• Welcome to Crohn's Forum, a support group for people with all forms of IBD. While this community is not a substitute for doctor's advice and we cannot treat or diagnose, we find being able to communicate with others who have IBD is invaluable as we navigate our struggles and celebrate our successes. We invite you to join us.

Anti-MAP Therapy Support Group

Regarding rifabutin, there may have been some confusion early on about rifabutin vs. rifampin dosage. I clarified with Dr. Chamberlin recently, and he said it was generally 300 mg daily rifabutin, 600 mg daily of rifampin. Patients take one or the other. However, he also mentioned RedHill would sometimes use 450mg rifabutin, and they have done a lot of research on dosages. So definitely not 600mg rifabutin!
I was reading Dr Chamberlains Q&A, and he mentions the herxheimer reaction.

Typically, it's low level sepsis.

That's fever, tachycardia, etc. It's the same "side effect" you get from vaccines (some people). Even non-vaccines will do it (obviously, since AMAT does it).

Crohn was trying to vaccinate people with anti-dysentery serum, and he found it only reduced symptoms, induced remission in people who had a reaction, much like the herxheimer. Other GIs of the time (Hurst, for example) then tried the same thing using silver/mercury/even horse serum. Same results. Only a response following the "serum shock"...

There is also the possibility that the antibiotic is efficiently killing alot of microbes, thus rendering the resulting broken up bacteria to be exposed and taken up through the intestinal wall and into the blood stream, and inducing "serum shock/herxheimer etc", which "resets" the immune system much in the same way Dr Chamberlain says.

It is more than possible that, in addition to hypothesising AMAT therapy works by targeting MAP, it also is equally possible, I suppose, that it is the mass wave of antibiotics killing any and all microbes and thus exposing the body to such a wave of antigenic diversity induces the herxheimer reaction which itself is the "culprit" for the clinical response. Whilst at this point all cards are on the table and each horse has a shot at winning, I lean towards this idea simply because it ties in across a spectrum of diseases (even cancer). But in the end, it's only the scientist in me that cares about that, the patient in me just wants something to work! :)
 
I came down an enterovirus this week that landed me in the hospital. They ran a CT scan as a precaution and it showed that I have extensive small bowel inflammation. My stool tests are negative for c. diff and other obvious pathogens. Based on my recent history, it's likely that the antibiotics have been ravaging my gut. I have been taking probiotics this whole time but they obviously aren't helping.

On the advice of doctors and more importantly my own intuition, I've had to stop AMAT. My small bowel is in a lot of pain and my food absorption status is questionable. I've had to revert to taking morphine again.

The preliminary assumption is that the antibiotics have been corrosive to my bowel and productive of new inflammation. Once the enterovirus hit, everything exploded. My CRP in the hospital was 120 despite no signs in my colon. For the first 4 weeks of AMAT I was also on prednisone. In the last 2 weeks all the pain and discomfort I was experiencing were probably the previously masked side effects of the abx coming to light once my pred taper was complete.

It's interesting that at the beginning of December I had perfect stools and it seemed like everything was normal, but it then turned to constipation and renewed inflammation. I still cannot explain this anomaly.

The one thing I really need to say to the IBD / AMAT community at large that really is driving me crazy is that people need to STOP always calling symptoms "die off" when somebody complains about a set of symptoms. It's highly unlikely that you're having massive die off symptoms after a month of being on full dose AMAT. The majority of die off is going to happen in the initial stages as the active MAP + your gut flora are all dying. After that, "die off" events are more than likely something else, like your own native body tissue becoming inflamed, detox reactions from the antibiotics themselves, etc. When I told the ER doctors that I had been on Clarithromycin for 6 weeks they just shook their heads and said that it's a powerful antibiotic that is very harsh on the guts of most healthy people, let alone someone with IBD. I knew this going on, it's not news to me... but seeing the results in technicolour is another story!

I am glad I gave this a try. I'm upset that I probably still have MAP but have no real way to deal with it now. I wasn't able to stay on AMAT long enough to look for evidence that my IBD was improving with it. What I should have originally done was waited 6+ months for my flare damage to heal before trying AMAT. It may also just be that I can't handle long-term antibiotics like this.

The radiologist who examined my CT scan wrote in his report that I show Crohn's signs, but this should be re-assessed by a GI doctor. There are signs in the terminal ileum. The problem is that enteroviruses can also cause these signs so it's hard to distinguish. I will need follow up endoscopes. It's also possible that the antibiotics have been severely irritating to my gut but it was not possible to know due to simultaneously prednisone use.

I will come back to give an update once I have more information. I am super depressed that this treatment avenue has turned out this way. I feel like the answers are all still unclear. If I do indeed have Crohn's then it means my original diagnosis was wrong or my UC has progressed to Crohn's, which would fit with the MAP picture. Unfortunately now that I have stopped AMAT, future resistance to AMAT antibiotics is likely. FMT is really my last treatment avenue... after that, I have nothing left to throw at my UC. I've done it all.
Hi Connor

We haven't met but I was reading essentially the entirety of this message trail so by the end with this bad news it's like I'm feeling sorry for someone I know already! I'm really sorry things didn't work out for you like with others. I really hope you get a diagnosis soon and get a treatment plan in place. I remember being in that space of not knowing one way or another and also having to deal with pain etc. I hope you find, if not a way out of CD/UC land (we should find some musicians on this board, make a heavy metal PAIN band, and call them CD/UC (like AC/DC?)), then a way to get comfortable which is what all of us had to do at some point. There are some good and great people here who'll listen to you with more care than anyone in your life since we all know what your going through, and when we say "I understand" we really mean it!

Hope you feel better soon!
 
Now that I've stopped the antibiotics and have been doing intensive probiotics, my bowels have become a lot more regular. Solid stools, no blood, although I'm still going 4-5 times daily and there is pain from the recent rawness. I figure that will get better as time goes on. I was even able to start going back to the gym today.

I have been wondering if maybe the 6 weeks of antibiotics cleared other things out that I'm not aware of. I'm also concerned that if my UC is MAP related, that the abx temporarily scaled back the numbers which is why I'm feeling so good. My research into mycobacterial infections has shown that most patients feel better within 1-3 months which tempts them to the stop the treatment because they think they're cured. Then the mycos come back and they're antibiotic resistant.

It's such a shame because underneath the antibiotics, it seems like I have a fairly healthy bowel now. It's possible that if I didn't have such a harsh reaction to the abx, that my current condition is what it would've been like while I was on them.

I'm not really sure how to proceed going forward. Stopping the abx felt right, but my MAP treatment is incomplete. I flare with predictability once per year. I have confirmed mycos in my blood, but whether or not they are IBD related is hard to say. Otakaro does not identify them as MAP, just as mycos.

So I don't really know what to do... that's where I'm at.
 
Connor once again thanks for taking time to share your findings with us, although the outcome was not what one would hope for.

Also, thanks for linking to that thread Crohns2357. I was not aware this topic was so well discussed/covered already back in 2015.
 
You're welcome OleJ. My plan is to see if my bowels achieve remission going forward. As I mentioned before, my UC is highly cyclical and refractory. I get a flare once per year like clockwork, but in between my bowels are very normal, so is my diet. So something is very amiss.

What I'm going to do is wait a couple months until the flare is well behind me, then I will re-test for mycobacteria at the Otakaro Lab. I want to see what my numbers look like under healthy conditions.

I also have the option of re-starting AMAT down the road. I might need a lower dose or a different combo of abx. All I know is that I don't want another life and death flare to strike again... I am so over it.

For now I'm taking LDN 3.5 every night before bed, DHEA, and Entyvio once monthly.
 
Hi all,
It's been a while and I wonder how you are all doing?
I'm doing fine, trying to stay on the lowest possible MTX dose (7,5mg/week + skipping some weeks).
As an experiment I have started to boil the tap water before I drink it. Reports (not from my country though) have shown that MAP can contaminate drinking water and exist for up to a year outside the cattle it comes from. So why not give it a try.
I wish there were more studies done on the possible MAP contamination of drinking water.
Also, I met my new GI last week (the old one quit and moved to another hospital). I asked him about MAP, and he did not know anything about the current research. It is a real problem for us here that GI's are not updated. I mean, I would be way more comfortable if he'd said "yes, I know about it and from what I have gathered, and conferring with my colleagues, we conclude there is not enough evidence to treat MAP as a trigger of intestinal inflammation". But the reality is they don't know about even the Selby study, the Redhill trial, or JHT's vaccine trials. I would have thought it was common knowledge for a GI.
The ones I have met so far have not even been interested.
Sighs.
 
Hi everyone. I just wondered if anyone in the UK had managed to get a Dr to agree to try the AMAT or LDN therapy? My Husband has severe crohns, had several operations, including a J pouch that was created around 18 years ago which is failing as its very scarred. Hes tried all biologics to no avail. We've been together for 9 years and he has not been in remission at all during this time. We saw his surgeon a couple of weeks ago who has suggested a permenant ileostomy but then went on to say he would have to take it above the internal pouch and leave the j pouch in situ because of the risks of taking it out (too many important nerves and blood vessels in the vacinity) but that there would be a 50/50 chance they would have to remove the j pouch anyway at a later date as they can become problematic (still making mucus) so in all he'd have a very high output stoma and the possability of serious issues with the surgery.

As you can probably guess, at 38 years old and with a 5 year old child this is not really an option that he feels he can take given the quality of life it could leave him with.

His Crohns Consultant (Dr Parkes at Addenbrookes in Cambridge, UK) has never offered any alternative to the many biologics he has tried and I am wondering why, given the circumstances, he has not offered this. Surely he should be able to at least try it?

