could get confused if the infections coexisted.

Then later when a hepatitis B vaccine is received the body would look not just for hepatitis but for herpes.....

note that it is not the vaccine that causes autoimmunity but the virus piece itself in the vaccine and the industry has pulled any vaccine that has reactions....the true trigger is the virus. I  advocate vaccinations.

The chicken pox virus aka vericella zoster virus incubates in the spinal cord.  The varicella zoster virus is the human herpes virus 3 based on homology.  To our immune system it is a herpes virus

Hypothesis:  If there is a history of genital herpes and hepatitis in the mother....and the child has had chickenpox (not the vaccine the actual disease)....then and only then could hepatitis vaccine could trigger myelitis in the child.

Antibodies can cross the blood barrier if the zoster virus (chicken pox virus) has already created holes and crossed. 

Possible? CDC will have to check case histories here.

Asperger's, Sjogren's, and Hashimoto's overlap?

Autoimmune Cross-targeting hypothesis:  The immune system triggers autoimmunity because two infections exist on one target.  One viral inside the target and one visable...like a fungus or bacteria on the outside of the target.

Candida seems to be the candidate for Sjogren's first infection which creates the first antibodies.  Then Hepatitis C virus or epstein barr seems to be the viruses that are involved in the cross-targeting triggering causing Sjogren's autoimmune attack at the lymphocytes.

 Hepatitis C and eptsein barr infect lymphocytes. Candida infects skin, mouth, eyes, lymph, bones, and joints.  The overlap target looks like the lymphocytes.

While I was researching the cross-targeting of Sjogren's this pattern emerged: Asperger's overlapping  Sjogren's and Hashimoto's.

Mother with Sjogren's, son with Asperger's? Or son had early diagnosis of thyroid disorder?
 Several forums...looking for a CDC study. If I can't find this I will request one.

Sjogren's with Hashimoto's  thyroid
http://www.ncbi.nlm.nih.gov/pubmed/23884987
http://www.ncbi.nlm.nih.gov/pubmed/16984944
http://www.ncbi.nlm.nih.gov/pubmed/8422556
http://www.ncbi.nlm.nih.gov/pubmed/9010968

Aspergers's with Hashimoto's thyroid? do they have low TSH causing OCD?
Asperger's have a form of obsessive compulsive disorder but it manifests differently then the tourettes form.
http://www.ncbi.nlm.nih.gov/pubmed/17354567

I had associated fungal infections or strep with Hashimoto's with the low Thyroid stimulating hormone TSH possibly triggering repetitive behavior.

Not associated with repetitive OCD behavior but rather ones kidneys is restless leg syndrome.

Restless leg syndrome with Asperger's
http://www.ncbi.nlm.nih.gov/pubmed/20738960
http://www.ncbi.nlm.nih.gov/pubmed/15450915

Restless leg syndrome with Sjogren's
http://www.ncbi.nlm.nih.gov/pubmed/8252317
http://www.ncbi.nlm.nih.gov/pubmed/17977584

The restless leg could be because of Kidney issues: http://www.ncbi.nlm.nih.gov/pubmed/15165541
Sjogren has been associated with kidney issues: http://www.ncbi.nlm.nih.gov/pubmed/23557013

So if a patient with Asperger's experiences restless legs is it the kidneys just like sjogren's?
Okay just to be cute I will post this: http://www.ncbi.nlm.nih.gov/pubmed/15079170
(i just went to Italy and Michelangelo is still on my mind)


Candida and type 1 diabetes exists for Sjogren...does type 1 diabetes appear in Asperger's?
Is this one type of Candida in particular that can lead to Asperger's?

Note that Asperger's was first diagnosed in 1944 which is a few years after the start of antibiotics.

Sjogren has IBS, does Asperger's have IBS? Irritable bowel syndrome

Forgive the sketchy outline I am starting with....I will update this as soon as I can.
 This theory also still fits with my earlier asperger's post....sjogren overlaps with type 1 diabetes and Candida.

