New MC research - bacterial aetiology??

[Zizzle]

Wow, Tex. Your Factual knowledge and opinions never cease to amaze me. Someone should bestow upon you an honorary medical degree (if you would accept it ;). I am a firm believer in molecular mimicry. In my case a teenage bout of mono, and the resulting Epstein Barr antibodies, may be to blame. I also blamed my post-partum autoimmunity on microchimerism, the idea that my body was battling my son's cells and DNA within me, which are obviously similar to mine.

Like Sara, I had a fairly healthy diet compared to most Americans, so it baffles me why the junk-food eating crowd doesn't get MC in greater proportions. I'm also curious why younger women are getting this (and IBS). Men must get the same adenoviruses and rotavirus exposures, no? Perhaps all the estrogen-mimicking chemicals are playing a role? Or do we succumb to certain pathogens while pregnant (and immune supressed), that a normal male body would fight off?

I also believe viruses play a much larger role in modern diseases than people give them credit for. I know someone dying from a virus-induced cancer. I know a child once diagnosed bipolar and OCD who turned out to have PANDAS--an autoimmune condition caused by strep bacteria (ok, not a virus). A friend's father diagnosed with celiac a few years ago just died after a brief, month-long battle with pancreatic cancer. And i just learned at least 24 vaccines are grown on cells from discarded human embryos, meaning we are being injected with human DNA and viruses and telling our immune systems to fight them. Oh yeah, and Pepsi continues to use human fetal cells to develop flavor enhancers, because they must to create appetizing products. I honestly don't trust the safety of ANYTHING anymore. I need to find a bubble to go live in.

Interesting about mycotoxind and rice being spared. Maybe that's one reason we tolerate it well? I read about oregano oil and plan to add it to my shopping list. At this point, nothing could make the D much worse, so I'll try anything. I dusted off the Culturelle sitting in my fridge too. I wish I could do the no grains, no sugar thing, but I think I would starve trying.

I've got $2000+ in medical flex spending to use again this year. Wondering where I should head next. Accupuncture? MRT testing? Naturopath? Rheumatologist or new GI?

I want to donate by live body to science! Why isn't anyone out there studying MC? Why are Crohns and UC researchers, with all their resources, still baffled??? We need a medical breakthrough, STAT!!

[mbeezie]

This is an interesting thread . . . the origins of diseases fascinates me. Like Zizzle, I think I noticed far more symptoms after being pregnant, but it was the flu vaccine that finally pulled the trigger in a big way - this I know for sure.

Sara,

I always ate a healthy diet too, or at least what I thought was healthy based on current advice from "experts". In hindsight I think I was eating reactive foods. I also think that we are eating far more chemicals than we realize, even when we are eating healthy foods. Our bodies just weren't designed to handle that much pollution. I have tried to reduce the amount of chemicals in my day to day life as much as possible . . . everything from personal care products to detergents and cleaning products to not burning scented candles. But it is impossible to escape everything, that is a fact of life.

I've also asked the question "why am I not more sick?" Of course I think I would be if I was still eating reactive foods. I went to a seminar last year on this very topic. While we can't prevent getting illnesses, research is showing that there are characteristics associated with people who have a smoother course of disease. Here is what the research says:

Who Stays Well

Anti-Inflammatory Nutrients: pro- and anti-inflammatory proteins, fruits, vegetables, starches, and fats; omega 3- and 6 fatty acids; resveritrol and related compounds; fish and the prevention of depression.
Regular Physical Activity: activities that enhance endurance, strength, and flexibility and reduce chronic inflammation; the dose response of exercise—how much, how often, how intense?
Depression Resistance: seeing challenges as temporary, solvable and impersonal.
The Type-B Personality: replacing hostility and urgency with caring and mindfulness.
Close Relationships: overcoming social rejection, loneliness and isolation; the protective effect of close friends and family.
Emotional Resilience: adaptively responding to thoughts that could trigger immune suppression; how thoughts influence physiology, the importance of expectation and the perception of control.
Mindfulness: ability to separate oneself from ongoing aversive states; ancient Buddhism meets modern neuroscience.
Optimism and Positive Affect: acquired optimism, positive expectations; the power of the placebo and reduction of immune symptoms and need for analgesics.
Meaning: the healing power of beliefs that are life supporting, mood enhancing, and meaning infusing; key research findings.

We had a previous thread on a similar subject (a book on Mind Body Connection that Polly read)\ http://www.perskyfarms.com/phpBB2/viewt ... connection

Mary Beth

[Polly]

Hi Z,

I enjoy reading your ideas and questions! Antibiotics were the trigger for my MC, I believe.