I would love for my Husband to be able to transfer to St Thomas in London to see Dr Sanderson as he supports the MAP Vaccine research (Dr Parkes will not even entertain the idea) but I am not sure how we would go about getting a referal?

Any help would be most appreciated before we run out of time.

Thank you
 
Hi Laura.
I am sorry to hear about your situation. In my opinion a good GI should either take an interest in the latest research and read up on it, or write a referral to another GI who is more knowledgeable in the field.
If I were you, I would schedule a meeting with my GI and push for a referral. I actually got one from my GI a while back, but I have not used it.
The referral is actually pretty straightforward, you can fill out most yourselves, but your GI does need to fill in a few fields and sign.
Maybe an idea could be to print and give your GI the consensus document from the latest MAP conference, as well as (some of) the information on the humanpara.org page regarding til AMAT protocol.
I hope your husband will get better soon!
 
Hi Laura.

You might want to contact with Human Paratuberculosis Foundation.
You can also write to Anti-MAP facebook groups.

You will probably get help from these sources, if you do write.
 
Last edited:
Hi Laura

I live in Ireland and wanted to try AMAT therapy so I paid to see Doctor Sanderson privately. I think it was around two hundred and fifty pound and that was two years ago.
He gave me all the info and wrote a letter to my GI detailing the meds. My GI didn't really believe in this therapy either but he gave me the prescriptions.
I did stay on infliximab and imuran with the rifabutin, clarithromycin and clofazamine as my disease was too severe at the time to risk removing them. Unfortunately it didn't work for me but maybe the other crohns meds hindered it's effectiveness or my disease was too active.
 
Nosebag, thank you for your report. The way AMAT and other drugs interact is yet another unexplored field I guess. I for one have never come across any data. I guess another reason could be that your case of CD is not caused / sustained by MAP in the first place?
 
NHS' recognition and permission for Anti-MAP therapy for treatment-refractory Crohn's patients who do not want to have surgery:


Date of Decision: April 2017
Date of Issue: May 2017
 
Thank you for sharing.

We've had a tough week, my Husband lost his mother last week and his Crohns has been relentless with bleeding and swelling - I guess due to the stress.

We have booked to see Professor Sanderson privately on 14th May, £300 for a half hour appointment but hoping it'll turn out to be a small price to pay for some kind of relief from his constant suffering.

We go on holiday on 21st May and he gets issues with the J-Pouch swelling during flights so really hoping it settles a bit before we go away
 
Thank you for sharing.

We've had a tough week, my Husband lost his mother last week and his Crohns has been relentless with bleeding and swelling - I guess due to the stress.

We have booked to see Professor Sanderson privately on 14th May, £300 for a half hour appointment but hoping it'll turn out to be a small price to pay for some kind of relief from his constant suffering.

We go on holiday on 21st May and he gets issues with the J-Pouch swelling during flights so really hoping it settles a bit before we go away
You're welcome. I assume you read this thread?
My 1st day on AMAT and how I got my funded treatment

Things like meditation, cannabis, diets can be helpful with stress and gut inflammation. Let us know about your husband's appointment.
 
Yes I have thank you.

He has tried various CBD Oils, both with and without the THC but it didnt help. He has also been on oral pred since February which usually helps but hasnt touched it this time (he also followed this with pred suppositories as they were still on his prescription request but no improvement).

We still have the AMAT, LDN and Stelara to try, after that I guess it will have to be the stoma, though he is also seeing Guys & St Thomas colorectal team the day after the appointment with Professor Sanderson to see if they are of the same opinion surgery wise or if they think they will be able to strictureplasty the stricture above his J-Pouch, then at least we have done all we can to try and find a better solution to improving his life.
 
I have read some patients use an anti-tnf biologic with anti-map therapy. I think this can increase the possibility of remission. Might be worth mentioning the doctor.

As always, you can ask for other patients' experiences in the anti-map Facebook groups, they are helpful people. You can also contact Human Paratuberculosis Foundation to ask your questions, they may be able to get in contact with doctors who have knowledge/experience in anti-map therapy and ask your questions to them on your behalf.
 
“Top-line results from the Phase III study with RHB-104 for Crohn’s disease are expected to be announced in approximately three months”

...

“RedHill will host an Analyst and Investor Webcast on RHB-104 for Crohn’s disease on Tuesday, May 15, 2018, at 8:00 a.m. EDT.

Members of RedHill’s executive team will be joined by key opinion leaders who will discuss RHB-104, the MAP US study, Crohn’s disease, the current treatment landscape and potential market. A question and answer session will be held following the presentations.

The conference call, including a slide presentation, will be broadcasted live and available for replay on the Company's website, http://ir.redhillbio.com/events, for 30 days. Please access the website at least 15 minutes ahead of the conference call to register, download, and install any necessary audio software.

Participants who wish to ask questions during the event can do so by telephone. To participate in the conference call, please dial one of the following numbers 5-10 minutes prior to the start of the call: United States: +1-800-263-0877; International: +1-646-828-8143; and Israel: +972-3-376-1315. The access code for the call is 1951893.”

https://www.redhillbio.com/RedHill/Templates/showpage.asp?DBid=1&LNGid=1&TMid=178&Fid=1384&Pid=0&Iid=7173
 
very exiting news on the RHB-104 study. I am just now listening to a webcast presentation on their website. They claim that quote:

"Blinded blended (all patients) remission rate are superior to pre-specified assumptions"

My only worry is that they allow participents to be in treatment with 6-MP and Methotrexate. Given these drug's AMAT properties I fear the picture will be muddy (the effectiveness of RHB-104 will appear less than it is in reality, because of the MAP suppression going on in the control arm).
 
It went really well thank you, amat is a possibility and he's also got him in with a good dietician and on his nhs list for guys hospital so will do his scopes etc and decide the best way forward but he said surgery was definitely not required. Couldn't be happier that he may actually get his life back. He's a great guy and has given us hope when we felt like time had run out
 
RedHill is conducting a first Phase III study of RHB-104 in Crohn’s disease (the MAP US study). The last patient enrolled in the study completed 26 weeks of treatment for primary endpoint evaluation in early May 2018, and top-line results from the study are expected to be announced in the coming weeks.
If the MAP US study results are positive, RedHill will meet with key opinion leaders and the U.S. Food and Drug Administration (FDA) to present the data package and discuss the preferred path to potential approval.
https://globenewswire.com/news-release/2018/07/02/1532291/0/en/RedHill-Biopharma-Announces-Allowance-of-Two-New-RHB-104-Patents-Ahead-of-Top-Line-Phase-III-Results-for-Crohn-s-Disease.html
 
Thanks for sharing. That is really exciting news. Let’s be sure to give the result a thorough review in this thread (or maybe a new one) and remember to present it to our GIs when it arrives :) regardless of the conclusion!
 
I think these are great results, and very comparable to all of the other conventional drug approvals out there for CD. One thing to keep in mind when comparing numbers. All of the biologics are allowed to skew their numbers by giving subjects a loading dose first, and then after 2 weeks, only enrolling the subjects who responded favorably initially. But clearly, that's not a true ITT analysis!

When someone told me this, I coukd 't believe it. So I actually read the two big Humira and Remi studies they used for approval (ex: CHARM). And what do you know - it's true. You have to dig in the appendices sometimes to get the raw data, but about 30-40% of the subjects who got the loading doses were weeded out after 2 weeks due to nonresponse! So I crunched the numbers again adding those people back in, and the remission rates were closer to 30%. So a 37% figure for RedHill is pretty darn good!

Also, this was an add on study with other therapies as well, since the FDA was nervous about the placebo group being off everything for 26 weeks (understandably). They mentioned this in the webinar. But anecdotally from what I've heard from others, AMAT may work best when nothing else is used. I'm interested to see if there is a subpopulation of people on nothing who responded more favorably, and also to see what their secondary endpoint data shows in regard to MAP levels and endoscopic healing.

Either way, this is a hallmark day for patients who can hopefully now look forward to a new therapy which works on a different theory. Hope this will spur further CD research in this area!
 
Irishgal: I think a lot of people (including investors who made the stock fall yesterday and today) were confused about the nature of this study.

1. The majority of participants have had Crohn's for 5+ years, are receiving standard treatment, yet still have high CDAI scores. These are well established and tricky Crohn's cases.

2. The placebo group isn't really just getting a placebo. They're also continuing on standard treatment eg remicade.

So getting a moderate response by adding on a treatment is pretty good in this group, and that's exactly what they found. 37% remission vs. 23% on placebo is a significant improvement and comparable to other widely used treatments.

My guess is that the results would be substantially better in an easier to treat group of patients.

People also looked at the 52 week remission numbers and were disappointed (I think it was 27% or 29% vs. 20% on placebo). It may not be a miracle drug for most patients, but I think they really succeeded in showing that it truly can help some people.
 
Were the study participants (Crohn's patients) tested for MAP, does anyone know?

The antibiotic cocktail has a broad spectrum effect. Reduction in the gut microbiome population does result in healing and reduction in CDAI in Crohn's Disease; regardless of MAP.
 
I think the disappointment for me was this avenue of research targeting this bacteria was kind of talked about as a possible cure avenue and these numbers do not reflect that. The remission rates of remicade and humira are not ideal. I guess I was hoping for much higher remission rates in this trial. I read somewhere that these results are similar to the findings when Crohn's patients are prescribed general antibiotics. Haven't investigated that to find out if there is any truth in it though.
It is also frustrating they are using subjective outcomes, but irishgal said objective results are on their way.
 
