Fecal transplants result in flares in crohn's disease, study stopped.

[kiny]

10 patients with CD given FMT.

No improvement in fecal calprotectin and SES CD score in any patient.

2 out of 10 patients flared due to the fecal transplant, requiring escalation of therapy, study was cancelled.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6620877/
2019 Jul

Department of Medicine, University of California San Francisco, San Francisco, CA, USA

Fecal microbiota transplant for Crohn disease: A study evaluating safety, efficacy, and microbiome profile

''We performed a prospective, open-label, single-center study. Ten CD patients underwent FMT and were evaluated for clinical response (defined as decrease in Harvey-Bradshaw Index score ≥3 at one month post-FMT) and microbiome profile (16S ribosomal RNA sequencing) at one month post-FMT.

The study was halted prematurely because of a presumed CD flare in two patients within a few days of undergoing FMT.

The first patient was a 37-year-old woman with colonic CD who had been diagnosed 10 years prior to enrollment in this trial. Her previous therapies included mesalamine and steroids. She was not on any therapy at the time of FMT. Within a few days of the procedure, she developed worsening abdominal pain and diarrhea. Her fecal calprotectin increased from 475 to >2000 µg/g. CRP increased from 2 to 15.5 mg/l and HBI increased from 3 to 16.

The second patient was a 32-year-old woman with colonic CD. She had been diagnosed 16 years prior to enrollment in the study. She had previously failed adalimumab and infliximab (responded initially with subsequent loss of response) and was on certolizumab at the time of FMT. She had required courses of steroids on several occasions but none in the last year prior to FMT. The day following FMT, this patient experienced increased abdominal pain and diarrhea severe enough to require inpatient admission for intravenous hydration and steroids. Her HBI increased from 11 to 13 post-FMT. CRP increased from 18.3 to 33.1 mg/l.

In this prospective, open-label study of FMT in CD, 30% of patients achieved the primary outcome of improvement of HBI ≥3 points one month post-FMT; however, there was no significant improvement in objective measures of inflammation such as fecal calprotectin and SES CD score.

Two patients in this cohort experienced adverse events requiring escalation of therapy within a few days of FMT that prompted early termination of the study.

Conclusions
Single-dose FMT in this cohort of CD patients showed modest effect and potential for harm''

 

[kiny]

I said it many times, if you know a doctor performing fecal transplants in CD patients, or even suggesting it, run and find another doctor.

These doctors are actively harming crohn's disease patients.

We have known for 3 decades that the fecal stream is causing the inflammation. These doctors should immediately be relieved of their function.

 

[kiny]

I would also suggest to simply be careful with those ''millions of good bacteria'' probiotics.

There is no reliable data that shows that probiotics are beneficial in crohn's disease. Nor are there any reliable studies that show that they are safe for crohn's disease.

The immune system in crohn's disease is responding to bacterial content. Introducing bacteria in the form of probiotics might be harmful instead of helpful.

UC and Crohn's disease are very different diseases. Things that work for UC, might be very harmful in Crohn's disease patients.

 

[wild_one353]

30 patient were given FMT .

26/30 achieved clinical improvement 23/30 achieved remission based on clinical activity
which was higher than other assessment points within 15-month follow-up.

Patients' body weight increased after FMT, and the lipid profile improved as well. FMT also showed a fast and continuous significant effect in relieving the sustaining abdominal pain associated with sustaining CD.

CONCLUSION:
This is a pilot study with the largest sample of patients with refractory CD who underwent single FMT. The results demonstrated that FMT through mid-gut might be a safe, feasible, and efficient rescue therapy for refractory CD.

https://www.ncbi.nlm.nih.gov/pubmed/25168749

 

[kiny]

26/30 achieved clinical improvement 23/30 achieved remission

Nanjing Medical University, Nanjing, China.

