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07-13-2015, 05:12 PM   #31
JMC
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Application of multiple laboratory tests for Mycobacterium avium ssp. paratuberculosis detection in Crohn's disease patient specimens.

http://www.ncbi.nlm.nih.gov/pubmed/26147146

The difficulties involved in detecting and enumerating Mycobacterium avium subsp. paratuberculosis (MAP) as a pathogen potentially involved in Crohn's disease (CD) are well known. This study aimed to improve this situation through the application of multiple laboratory diagnostic tests to detect and isolate this bacterium from different specimens collected from CD-patients and non-CD subjects as controls. A total of 120 samples (terminal ileum and colon biopsies, blood and stool) were obtained from 19 CD-patients and from 11 individuals who did not have a clinicopathological diagnosis of CD (non-CD controls) attending for ileocolonoscopy. All samples were processed by staining techniques, culture on both solid and liquid media, and Insertion Sequence 900/F57 real-time PCR. The MAP frequency in CD-patients was found in a significantly greater proportion than in non-CD subjects; the most positive samples were biopsies from CD-patients tested by real-time PCR. MAP detection in biopsies, and in the other samples, by applying multiple and validated laboratory diagnostic tests, could be a marker of active infection, supporting MAP involvement in CD.
07-14-2015, 02:31 PM   #32
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It's interesting how MAP was detected at the same levels in the blood and stool of both CD patients and healthy control group, suggesting that the bacteria may be present in the environment and carried in most humans, but that somehow the inability of macrophages in CD patients to kill it may contribute to the disease state.

I also learned that MAP can be present in both a cell-wall defective and cell-wall intact form, to which different staining techniques exhibit different results and perhaps why it is difficult to detect in conventional lab environments. They were able to make the highest correlation in active CD patients (94.7%) only when using real-time PCR of biopsy samples.
07-14-2015, 04:07 PM   #33
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I also learned that MAP can be present in both a cell-wall defective and cell-wall intact form, to which different staining techniques exhibit different results and perhaps why it is difficult to detect in conventional lab environments.
This is something that was noted by Prof Hermon-Taylor a long time ago. It is also why a lot of the earlier MAP studies produced contradictory results.
07-16-2015, 04:35 AM   #34
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New info from Brazil.
Old Mike
http://www.ncbi.nlm.nih.gov/pubmed/26176833

Presence of Mycobacterium avium subsp. paratuberculosis (MAP) in Brazilian patients with inflammatory bowel diseases and in controls.

Carvalho IA1, Schwarz DG2, Pietralonga PA2, Faria AC2, Braga IF2, Carvalho GD3, Valente FL2, Machado JP1, Guimarães LM4, Ferrari ML4, Silva Júnior A2, Moreira MA2.



Author information






Abstract

CONTEXT AND OBJECTIVE:

Mycobacterium avium subsp. paratuberculosis (MAP) has attracted the interest of researchers because of similarities between paratuberculosis and Crohn's disease (CD). The aim of this study was to evaluate the frequency of MAP through cultures, histology and polymerase chain reaction (PCR) on intestinal biopsies from Brazilian CD patients. Quantitative real time PCR (qRT-PCR) was performed on positive samples.

DESIGN AND SETTING:

Analytical cross-sectional study with control group at two federal universities.

METHODS:

Fresh samples were collected from 25 patients; five with CD, eight with ulcerative colitis (UC) and 12 controls with non-inflammatory bowel disease (nIBD). Formalin-fixed paraffin-embedded (FFPE) samples from 143 patients were also collected: 44 CD, 49 UC and 56 nIBD.

RESULTS:

None of the fresh samples was positive for MAP. Five FFPE samples (one CD, two UC and two nIBD) and three fresh samples (one in each group) were positive through IS900-PCR. qRT-PCR was performed on these eight samples. Among the FFPE samples, there were 192.12 copies/μl in the CD group, 72.28 copies/μl in UC and 81.43 copies/μl in nIBD. Among the fresh samples, there were 432.99 copies/μl, 167.92 copies/μl and 249.73 copies/μl in the CD, UC and nIBD groups, respectively. The highest bacterial load was in the CD group.

CONCLUSION:

This study does not provide evidence for a role of MAP in the etiology of CD, although MAP DNA was detected in all three patient groups. This is the first report of MAP presence in human intestinal biopsies in Brazil
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07-17-2015, 07:05 AM   #35
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Great thread. This isn't really a research article, but a cool beststory.ca article about Dr. Borody and tons of other into on MAP and Crohns. Well worth the 40 cents.