Last edited:
RedHill Biopharma (NASDAQ:RDHL) says the market may be "confused" with the week 52 remission secondary endpoint from its Phase 3 clinical trial evaluating RHB-104 in Crohn's disease patients. Shares, initially up, sold off in apparent reaction to the endpoint which appeared to show only a modest separation from placebo.

The company says the endpoint measured "late induction of remission" and did not evaluate the preservation of remission over time. In other words, the endpoint meant to capture those patients who may have needed more than 26 weeks of therapy for initial induction of remission.


From: https://seekingalpha.com/news/3376619-redhill-clarifies-52-week-data-phase-3-study-rhbminus-104-crohns

Regarding the standalone week 52 remission secondary endpoint, we believe there may have been some confusion. The standalone week 52 remission endpoint measures “late induction of remission” and does not evaluate preservation of remission over time. As such, this specific endpoint is neither a clinical nor a regulatory relevant endpoint. The standalone week 52 remission secondary endpoint was merely included by RedHill in the study to investigate whether certain individual patients might require more than 26 weeks of therapy for initial induction of remission. Accordingly, the analysis of standalone week 52 remission is an isolated exploratory outcome.

To emphasize, the clinically and regulatory relevant endpoint pertaining to week 52 is “maintenance of remission”, which by definition evaluates the maintenance (preservation) of remission from the induction of remission or response at an earlier time point to week 52. This “maintenance of remission” endpoint, in conjunction with a separate early “induction of remission” endpoint, has served as the basis for approval of current standard-of-care therapies for Crohn’s disease. In this endpoint, maintenance of remission from the induction of remission at week 16 to week 52, RHB-104 was twice as effective as placebo with high statistical significance (25% vs. 12%, RHB-104 and placebo, respectively, p= 0.007).


From: https://seekingalpha.com/pr/17232359-redhill-biopharma-elaborates-announced-positive-top-line-results-phase-iii-study-rhbminus-104
 
Were the study participants (Crohn's patients) tested for MAP, does anyone know?

The antibiotic cocktail has a broad spectrum effect. Reduction in the gut microbiome population does result in healing and reduction in CDAI in Crohn's Disease; regardless of MAP.
Were all/majority of the study participants tested for MAP before or during enrollment, and which testing procedure was used (the old ones or the newly developed ones)? How many of them were tested positive for MAP? Why not all of them were tested positive for MAP, if MAP is the causative agent? How many of the MAP positive subjects responded to the anti-MAP treatment, and how well did they respond?

What do these data say to us for the age-old MAP problem, and also the possibility of a cure for Crohn's?

Reduction in the gut microbiome population does result in mucosal healing and reduction in CDAI; regardless of MAP. So, even if MAP is completely irrelevant, a positive effect from the antibiotics is expected.

I think the distinction between the reduction of commensal bacteria (bacterial burden) or "anti-map effect" should be made when analyzing the trial data and the effectiveness of the antibiotics.

I will wait for the anti-MAP vaccine trials for a better answer to the MAP problem.
 
Were all/majority of the study participants tested for MAP before or during enrollment, and which testing procedure was used (the old ones or the newly developed ones)? How many of them were tested positive for MAP? Why not all of them were tested positive for MAP, if MAP is the causative agent? How many of the MAP positive subjects responded to the anti-MAP treatment, and how well did they respond?

What do these data say to us for the age-old MAP problem, and also the possibility of a cure for Crohn's?

Reduction in the gut microbiome population does result in mucosal healing and reduction in CDAI; regardless of MAP. So, even if MAP is completely irrelevant, a positive effect from the antibiotics is expected.

I think the distinction between the reduction of commensal bacteria (bacterial burden) or "anti-map effect" should be made when analyzing the trial data and the effectiveness of the antibiotics.

I will wait for the anti-MAP vaccine trials for a better answer to the MAP problem.
Agree with all of this.
 
I don't necessarily agree with the above and here's why:

First, RedHill did test for MAP levels throughout, and they said that data is still to be released. That will answer a lot of your above questions in regard to MAP in this study. Which the validity of which has to be balanced against their MAP test, and they will hopefully release details of their methodology in a peer reviewed journal. Those results will help move MAP science forward I think.

Secondly, I don't think anyone but the MAP vaccine folks term any of this a cure. I look at the RedHill trial as another weapon in the arsenal against CD. It may be MAP only affects a subpopulation of CD patients, and for those patients who are miracle responders, long term healing could approach a “functional cure”, defined as being off all meds for a long period of time without any relapse of CD symptoms. There are some who have achieved this via Prof. Borody's center. They are not the majority, but there are enough of them that it's a possibility for some. But we need more long term data to determine any of this.

Lastly, I don't think you can make the assumption that overall reduction in the microbiome will help CD patients, and therefore antibiotics work generically and not specifically on MAP. This has been one of the huge questions in MAP science and it remains unanswered. However, these antibiotics specifically target mycobacteria. They may work on some others, but it is not true that all antibiotics work to reduce all bacteria. Antibiotics have a specific target, and these are ideal for mycobacteria. Again, we need data for this, and I'm hopeful that this first study will lead to more funding for MAP research so we can answer these data gaps. From a drug company's perspective and on some level to the patient, it doesn't matter WHY the treatment works, only that it DOES. Sure it would be nice to know the why, especially in the case of MAP, but in the meantime, RedHill will hopefully get this therapy FDA approved and then anyone can get it easily! I see this study as a huge win.

I know you are waiting for the MAP vaccine, as are many others, but there have been no peer reviewed papers on this in probably around a decade. This is not the way standard medical research is done. I'm not sure where this project is going and I have doubts about the science of it. I wish them the best, but I'm not counting on it as a treatment option in the next 10 years. RedHill released results now and has given a very detailed path forward, and that's something I CAN count on.
 
Hey irishgal. I agree with what you are saying. I think the thing is with the MAP theory there is a lot of buzz around it because it held/holds the potential to explain the cause of Crohn's in some/all. There aren't really many other avenues being explored right now as the underlying cause of Crohn's. It really would be amazing if the cause was due to a bug just like helicobacter pylori. If they knew the cause to be a bug like that, then a cure would be imminent. We all want to get off immune suppressing drugs.

I see that you say that no one really ever viewed this as a cure except the MAP vaccine folks, and that is fair enough. However, I guess I was hoping for more people to have the "functional cure" you speak of in the trial. I was hoping for numbers more like 77% in remission as opposed to 37%. As I said, the numbers in remission on remicade / humira etc are not ideal. I think we all want meds that help a majority of people, not less than half of people.

It's interesting the point you make about the MAP vaccine - with there being no peer reviewed papers in around a decade. I do find that concerning. It is excellent that Redhill are paving the way for more studies and hopefully approval for this drug. The more drug options we have, the better. I have my fingers crossed that endoscopic data strengthens their findings and does not weaken them.
 
Location
San Diego
I find the result both encouraging and disappointing at the same time - for most of the same reasons mentioned in the discussion above. It will be good to possibly have another tool to help manage Crohn's, but it's miles from being the big cure that MAP true believers have been expecting.

I look forward to eventual FDA approval and having one more option to consider when and if the more effective medications stop working or were not enough in the first place.
 
I find the result both encouraging and disappointing at the same time - for most of the same reasons mentioned in the discussion above. It will be good to possibly have another tool to help manage Crohn's, but it's miles from being the big cure that MAP true believers have been expecting.

I look forward to eventual FDA approval and having one more option to consider when and if the more effective medications stop working or were not enough in the first place.
I agree.
 
For me personally, I tend to hope for the best, but plan for the worst in all areas of life. True CD patient, right! MAP seems like a tough bug to crack, so I was never hoping for huge numbers or a cure out of this. With some tweaking or with another to be created combo therapy, maybe. But these results are about on par with all of the other approved CD drugs. AMAT has provided me nearly 4 years of no CD, and I'm currently on 2 meds, full strength, every other week to hopefully keep whatever I have left in dormancy. I'll take what I can get to beat this horrible disease! I got before and after MAP tests though from Otakaro, so I know for sure my issue was mycobacteria. Maybe others have other issues.

There is currently a debate about what percentage of CD patients have MAP as their primary issue, and that number ranges from about a third, to 100%. The current data, which is hard to consider fully reliable, tests around 30-40% I think. And if you see the RedHill results showed around that number too. Unlike the biologics, they didn't “prime” people for a few weeks with the drug and then only take the ones that responded. Their figures at the 16 week mark were good, and the subset of people who responded at 16 weeks had significantly increased remission rates at 52 weeks.

Also, and this is just a hunch of mine, but I really think AMAT works best when tried 1) as a first line therapy and 2) without any other meds. This was not the study run by RedHill for a bunch of reasons, but they talked about doing this type of study eventually. I think the biologics create dormant, resistant MAP, and that could explain some of these results. I'd be curious to see results of this used first line.

All of this to me adds up to that some people respond really well to AMAT, and some just don't. Whether it is only MAP and those are resistant strains, or whether MAP is only a subset of CD patients remains to be seen. Very excited about their secondary data endpoints, like the MAP levels. I have a feeling this first study will spawn many more and we'll start working on a complete picture of MAP's role in CD. Funding has been a serious issue and has held the science back for a very long time.
 
Location
San Diego
One interesting line of research I would like to see tried would be combo therapy. Treat treatment-naïve patients with the Redhill drug regimen or something similar in combination with say azathioprine or infliximab, or usetekinumab - to battle the disease at the front end and the back end both at the same time.
 
To those of you who have had AMAT, how did you get it? I would be particularly interested if anyone from the UK has managed to get it.