As Tex noted, he and I have always suspected an infectious etiology. In particular, we wonder about Mycobacterium paratuberculosis. I don't have time to reference our old discussions on this, but perhaps Tex will have some extra time today. This bug has long been associated with an MC-type disease in cattle (I think it's Jonne's disease ((SP?))). It is stubborn to treat because it can change form - it takes multiple antibiotics over years even to treat it. It is also almost impossible to culture.

I hope you were just kidding about the "nuclear option". One of the causes of my MC, I believe, was weeks of antibiotics (doxycycline) wiping out my gut bacteria. Apparently, once we wipe out those strains that we have had colonized since birth, we can never really replace them. The bacteria that we get from our mothers during the birth process has somehow been "sensitized", and once it is gone, it can never be replaced. That's why probiotics have to be continually replaced - they have not been sensitized by going through a human GI tract. (We have read about a company in England that is trying to do this with a probiotic). This is the basis for that fecal transplant treatment (from another human) that has been successful for some.

Mary Beth, great list!

Keep these ideas coming!

Hugs,

Polly

[Deb]

Wow, this is an amazing thread. I know that no matter how good my LC symptoms are I will still be here learning all of this fascinating information.
Thanks to all of you for your willingness to share. The more I know the more I realize how little I really do know!

[tex]

It is stubborn to treat because it can change form - it takes multiple antibiotics over years even to treat it. It is also almost impossible to culture.

And apparently, the incubation period can span many years, which makes tracking the source/vector/carrier of the disease even more difficult. Here are a few of the past discussions that Polly mentioned:

http://www.perskyfarms.com/phpBB2/viewtopic.php?t=2791

http://www.perskyfarms.com/phpBB2/viewtopic.php?t=3183

http://www.perskyfarms.com/phpBB2/viewtopic.php?t=10895

http://www.perskyfarms.com/phpBB2/viewtopic.php?t=12392

Tex

[tex]

The more I know the more I realize how little I really do know!

That's so true for all of us, I believe. I know that's probably the main reason why I'm always eager to log onto the board each day.

Tex

[Zizzle]

Thanks for the links to the Mycobacterium Paratuberculosis threads. This website linking it to Crohns was very interesting. Seems there are many examples of patients being successfully treated with many antibiotics over time. But,

To date, no controlled drug trial has been conducted that uses a multi-drug anti-mycobacterial regime that includes macrolide antibiotics. Given the evidence of the studies quoted above, it is likely that such a trial would demonstrate that this is an effective method of treating Crohn's Disease.

http://crohn.ie/archive/chemo.htm

Most of their data is old, and I wonder who, if anyone, is futhering this line of research?

I note that perhaps MCers would be considered as having

The contained "nonperforating" form. This form of Crohn's comes about when the immune system of the sufferer is strong enough to control the mycobacterial infection. However, this immune success comes at a high cost, since inflammation and granulomas are the result. Granulomas are formed when the immune system seals the mycobacteria inside hard shells. Over time, as the body is exposed to infection by Mycobacterium paratuberculosis again and again, more and more of these granulomas form in the intestines, eventually leading to obstruction (blockage) of the intestines. Crohn's patients with the contained nonperforating form of Crohn's disease may not benefit as much from treatment with antibiotics, since their infection may already be under control.

Is there any evidence of granuloma formation in MC?

Interestingly, I came across a group of researchers who were warning about the DANGERS of Vitamin D supplementation in autoimmune diseases like Lupus and Crohns. It had to do with the granulomatous nature of these diseases. Apparently Vit D makes it worse. Now it makes sense to me, that by improving immune function with Vit D, you may be increasing the formation of granulomas around these infections. Wow! So these patients should just supress their immune systems and let the mycobacteria take over?? I don't think so!! It's no wonder people's symptoms and flares come raging back after stopping steroids and related meds. The mycobacteria have been throwing a party in the absence of immune system law and order!!

Interestingly, the website says 40% of cattle are infected. In that case, I would imagine a far greater number of our population would harbor this bug. If so, why doesn't everyone get sick from it? I suppose it's the opportunistic nature, but I would argue that many healthy people have had as many antibiotic/infectious/stressful events as we have, and share many of the same sensitivity genes, and yet they remain well. Can you tell I'm becoming envious of these people?? I'm getting angrier by the minute about this whole thing! Why are we still reading research from 10+ years ago. Where is progress?!?!?

Incidentally, years ago I became fascinated with the Brown Protocol for treating RA. This is a method of pulsing antibiotics long-term to cure RA. Converts talk about experiencing uncomfortable Herxeimer reactions -- from the die off of bacteria, but they do achieve remission eventually. I'm not sure if that means they take antibiotics for life to maintain the remission, and what if any side-effects that may cause (probably MC!). There are rheumatologists across the country who are trained in this method, and I have thought about finding one near me, just to see if it may apply to MC (and my other autoantibodies). It occurs to me that if you are producing Anti-Nuclear Antibodies, your body may be waging war on a mycobacterium that has taken shelter inside your cells. It makes perfect sense to me, but maybe I'm crazy.