POSTED: JUNE 2015
Medical pioneer from Down Under leads world in Crohn’s treatment
Analysis by WARREN PERLEY
Writing from Montreal

Dr. Thomas Borody of Australia enjoys the highest remission rate of any doctor in the world when it comes to treating Crohn’s patients. Now he and U.S.-based Dr. William Chamberlin, who like Dr. Borody treats Crohn’s as an infectious disease, talk about the antibiotic formulas they use, their success rates, and their views on the future direction of Crohn’s treatments. Microbiologist Dr. Saleh Naser of the University of Central Florida explains why the connection between MAP bacterium and Crohn’s continues to confound most microbiologists and gastroenterologists.
08-12-2015, 12:20 PM   #36
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Here is a video on crohns autoimmune or infectious
https://www.youtube.com/watch?v=7x3l...ature=youtu.be

here is the lab site
https://www.mcgill.ca/molepi/

Old Mike
08-12-2015, 03:21 PM   #37
xeridea
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Here is a video on crohns autoimmune or infectious
https://www.youtube.com/watch?v=7x3l...ature=youtu.be

here is the lab site
https://www.mcgill.ca/molepi/

Old Mike
Here's a recent report where the doctor they interview (at 1:00 mark) says that though it parallels many of the symptoms as autoimmunity, Crohn's is not an autoimmune disease, but rather, a chronic inflammatory disease. It's refreshing to see a shift away from the autoimmune mislabeling of CD.
08-12-2015, 04:06 PM   #38
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This is exactly what the docs who have helped me say! They just put up a core research pack on their symposium website which has the best studies illustrating this. It's a great resource to bring to your doc!

http://thecrohnsinfection.org/core-research-pack/
08-13-2015, 05:15 PM   #39
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Here's a recent report where the doctor they interview (at 1:00 mark) says that though it parallels many of the symptoms as autoimmunity, Crohn's is not an autoimmune disease, but rather, a chronic inflammatory disease. It's refreshing to see a shift away from the autoimmune mislabeling of CD.
Crohn's is not and never has been an autoimmune disease. Any medical practioner who tells you Crohn's is an autoimmune should be avoided immediately. The best explanation is given by Prof Marcel Behr in this youtube video which is worth an hour of anybody's time: https://youtu.be/7x3lq8QEg5g
08-13-2015, 05:20 PM   #40
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To put it in perspective, even Wikipedia reflects the fact that Crohn's is not an autoimmune disease. That Crohn's is a "multi-factorial" disease with genetic and environmental elements is now mainstream, whereas even 5 years ago, most people would have described it (wrongly) as an autoimmune disease.
08-13-2015, 06:45 PM   #41
xeridea
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To put it in perspective, even Wikipedia reflects the fact that Crohn's is not an autoimmune disease. That Crohn's is a "multi-factorial" disease with genetic and environmental elements is now mainstream, whereas even 5 years ago, most people would have described it (wrongly) as an autoimmune disease.
No disagreement from me that it's not an autoimmune (AI) disease. I'm more of the persuasion that it's something related to the innate immune system activating the adaptive one. I posted the video on other boards too, where some still regard CD as AI, thought maybe some here would appreciate it too.
09-22-2015, 04:29 PM   #42
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Another interesting piece in the puzzle...

Mechanism of action of the tuberculosis and Crohn disease risk factor IRGM in autophagy.

http://www.ncbi.nlm.nih.gov/pubmed/26313894

Polymorphisms in the IRGM gene, associated with Crohn disease (CD) and tuberculosis, are among the earliest identified examples documenting the role of autophagy in human disease. Functional studies have shown that IRGM protects against these diseases by modulating autophagy, yet the exact molecular mechanism of IRGM's activity has remained unknown. We have recently elucidated IRGM's mechanism of action. IRGM functions as a platform for assembling, stabilizing, and activating the core autophagic machinery, while at the same time physically coupling it to conventional innate immunity receptors. Exposure to microbial products or bacterial invasion increases IRGM expression, which leads to stabilization of AMPK. Specific protein-protein interactions and post-translational modifications such as ubiquitination of IRGM, lead to a co-assembly with IRGM of the key autophagy regulators ULK1 and BECN1 in their activated forms. IRGM physically interacts with two other CD risk factors, ATG16L1 and NOD2, placing these three principal players in CD within the same molecular complex. This explains how polymorphisms altering expression or function of any of the three factors individually can affect the same process - autophagy. Furthermore, IRGM's interaction with NOD2, and additional pattern recognition receptors such as NOD1, RIG-I and select TLRs, transduces microbial signals to the core autophagy apparatus. This work solves the long-standing enigma of how IRGM controls autophagy.
09-22-2015, 04:31 PM   #43
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The potential Public Health Impact of Mycobacterium avium ssp. paratuberculosis: Global Opinion Survey of Topic Specialists.