Right....the same hospital in Nanjing China that treats IBS with acupuncture and herbal tea...

https://www.ncbi.nlm.nih.gov/pubmed/31110553
and treats crohn's disease with herb extracts...herbs lead to clinical remission in crohn's disease...

https://www.ncbi.nlm.nih.gov/pubmed/26473333
The results this Chinese hospital seems to get with herbs is amazing. They can apparently get people in remissions with herbal teas or herbal extracts. If that doesn't work, they also use acupuncture. And fecal transplants. Maybe they can try massage next..nm they already tried that, it worked apparently.

In other news, 80% of clinical trials coming out of China are apparently completely fabricated.

 

[wild_one353]

So im looking into this China research fraud thing and I found an article about it but it was for pharmaceuticals and FMT doesn't seem like a pharmaceutical, so I'm not sure if that investigation would apply to the work at nanjing university where that FMT study was done. But there is always that possibility that it is not trustworty, but FMT is cheap and natural not a patented pharmaceutical.
https://www.sciencealert.com/80-of-the-data-in-chinese-clinical-trial-is-fabricatedhttps://www.nju.edu.cn/EN/wbout/main.htm

 

[kiny]

Studies coming of out China are highly unreliable. Crohn's disease is much more rare in China, pysicians lack diagnostic tools and experience, which leads to misdiagnosis and rampant abuse of antibiotics. The first and usually only assumption in China if a patient shows ileal granulomatous inflammation is that they have intestinal TB.

Not only should one question all those sensational studies from China that successfully treat crohn's disease with herbs, acupuncture, fecal transplants etc...but wonder if these patients even have crohn's disease to begin with.

When fecal transplant studies from that same hospital in Nanjing China claim sensational remission rates for crohn's disease, that are higher than infliximab treatment.... yet every study in the West seems to result in no remissions and worsening of disease....then someone is wrong.

Either the data coming out of that Chinese hospital is wrong, or all the data from Western studies is wrong. I know which data I trust more, you'll never see me reference a study out of China.

 

[wild_one353]

Studies coming of out China are highly unreliable.

Not only should one question all those sensational studies from China that successfully treat crohn's disease with herbs, acupuncture, fecal transplants etc...but wonder if these patients even have crohn's disease to begin with.

When fecal transplant studies from that same hospital in Nanjing China claim sensational remission rates for crohn's disease, that are higher than infliximab treatment.... yet every study in the West seems to result in no remissions and worsening of disease....then someone is wrong.

Either the data coming out of that Chinese hospital is wrong, or all the data from Western studies is wrong. I know which data I trust more, you'll never see me reference a study out of China.

You are aware of the success of FMT for C. difficile though right? And are you aware of the state of the therapy in USA?
FMT has been approved by the FDA for the last 5 years to be used for antibiotic refractory c diff. or in other words c diff that has not responded to a round of antibiotics, and openbiome has been shipping frozen stool samples all over the country to clinics and hospitals all that time? https://www.openbiome.org/

So if FMT already has a place in treating c. diff ,it is not that much of a stretch to believe that FMT has a place for another gi condition like IBD, therefore the studies coming out of Nanjing University could be true.

Also If Nanjing university has such a bad reputation then why would professor Thomas J. Borody ,the first expert on FMT, be working so closely with their staff?

Prior to the conference Prof. Borody visited the FMT Bank in Nanjing with China's FMT leader Professor Faming Zhang, who was the first to perform FMT in China and has carried out over 1600 treatments to date. Prof. Borody has collaborated closely with Professor Faming Zhang, who is the Director of Intestinal Diseases Center at the 2nd Affiliated Hospital, Nanjing Medical University.

https://www.biospace.com/article/re...t-clinical-trials-to-fight-serious-diseases-/
For those reasons, I believe the research at Nanjing to be at least considered with some value. The fact that it is from china alone is not enough to prove they automatically can't be believed. If anything they are ahead of us a little bit as the successful FMTS indicate a better understanding.

 

[kiny]

You are aware of the success of FMT for C. difficile though right?

I am aware, what does it matter, it's a disease completely unrelated to crohn's disease.

