The incidence of TB may have been overestimated, because empirical treatment was included in this study. Finally, our study was not designed according to any protocol, and there may have been selection bias. Author contributions: SNH: study concept and design, analysis and interpretation of data, statistical analysis, drafting of the manuscript.
HJK: study concept and design, acquisition of data, analysis and interpretation of data. HSA: study concept and design, acquisition of data, analysis and interpretation of data, critical revision of the manuscript for important intellectual content, study supervision. Volume 45 , Issue 2. The full text of this article hosted at iucr. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account. If the address matches an existing account you will receive an email with instructions to retrieve your username.
Original Article Free Access. Ahn Corresponding Author E-mail address: ahnhann gmail.
Johne's and Crohn's disease: The role of Mycobacterium avium | RSB
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Share full text access. Please review our Terms and Conditions of Use and check box below to share full-text version of article. Summary Background The low incidence of Mycobacterium tuberculosis infection and lack of adequate controls have prevented researchers from estimating tuberculosis TB risk in inflammatory bowel disease IBD patients. Introduction Inflammatory bowel diseases IBDs , including ulcerative colitis UC and Crohn's disease CD , are thought to be caused by dysregulated mucosal immune responses to intestinal microbiota.
Inflammatory bowel disease a a 3. Figure 1 Open in figure viewer PowerPoint. Incidence rates and standardised incidence ratio of incident Mycobacterium tuberculosis in patients with inflammatory bowel disease according to subtype, gender, and age decades. Figure 2 Open in figure viewer PowerPoint.
Is Crohn’s Disease a Mycobacterial Disease?
Incidence rates and standardised incidence ratio of incident Mycobacterium tuberculosis in patients with inflammatory bowel disease a , ulcerative colitis b , and Crohn's disease c according to prescribed medication. TB, Mycobacterium tuberculosis ; s. Acknowledgement Declaration of personal interests: None. Current Opinion in Gastroenterology. Borody T. Taylor, J.
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Digestive and Liver Disease. American Journal of Gastroenterol. Inflammatory Bowel Diseases. Mycobacteria in water, soil, plants and air: a review. Veterinarni Medicina. Future Microbiol. Naser SA et al. Mycobacterium avium subspecies paratuberculosis causes Crohn's disease in some inflammatory bowel disease patients.
In June , panendoscopy was normal. A thorough infectious disease work up was done, including investigations for unusual pathogens such as tuberculosis TB. The patient remained symptomatic. In September , an empiric steroid trial was instituted with a dramatic 2-week response, including significant improvement in bloating and resolution of nights sweats. The steroid taper was followed by a return of symptoms incompletely mitigated by mesalamine.
In March , a magnetic resonance enterography MRE was consistent with ileitis. This was followed by a second colonoscopy in March , including visualization of the terminal ileum, which again showed no mucosal lesions and a negative biopsy for microscopic colitis.
The clinical diagnosis of CD was made in April , and the patient was treated with steroids plus tumor necrosis factor TNF blockers adalimumab followed by infliximab without a sustained clinical response. She continued with drenching night sweats and postprandial bloating.
In January , 6-mecaptopurine was added and not tolerated. In March , a repeat MRE was done that showed less enhancement of the terminal ileum but thickening. This led to laparotomy in April She received an intravenous dose of ceftriaxone and metronidazole preoperatively. A section of terminal ileum was pale and flaccid and was resected. The remainder of the intestines appeared normal. The pathology showed lymphoid hyperplasia with drug-induced modulation of associated lymphoid tissue and reduction in neural ganglia cells. Nevertheless, her night sweats returned 7 days postoperative.
All of her laboratory and pathology samples were reviewed—special stains looking for infectious agents were repeated and all were negative. She was also recultured for TB.
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In June , a buffy coat blood sample nucleated cells was obtained for culture at a specialized laboratory using modified media [ 1 ]. The only medication the patient was taking was a tapering dose of prednisone. Contemporaneously, she was started on an empiric 5-drug regimen rifampin, ethambutol, azithromycin, isoniazid, and levofloxacin for presumed mixed mycobacterial infection. Within 10 days, the night sweats decrementally improved; and within 6 weeks of treatment resolved completely. Nine weeks after blood sample collection, the culture reading was positive for MAP 1.
We postulate that a MAP infection likely caused an ileitis with destruction of the neural ganglia, which caused the terminal ileum to become atonic. The patient was treated as having CD and was given high-dose steroids, TNF blockers, and immunomodulators without sustained clinical response.
Finally, persistent right lower quadrant pain, polychezia, bloating, and night sweats led to ileal resection with resolution of the GI symptoms but not the night sweats. These have resolved with anti-MAP antibiotics. We recognize case reports as one of the lowest levels of evidence; nonetheless, they have an important role in medical advances [ 3 ], such as acquired immune deficiency syndrome being described in Los Angles in The Helicobacter story reminds us that commensals once considered to be harmless can, under certain clinical conditions, cause disease.
These case reports inspired our curiosity to explore the unexpected.
Unlike typical CD, no mucosal changes were ever discovered, but damage occurred to the ganglionic cells that led to an atonic terminal ileum. Removal of the atonic segment remedied the functional postprandial bloating and other GI symptoms. Intravenous ceftriaxone and metronidazole at surgery may have temporarily been responsible for 1 week of night sweats abatement.
However, until MAP was treated with a sustained multidrug regimen, the night sweats continued. A mixed mycobacterial infection was also considered as a cause, perhaps Mycobacterium bovis ; however, we were unable to culture this, and both her purified protein derivative and QuantiFERON Gold tests were negative.
Transmission from cow to calves by milk is known to occur. Mycobacterium avium paratuberculosis is not routinely killed by pasteurization, and even infant formula can be found to occasionally contain MAP [ 6 ]. A Australian, randomized, prospective, clinical trial of anti-MAP antibiotics versus placebo concluded that MAP was not causative [ 7 ], and this has been generally accepted by the GI community despite multiple criticisms on experimental design as well as using subtherapeutic antibiotic dosing [ 8 ].
There are reasons to believe that MAP soil commensal is a causative pathogen.