http://www.ncbi.nlm.nih.gov/pubmed/26272619

Global research knowledge has accumulated over the past few decades, and there is reasonable evidence for a positive association between Mycobacterium avium spp. paratuberculosis and Crohn's disease in humans, although its role as a human pathogen has not been entirely accepted. For this reason, management of public health risk due to M. paratuberculosis remains an important policy issue in agri-food public health arenas in many countries. Responsible authorities must decide whether existing mitigation strategies are sufficient to prevent or reduce human exposure to M. paratuberculosis. A Web-based questionnaire was administered to topic specialists to elicit empirical knowledge and opinion on the overall public health impact of M. paratuberculosis, the importance of various routes of human exposure to the pathogen, existing mitigation strategies and the need for future strategies. The questionnaire had four sections and consisted of 20 closed and five open questions. Topic specialists believed that M. paratuberculosis is likely a risk to human health (44.8%) and, given the paucity of available evidence, most frequently ranked it as a moderate public health issue (40.1%). A significant correlation was detected between topic specialists' commitment to M. paratuberculosis in terms of the number of years or proportion of work dedicated to this topic, and the likelihood of an extreme answer (high or low) to the above questions. Topic specialists identified contact with ruminants and dairy products as the most likely routes of exposure for humans. There was consensus on exposure routes for ruminants and what commodities to target in mitigation efforts. Described mandatory programmes mainly focused on culling diseased animals and voluntary on-farm prevention programmes. Despite ongoing difficulties in the identification of subclinical infections in animals, the topic specialists largely agreed that further enhancement of on-farm programmes in affected commodities by the agri-food industry (68.4%) and allocation of resources by governments to monitor the issue (92%) are most appropriate given the current state of evidence.
09-22-2015, 04:43 PM   #44
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Including this paper because I had doubts about whether MAP caused the fistulating form of Crohn's and it appears tuberculosis (rather than paratuberculosis) can cause fistulas which are hard to distinguish from Crohn's. Although not conclusive it suggest to me MAP could also cause fistulas.

Clinical features of tuberculous versus Crohn's anal fistulas in Korea.


http://www.ncbi.nlm.nih.gov/pubmed/26374663


TB anal fistula is clinically very similar to CD anal fistula. In Korea, the incidence of CD anal fistula has recently increased in prevalence, while the prevalence of TB anal fistula is decreasing but is still persistent. We recommend that clinicians should prepare for a possibility of TB as well as CD anal fistula in TB-endemic countries including Korea.
09-22-2015, 05:30 PM   #45
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JMC - love the Potential Public Health Impact article. I found the entire thing as linked below and am planning on reading it when I have a few minutes. It clearly shows that most people familiar with MAP think it's a problem and that the govts should contain it.

http://www.researchgate.net/publicat...ic_Specialists
09-22-2015, 10:07 PM   #46
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thanks JMC - very informative. I wonder how long it will be until there is a MAP diagnostic test available to us??? To tell if we have MAP in our bodies…or not. Any news from london?
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09-23-2015, 05:34 AM   #47
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happy poo poo - you can get tested now via John Aitken's lab in New Zealand if you'd like. I went this route almost a year ago and was quite pleased. Contact him via his web site:
http://www.otakaropathways.co.nz/contact
09-23-2015, 08:44 PM   #48
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Dr. Chamberlin's Immunikas and EpiBro talk is up! Dr. Amy and the MAP vaccine are next.