Also If Nanjing university has such a bad reputation then why would professor Thomas J. Borody ,the first expert on FMT, be working so closely with their staff?

Ah yes, Thomas Borody, the magician from Australia. Famous anti-MAP cocktail advocate and advocate of fecal transplants to treat everything.

When other studies in the US or Europe try to recreate his ''successes'' they always come up short somehow. I am not surprised he is now working in China.

 

[kiny]

Regarding Thomas Borody, the magician from Australia that could cure people with Crohn's, now (not surprisingly) working with the herbal magician team in China.



Thomas Borody claimed his anti-MAP treatment caused remission in ALL 9 out of 9 patients with fistula.

And he claimed he could treat active Crohn's Disease, with 6 OUT OF 12 patients were in remission with his anti-MAP treatment., with many of them being ''cured''.

https://www.ncbi.nlm.nih.gov/pubmed/11926571
''RESULTS:
Follow-up data were available for up to 54 months of therapy Six out of 12 patients experienced a full response to the antiMycobacterium avium subspecies paratuberculosis combination. ''



In another study, the magician again claimed the same thing. Anti-MAP treatment caused remission in 54% of patients.

https://www.ncbi.nlm.nih.gov/pubmed/17369114
''RESULTS:
Twenty-two patients (56.4%, 22/39) healed with unusual scarring, which appeared as branched, ribbon-like, elevated lines.''




Yet a study in 2007 by another team, tried to recreate Borody's magic, WITH 213 PATIENTS, and found more people on the treatment actually relapsed than on the placebo.

https://www.ncbi.nlm.nih.gov/pubmed/17570206
''CONCLUSIONS:
Using combination antibiotic therapy with clarithromycin, rifabutin, and clofazimine for up to 2 years, we did not find evidence of a sustained benefit. This finding does not support a significant role for Mycobacterium avium subspecies paratuberculosis in the pathogenesis of Crohn's disease in the majority of patients. Short-term improvement was seen when this combination was added to corticosteroids, most likely because of nonspecific antibacterial effects.''

 

[kiny]

Wildbill, do no alarm bells go off when a doctor in Australia like Thomas Borody does lots of trial in his own private clinic....with results that no one in another hospital can recreate...and then teams up with a Chinese team that also has spectacular results that no one can recreate.

Do no alarm bells go off, when these people always want ''extra funding'' for research.

 

[wild_one353]

I am aware, what does it matter, it's a disease completely unrelated to crohn's disease.

Not true, both conditions have functional changes in the microbiome and less diversity then healthy controls, c. diff is easier to correct while IBD is not as easy. Improvements in both diseases are correlated with the restoration of similar species of microbes, the logic is very similar but the differences are yet to be explained and understood.

 

[kiny]

Not true, both conditions have functional changes in the microbiome and less diversity then healthy controls, c.

Intestinal tuberculosis results in dysbiosis too if left untreated. Do you suggest we treat intestinal tuberculosis with fecal transplants?

Every intestinal disease that features inflammation in the intestine results in dysbiosis. Inflammatory conditions leads to bacterial populatons experiencing stress and others having a fitness advantage, this leads to changes in the microbiome.

When the inflammation in crohn's disease subsides, dysbiosis is no longer observed.

We don't know if dysbiosis is the result or cause of the inflammation in crohn's disease, but I believe it to be a result, and not the cause of crohn's disease. If it was the cause of crohn's disease, fecal transplants should be a straightforward solution to a cure, it is not.

 

[wild_one353]

Intestinal tuberculosis results in dysbiosis too if left untreated. Do you suggest we treat intestinal tuberculosis with fecal transplants?

Every intestinal disease that features inflammation in the intestine results in dysbiosis. Inflammatory conditions leads to bacterial populatons experiencing stress and others having a fitness advantage, this leads to changes in the microbiome.

When the inflammation in crohn's disease subsides, dysbiosis is no longer observed.