Vitiligo which is the lack of pigment has been associated with Addison's disease. Addison's disease I associate with Candida, viral, and genetic susceptibility. Here is a website where someone is trying to directly link candida and vitiligo: http://blog.probacto.com/vitiligo-and-candida-connection/ 

Here is a paper linking sjogren and vitiligo
http://www.pagepress.org/journals/index.php/rr/article/view/rr.2009.e7/1393

Candida makes a melanin pigment: http://ec.asm.org/content/9/9/1329.full 
Thus if the immune system was after candida and melanin...it could confuse melanin and melanocytes....thus the vitiligo.

  I am bringing this up wondering if pigment issues appear in Asperger's and how much of an overlap exists between albino issues and Asperger's.  Deafness can occur with albino's...can deafness occur from on autoimmune attack on melanin.

I found a personal blog by a mother named Nell with an asperger's child who noticed a huge improvement when her child had gone on Anti-virals.  (vira-stop) Her son Julian had tested for extremely high levels of epstein-barr virus.

Epstien-barr virus is a culprit underconsideration by researchers as an instigator of melanoma...this virus infects melanocytes.  It seems very likely to  me that this could be the cross-targeting that causes Asperger's to be an autoimmune disease.  Candida makes anti-melanin antibodies that focus on melanocytes but our immune system won't attack until a virus also marks it....it is then possible that melanin used in other areas of the the body could be attacked.  Because hearing involves melanin the immune system could cause deafness....some areas of the brain have melanin....but the blood brain barrier must develop a hole....i am not sure how this will develop but at least we have a starting place.

The top most part of the brainstem the mesencephalon is made up of the tectum and the cerebral peduncles. The cerebral peduncles are nerve fibers that carry melanin. Is this area of the brain vulnerable to antibodies or does the blood brain barrier protect it?  Would an autoimmune attack on melanin involve these nerve fibers?  This is the region of the brain for processing the control of eye movements and auditory input.... and quick responses.

As for the cross-targeting Epstein-barr has been known to infect the brainstem region and cause encephalitis. http://www.ajnr.org/content/27/7/1447.long

I have read that asperger's can coexist with dyslexia and that some asperger's kids have coordination issues.  Could this explain what is going on? would immune suppression help? I have them as different groups.

Is Asperger's an autoimmune disease of melanin containing tissue/nerves of the brainstem?  Candida/aspergillus causing antibodies marking the target then the epstein-barr virus infecting the target?





NONE of this could be true..hypothesis...but my imagination can't help but generate possible connections like this for us to look at.  I hope my thoughts help research.

Bipolar disorder is not autoimmune but it could be caused by Graves which is autoimmune

Most of this Blog focuses on an autoimmune hypothesis where 2 infections cross-target on a cell type then autoimmunity develops.

When I looked at bipolar I realized it was not itself autoimmune but from autoimmune thyroid disease not under control.  Thyroid issues need to be identified quickly and continuously monitored so health does not become worse.

Bipolar disease patients have increased monoamine neurons in their brains. Thyroid hormones are involved in the development and regeneration of brain cells. http://www.ncbi.nlm.nih.gov/pubmed/?term=monoamine+bipolar+neurons+Zubieta

Graves disease which is a hyper thyroid disorder where excess thyroid hormone is produced. Bipolar patients have a history of Graves disease. (references coming soon page under construction still)
http://www.ncbi.nlm.nih.gov/pubmed/22842504
http://www.ncbi.nlm.nih.gov/pubmed/22520715
http://www.ncbi.nlm.nih.gov/pubmed/15763125
http://www.ncbi.nlm.nih.gov/pubmed/16271661

Graves disease I have as an autoimmune disorder connected with the mycoplasma infection group: RA, LUPUS, chronic asthma, and some type 1 diabetes.
http://www.ncbi.nlm.nih.gov/pubmed/?term=mycoplasma+graves 
http://www.ncbi.nlm.nih.gov/pubmed/11128659
http://www.ncbi.nlm.nih.gov/pubmed/8943749

Unlike schizophrenia where infections have a direct involvement triggering the autoimmunity to the brain, bipolar I believe is a result of the hyper thyroid.....autoimmunity at the thyroid not at the brain. The thyroid telling the brain cells to grow in excess.