http://thecrohnsinfection.org/symposium-information/
10-01-2015, 04:26 PM   #49
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JMC, anecdotally, when I consulted with Dr. Chamberlin and mentioned fistulas, he said having them was another indication that it is MAP, and initially suggested AMAT, saying that it would also help to heal them. He convinced me, but upon learning that antibiotics were poorly tolerated and dangerously so, he suggested Remicade. In the end, it was surgery, Humira and luck that seems to have worked ... at least for now.
10-01-2015, 04:32 PM   #50
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JMC, anecdotally, when I consulted with Dr. Chamberlin and mentioned fistulas, he said having them was another indication that it is MAP, and initially suggested AMAT, saying that it would also help to heal them.
The reason why I questions whether MAP caused fistulas is that it is not a feature of Johnes disease which is closer in nature, as I understand it, to the stricturing form of Crohn's. I know diseases do not present with identical symptoms in all species, but you do have to wonder why there appears to be distinct variants of Crohn's. I have not read any papers which can directly explain why that should be the case, if anyone else has, I would be interested to know.
10-01-2015, 05:25 PM   #51
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In retrospect I should have asked that he point me to a paper to support his opinion. I did come across a study that I am sure you have already read about mouth ulcers which were infected with MAP: http://www.biomedcentral.com/content...-4749-5-18.pdf

I agree, it is curious that Crohn's has such varied manifestations. Perhaps genetics plays a role? MAP being the underlying cause, but depending on genetic mutations, it manifests differently? In time hopefully, we will have most of the answers, if not all.
10-03-2015, 06:39 PM   #52
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Has anyone heard of hematomas on vocal chords as a part of Crohn's
10-25-2015, 10:19 AM   #53
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Mycobacterium paratuberculosis as a cause of Crohn's disease.

http://www.ncbi.nlm.nih.gov/pubmed/26474349

Crohn's disease is a chronic inflammatory bowel disease of unknown cause, affecting approximately 1.4 million North American people. Due to the similarities between Crohn's disease and Johne's disease, a chronic enteritis in ruminant animals caused by Mycobacterium avium paratuberculosis (MAP) infection, MAP has long been considered to be a potential cause of Crohn's disease. MAP is an obligate intracellular pathogen that cannot replicate outside of animal hosts. MAP is widespread in dairy cattle and because of environmental contamination and resistance to pasteurization and chlorination, humans are frequently exposed through contamination of food and water. MAP can be cultured from the peripheral mononuclear cells from 50-100% of patients with Crohn's disease, and less frequently from healthy individuals. Association does not prove causation. We discuss the current data regarding MAP as a potential cause of Crohn's disease and outline what data will be required to firmly prove or disprove the hypothesis.
10-25-2015, 10:22 AM   #54
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My understanding of this article is that previous exposure to MAP changes the response of the immune system to subsequent exposure. I would be interested in other views who have greater expertise than I do.

Macrophage polarization in cattle experimentally exposed to Mycobacterium avium subsp. paratuberculosis

http://www.ncbi.nlm.nih.gov/pubmed/26454271

Mycobacterium avium subspecies paratuberculosis (MAP), the causative agent of Johne's disease (JD) in cattle, has significant impacts on the livestock industry and has been implicated in the etiology of Crohn's disease. Macrophages play a key role in JD pathogenesis, which is driven by the manipulation of host immune mechanisms by MAP. A change in the macrophage microenvironment due to pathogenic or host-derived stimuli can lead to classical (M1) or alternative (M2) polarization of macrophages. In addition, prior exposure to antigenic stimuli has been reported to alter the response of macrophages to subsequent stimuli. However macrophage polarization in response to MAP exposure and its possible implications have not previously been addressed. In this study, we have comprehensively examined monocyte/macrophage polarization and responsiveness to antigens from MAP-exposed and unexposed animals. At three years post-exposure, there was a heterogeneous macrophage activation pattern characterized by both classical and alternate phenotypes. Moreover, subsequent exposure of macrophages from MAP-exposed cattle to antigens from MAP and other mycobacterial species led to significant variation in the production of nitric oxide, interleukin-10 and tumour necrosis factor α. These results indicate the previously unreported possibility of changes in the activation state and responsiveness of circulating monocytes/macrophages from MAP-exposed cattle.

