What Tuberculosis and Crohn’s Have in Common
It wouldn’t seem as if leprosy, tuberculosis, and Crohn’s disease would have much in common. But increasing evidence points to all three diseases being caused by closely related species of Mycobacterium, a germ that’s notoriously difficult to treat with antibiotics.
We know, of course, that tuberculosis (which is present, clinically or subclinically, in one out of three people in the world) is caused by Mycobacterium tuberculosis. Leprosy, with 200,000 new cases reported per year worldwide, is not only bacterial, it was in fact the first disease to be definitively associated with a bacterium (namely Mycobacterium leprae) back in 1873. The shocker is that a growing body of evidence now associates M. avium subspecies paratuberculosis (MAP, for short) with occurrences of Crohn’s disease and ulcerative colitis, two bowel disorders that are increasingly prevalent in developed countries, with U.S. prevalence running at around 201 cases per 100,000 persons for Crohn’s and 238 for ulcerative colitis (2007 stats).
The conventional dogma for Crohn’s is that it is a genetic disorder involving the immune system. The fact that some people are more genetically predisposed to the condition does not rule out an infectious agent, however, and Mycobacterium infections are famous for eliciting a complex immunological response. When Dr. Robert J. Greenstein of the VA Medical Center in the Bronx, NY wrote an article in Lancet in 2003 suggesting an etiological role for MAP in Crohn’s disease, the only trials investigating the effectiveness of antibiotics for Crohn’s disease had produced negative results. But the trials, up to that time, had all used antibiotics that are ineffective against Mycobacterium. Since then, other studies have been done using appropriate antibiotics, and a recent meta-analysis of results found:
Long-term treatment with nitroimidazoles or clofazimine appears to be effective in patients with Crohn’s disease.
What about the familiar claim that Crohn’s runs in families? Spokane pathologist Ellen S. Pierce, writing in Gut Pathogens 2010, 2:21, describes case studies in which the children of a family develop Crohn’s, followed by one parent, followed by the other parent. She describes cases where one parent develops Crohn’s and the other (of course genetically unrelated) parent develops ulcerative colitis (UC), and some cases where both parents develop UC. The common thread? Food and water. Specifically, milk, and bath water. MAP can occur in either.
It turns out, under current U.S. standards for dairy products, MAP bacilli are not reliably killed by pasteurization. But you don’t have to drink milk to be exposed. MAP is also prevalent in potable water. In one study, faucets and shower heads in a hospital were sampled for MAP. Eleven of 16 hot water taps (including shower heads putting out 55-degree-C water) tested positive for a medically important serotype of MAP.
Just as M. tuberculosis doesn’t cause frank disease in everyone who carries it, neither does MAP. Which is good, because a course of antibiotic treatment can take six months and involves a risk of bowel obstruction. But in the U.S., you probably won’t be offered antibiotic therapy, since there is reluctance in the medical profession to consider Crohn’s or ulcerative colitis bacterial diseases, just as there was reluctance to consider peptic ulcers to be the result of infection.
Nevertheless, if you or someone you know has Crohn’s or ulcerative colitis, you should read the latest research (start with Pierce’s paper) and come to your own conclusions. Don’t wait for the medical community to “come around.” You might be in for a very long (and painful) wait.