We don't know if dysbiosis is the result or cause of the inflammation in crohn's disease, but I believe it to be a result, and not the cause of crohn's disease. If it was the cause of crohn's disease, fecal transplants should be a straightforward solution to a cure, it is not.

You got a few good points here. Not all of them are certainly true though, such as

When the inflammation in crohn's disease subsides, dysbiosis is no longer observed.

I can think of one study that examined that and even in remission a lack of diversity exists in crohn's, but yes the bacterial profile will change somewhat with levels of inflammation. I'll have to find that reference though it does exist.

dysbiosis may not be the most accurate term to describe changes in microbiome, lack of diversity is another related term, dysbiosis could just represent a shift/unbalance of some sort in micro-organisms, while having no change in diversity.

please acknowledge the points I've brought up as well, sorry I have no references at the moment to back them up better, c diff and ibd have many similarities therefore, FMT could treat both, not just more but ,better, research is needed.

 

[Pangolin]

I don't think it's clear whether more or less diversity is in fact a good thing.

 

[wild_one353]

I don't think it's clear whether more or less diversity is in fact a good thing.

You're right its not that clear, but its probably the case. Something needs to be there, we just don't know exactly what yet, so is more better? more often then not more is better but there could just be more pathogens or passive travelers!! So determining which ones are doing what is a prime goal of microbiome research.

Greater diversity is associated with better health, this seems to be the case when comparing IBD patients to healthy controls crohn's is even less diverse then UC.

 

[Pangolin]

I would take any claims of an association between higher microbiome diversity and better health with a grain of salt. I've also seen studies that indicate the opposite. It's just totally unknown, imo.

 

[wild_one353]

There were studies comparing ulcerative colitis patients to crohns patients and found less diversity in crohns, and even less in people with crohn's that have intense fatigue as a symptom. So even within the spectrum of ibd there is a difference in diversity as well as compared to a healthy patient. And in non westernized countries where all rates of chronic disease is lower, the diversity is much much higher compared to our healthiest microbiomes, so its a pretty good general measure of microbiome health, or as far as we know at the moment.

 

[wild_one353]

This study looked at the diversity of only a specific species of bacteria in Crohn's and U.C. vs. healthy controls and found less diversity. This is not overall diversity, only a group of bacteria suspected to be implicated in the regulation of inflammation. So it's a study that is replicating or confirming previous findings, there is consensus that is growing in the concept of diversity, and more specifically to clostridium leptum which may have been renamed as clostridium cluster xiva.

https://bmcgastroenterol.biomedcentral.com/articles/10.1186/1471-230X-13-20

 

[Mommabear]

Regarding Thomas Borody, the magician from Australia that could cure people with Crohn's, now (not surprisingly) working with the herbal magician team in China.



Thomas Borody claimed his anti-MAP treatment caused remission in ALL 9 out of 9 patients with fistula.

And he claimed he could treat active Crohn's Disease, with 6 OUT OF 12 patients were in remission with his anti-MAP treatment., with many of them being ''cured''.

https://www.ncbi.nlm.nih.gov/pubmed/11926571
''RESULTS:
Follow-up data were available for up to 54 months of therapy Six out of 12 patients experienced a full response to the antiMycobacterium avium subspecies paratuberculosis combination. ''



In another study, the magician again claimed the same thing. Anti-MAP treatment caused remission in 54% of patients.

https://www.ncbi.nlm.nih.gov/pubmed/17369114
''RESULTS:
Twenty-two patients (56.4%, 22/39) healed with unusual scarring, which appeared as branched, ribbon-like, elevated lines.''




Yet a study in 2007 by another team, tried to recreate Borody's magic, WITH 213 PATIENTS, and found more people on the treatment actually relapsed than on the placebo.

https://www.ncbi.nlm.nih.gov/pubmed/17570206
''CONCLUSIONS:
Using combination antibiotic therapy with clarithromycin, rifabutin, and clofazimine for up to 2 years, we did not find evidence of a sustained benefit. This finding does not support a significant role for Mycobacterium avium subspecies paratuberculosis in the pathogenesis of Crohn's disease in the majority of patients. Short-term improvement was seen when this combination was added to corticosteroids, most likely because of nonspecific antibacterial effects.''

