Leprae is indeed difficult to culture. However, as I discussed with you about one year ago in a post in another thread, Gerhard Henrik Armauer Hansen in Norway had announced back in 1873 the discovery of Mycobacterium leprae in the tissues of all sufferers, with just a "new and better" microscope, without the special stains developed by Albert Neisser and others later. Here, I would like to repost that post here.
“Thanks kiny for sharing the thoughts. I admired the great efforts you and many other patients in this forum took, trying so hard to understand the disease. The body is very complex. Apparently, it is not easy to read through the many research papers with the many jargons.
Frankly, my intention is not to provoke sentimental arguments, although I have a lot of strong “scientific” evidences for both sides of the MAP controversy for an endless debate. Rather I think we should ponder thoroughly, deeply and carefully over the many conflicting “facts” to make a more accurate assessment and insightful judgments to figure out the likely true nature of the disease.
I do not think finding MAP in the blood is a trivial thing. The long lasting MAP controversy would actually largely attribute to the scarce of MAP found in the patients, which is in fact in great contrast with the situations in the Johne’s disease, M Leprae and H Pylori. Yes, we still failed to find out the right condition for culturing M Leprae in vitro. However, Gerhard Henrik Armauer Hansen in Norway had announced back in 1873 the discovery of Mycobacterium leprae in the tissues of all sufferers, with just a "new and better" microscope, even without the special stains developed by Albert Neisser and others later (http://en.wikipedia.org/wiki/Gerhard_Armauer_Hansen). This had been also before the discovery of Mycobacterium tuberculosis by Robert Koch in 1882 (http://en.wikipedia.org/wiki/Mycobacterium_tuberculosis) and the discovery of Johne’s disease by Heinrich A. Johne in 1905 (http://en.wikipedia.org/wiki/Paratuberculosis). The existence of H. Pylori (the spiral-shaped bacteria) in the lining of the human stomach had been found by German scientists back to 1875, a century before Barry Marshall and Robin Warren approved they are the key causative factors for peptic ulcers in 1980s (http://en.wikipedia.org/wiki/Helicobacter_pylori) . As we know, large amounts of MAP can easily be found in the feces and tissues of Cattle with Johne’s disease and cultured with the standard methods established long time ago. It is the scarce of MAP in the feces and tissue of Crohn’s disease made the report of successful culture of higher rates of viable MAP in the blood of Crohn’s patients become quite an important event. And only the consistent, reproducible differences between the patients and controls may suggest the existence of a possible link.
I also do not agree with the notion that Crohn’s disease is more closely linked to diseases like leprosy rather than ulcerative colitis. There is no misdiagnosis between CD and leprosy at all. However, no matter how splendid the hospital, how good the doctor and how hard they try, there is always a portion of cases Non-Differentiable as either CD or UC. In addition, CD and UC but not leprosy also shared many similarities in epidemiological distribution, treatments, etc.”
