Crohn'sCanada
  Addressing the alarming rise of the bacterium "Mycobacterium avium Paratuberculosis"
 
in the environment and the growing evidence linking this bacterium to Crohn's
disease.

Founders: Diane and Michael Fagen

Contact Info: dianef84@yahoo.com

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La Presse,  April 8, 2001,  Never in My Milk? by Marie France Coutu

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Does Mycobacterium Paratuberculosis cause Crohn's disease by Alan Kennedy  

(PARA) PARATUBERCULOSIS AWARENESS & RESEARCH ASS.,INC



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Dr. B. Crohn

Got Milk? by Michael Greger, MD Updated January 2001

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Disease A wake-up call for the dairy industry?

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Internation Association for Paratuberculosis

Ninth International Colloquium on Paratuberculosis Session 6: Public health

Greetings all,

The abstracts from the Ninth International Colloquium on Paratuberculosis (9ICP) have been published online. As with previous ICP, the number of papers presented on the relationship between Crohn's Disease and Mycobacterium Paratuberculosis has grown, as knowledge of this complex organism and its potential to cause disease in humans, has grown. The list of 9ICP presentations in the "Public Health" segment of the Colloquium are listed here http://www.paratuberculosis.org/pubs/proc9/section6.htm As acceptance of the relationship between MAP and CD grows, related papers are now being presented outside of the dedicated "Public Health" segment. The following paper discusses how the pathogenetic mechanisms of paratuberculosis in Johnes Disease and Crohn's Disease can be compared in order to increase understanding of both; it was presented in the "Pathogenesis and Immunology" segment. Role of Mycobacterium avium subsp. paratuberculosis in the pathogenesis of Crohn's disease http://www.paratuberculosis.org/pubs/proc9/abst4a.htm Also of interest is the growing evidence that Mycobacterium avium subsp paratuberculosis may be a cause of Type-1 diabetes. Association of Mycobacterium avium subsp. paratuberculosis with Type-1 diabetes, a possible trigger http://www.paratuberculosis.org/pubs/proc9/abst181f_o3.htm Paratuberculosis and Type I Diabetes -Mapping the TRIGR- http://www.paratuberculosis.org/pubs/proc8/abst3b_o20.htm

Alan.

 

Another piece of research which establishes the anti-paratuberculosis antibiotic activity of molecules which are currently thought to have an immuno-suppressant effect in Crohn's Disease. Alan

. ====================================== BACKGROUND: We have shown that the "immuno-modulators" methotrexate and 6-MP and the "anti-inflammatory" 5-ASA inhibit MAP growth (www.PLoSONE.org) and concluded that their most plausible mechanism of action in several idiopathic diseases is as antiMAP antibiotics. Thalidomide is an "immunomodulator" used in multiple "auto-immune" and "inflammatory" diseases and the mycobacterial diseases leprosy and tuberculosis. We now test the hypothesis that thalidomide inhibits MAP growth.

METHODS

Thalidomide () and (+) and (-) and its two components, phthalimide and 1-hydroxy 2,6 piperidine dione (HPD) were evaluated in culture of two strains each of MAP (ATCC 19698 [bovine] & Dominic [human]) and M. avium subspecies avium (ATCC 25291 & 101.) We used a radiometric (14CO2 Bactec(R)) detection system. Inhibition is indicated by "percent decrease in cumulative Growth Index" (%-DcGI) from control.

RESULTS:

Phthalimide has no dose dependent inhibition on any strain. There was no dose dependent inhibition on either M. avium strain with thalidomide or its components. With the two MAP strains, there is dose dependent inhibition with thalidomide (); Dominic (31%-DcGI) and ATCC 19698 (26%-DcGI) at 64g/ml. Thalidomide (+) is more inhibitory than (-). HPD is, on a weight for weight basis, the most inhibitory agent evaluated; Dominic (46%-DcGI) and ATCC 19698 (44%-DcGI at 64g/ml)

CONCLUSIONS:

We show in vitro heretofore-undescribed inhibition of MAP growth by racaemic thalidomide. Thalidomide (+) is more potent than (-). Of thalidomide's two moieties, phthalimide has no antiMAP activity and HPD is the active component in inhibiting MAP growth. We suggest that since 1942, initially with 5-ASA, the medical profession has unknowingly been treating MAP infections. These data are compatible with our concern that MAP is zoonotic. We conclude that all idiopathic "autoimmune" and "inflammatory" diseases, empirically treated with medications that we show are active against MAP, should now be evaluated for MAP as the etiological agent. http://www.paratuberculosis.org/pubs/proc9/abst185f_o4.htm