Here's the website for the Roadback Foundation dedicated to this method. I encourage you all to take a look. After all, we know most autoimmune diseases are related.

http://www.roadback.org/

[Sheila]

Wow, this is interesting and completely confusing at the same time. I am learning some things that surprised me. Before the Really Big Flare 2010, I had conjunctivitis again! I have not had "pink eye" since I was a child and now I seemed to be getting "sticky" eyes frequently. This time I used my husband's prescription anti-biotic drops for conjunctivitis and immediately the flare began. So, did I "catch" conjunctivitis from my husband who had it a few years ago? Did the antibiotics in the eye drops cause the flare to start? My doc thought that was possible. Or was the conjunctivitis just the forerunner of a major CC flare?

I had one major bout of very serious D 2 years ago that started with antibiotics for an ear infection. I think that was the start of CC. The big flare after Christmas 2010 was blamed on C diff but the lab results (twice) were showing a lot of white cells but no definite C diff. The doc felt that I did have it and kept me on the flagyl for weeks and weeks on end until the D finally slowed down. In the meantime, I'm having this damn problem with my eyes. What is the connection between MC and conjunctivitis?

My mother, who had CC, had a chronic problem with her eyes "running". She was always dabbing at them. The doc said it had to do with her tear ducts. Could it have been her CC causing her eye problems?

THanks.

[Zizzle]

Sheila,
MC is often accompanied by autoimmune eye issues such as Sjogren's (dry eyes) and uveitis.

[Zizzle]

From the Roadback group, here's an explanation about mycoplasmas in autoimmune disease. I wonder if low-dose intermittent antibiotics is causing MC-like symptoms in people following this protocol? I know if I eventually develop RA, I would fully pursue this path.

DISCLAIMER: This is about a treatment for RA and Scleroderma, not MC, but I think it may offer insights into our own disease process and aetiology. They mention several mycoplasma, but not the MAP we've been discussing. Interesting.


About the Antibiotic protocol:
http://www.roadback.org/index.cfm/fusea ... d/145.html

This therapy is not a cure; it is, however, a highly effective treatment. Response varies and is affected by many factors: the strength of your immune system, what your previous medications have been, what medications you might still be using, how long you have had your disease, how severe it is, etc. Some people see almost instant improvement, others get worse before they get better (a response called a Jarisch-Herxheimer reaction). Usually improvement is slow and gradual, often even subtle, but eventual remissions are not uncommon with antibiotic therapy.

http://www.roadback.org/index.cfm?fusea ... lay_id=108

~ KEYS TO TREATMENT ~

* Pathogenicity is a complex set of conditions that regulate the host-parasite relationship.

* Excessive long-term dosage can permanently damage organ functions. Small doses can stimulate the antibiotic effect; large doses can suffocate. Titrate the dose based on host response and tolerance.

* When it is intracellular, the mycopalsma cannot be cultured nor will it respond to antibiotics or antisera.

Only when the mycoplasma is released (cellular death of host cell) can it be isolated and respond to antibiotics.

* Dosage varies with the location of the mycoplasma. ie, clearing the fatty synovium tissue may require higher dosages than clearing the genital tract.

[tex]

Most of their data is old, and I wonder who, if anyone, is futhering this line of research?

Probably no one, because I doubt that Big Pharma is interesting in finding a way to cure the disease by using existing antibiotics. They're content to continue to sell all the drugs that they are marketing to treat flares, by limiting symptoms. Diseases that require lifetime treatment are extremely profitable for the drug companies.

Is there any evidence of granuloma formation in MC?

Yes. http://www.ncbi.nlm.nih.gov/pubmed/15228447

http://www.docguide.com/microscopic-col ... apy?tsid=5

http://www.palpath.com/MedicalTestPages/colitides1.htm

110 patients (67.9%) with normal histology, microcopic colitis not otherwise specified, and isolated small granulomas; 17 (10.5%) patients had findings of borderline diagnostic significance, including possible collagenous colitis, some features of lymphocytic colitis and melanosis coli; and 35 (21.6%) patients, with diagnostic significant histologic findings as collagenous colitis, lymphocytic colitis, minimal change microscopic colitis, eosinophilic colitis, pericrypt eosinophilic enterocolitis, intestinal spirochetosis, schistosomiasis, and Crohn’s disease. Of the 52 patients with either borderline or significant diagnostic abnormalities, in 8 (15.4%) the diagnosis was done only with a proximal study (ascending, transverse, or descending colons).