This Selby trial was flawed though. One of the meds didn’t dissolve and I believe the dosage of one of the others was very low, much lower than what those who follow Borody’s protocol get.

This is the first time I have heard criticism about Borody. He has a huge following, a year’s waiting list to see him. I can’t imagine he would be so popular if he didn’t produce results. And his protocol makes sense to me. He uses biologics initially to reduce inflammation and then AMAT followed by FMT. That seems to work for many. But I agree, and have wondered why others elsewhere cannot match his success rate, particularly since he is very open about his treatment protocol.

Anecdotal I realize, so not scientific but I know people who failing all other treatments have responded very well to AMAT. If it isn’t MAP, why would this targeted therapy work?

I really hope we have a publication from Redhill soon regarding their trial...

 

[Mommabear]

I would also suggest to simply be careful with those ''millions of good bacteria'' probiotics.

There is no reliable data that shows that probiotics are beneficial in crohn's disease. Nor are there any reliable studies that show that they are safe for crohn's disease.

The immune system in crohn's disease is responding to bacterial content. Introducing bacteria in the form of probiotics might be harmful instead of helpful.

UC and Crohn's disease are very different diseases. Things that work for UC, might be very harmful in Crohn's disease patients.

Aren’t the best probiotics simply fermented foods (SCFAs) high in fiber like sauerkraut, which produce butyrate that has shown to be quite beneficial for gut health, including immune regulation?

 

[kiny]

Anecdotal I realize, so not scientific but I know people who failing all other treatments have responded very well to AMAT.

If it isn’t MAP, why would this targeted therapy work?

Any limited benefit from anti-MAP therapy is likely due to its very limited capacity to kill AIEC within the activated macropohage.

Most people with ileal crohn's disease respond to macrophage penetrating antibiotics. They respond especially well to ciprofloxacin, much less so to those anti-MAP cocktails (clarithromycin, rifabutin, and clofazimine) which are far less effective in killing gram neg. E coli. But people simply relapse shortly after.

Mycobacteria are not like AIEC E Coli, MAP cocktails are very ineffective at killing E Coli. Mycobacteria are gram pos bacteria with a very different cell wall than gram neg E Coli. If you use anti-MAP cocktails while the inflammation is being caused by AIEC invading the epithelial barrier, you will not help the patient, you will just create resistance. I don't think anti-MAP cocktails are very effective.

Cipro is more effective, it is most likely killing macrophage penetrating AIEC that has entered through the peyer's patches, not MAP. But antibiotics are not a solution, because people simply relapse on antibiotics, AIEC becomes resistant and depleting the gut flora with broad spectrum antibiotics will simply give AIEC a fitness advantage.

It's good to know antibiotics can cause short term remissions though, we know that bacteria are causing inflammation, we know we can't mimmick crohn's disease in mice in sterile environments and we know that removing the fecal stream high in bacterial load results in remission.

Instead of using antibiotics, you want to go after AIEC by either blocking FimH, or by actually going after the bacteria with bacteriophages, penetrate the biofilm and just kill it through lysis.

Both anti-Fimh and bacteriophages are in development to treat crohn's disease by going after AIEC.

 

[kiny]

Regarding the question, why I think AIEC (E coli) is more likely driving the inflammation and not MAP.

Because studies consistently find E Coli DNA in CD granuloma, not so for mycobacteria DNA. 88% of patients with Crohn's disease have E Coli DNA in their granuloma. (also now isolated from dogs with intestinal inflammation)

We do sometimes find mycobacteria DNA in crohn's disease granuloma, but far less frequent, nowhere near the rates that we are seeing of E Coli. Nowhere near consistently enough to justify widespread use of (rather ineffective) anti-MAP cocktails.