 

It appears that some Azathioprine and 6-MP, which are used for the treatment of Crohn's Disease, and whose mechanism of action is currently unknown, have antibiotic activity against Mycobacterium avium subspecies paratuberculosis (MAP)

. As noted by the authors, "These data may partially explain the paradoxical response of Crohn's disease patients infected with M. paratuberculosis to treatment with immunosuppressive thiopurine drugs i.e. they do not worsen with anti-inflammatory treatment as would be expected with a microbial etiologic pathogen." Alan.

====================================== The in vitro susceptibility of human and bovine-origin Mycobacterium paratuberculosis to the thiopurine drugs 6-mercaptopurine (6-MP) and azathioprine (AZA) were established using conventional plate counting methods and the MGIT 960 ParaTB culture system. Both 6-MP and AZA had antibacterial activity against M. paratuberculosis; isolates from Crohn's disease patients tended to be more susceptible than were bovine-origin isolates. Isolates of Mycobacterium avium, used as controls, were generally resistant to both AZA and 6-MP even at high concentrations (=64.0 g/mL). Among rapidly growing mycobacteria, M. phlei was susceptible to 6-MP and AZA whereas M. smegmatis strains were not. AZA and 6-MP limited the growth of, but did not kill, M. paratuberculosis in a dose-dependent manner. Anti-inflammatory drugs in the sulfonamide family (sulfapyridine, sulfasalazine, and 5-amino- salycilic acid (mesalamine)) had little or no antibacterial activity against M. paratuberculosis. The conventional antibiotics azithromycin and ciprofloxacin (CPX) used as control drugs were bactericidal for M. paratuberculosis, exerting their killing effects on the organism relatively quickly. Simultaneous exposure of M. paratuberculosis to 6- MP and CPX resulted in significantly higher CFUs as compared to use of CPX alone. These data may partially explain the paradoxical response of Crohn's disease patients infected with M. paratuberculosis to treatment with immunosuppressive thiopurine drugs i.e. they do not worsen with anti-inflammatory treatment as would be expected with a microbial etiologic pathogen. These findings also should influence the design of therapeutic trials to evaluate antibiotic treatments of Crohn's disease: azathioprine drugs may confound interpretation of data on therapeutic responses both antibiotic-treated and control groups.

Liverpool, UK - 10 December 2007: Scientists at the University of Liverpool have found how a bacterium, known to cause illness in cattle, may cause Crohn's disease in humans. http://www.liv.ac.uk/newsroom/press_releases/2007/12/crohns-disease.htm

Crohn's is a condition that affects one in 800 people in the UK and causes chronic intestinal inflammation, leading to pain, bleeding and diarrhoea.

The team found that a bacterium called Mycobacterium paratuberculosis releases a molecule that prevents a type of white blood cell from killing E.coli bacteria found in the body. E.coli is known to be present within Crohn's disease tissue in increased numbers.

It is thought that the Mycobacteria make their way into the body's system via cows' milk and other dairy products. In cattle it can cause an illness called Johne's disease - a wasting, diarrhoeal condition. Until now, however, it has been unclear how this bacterium could trigger intestinal inflammation in humans.

Professor Jon Rhodes, from the University's School of Clinical Sciences, explains: "Mycobacterium paratuberculosis has been found within Crohn's disease tissue but there has been much controversy concerning its role in the disease. We have now shown that these Mycobacteria release a complex molecule containing a sugar, called mannose. This molecule prevents a type of white blood cells, called macrophages, from killing internalised E.Coli."

Scientists have previously shown that people with Crohn's disease have increased numbers of a 'sticky' type of E.coli and weakened ability to fight off intestinal bacteria. The suppressive effect of the Mycobacterial molecule on this type of white blood cell suggests it is a likely mechanism for weakening the body's defence against the bacteria.

Professor Rhodes added: "We also found that this bacterium is a likely trigger for a circulating antibody protein (ASCA) that is found in about two thirds of patients with Crohn's disease, suggesting that these people may have been infected by the Mycobacterium."

The team is beginning clinical trials to assess whether an antibiotic combination can be used to target the bacteria contained in white blood cells as a possible treatment for Crohn's disease.

The research was funded by Core and the Medical Research Council and is published in Gastroenterology.