10-25-2015, 10:25 AM   #55
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The Hruska postulate of Crohn's disease.


http://www.ncbi.nlm.nih.gov/pubmed/26432629

Crohn's disease is due to the loss of immunological tolerance within the gastrointestinal tract to the antigenic array of Mycobacterium avium subspecies paratuberculosis (MAP) and closely related polymorphic variants. The loss of immune tolerance results in an effector cytokine responsive upon re-exposure to MAP. For immune tolerance to MAP to be induced, infection must occur when acquired immunity is markedly underdeveloped.
10-25-2015, 10:39 AM   #56
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More on Hruska:

https://books.google.co.uk/books?id=...tulate&f=false
10-25-2015, 12:22 PM   #57
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Crohn’s disease and related inflammatory diseases: frommany single hypotheses to one “superhypothesis”

http://vri.cz/docs/vetmed/59-12-583.pdf

The aetiology of Crohn’s disease and paratuberculosis are the subjects of intensive study and also frequently, of dispute. However, a number of other nosological entities have a similar history, namely type 1 diabetes, multiple sclerosis, sarcoidosis, asthma, psoriasis, spondylarthritis, Blau syndrom etc. The zoonotic risk of Mycobacterium avium subsp. paratuberculosis (MAP) has been discussed for more than one hundred years. „The problem remains open, further research is needed“, is the sentence which seems to be obligatory in the conclusions of many scientific articles. A number of hypotheses have been suggested, all with a grain of truth in them.
The infection hypothesis has many supporters and opponents, but it does not fit to all Crohn’s disease cases. The contribution of the genetic factor has been admitted a long time ago and has been experimentally confirmed by recent excellent studies. An environmental factor is expected and has been often mentioned, but has yet to be
discovered. Muramyl dipeptide, derived from peptidoglycans of the bacterial cell wall is one of the triggers, mentioned in connection with chronic inflammatory diseases. The immunomodulatory ability of this compound has been recognised for decades and is exploited in Freund’s adjuvant. A critical amount of muramyl dipeptide can affect immunity during some bacterial infections but the long latent period between infection and onset of the clinical form of the disease could explain why a causative relationship between the primary infection and chronic inflammation is not considered. Different species of mycobacteria can be found in the environment, in water, dust,
soil and aerosol. Although severe infections with mycobacteria have been described, these species are not thought to be typical zoonotic pathogens. Muramyl dipeptide derived from mycobacteria obviously plays a starring role as a bacterial trigger in the aetiology of many autoimmune and autoinflammatory diseases. Paratuberculosis in
cattle and other ruminants is a source of enormous contamination of the environment but also of milk and meat by MAP. Muramyl dipeptide from mycobacteria, namely MAP, and Crohn’s disease as a representative of diseases often called civilization threats, are important pieces of the gigantic puzzle. Mycobacteria in the environment and foodstuffs have to be acknowledged as a public health risk, which can never be completely eliminated. There is no reason to push the panic button, but we must learn how to live together with this microorganism, how the pool of immunomodulator sources can be diminished, and how the pathogenic relationship between triggers and target tissues can be disrupted. The dissemination of knowledge, the availability of rapid and inexpensive tools for identification of mycobacteria in different matrices, and the establishment of a maximal allowed limit for mycobacteria in milk and meat should contribute to food safety and consumer protection.
11-10-2015, 04:20 PM   #58
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New paper from Thomas Borody demonstrating remarkable success with curing fistulas by combining anti-Map therapy with Infliximab and a new hyperbaric oxygen therapy.

http://www.future-science.com/doi/fu...4155/fso.15.77

Combining infliximab, anti-MAP and hyperbaric oxygen therapy for resistant fistulizing Crohn's disease

Background: Fistulizing Crohn's disease (CD) presents a therapeutic challenge as fistulae are notoriously difficult to heal. Mycobacterium avium ss paratuberculosis (MAP) treatment in CD is gaining attention. Aim: We evaluated healing of CD fistula(e) using a novel combination therapy. Study: Nine consecutive patients who failed to heal fistulae on conventional treatment including anti-TNF, were treated with at least three doses of infliximab, 18–30 courses of hyperbaric oxygen therapy and anti-MAP antibiotics comprising rifabutin, clarithromycin and clofazimine. Results: All patients achieved complete healing of fistulae by 6–28 weeks and follow-up for mean 18 months. Conclusion: Combining infliximab, hyperbaric oxygen therapy and anti-MAP, seems to enable healing of recalcitrant fistulae and although a small case series, all nine patients achieved complete healing.
11-10-2015, 07:15 PM   #59
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thanks, this is what I need to show my doctor who wants to put me under the knife.

Thanks
12-06-2015, 02:46 PM   #60
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New post by John Aitken: Victory
http://thecrohnsinfection.org/presenter-blog/

Sorry if you're seeing this multiple times. Just wanted to post on a few threads so everyone would have access.
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