I have had Crohn's for around a year now, it is active at the moment but not severely. Although the odds are it will get worse at some point in the future in my life.

I have asked several consultants about having AMAT, but their response has been along the lines of: We only give this in severe cases. You haven't tried Methotrexate, Azathioprine, Anti-TNF therapy yet, and we'd only consider AMAT if you had tried those and didn't respond.

For someone who believes that MAP is the cause of Crohn's, this logic seems backwards. If someone had a TB infection that wasn't severe (like latent TB) the doctors wouldn't say, "We're not going to treat your TB infection with antibiotics yet because it's not severe, we're just going to give you drugs that mask the symptoms for now".
What you would want to do is kill the infection as soon as possible with all you've got.

My mind is made up. I have read enough studies to convince me that AMAT is more effective, and also has fewer side effects than other treatments like Mtx, Aza, Anti-TNF and steroids.

Can anyone put me in contact with a doctor in the UK who we know is willing to try this? Or give me any advice on how I would look for one?

Edit: Dr. Sanderson of Guy's hospital was mentioned in a previous post. I would be really grateful if I could have some more info about him.
 
Dr. Sanderson may be your best bet. He sees patients privately at the Shard Building in London. I've heard he is a very good doc.
 
I have emailed Dr. Sanderson. I would happily pay to see him privately after the many positive testaments I have read on this forum and others.
Let's hope he has the time to reply.
 
Do we know of anyone having anti-MAP therapy at the same time as a biologic or immunomodulator? (Infliximab, Adalimumab or Azathioprine)?

I remember something that Dr. Borody mentioned in one of his interviews was that it would be interesting to see the results if this was the case. Since biologics and Azathioprine trigger apoptosis (self destruction) of macrophages where the MAP is hiding, it would seem logical that it would make the antibiotics more effective and faster to induce a response.

Although an increased chance of liver toxicity would be a concern.
 
Hello everyone,

I have started the anti-map treatment 2 weeks ago. I am on 200mg Rifampicin daily, 100mg Clofazimine and 750mg Clarythromicin.

I would like to ask people who tried or are currently on the treatment how it went the first couple of weeks / months. When can I start expecting results? I feel terrible at the moment (no energy, headaches, pressure behind my eyes,...), did you experience any side-effects and did they go away? If yes after how long?

I was joyful when I read the results of the Redhill study. However, people in the study only noticed effects after 4 months and achieved remission in 6 months. Will it be the same for us? I think the participants were on lower dosages.


kind regards,

Xavier
 
Hi Xavier - my case was fast in that I started to see improvement by 2 weeks. Still kind if felt horrible (like what you are describing) but I was on higher doses right from the start. It sounds like you are having the typical flu like symptoms. The only thing you may want to get checked out is the eye pressure. Have not heard of that before. When I went through this period, my doc told me to baby myself, take it easy, lay on the couch and watch movies, eat well, and not expect too much. He said symptoms will slowly start melting away, and that was a very accurate description. I found it helpful to keep a journal about how I felt each day, so each week I could track if I was getting better.
 
Thanks for your reply Irishgal. How long did this off-period last for you and what were your negative side-effects? When I look in the mirror now I see a zombie... Also, could I ask what the first symptoms of improvement were that you experienced?

My case is quite special, I'm currently on Vedoluzimab for almost a year now. On paper, my inflamation values are very good. So my doctor keeps telling me I'm in remission. However, none of the Crohn's side effects went away. I'm chronically fatigued, can't gain a single kilo (I'm 7kg's under weight) and my diarrhea never went away. So hoping the improvement from the Anti Map treatment will include energy, weightgain and less diarrhea.

Thank you for the tip on the journal. Will do this!
 
Yes - zombie is a good way to describe it initially. Exhausted, running back and forth to the bathroom, horrible nausea, stomach pain, fever, chills, lack of wanting to do anything other than curl up in a down comforter and hide in bed (it was winter when I started!) After a few weeks I noticed my skin form of CD starting to heal rapidly. That was amazing, since the skin part was hugely painful and almost worse than the GI symptoms, which I was used to after 25 years.

After the nausea went away, I got intensely hungry and ate a ridiculous amount. By 6 weeks I had gained 10 pounds. I also had night sweats for months, which I think was my body's way of getting rid of toxins. I think the things you want to achieve are possible if the therapy works, so just take it easy. It may take a few months. The D was the last symptom of mine to resolve, and while the trips to the bathroom were reduced over time, to get the D to fully go away took about 9 months I recall.

And my doc would soemtimes tell me I was doing OK due to low-ish inflammatory markers, but I still felt terrible. That was addressed a little at the conference this weekend. The markers of healing and inflammation don't always correspond exactly to how the patient feels, which is interesting. I'd also recommend trying to do everything you can to help your body recover, like getting enough sleep, doing some exercise, eating well and avoiding trigger foods and things like sugar and fried or processed junk food. That seemed to help me a lot initially. Ginger and peppermint tea were also very helpful. Keep in touch with your doc if you feel like there's something really horrible or out of the ordinary going on as well!
 
Yes - zombie is a good way to describe it initially. Exhausted, running back and forth to the bathroom, horrible nausea, stomach pain, fever, chills, lack of wanting to do anything other than curl up in a down comforter and hide in bed (it was winter when I started!) After a few weeks I noticed my skin form of CD starting to heal rapidly. That was amazing, since the skin part was hugely painful and almost worse than the GI symptoms, which I was used to after 25 years.

After the nausea went away, I got intensely hungry and ate a ridiculous amount. By 6 weeks I had gained 10 pounds. I also had night sweats for months, which I think was my body's way of getting rid of toxins. I think the things you want to achieve are possible if the therapy works, so just take it easy. It may take a few months. The D was the last symptom of mine to resolve, and while the trips to the bathroom were reduced over time, to get the D to fully go away took about 9 months I recall.

And my doc would soemtimes tell me I was doing OK due to low-ish inflammatory markers, but I still felt terrible. That was addressed a little at the conference this weekend. The markers of healing and inflammation don't always correspond exactly to how the patient feels, which is interesting. I'd also recommend trying to do everything you can to help your body recover, like getting enough sleep, doing some exercise, eating well and avoiding trigger foods and things like sugar and fried or processed junk food. That seemed to help me a lot initially. Ginger and peppermint tea were also very helpful. Keep in touch with your doc if you feel like there's something really horrible or out of the ordinary going on as well!
Thank you so much for your detailed response. I guess all I can do is wait and see what happens. How long did it take for your tiredness to go away? The reason I'm trying this is to get rid of it, but now that it became even worse I'm hoping it will fade away. I don't have fever, chills, more diarrhea, nausea,... however.

Oh and I see that you take (or took) LDN. Would you recommend this?
 
I can't recall exactly on the exhaustion when it started going away. Maybe a few months? I have little kids though, so constantly live in a state of semi-exhaustion. I have a lot more energy now that I'm better though, so the exhaustion from the CD has probably resolved now, but the exhaustion from kids, work, not enough sleep and daily life is probably self imposed.

And yes - I started LDN arund 6 months into treatment when Levo failed. I was prett much better by then, so it's hard to know if it's doing anything. My integrative doc recommended it to help my immune system. So far I'm well, so not rocking the boat!
 
Xavke91, I have tried LDN in the past. My disease was very severe and nonresponsive to the immunosuppressives, biologics, and the combination therapies. The LDN significantly lowered my CRP count (more than any other drug), but it didn't give me remission. My symptoms were a little better; but not much change. I took 4.5 mg right from the beginning, and took it for about four months, if I remember correctly.

As for recommendation, If you make a thorough research about it yourself, and think it would be good for you; then why not? It seemed to me safe back then. I don't know how the anti-map and LDN interact, maybe look into "Drug Interaction Checker" links for naltrexone and the antibiotics used for the anti-map therapy. Ask about it in the anti-map facebook groups, and the other online forums.
 
Last edited:
I can't recall exactly on the exhaustion when it started going away. Maybe a few months? I have little kids though, so constantly live in a state of semi-exhaustion. I have a lot more energy now that I'm better though, so the exhaustion from the CD has probably resolved now, but the exhaustion from kids, work, not enough sleep and daily life is probably self imposed.

And yes - I started LDN arund 6 months into treatment when Levo failed. I was prett much better by then, so it's hard to know if it's doing anything. My integrative doc recommended it to help my immune system. So far I'm well, so not rocking the boat!
Hi Irishgal, I have a quick question. My doctor wants to prescribe me steroids for inflammation that is going up again. Is it safe to take corticosteroids with amat? I read in a pamflet online that amat and steroids can be prescribed together. They want to give me Budesonide, but when I look online I see written that clarythromicin and Budesonide should be avoided? Do you know anything more? Thank you!
 
Xavke91, I have tried LDN in the past. My disease was very severe and nonresponsive to the immunosuppressives, biologics, and the combination therapies. The LDN significantly lowered my CRP count (more than any other drug), but it didn't give me remission. My symptoms were a little better; but not much change. I took 4.5 mg right from the beginning, and took it for about four months, if I remember correctly.

As for recommendation, If you make a thorough research about it yourself, and think it would be good for you; then why not? It seemed to me safe back then. I don't know how the anti-map and LDN interact, maybe look into "Drug Interaction Checker" links for naltrexone and the antibiotics used for the anti-map therapy. Ask about it in the anti-map facebook groups, and the other online forums.
Which are the anti-map facebook groups? Thanks!
 
