Throughout 1997 and 1998 the most comprehensive treatment of this was published on the Internet by Alan Kennedy, and it should be the starting point for all researching this. The topic is still very controversial since there are studies that found Mycobacterium in Crohn's patients, and there are ones that did not. The truth may be that both of them were right, and that this agent may be implicated in certain percentage of occurrences. In addition to Alan's page, I'll list some other references that may be of interest for the reader.
NEWS!!!NEWS!!! University of Central Florida has some exciting
new research going on:
detection
of M paraTB in Crohn's patients and new
drugs development.
THALIDOMIDE - an old drug, a new indication: read all about it on CCFA page (clinical trial in progress in Chicago), and medical papers on Thalidomide.
Acting on DNA evidence that implicates Mycobacterium paratuberculosis as a possible cause of Crohn's disease, a team led by John Hermon-Taylor, MD( j.hermon-taylor@sghms.ac.uk ), a Crohn's disease researcher here, used a combination of rifabutin and clarithromycin (Biaxin, Abbott) to treat 46 patients with Crohn's disease. The investigators did not determine whether patients were infected with M. paratuberculosis.After patients started antibiotic treatment, they continued to take steroids, a conventional treatment, at their usual dosages for four to six weeks. After that, they gradually reduced the steroids until they were off them completely. Data from this uncontrolled study suggest that patients who took the antibiotics had a much longer remission than patients who received conventional treatment alone. About 80% of the patients who could take the treatment had "a profound and lasting remission" of their illness, said Hermon-Taylor, who is professor of surgery at St. George's Hospital Medical School, London.
Hermon-Taylor and his colleagues are not the only investigators who have tested antibiotics as a treatment for Crohn's disease. David Graham, MD, of Houston, and colleagues conducted a placebo-controlled trial looking at the efficacy of clarithromycin as a treatment for Crohn's disease. They randomly assigned 17 people with severe Crohn's disease to receive either conventional therapy plus a placebo or conventional therapy plus clarithromycin. They did not determine whether the patients harbored M. paratuberculosis. Forty percent of the patients in the antibiotic arm became well and stayed well for up to three years, said Graham, who is chief of gastroenterology at the Veterans Administration Medical Center in Houston. In contrast, one person in the placebo arm became well but did not remain well. To confirm their findings, Graham and colleagues are conducting a larger placebo-controlled study looking at the efficacy of clarithromycin plus ethambutol.
Crohn’s research being done at the University of Central Florida in Orlando. (This is from a post-baccalaureate student working under Saleh A. Naser, Dept. of Molecular Biology and Microbiology and Ira Shafran, M.D. gastroenterology, Orlando.) "Generally speaking, the work we’re doing know is an extension of (humoral) immune response work published by Dr. Saleh A. Naser (Ph.D, Dept. of Microbiology and Molecular Biology, University of Central Florida), et.al. in 1994, which lent evidence to the association of M. paraTB to Crohn’s disease. The current research is supported clinically by Ira Shafran, M.D.(Orlando, FL). We have shown a 92% positive rate for the presence of antigens specific to M. paraTB in the blood sera of 50+ patients confirmed to have CD. In contrast, our control sample of individuals presumed free of gastrintestinal disease showed a 27% positive rate, with no individual positive for more than one M. paraTB-specific antigen. Over 70% of CD patients tested positive for more than one antigen. We are continuing our study by testing sera of different types of control samples, amplifying M. paraTB DNA existing in CD patient tissue, and culturing M.paraTB cells from CD tissue."
In reference to a possible link of Johnes to Crohn’s disease, there was an interesting article in the Canadian Journal of Veterinary Research, 1991;55:199-202 entitled EXPERIMENTAL DISEASE IN YOUNG CHICKENS INDUCED BY A MYCOBACTERIUM PARATUBERCULOSIS ISOLATE FROM A PATIENT WITH CROHN’S DISEASE (H.J. Van Kruiningen, B. Ruiz and L. Gumprecht, Dept of Pathobiology, U. of Connecticut, Stoors, CN 06269): Two week old Leghorn-Cochin chicks were inoculated with strain Linda. Six birds received 10**7 organisms orally, six intraperitoneally, and five intracardially. Six uninoculated birds served as controls. Birds from each group were necropsied at two-week intervals. Focal granulomatous lesions occurred in two of six chickens which were inculated orally, six of six inoc. intraperitoneally, three of five intracardially, bun in none of the six controls. Of the 11 birds with lesions, acid-fast bacilli were demonstrated in five. Immunoperoxidase reactivity paralled the presence of acid-fast bacilli.
Also, in J Clin Microbiol, 1992 Aug, 30:8, 2013-8 a paper "Immunoglobulin A (IgA) and IgG serum antibodies to mycobacterial antigens in Crohn's disease patients and their relatives" (Wayne LG; Hollander D; Anderson B; Sramek HA; Vadheim CM; Rotter JI; Tuberculosis Research Laboratory, Department of Veterans Affairs Medical Center, Long Beach, California 90822): "Sera from patients with Crohn's disease, their relatives, their spouses, and unrelated healthy controls were assayed by enzyme-linked immunosorbent assay for immunoglobulin G (IgG) and IgA antibodies to Mycobacterium tuberculosis, M. avium, and M. gordonae. The patients had significantly higher IgA responses to mycobacterial antigens than did either their relatives or the controls. On the other hand, both the patients and their relatives had significantly higher IgG responses against these antigens than did the controls. The elevated IgA response was more pronounced against isopentanol-extracted whole bacterial cells than it was against soluble protein extracts, and it appeared to be directed against fixed surface antigens that lie under the loosely bound peptidoglycolipid or glycolipid antigens of mycobacteria.