This fits with my theory of Alzheimer's and growth.  Thyroid stimulating hormone receptor is over expressed in the brain of patients with Alzheimer's and Down syndrome, those with mitochondrial defects where neuron growth would be stifled and the brain would attempt to over ride the system and increase growth.  (I have suggested that the APP protein is a growth-on serine protease encouraging neuron growth)

Overlaps and misdiagnosis of the elderly between Bipolar and Alzheimer's disease has occurred because of an overlap in memory loss and mood swings.  Perhaps by comparing these 2 different diseases we may figure out how they work faster...giving clues to the normal functioning system and revealing how the thyroid controls brain cell growth.

Another interesting tangent has to do with Hypothyroid, Hashimoto's disease. What if OCD was linked to the hypothyroid condition...I am looking for references to confirm.  Genetically altered mice with a point mutation in the receptor for thyroid stimulating hormone had less of the neurons and developed repetitive movement disorders.  http://www.ncbi.nlm.nih.gov/pubmed/11530227  Autoimmune hypothyroid I have weakly linked to the fungal infections like aspergillus and candida. 

Strep has been associated with OCD which made me wonder if it effected the thyroid: yes it does. http://www.ncbi.nlm.nih.gov/pubmed/23435638 Streptococcus anginosus infections suppressed the TSH of the thyroid in both of these patients.

The other interesting overlap I have stumbled upon here: stuttering & low TSH.  Autistic kids given the Alzheimer's drug Memantine started stuttering....which makes me think that Memantine is not just a NMDA receptor antagonist but a TSH receptor antagonist.....? 

I hope these thoughts spark research, hope, and stop the worsening of biopolar or OCD in patients.
Angela Biggs

Ulcerative colitis & C. sordellii?

Intestinal infections can develop into autoimmune disease: E.coli can turn into Celiac disease and Sutterella can turn into Autism when a secondary virus causes cross-targeting.

 I wonder if  other infections like the mycobacteria associated with crohn's  or he C. diff developing into ulcerative colitis...have the potential to become autoimmune disease.  I think these are considered inflammation states. (like psoriasis and eczema of the skin)  I will be researching for overlapping autoimmune disorders.

This page is still under construction.

Ulcerative colitis and c. diff
http://www.ncbi.nlm.nih.gov/pubmed/22508484
http://www.ncbi.nlm.nih.gov/pubmed/18484669
http://www.ncbi.nlm.nih.gov/pubmed/19913210
http://www.ncbi.nlm.nih.gov/pubmed/19944802
http://www.ncbi.nlm.nih.gov/pubmed/21915178
http://www.ncbi.nlm.nih.gov/pubmed/22405170

allergy and ulcerative colitis
http://www.ncbi.nlm.nih.gov/pubmed/10912663

Leukocytes and c. diff
http://www.ncbi.nlm.nih.gov/pubmed/22421720

C.diff appearing in low risk populations outside the hospital
http://www.ncbi.nlm.nih.gov/pubmed/17482995 

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.

I wish I could tell if c.sordellii is one of the few that can use Casein.
 http://www.bd.com/ds/productCenter/221858.asp

Other thoughts:
Daisy/chamomile allergy
The natural treatment of ulcerative colitis is chamomile and people I know with ulcerative colitis have Daisy/mum/chamomile allergies. I wonder what is going on.  There are more thoughts on the earlier ulcerative colitis page

Mycobacteria Diseases: Psoriasis, Crohn's, Parkinson's, Panda's, type 2 diabetes ? Cross-targeting autoimmune diseases ?