The risk with taking clarithromycin and budesonide together is that the clarithromycin may inhibit the breakdown of the budesonide and allow it to escape the first pass metabolism and become more of a systemic steroid than a localised one.
In short it may mean that the budesonide acts more like prednisone and has effects on the whole body rather than just the gut like it usually does.
If you take the budesonide first thing in the morning and then the clarithromycin at least 3-4 hours afterwards you will lessen the risk as most of the budesonide should have been processed by then anyway.
Some other anti-MAP antibiotics that have this same effect include rifampin and isoniazid.
I have taken this combination together myself and been fine. There is the potential for many interactions with anti-map antibiotics, the drugs.com interaction checker is a good resource.

But as always, don't rely solely on my advice or that of the interaction checker, always ask your doctor if you are unsure.
 
Hi Irishgal, I have a quick question. My doctor wants to prescribe me steroids for inflammation that is going up again. Is it safe to take corticosteroids with amat? I read in a pamflet online that amat and steroids can be prescribed together. They want to give me Budesonide, but when I look online I see written that clarythromicin and Budesonide should be avoided? Do you know anything more? Thank you!
Not totally sure on the interactoins. Not a doc, but sounds like there may be some issues from the other posts. I do know people taper off of steroids by introducing AMAT, but not sure which form of steroids they were talking about. Maybe just straight pred. When in doubt, I'd always ask the doc!
 
Letter to NICE regarding Crohn's Disease management update CG152

Dear Sir / Madam,

As a group of patients with Crohn’s Disease, close family members and friends or doctors with an interest in Inflammatory Bowel Disease, we would like to request that your current review of the guidelines for post-surgical Crohn’s disease management include discussion of the option of anti-MAP antibiotic therapy (AMAT) for the treatment of Crohn’s. AMAT is a treatment combining the antibiotics Clarithromycin, Rifabutin and Clofazimine to target Mycobacterium avium subspecies paratuberculosis (MAP). The rationale for this treatment is based on increasing evidence supporting the hypothesis that Crohn’s disease is caused by MAP in susceptible patients.

In particular, we would request that the panel review the recent data from the phase III randomised controlled trial ‘Efficacy and Safety of Anti-MAP Therapy in Adult Crohn's Disease’ (MAPUS) led by Redhill Biopharma (https://tinyurl.com/RedhillRHB104) and consider whether AMAT should be included as an additional treatment option in the updated guidelines. These recent trial data suggest both safety and efficacy of this treatment over standard care including corticosteroids, immunosuppressants, oral 5-ASA compounds and biologics (infliximab or adalimumab). Of note, AMAT does not carry the rare but life-threatening risks associated with biologics (e.g. lymphoma) nor the risks associated with long-term immunosuppression. At a cost of £4660 for a 12-month course, the treatment compares favourably to current therapies in terms of cost-effectiveness.

Given these data are in the public domain, it seems likely that many patients will seek information and guidance on this new treatment option. It is therefore important that national recommendations provide guidance for doctors making difficult decisions together with patients who may have exhausted all other treatment options.

We thank you in advance for your consideration and look forward to your response.
 
https://www.sciencedirect.com/science/article/pii/S1590865807000138

Anti-mycobacterial therapy in Crohn's disease heals mucosa with longitudinal scars
T.J.BorodyS.BilkeyA.R.WettsteinS.LeisG.PangS.Tye

Abstract
Background
A possible causative link between Crohn's disease and Mycobacterium avium ss paratuberculosis has been suggested.

Aim
To report unique scarring in Crohn's disease patients treated with anti-Mycobacterium avium ss paratuberculosis therapy.

Patients
A retrospective review of 52 patients with severe Crohn's disease was conducted. Thirty-nine patients who had at least one follow-up colonoscopy during treatment were included.

Methods
Patients received rifabutin (up to 600 mg/day), clofazimine (up to 100 mg/day) and clarithromycin (up to 1 g/day) – anti-Mycobacterium avium ss paratuberculosis therapy – for 6 months to 9 years. Ramp-up dosing was used. Colonoscopies and histological analyses monitored progress.

Results
Twenty-two patients (56.4%, 22/39) healed with unusual scarring, which appeared as branched, ribbon-like, elevated lines. In 2/6 patients (33.3%) who had >3 years of treatment after scarring occurred, scars receded, becoming imperceptible as full healing occurred. Histologically, a marked reduction in inflammation occurred in 15/39 patients (38.5%). Of these, 6/15 patients (40%) displayed restoration of normal mucosa. Longitudinal scarring occurred in 12/15 patients (80%) with improved histology.

Conclusions
The presence of scarring fading to normal mucosa on anti-MAP therapy implies a more profound healing not seen with standard anti-inflammatory and immunosuppressant drugs. Longitudinal scarring and consequent healing with normal histology should become a standard treatment goal for Crohn's disease.
 
I forgot about this post for a while but I am doing very well now.
Within a week of starting the infliximab all of my symptoms went completely away and I started putting weight back on. I was previously underweight.
My calprotectin went from being around 1100 to low 20s within 3 weeks.
I have now been in total remission for around 2.5 months and have put on around 5kg in weight.
This is quite significant considering that a few months ago, in the words of my consultant, I had severe pan-enteric crohn's disease with lesions in the stomach, duodenum, ileum, terminal ileum and right side of the colon.
I will never know whether I would have had such a good response without the anti-map but my consultant says that my response has been faster and better than you would usually see with infliximab alone.
My plan is to continue the infliximab maintenance indefinitely or until I lose response to it. I plan to continue the azathioprine at full dose, and if I reach 6 months of remission, go down to half the dose of azathioprine since there is some research which suggests full dose is no more effective than half dose after 6 months of remission in combination therapy.
I plan to continue the anti-map for 1-2 years depending on whether or not I stay in remission.
Another "I started Anti-MAP" thread
 
Hi

I am currently on Anti map therapy the last 4 weeks 150mg of rifabutin twice daily, 500mg clarithromycin once daily and 100mg of clofazamine daily. My weight is around 120lb or 54kg. Is the dosage of my medication correct for my weight?
I still take stelara every 4 weeks also. I don't know if the anti map is working as of yet or if I am on the correct dose.
If anyone knows the answer I would be grateful.
 
Hi Nosebag. A good reference for the drugs and dosages are here: https://humanpara.org/for-clinicians-chamberlin-amat-protocol/
Your dosages are correct apart from the clarithromycin which should be 500mg twice daily instead of once.
How did you get the Anti-map?
Hopefully you should see improvements in the next few weeks.
Are you on an immunomodulator as well such as methotrexate or azathioprine/6MP?
Anti-Map with ustekinumab may be a good combination.
 
Hi Nosebag. A good reference for the drugs and dosages are here: https://humanpara.org/for-clinicians-chamberlin-amat-protocol/
Your dosages are correct apart from the clarithromycin which should be 500mg twice daily instead of once.
How did you get the Anti-map?
Hopefully you should see improvements in the next few weeks.
Are you on an immunomodulator as well such as methotrexate or azathioprine/6MP?
Anti-Map with ustekinumab may be a good combination.
Hi Kas8173

I tried it a few years ago and it didn't work. Doctor Jeremy Sanderson prescribed my dose and gave me information to give to my GI.That was the dose he prescribed at the time so I thought it was based on my weight. I have high liver counts previously so I hope they will allow me up the dosage.
I have taken Imuran and different biologics previously and they failed. My large bowel is diverted and I have an ileostomy but crohns has returned in both areas.
Thanks for your help.
 
Scafo88, I am adding your first post here, so that more people can see it. Maybe someone will give you a good information.

Hi All -

My son (10) started anti-map therapy a week ago. I would love to hear any other parents/folks experience. A little about my son. He was dx at 6 with UC then it changed to Crohns and now we sit at Indeterminate colitis. I sent his blood off to New Zealand to culture for MAP. It came back highly suggestive of MAP. My son previously failed, steriods, 6mp and remicade.

He has always been a bleeder and that has been one of our biggest issues. He doesn't have small intestine involvement (thank goodness) but does have joint pain, uclers and developed seizures which we had to medicate for. Please don't go into the neuro-toxicity of anti map or other meds because I am well aware of all of it.

I want to know how long it took to see bleeding stop on Antimap? My son has been super weepy which is not like him and I attribute that to the therapy as well. Anything you can offer would be greatly appreciated!

Thank you
I am not a medical doctor, nor licenced to give medical advice, I am a Crohn's patient like others here, and reading what you wrote about your son, if I were in your shoes, I would definitely consider the anti-map therapy. It seems well justified in his case: The disease looks severe (or at least problematic); lab results for MAP came back "highly suggestive"; his disease has not responded to the conventional immunosuppressant treatments; he is young and still at the developmental age and needs good nutrition, absorption, and his inflammation to be down as soon as possible; he has seizures (I have read MAP might also cause neurological disorders) which might become better with the antibiotics.

Regarding how long the anti-map therapy takes to work, I think it depends on the person. I assume, since he is a child and his lab results came back high, he might have a quick response (if he is to respond, that is).

In the first post of this support group, I provided many useful links, some of which contain useful and practical information about this therapy while the others are links to other support groups (facebook groups, and a forum for patients who use/consider to use the anti-map therapy). I would consider being a member to them and asking my questions in those pages too. You can also contact Human Paratuberculosis Foundation by clicking this link to ask your questions. They might help you.

If you decide to start him the therapy, definitely do this under a doctor's supervision. If you describe your situation to the Human Paratuberculosis Foundation and ask for a doctor's name who is near you and is willing to use this therapy, they might provide you that information. I believe irishgal might also provide you this information, you can send a private message to her through this link. She has first hand experience with the anti-map therapy, is knowledgeable about many of the practical questions regarding the anti-map therapy, and she is helpful.