Anti-MAP therapy is far less effective than simply giving people cipro. But both will result in a relapse.

 

[Mommabear]

Any limited benefit from anti-MAP therapy is likely due to its very limited capacity to kill AIEC within the activated macropohage.

Most people with ileal crohn's disease respond to macrophage penetrating antibiotics. They respond especially well to ciprofloxacin, much less so to those anti-MAP cocktails (clarithromycin, rifabutin, and clofazimine) which are far less effective in killing gram neg. E coli. But people simply relapse shortly after.

Mycobacteria are not like AIEC E Coli, MAP cocktails are very ineffective at killing E Coli. Mycobacteria are gram pos bacteria with a very different cell wall than gram neg E Coli. If you use anti-MAP cocktails while the inflammation is being caused by AIEC invading the epithelial barrier, you will not help the patient, you will just create resistance. I don't think anti-MAP cocktails are very effective.

Cipro is more effective, it is most likely killing macrophage penetrating AIEC that has entered through the peyer's patches, not MAP. But antibiotics are not a solution, because people simply relapse on antibiotics, AIEC becomes resistant and depleting the gut flora with broad spectrum antibiotics will simply give AIEC a fitness advantage.

It's good to know antibiotics can cause short term remissions though, we know that bacteria are causing inflammation, we know we can't mimmick crohn's disease in mice in sterile environments and we know that removing the fecal stream high in bacterial load results in remission.

Instead of using antibiotics, you want to go after AIEC by either blocking FimH, or by actually going after the bacteria with bacteriophages, penetrate the biofilm and just kill it through lysis.

Both anti-Fimh and bacteriophages are in development to treat crohn's disease by going after AIEC.

I like your last sentence! I am super intrigued by the potential of bacteriophages for Crohn’s! If it is AIEC how do people become infected? Why are cases growing in Asia and South America? It must be in the food, hence why MAP seems plausible via increased dairy consumption. Is it possible that some people who have gone into remission through diet have done so by increasing good bacteria and eliminating the bad such as AIEC or MAP?

 

[Mommabear]

Regarding finding AIEC and not MAP in granulomas, from what I understand it is extremely difficult to detect and that’s why there is so much controversy. But there is a UK company: PBD Biotech that has created a test using bacteriophages to detect viable MAP. It is in the midst of testing TB patients with it. It would be great to see it used for MAP in Crohn’s patients. Maybe we would finally get the answer that way!

 

[D Bergy]

Naturopaths get rid of C-Diff just using a few drops of food grade hydrogen peroxide mixed in water. Its not that difficult to kill either C-Diff or E-Coli using any oxidizing treatment although C-Diff is the easier of the two being a true anaerobe.

But you run into that standard of care thing that pretty much amounts to “thou shall not use an unpatented non pharma product to resolve anything.”

It’s frustrating watching the contortions the orthodox medical community goes through to get rid of simple infections that those outside that institution can handle with little difficulty using readily available products.

I don’t know about anyone else but I would much rather take a few drops of hydrogen peroxide rather than get a fecal transplant.

In my experience as unorthodox as it is, very few people could benefit even if every bit of MAP was removed from the body. Some could but I am fairly certain the disease is most often polymicrobial and MAP is just one of many bacterium causing chronic inflammation.

Interesting thread for sure.

Dan

 

[kiny]

If it is AIEC how do people become infected?

We don't really know.

Maybe it's not an answer worth pursuing. We've known salmonella, campylobacter, listeria and yersinia cause disease too, and yet every store that sells food is full of them. It wouldn't change anything if we knew how exactly AIEC ends up in people's intestine.

It's important to know what AIEC is doing in Crohn's disease patients, but knowing how it got there wouldn't change anything for patients, nor would it stop future cases.

Is it possible that some people who have gone into remission through diet have done so by increasing good bacteria and eliminating the bad such as AIEC or MAP?