Autoimmune Hypothesis: 2 infections cross-target to trigger autoimmune disease. When Mycobacterias are the initial infection the autoimmune disease that develops depends on which virus is there to do the cross-targeting. All of these are mycobacteria diseases but not all of them are autoimmune; some are just inflammation.

Crohn's: Mycobacteria and norovirus like virus cross-targeting the intestine or is it just mycobacteria alone?
http://www.ncbi.nlm.nih.gov/pubmed/23128233
http://www.ncbi.nlm.nih.gov/pubmed/9228475
http://www.ncbi.nlm.nih.gov/pubmed/8174989
http://www.ncbi.nlm.nih.gov/pubmed/23971052  (psoriasis and IBS)

similarity between crohn's and Johne's disease
http://www.ncbi.nlm.nih.gov/pubmed/24494172

Psoriasis: Mycobacteria  this not an autoimmune disease just inflammation of the skin from mycobacteria
http://www.ncbi.nlm.nih.gov/pubmed/23675972
http://www.ncbi.nlm.nih.gov/pubmed/23278714
http://www.ncbi.nlm.nih.gov/pubmed/23157912
http://www.ncbi.nlm.nih.gov/pubmed/23036486
http://www.ncbi.nlm.nih.gov/pubmed/22208431 
http://www.ncbi.nlm.nih.gov/pubmed/24050284

Psoriatic arthritis and mycobacterias...could be autoimmune so i will look for a virus next.
http://www.ncbi.nlm.nih.gov/pubmed/22751601
http://www.ncbi.nlm.nih.gov/pubmed/23473929
http://www.ncbi.nlm.nih.gov/pubmed/22413775
http://www.ncbi.nlm.nih.gov/pubmed/22208431

Parkinson's: Mycobacteria (called Nocardia?) crossed over the bloodbrain barrier then a bird flu virus  H5NI then must trigger the cross-targeing of the immune system
Looking for references, this is close:
http://www.ncbi.nlm.nih.gov/pubmed/22821065
http://www.ncbi.nlm.nih.gov/pubmed/12208174
http://www.ncbi.nlm.nih.gov/pubmed/8420152
http://www.ncbi.nlm.nih.gov/pubmed/16257505

(see older post "is parkinson's an autoimmune disease?" while this page is under construction)

Mycobacteria and Multiple Sclerosis (with herpes viruses causing the cross-targeting)
 http://www.ncbi.nlm.nih.gov/pubmed/21409957
http://www.ncbi.nlm.nih.gov/pubmed/14616302
also
http://www.ncbi.nlm.nih.gov/pubmed/15150306 and http://rheumatology.oxfordjournals.org/content/39/8/930.full (which I think psoriatic athritis and psoriasis are mycobacterias)

Type 2 diabetes: raised Il-6 caused by inflammation over mycobacteria. Not all type 2 will be this but perhaps a large group where lifestyle doesn't seem to be a factor in the disease.

Asthma or sinus

PANDAS:  Mycobacteria and strep cross-targeting the basal Ganglia

Mycobacterias are gluten sensitive, changing morphology with the presence of gluten so Psoriasis, this form of parkinson's, this form of asthma....they should all be gluten sensitive.

Psoriasis and gluten
http://www.ncbi.nlm.nih.gov/pubmed/8286249
http://www.ncbi.nlm.nih.gov/pubmed/10651693
http://www.ncbi.nlm.nih.gov/pubmed/14690336
http://www.ncbi.nlm.nih.gov/pubmed/8547041
http://www.ncbi.nlm.nih.gov/pubmed/21418272
http://www.ncbi.nlm.nih.gov/pubmed/16436335


Mycobacterias are sensitive to green tea's  EGCG. Caution should be taken with it. Killing off mycobacteria should help the situation but "kill off" my also trigger allergic responses.

THIS PAGE IS STILL UNDER CONSTRUCTION.

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