Good luck, and let us know.
 
Last edited:
Based on my personal experience, my risk/benefit made it very clear it was worth a try. Although it has not induced a permanent remission it has improved my symptoms greatly and kept me in a stable state.
 
David Graham, MD, a professor of medicine, molecular virology and microbiology at Baylor College of Medicine, in Houston, and his colleagues at 92 sites around the world conducted the MAP U.S. study, in which they randomly assigned 331 patients with moderately to severely active Crohn’s disease to receive either 95 mg of clarithromycin, 45 mg of rifabutin and 10 mg of clofazimine (RHB-104, RedHill Biopharma Ltd.) administered as five capsules twice daily for up to 52 weeks, or the same regimen of placebo pills.

“MAP U.S. is the first global, randomized trial to assess the efficacy of anti-MAP therapy in active [Crohn’s],” the team stated in an abstract they presented at the 2018 United European Gastroenterology Week (abstract LB06).

After 16, 26 and 52 weeks of treatment, Dr. Graham and his colleagues evaluated patients for clinical remission, which they defined as a Crohn’s Disease Activity Index (CDAI) score lower than 150. They also assessed clinical response, which was defined as a decrease of at least 100 points from baseline on the CDAI. Study participants continued any existing treatments throughout the trial.

According to the researchers, 42% of participants who received anti-MAP therapy along with their existing treatment achieved clinical remission at week 16, compared with 29% of placebo recipients (P=0.015). After 26 weeks, 37% and 23% of the two groups, respectively, were in clinical remission (P=0.007), whereas 44% of patients who received anti-MAP therapy achieved clinical response at 26 weeks, compared with 31% of placebo recipients (P=0.017).

Dr. Graham’s team found that 25% and 12% of anti-MAP and placebo recipients, respectively, were in clinical remission at the one-year mark of the study (P=0.003).

“RHB-104 was safe and well tolerated and could provide a new oral antibiotic therapy for use across a broad spectrum of Crohn’s disease patients,” Dr. Graham’s team concluded.

Although he welcomed the results, Dr. Shafran said he believed the study could have demonstrated a larger treatment effect if it had been designed differently.

“This trial included all-comers, not necessarily only those with MAP detected in their serum,” he said, adding that selecting only patients with confirmed MAP infection could have led to better outcomes.

Ira Kalfus, MD, a medical director at RedHill, said the study did not look at MAP status because no validated diagnostic tests are capable of accurately and reproducibly diagnosing the infection in humans.

“Detection of MAP via serological assays is challenging due to the low sensitivity of commercially available” tests, Dr. Kalfus said. “In humans, MAP is thought to reside intracellularly within macrophages, and serological antibody tests have limited utility in this situation.”

He said RedHill is researching whether polymerase chain reaction can be used to detect MAP in tissue samples.

Dr. Shafran also said that treating MAP early in the disease course could dramatically improve results. Many treatments for Crohn’s have relatively low rates of success, and patients who achieve initial response or remission often relapse within one year of treatment initiation.

“Antibiotics with a similar level of efficacy may be a good option to have for these patients,” Dr. Shafran said.

RedHill is completing a final analysis of the study data and meeting with FDA officials to discuss the results and determine how to move forward toward a New Drug Application.

“As soon as these discussions have been finalized, we will make them public,” Dr. Kalfus said.
https://www.gastroendonews.com/In-the-News/Article/01-19/Anti-MAP-Treatment-Tops-Placebo-in-Large-Crohn-s-Trial/53847
 
The Crohn's MAP vaccine is being tested on healthy people now, and the trial on Crohn's patients will begin soon.

Article said:
Volunteers, mainly made up of Crohn’s patients and their families also raised £700,000 for a diagnostic blood test to run in conjunction with the vaccine trials. Fundraising is still taking place to take the trials to completion.

The website says: “Historically, MAP in humans has been difficult to study as it cannot be seen under an ordinary microscope and is very difficult to grow.

“Testing for MAP by the presence of its DNA (using PCR) has found MAP in up to 92% of Crohn’s patients but until now no-one has developed a test to show MAP in-situ in the tissues of people with Crohn’s disease.

“With the new MAP test developed by Professor Hermon-Taylor, we are seeing it in intricate detail for the very first time.

“The test is an essential ‘companion diagnostic’ for the Vaccine trial; a simple blood test allowing doctors to confirm MAP infection prior to vaccination and monitor patients’ responses to the vaccine. Validation of the new test is almost complete”.

Phase one trial of the second component of the vaccine is now underway on healthy volunteers and it is hoped phase two on Crohn’s patients will run in tandem, beginning at the end of April this year.

If all goes according to plan, trials should be completed by the middle of 2020.


The vaccine has garnered huge support on social media sites including Facebook, Twitter and Instagram.

To find out more, visit www.crohnsmapvaccine.com
https://www.edinburghnews.scotsman.com/news/health/vaccine-hope-to-treat-crohn-s-disease-is-one-step-closer-1-4890394


Info on entry criteria:

CMV Website said:
Can I be involved in the Vaccine trial? And when is the Vaccine likely to be available?

A phase I safety trial in healthy human volunteers began in March 2017. This will be followed by a Phase IIa trial, anticipated to begin in the first half of 2019. The Phase IIa trial will be a single-centre trial based at St. Thomas’s Hospital, London, UK in 20 adults with Crohn’s Disease and will last 1 year. The estimated timeline of the Vaccine manufacture and trials is shown in the Gantt Chart below. The patients recruited to this trial will need to meet strict entry criteria; there are stringent regulations which we have to obey and the trial will be governed by the close scrutiny of the regulators. Regrettably we cannot invite people to take part in the trial at this time. However, the results of the trial will be analysed in real time as it proceeds. As soon as there is evidence of safety and efficacy, we can apply for use of the vaccine on compassionate grounds; this will enable people who wish to have the vaccine but are unable to be part of the trial to access it on a named-patient basis outside of the trial. Indeed, under the newly proposed ‘Early Access to Medicines’ scheme in the UK, severely ill patients who have failed existing treatments may be granted access to new medicines that are proven to be safe, even before efficacy has been fully established. In addition, following the demonstration of safety and efficacy, it is anticipated that the Vaccine technology would be licenced to a pharmaceutical company to make it available to all who need it through health services worldwide -as part of this, larger Phase 3 trials inviting wider participation would be expected. The manufacture and trial of the Vaccine is being funded through investment in the company HAV Vaccines Ltd (HVL) -completion of the trial according to this timescale is dependent on HVL to secure the remainder of the funding required.



Timelines are current best estimates and are not set in stone. Delays are commonplace in research due to the unpredictable nature of organising and running trials (last updated 03.01.2019)
From: http://www.crohnsmapvaccine.com/faq/
 
Last edited:
Just curious if anyone could help me interpret my Otakaro Pathways (prelim) results. There are just too many specific and technical terms for me to nail down with proper certitude what the report is telling me. Thanks
 
Location
San Diego
Just curious if anyone could help me interpret my Otakaro Pathways (prelim) results. There are just too many specific and technical terms for me to nail down with proper certitude what the report is telling me. Thanks
I can try. Do you have a link to the results?
 
I can try. Do you have a link to the results?
I just have the PDF John emailed me. I'll add the info to this post. Not sure I should try posting the chart as I have a feeling the formatting will go haywire. If you think that will be helpful let me know and I'll see what I can do. Thanks!


Comments
No persister forms were seen, but several single large forms were noticed. This sometimes suggests latency of the
organism as a result of prior exposure to anti-TNFs (remicade, humira etc)
Persister forms
One possible grouping of a single mother -daughter cell was seen on extended screening
Daughter cells
There is a slight increase in ruptured forms when the 8 day reading is compared with the 30 day reading
Ruptured forms
Only one group of large forms was seen.
Large forms
The appearances are similar to those seen in Crohn's disease where the patient is not experiencing a flareup, but is on
sub-optimal therapy. The 7DN medium, which we are evaluating as a biomarker, was positive, and variant forms we
associate with Crohn's disease were seen.These variant forms were not robust in morphology and few in number. I have
seen similar appearances in treatment-resistant Crohn's disease -This can occur when most available therapies have
been exhausted. In that scenario, the patient may be experiencing a flareup, but the CWDM are difficult to culture.
Further culture work is planned.
Conclusions
INTERPRETATION

This was from the email:
This is a difficult sample to interpret, as there is little growth unless I look closely. (which I did). I am going to get some more cultures going, using novel growth promotants, to try and grow more DNA. Please contact me if you have any quesitons at this stage

It does seem odd that he mentions there is such little growth but also it appears similar to Crohn's and sub-optimal therapy. Seems like at least some tension between those two statements if not some contradiction. Also, this does seem like he found evidence of mycobacteria in general, not necessarily MAP specifically, is that correct?

I haven't ever been on any anti-TNF drugs but did mention to him I consume DMSO which I've read at least one paper showing evidence it acts as a potent anti-TNF agent.
 
Location
San Diego
It does seem odd that he mentions there is such little growth but also it appears similar to Crohn's and sub-optimal therapy. Seems like at least some tension between those two statements if not some contradiction. Also, this does seem like he found evidence of mycobacteria in general, not necessarily MAP specifically, is that correct?
I don't see those two statements as necessarily contradictory, He appears to be saying that the specimen does not show signs of frank disease but does not look entirely normal either - perhaps some residual or latent disease can be seen.

He doesn't say anything one way or the other about whether it is specifically MAP.
 