Not for MAP. MAP is within tissue.

Maybe it's possible for AIEC but I doubt it. AIEC enters tissue, but it also sticks to the intestinal wall where it competes with other bacteria for nutrients. You could argue that if you drastically change your diet, you would somehow cause a shift in bacterial populations that would hinder AIEC. But we've seen that those bacterial shifts in response to changes in diets are temporary.

I don't think diet really help in crohn's disease. Elemental diets help, but just changing diets, I don't think that has much of any effect on AIEC, it certainly won't affect MAP.

 

[kiny]

Regarding the long term remission.


AIEC thrives when there is inflammation. AIEC enters the intestine of people with crohn's disease, through peyer's patches for example. This activates macrophages in the lamina propria, which causes inflammation.

Due to innate immunodeficiencies and autophagy deficiencies at the macrophage level, AIEC isn't killed. This causes the inflammation to become chronic, which then causes the mucosal barrier to break down, which allows AIEC even more access to intestinal tissue.

It stops when the inflammation subsides, which causes intestinal healing and prevents further tissue penetration of AIEC.

It is a viscious circle.

People in long term remission somehow broke that viscious circle.

 

[Mommabear]

Regarding the long term remission.


AIEC thrives when there is inflammation. AIEC enters the intestine of people with crohn's disease, through peyer's patches for example. This activates macrophages in the lamina propria, which causes inflammation.

Due to innate immunodeficiencies and autophagy deficiencies at the macrophage level, AIEC isn't killed. This causes the inflammation to become chronic, which then causes the mucosal barrier to break down, which allows AIEC even more access to intestinal tissue.

It stops when the inflammation subsides, which causes intestinal healing and prevents further tissue penetration of AIEC.

It is a viscious circle.

People in long term remission somehow broke that viscious circle.

Does AIEC cause fistula and fissures? When my son was initially diagnosed he was tested for e-coli but it came up negative...

 

[kiny]

The deep transmural inflammation seen in some crohn's disease patients causes fistula. It's not seen in UC for example because they don't have transmural inflammation, that's also why they don't have major wall thickening.

The trigger for that inflammation is probably bacterial in crohn's disease, that chronic inflammation then leads to fistula in some patients.

 

[kiny]

he was tested for e-coli but it came up negative...

Well, you can't test for the presence of crohn's associated adherent invasive E Coli (AIEC) right now, not in any normal setting.

You need a genetic marker that you can identify test after test to start screening patients for AIEC, that test simply doesn't yet exist. Hospitals will never do the elaborate testing you see in studies, they want a reliable ready made test and protocol.

What we do have is anti-OmpC testing, which is positive in most people with ileal CD, and negative in almost everyone with UC. We also have bacterial flagellin tests, which are again positive in most people with ileal CD and negative in UC.

Most people with ileal crohn's disease harbour AIEC, will have a positive anti-OmpC test, and positive bacterial flagellin test.

 

[Mommabear]

Well, you can't test for the presence of crohn's associated adherent invasive E Coli (AIEC) right now, not in any normal setting.

You need a genetic marker that you can identify test after test to start screening patients for AIEC, that test simply doesn't yet exist. Hospitals will never do the elaborate testing you see in studies, they want a reliable ready made test and protocol.

What we do have is anti-OmpC testing, which is positive in most people with ileal CD, and negative in almost everyone with UC. We also have bacterial flagellin tests, which are again positive in most people with ileal CD and negative in UC.

Most people with ileal crohn's disease harbour AIEC, will have a positive anti-OmpC test, and positive bacterial flagellin test.

Mark Davis from Stanford has a project (pending funding) to determine what exactly the T-cells are targeting in Crohn’s. Do you think his results will mostly show AIEC, maybe with scattered MAP, fungus, etc. here and there? I should think it would be a huge help in figuring out what the cause is.

For those who are infected with MAP and not AIEC, do you think the vaccine has a chance of working? If not, why?

 

[kiny]

I have no idea to be honest.