Apparently, according to the article, 13.6% of people in the study who had chronic diarrhea, had isolated granulomas.

http://www.sovegastro.com/pdf/DIARREA%2 ... OGICOS.pdf

Recently non-necrotizing pericryptal granulomas have been described in cases of microscopic colitis. These cases should not be confused with Crohn's disease.

http://www.histopathology-india.net/MCo.htm

Tex

[sarkin]

Innnnteresting indeed.

Suddenly I am ever so slightly less opposed to having a colonoscopy when I'm more healed. Presumably if there are granulomata, they would still be present, even if collagen is lessened or gone.

That would be worth knowing. Would this be visible (unlike mast cell involvement) without special techniques other than those looking for MC?


I didn't understand this exactly - colonoscopic findings were consistent with microscopic colitis, but histopathological examination revealed granulomatous inflammation. (weren't the findings consistent w/MC also histological? is 'but' the only word I don't grasp?)

And this gave me pause: In two of the patients symptoms have continued for more than 10 years. One patient died as a result of medical complications relating to severe diarrhoea and dehydration.

Do they discuss how many had LC vs. CC?

One article mentions tenascin, which I had learned about on some other research expedition, but have forgotten the context. You guys are doing great - I'm on tenterhooks to see how this turns out, and paddling as fast as I can to keep up.

Love,
Sara

[Joefnh]

Its interesting Zizzle that you mention Epstein Barr as the trigger for your MC. After a trip to Hong Kong in November of 1995, I got really sick and was out of work for 6 months. I had a fever of 101 and massive fatigue that would not stop for almost 4 months and it took an additional 2 months to get back to work. It took almost 2 months from the start for the doctors to diagnose me with the full blown Epstein Barr virus.

I never had mono as a kid and I heard that if you contract mononucleosis (a subset of EBV) then you are most likely to get the full blown more dangerous EBV infection.

It was right after that time period that the 'FMS' diagnosis, the Raynauds syndrome, various allergies and unexplainded boughts of D started. Prior to that event I was an avid long distance runner and competitive skier.... I have never been able to get enough energy to participate in those activities since then.

Joe

[Zizzle]

Sara,

I didn't understand this exactly - colonoscopic findings were consistent with microscopic colitis, but histopathological examination revealed granulomatous inflammation. (weren't the findings consistent w/MC also histological? is 'but' the only word I don't grasp?)

In that example, I believe the author thinks granulomas are not a common finding in MC, since granulomas are generally viewed as a feature of Crohn's. Interesting how close the 2 conditions can be...

Joe,
EBV is implicated in most major autoimmune diseases, so it could definitely be your trigger.

I'm trying to synthesize some of the mental gymnastics I've been doing the past 2 days. Tex, thanks for bearing with me. And all, sorry for all the confusion and unanswered questions!!

I have always been a firm believer that "auto-immune" disease, commonly described as the body erroneously attacking itself, does not exist. Much like I don't believe IBS exists. These are the medical establishment's way of trying to label and treat something they simply don't understand and can't cure. I truly believe our immune systems are trying to attack a pathogenic organism that has taken up residence in our cells. These are organisms we either can't find or can't erradicate. Drug-induced self-limiting LC does not seem to fit this theory, but perhaps the drug irritants create the opportunity for dormant microbes to take over temporarily, until the drug irritatant is discontinued?

One conclusion I am drawing is that even though some unknown mycobacterium or virus is my ultimate foe, there appears to be nothing I (or the medical community) can do to get rid of it for good. So maybe pondering all the microbial suspects is a pointless exercise. If my MC were as debilitating as RA, I might take intermittent antibiotics to feel better, but I'm not that sick, so I won't. Research does show that LC is the body reacting to antigens in the digestive tract, so that brings me back to where we all started, sorting out all my various food intolerances. On to MRT testing, I guess...

[tex]

Would this be visible (unlike mast cell involvement) without special techniques other than those looking for MC?

Yes, those show up quite well with normal staining.

I didn't understand this exactly - colonoscopic findings were consistent with microscopic colitis, but histopathological examination revealed granulomatous inflammation. (weren't the findings consistent w/MC also histological? is 'but' the only word I don't grasp?)

Which article are you referring to?

And this gave me pause: In two of the patients symptoms have continued for more than 10 years. One patient died as a result of medical complications relating to severe diarrhoea and dehydration.

Which article are you referring to?

Do they discuss how many had LC vs. CC?

Which article are you referring to?

If it's the 4th one, (the one from Brazil), of the 162 patients:

37 had MC, (not otherwise specified)
9 had CC
7 had LC
12 had minimal change MC
10 had possible CC
5 had "Some features of LC"

Looking at all the "possibles", "some features", "minimal change", etc., is it any wonder that even pathologists misdiagnose this disease when they are looking right square at the evidence under the microscope.

Love,
Tex