I don't see those two statements as necessarily contradictory, He appears to be saying that the specimen does not show signs of frank disease but does not look entirely normal either - perhaps some residual or latent disease can be seen.

He doesn't say anything one way or the other about whether it is specifically MAP.

Thanks Scipio, that’s what I was afraid of on the second part. I was hoping it would be a definitive finding of MAP.
 
P550 Anti-mycobacterium paratuberculous therapy in Crohn’s disease: outcomes from tertiary IBD referral centres
E Johnston S Honap B Al-Hakim J Sanderson

Journal of Crohn's and Colitis, Volume 13, Issue Supplement_1, March 2019, Page S389, https://doi.org/10.1093/ecco-jcc/jjy222.674
Published: 25 January 2019

Abstract

Background
Mycobacterium avium paratuberculosis (MAP), an obligate intracellular pathogen, has long been proposed as an aetiological factor in Crohn’s disease. Prolonged, combination antibiotic therapy has shown beneficial effect in the induction and maintenance of remission in a small number of studies but was not replicated in an RCT.1 However, the evidence remains conflicting, particularly with criticisms on experimental design and subtherapeutic antibiotic dosing in the latter. We report the outcomes of this therapeutic option in a selected cohort of patients at our institutions.

Methods
A retrospective study was conducted by examining the records of adult patients commenced on anti-MAP therapy (AMT) at both Guy’s and St. Thomas’ Hospitals and London Bridge Hospital, between February 2011 to December 2017. Treatment regimens were slightly varied but standard therapy was clarithromycin 750 mg OD, rifabutin 450 mg OD and clofazimine 100 mg OD. Hospital notes were used to capture demographic data, disease characteristics and therapy details including indications and duration of therapy. Objective measures of response included at least one of; reduction in CRP or faecal calprotectin, improvement in endoscopic or radiological appearances. Statistical analysis was performed using GraphPad Prism.
Results

In total, 62 patients were prescribed AMT over the study period, 21 were excluded due to insufficient outcome data. 21/41 (51%) were male and median age was 28 (range 18–63) at the time of commencing therapy. The cohort had moderate to severe Crohn’s disease with 26 (63%) having stricturing or penetrating disease and 18 (44%) with previous surgery. Thirty-one (76%) had previously received biologic therapy. AMT was commenced in 26 (63%) patients due to failure of conventional therapy, 3 (7%) in patients where conventional therapy was not appropriate and the remaining due to patient preference. AMT was well tolerated with only 5 (12%) patients stopping therapy due to adverse effects. Nineteen patients (46%) demonstrated at least partial benefit, corroborated by objective evidence in 13/19 (68%). Response was not associated with disease phenotype and duration, previous therapy or use of clofazimine. Those patients who responded had a longer duration of therapy (median 24 months compared with 14 months; p = 0.04) than patients who did not respond.

Conclusions
Our study demonstrates that in a cohort of patients in which the majority failed conventional treatment, AMT was well tolerated and a response was seen in 46%. Patients who responded were on AMT a median 24 months which supports the current recommendation of a 24-month duration of treatment. Limitations include a small, heterogenous cohort of patients.

Reference

1. Selby WS, Pavli P, Crotty B, et al. Two-year combination antibiotic therapy with clarithromycin, rifabutin, and clofazimine for Crohn’s disease. Gastroenterology 2007;132:2313–9.
 
British Society of Gastroenterology updates guidance on Crohn’s
We are pleased to share the recently published updated guidance on Crohn’s and Ulcerative Colitis for adults over sixteen from the British Society of Gastroenterology. It includes the first ever mention of RHB-104, the combined antibiotic pill which has been successfully trialled by Redhill Biopharma; this large RCT addresses the mycobacteria which we believe is at the root of the Crohn’s disease and which the Crohn’s MAP Vaccine is also designed to target. We are delighted to see antibiotic treatment included in the new guidance and hope that the BSG will be following the progress of the vaccine trials with interest!
 
Son was tested by Otakaro Pathways, and subsequently became a patient of Prof. Tom Barody (CDD, Sydney), using anti-biotic anti-map therapy. Unfortunately, our son is not one of the success stories, but there are many for whom this treatment does work. Research does back the theory, with the para-physiology of Johnnes in cattle identical to Crohns in humans. Toms "poster" patient is a woman now in her 30's, living a full life in complete remission for years. Kimberly was 17 when she became one of Tom's first patients, when anti-map was in its infancy. She had been told she needed a total colectomy as her lower GI was beyond repair, and she would never have children. A remarkable success story indeed.

I am pleased we partook in the treatment, for though it was unsuccessful for our son, if we had not tried, it would always have been a "what-if" for us. (And I do wonder whether there were other factors involved in his particular lack of success with the treatment, but this is another story all together)

The research into gut bacteria and the implications on our health is being more widely researched now, with strong links to other diseases, including the likes of Parkinsons, Alzheimers and even cardio-vascular implications
 
Crohn's MAP Vaccine March 2019 newsletter said:
Phase 2 Clinical Trial in people with Crohn's disease

The trial will be conducted at Guy’s and St Thomas’s Hospitals in patients with mild Crohn's Disease (with a positive test for MAP) aged between 18-50 years who are not taking any immunosuppressant medications or biologics and are resident in the UK. The trial design will be similar to the Phase 1 Clinical Trials in Oxford and will concentrate again, as required, on Safety and Immunogenicity. We will be using our new MAP test to assess MAP levels before and after vaccination. Further details of the eligibility criteria will be published online when the trial opens for recruitment. Please note that recruitment has not yet started, so we therefore ask our supporters not to contact us or St Thomas’ Hospital about this.
 
Last edited:
CLOFAZIMINE: PRACTICAL CONSIDERATIONS FOR PATIENTS

The information provided is not intended or implied to be a substitute for professional medical advice, diagnosis or treatment. You are encouraged to confirm any information obtained from or through this website with other sources, and review all information regarding any medical condition or treatment with your physician. Human Paratuberculosis Foundation does not recommend, endorse or make any representation about the efficacy, appropriateness or suitability of any specific tests, products, procedures, treatments, services, opinions, health care providers or other information that may be contained on or available through this website.
Introduction
Due to the recent success of RedHill Biopharma’s Stage 3 trial of RHB-104, more patients and doctors have become interested in Atypical Mycobacterial Antibiotic Therapy (AMAT) as a treatment option for chronic immune conditions, such as Crohn’s disease and multiple sclerosis. RHB-104 contains a triple combination of antibiotics that showed significant effectiveness in Crohn’s disease, and includes clarithromycin, Rifabutin and clofazimine. While clarithromycin and Rifabutin are easily available worldwide, clofazimine is not.
Limited Availability of Clofazimine
Clofazimine was first developed by researchers at Trinity College in Dublin, Ireland. It’s primary use is for the treatment of leprosy. It is also used to treat nontuberculous mycobacterial infections. With its inclusion in RHB-104, there developed a growing niche for the drug in Crohn’s disease. But this medication is not readily available at pharmacies or chemists, because few cases of leprosy exist in the Western world.
Clofazimine has been classified as an orphan drug, which means that few companies produce the medication due to limited potential for profitability. It does not mean that the drug is illegal, or has been banned. A community member has kindly provided Human Para with a variety of options he considered on his quest to legally obtain clofazimine.

Option 1: FDA SPIND (Single Patient Investigational New Drug) via Expanded Access
In recent years, the United State Food & Drug Administration (FDA) has taken a more lenient approach in allowing doctors and their patients to make decisions about treatments that have not yet received full FDA approval for a specified condition. This practice is known as Expanded Access, or Compassionate Use. While clofazimine is FDA approved for leprosy, it is not yet approved for use in Crohn’s disease. Prescribing an FDA approved drug for a secondary, unapproved condition is considered an “off label” use of that medication, and can be a legal gray area for doctors. If approval is granted, the FDA will issue a SPIND # to the investigating physician, for use with the patient named in the protocol.
In parallel, Novartis, the Swiss pharmaceutical manufacturer of clofazimine, has developed its own Managed Access Program. Through Managed Access, Novartis is able to work directly with physicians (but not patients) to guide them thru the necessary regulatory steps. Once the SPIND # is assigned by the FDA, they arrange access for your clinic to clofazimine.
In our case, our gastroenterologist developed her plan/protocol, based on the RedHill MAPUS Clinical Trial protocol and input provided by Prof. Borody. The University required signature approval of several of colleagues, which she received. The request was also approved by the Institutional Review Board (IRB).
Following IRB approval, our doctor submitted the package, along with a few other completed forms, to the FDA for approval under Expanded Access. This was a relatively straightforward process. From the time the protocol was developed it took 4-6 weeks to get IRB signatures, and FDA approval.
Novartis required hard copies (not email) of the various approvals, after which they arranged shipment of the clofazimine directly to the clinic. The approach is sometimes seen as a “trial of n=1.”
Option 2: Prof. Thomas Borody, Centre for Digestive Diseases in Sydney, Australia
Professor Borody’s clinic in Sydney has a relationship with a compounding pharmacy for providing clofazimine to Crohn’s disease patients worldwide. By contacting their office, your physician can work with the staff to complete case histories, prescriptions, and arrange 90-day shipments, at a fixed cost. NOTE: Your physician must contact the CDD directly via email, phone or fax. Due to the volume received, inquiries from patients cannot be answered.
Option 3: Order Online from Canadian Pharmacies
A Google search for clofazimine will reveal dozens of offers from Canadian online pharmacies, promising to provide clofazimine to United States patients, worry free. While there are hundreds of such online pharmacies, the (supposedly) most reliable have certification or approval from two agencies: CIPA and Pharmacy Checker.
CIPA, the Canadian International Pharmacy Association, has authorized 66 Canadian websites to display its seal, which sites are licensed and regulated by the government for safety.
Pharmacy Checker has a verification program where they check the licensing and industry standards of applicants to assure they are in good standing in the countries in which they are located. Unlike CIPA, Pharmacy Checker is open to pharmacies around the world. Pharmacies in certain countries are subject to onsite inspection.
We looked at every online pharmacy that had either CIPA approval, Pharmacy Checker approval, or both. Of more than 80 sites checked, only 8 offered clofazimine. Some of these sites appeared to be owned by the same person. A few of those that offered clofazimine accepted credit card payments, but some only accepted a check or payment via Paypal. This could be a consideration, and a possible red flag. The pharmacies we checked stated they received their supply from India. China is also another possible supplier.
While the easiest of the three options above, supply chain and verification methods may be an issue for some patients. Additionally, for Canadian patients, these online pharmacies are not available since they are (ironically) prohibited from shipping to Canadian residents. Lastly, any international mail order medication is subject to customs inspection, which may delay delivery.
Thank you to Kerry Schuster for sharing his journey and providing our community with this resource.
 
RedHill plans to meet with the FDA in the second half of 2019 to discuss the development path toward potential approval of RHB-104, including the design of a confirmatory Phase 3 study. The MAP US randomized, double-blind, placebo-controlled first Phase 3 study with RHB-104 for Crohn’s disease successfully met both its primary endpoint and its key secondary endpoints and presented the broad benefit of RHB-104 as an add-on therapy to standard-of-care treatments for Crohn’s disease, including anti-TNFs.
 
Expert Rev Clin Immunol. 2011 Nov;7(6):751-60. doi: 10.1586/eci.11.43.
Primary treatment of Crohn's disease: combined antibiotics taking center stage.
Chamberlin W1, Borody TJ, Campbell J.
Author information

Abstract

Although controversial, the use of properly chosen antibiotics in Crohn's disease appears beneficial. Evidence supporting the use of targeted antibiotic therapy comes in two forms: statistical evidence derived from meta-analyses of multiple formal studies and the documented clinical and endoscopic responses in patients treated with antibiotic combinations outside of formal clinical studies. This article reviews evidence from both categories that support the use of properly chosen antibiotic regimens in treating Crohn's disease, comments on the advantages and disadvantages of antibiotic therapy, and attempts to present a unifying hypothesis related to the role of enteric bacteria, mucosal immunity and antibiotic therapy. Relevant studies identified through a Medline search from 1976 to 2011 were assessed for inclusion by two independent observers who resolved any disagreements by consensus. References from all identified articles and recent review articles were cross-checked to ensure a thorough search. Papers were selected based on scientific merit as to which presented original contributions to the results.

In 2011, Dr. William Chamberlin, Prof. Thomas Borody and Dr. Jordana Campbell collaborated on a meta-analysis of the published Medline studies from 1976 to 2011 which discussed Crohn’s disease patients treated with antibiotic combination therapy. The article, Primary Treatment of Crohn’s Disease: Combined Antibiotics Taking Center Stage, gives unbiased data on the effectiveness of antibiotic use in Crohn’s disease. For those of you who are short on time or find this type of technical reading difficult, we have attempted to summarize the key points.

View Full Text:

Download Full Text:
 
Last edited:
I was diagnosed with Crohn’s Disease in 2004. After the ‘shock’ wore off, I began researching the disease and came across Borody’s and Hermon-Taylor’s research. This prompted me to ask my GI specialist for a blood test to check for MAP. He ignored my requests, dismissed the compelling evidence and continued treating me with steroids and 5-ASA’s. It wasn’t long before these treatments were no longer effective… not to mention the side effects. I took matters into my own hands and sought out Dr. Saleh Naser at UCF. After several months of communication, he finally agreed to test me for MAP (I can’t thank him enough!). Needless to say, I tested positive and finally had the proof. I took the results of the MAP positive test to an Infectious Disease specialist and he began treating me with anti-MAP antibiotics under the premise that I have an ‘atypical mycobacterium infection’. The logic being the MAC (Mycobacterium Avium Complex) is recognized as disease-causing in humans, thereby bypassing the Crohn’s/MAP argument. The protocol includes clarithromycin, rifabutin and clofazimine (the same combo found in RHB-104). Since beginning this treatment, I have been in remission. In short, I had to do an ‘end around’ on traditional thinking to get the correct treatment. While it has saved me from adalimumab and surgery, it has not been able to eradicate the infection. My hope is that it will sustain me until the vaccine is available. Thanks again to Amy and her father for their tireless efforts!!!

 
The recently published article describing the discovery of a MAP mutation that may lead to the development of a MAP vaccine for both animals and humans was received by our community with great interest. One of the researchers, Dr. William C. Davis, has provided Human Para with a summary of this highly technical article. A huge thanks to Dr. Davis and his colleagues for this piece, and for their contribution to MAP science.

...

"The results at this stage of our studies are very promising. The finding that deletion of a single gene cripples Map’s ability to establish a persistent infection led to the discovery of a peptide with potential for development of a peptide-based vaccine. Studies with the peptide in tissue culture show vaccination leads to development of immune cells that can kill Map inside macrophages, an essential requirement for a vaccine against intracellular pathogens. While this is being investigated in cattle, it could have implications for human health as well."


Research Summary

The long term objectives of our research program are to elucidate the mechanisms regulating the immune response to infectious agents and develop protective vaccines. To achieve these objectives, we continue to develop and use monoclonal antibodies and assays to study the immune response in domestic animals with a primary focus on ruminants. M. avium subsp. Paratuberculosis (Map) has been selected as the model pathogen for our investigations because of its economic importance and its potential for providing insight into the mechanisms regulating the immune response to Map and other intracellular pathogens. Map is the causative agent of Johne’s disease (JD) in cattle, a chronic wasting disease of the intestine. It causes significant economic loss to producers, especially the dairy industry, due to increase in forage consumption, decreased milk production and early culling due to poor health of affected animals. There is also a concern that Map is a zoonotic pathogen. Map has been isolated from human patients with Crohn’s disease (CD), a chronic inflammatory disease of the intestine. It is not clear whether Map is the etiologic agent causing Crohn’s disease. However, recent studies on CD and mycobacterial pathogens M. tuberculosis (Mtb) and Map have shown a similarity in the mechanisms of pathogenesis at the cellular and molecular level. The studies have revealed the cross regulation of the immune system by regulatory T cells and effector T cells mediating protective immune responses is dysregulated, giving rise to an imbalance that results in chronic inflammation of target tissues, and in the case of Mtb and Map dysregulation of protective immunity. To extend these observation we developed a bovine cannulated ileum model to conduct studies on the mechanisms of pathogenesis mediated by Map in the natural host, studies that cannot be conducted in humans. The model has offered an opportunity to study the interaction of Map during the early and late stages of infection. We have also developed and used a flow cytometric assay to analyze the immune response to Map and methods to elucidate the functional changes associated with dysregulation of the immune system. Use of these methods in conjunction with development of methods to monitor the intracellular killing of bacteria by cytotoxic T cells have facilitated analysis of the functional activity of cytotoxic T cells responding to Map and derived candidate antigens. Ongoing studies with a mutant of Map, with a deletion in relA, has shown deletion abrogates the capacity of the mutant to establish a persistent infection. Further studies have shown the target of the immune response is directed towards a membrane protein (MMP). Ex vivo studies have shown stimulation with the MMP leads to the development of cytotoxic T cells with the capacity to kill intracellular bacteria. This major finding indicates a peptide based vaccine is possible against a major pathogen. These findings will now be used to advance our studies to the next phase, development and validation of a virus vector containing the gene encoding the MMP as a vaccine for JD.


 
Last edited:
https://academic.oup.com/ibdjournal/article-abstract/25/4/711/5218864?redirectedFrom=fulltext

Inflammatory Bowel Diseases, Volume 25, Issue 4, April 2019

Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, ON, Canada.

Oberc, Fiebig-Comyn, Tsai CN, Ethenawy W, Coombed BK

Antibiotics Potentiate Adherent-Invasive E. coli Infection and Expansion

''BACKGROUND:

Crohn's disease (CD) is an inflammatory bowel disease with a complex etiology. Paradoxically, CD is associated with the use of antibiotics and with an increased abundance of an unusual phenotypic group of Escherichia coli known as adherent-invasive E. coli (AIEC). However, the impact of antibiotics on AIEC infection has not been well studied in controlled models of infection.

METHODS:
We infected mice with AIEC before or after treatment with a variety of different classes of antibiotics. We assessed levels of AIEC in the feces and tissues, AIEC localization by immunofluorescence microscopy, and tissue pathology.

RESULTS:
We found that a wide range of antibiotic classes strongly potentiated initial AIEC infection and expanded AIEC in chronically infected mice. We found that the ability of antibiotics to potentiate AIEC infection did not correlate with a stereotyped shift in the gut bacterial community but was correlated with a decrease in overall diversity and a divergence from the pre-antibiotic state. We found that antibiotic-induced inflammation provided a fitness advantage for AIEC expansion through their use of oxidized metabolites in the postantibiotic period.

CONCLUSIONS:
Our results show that antibiotics can render hosts more susceptible to initial AIEC infection and can worsen infection in previously colonized hosts. AIEC appears to exploit host inflammatory responses that arise in the postantibiotic period, highlighting a previously unknown interaction between CD risk factors.''
 
Top