Possible Infectious Causes Of Inflammatory Bowel Disease (IBD)

There are many similarities between the way IBD presents in the intestines and a number of specific infections caused by bacteria, viruses, and parasites. Well-recognized intestinal infections, caused by specific bacteria (such as Salmonella, Campylobacter, Yersinia, several strains of E. coli), by specific viruses (such as Norwalk virus and rotavirus), and by parasites (such as Entamoeba histolytica and Giardia), often produce intestinal inflammation and damage, along with the associated symptoms of abdominal pain, diarrhea, and rectal bleeding, but they do not usually last more than several days before they are cleared by the body's immune system. These microbes (bacteria, viruses, and parasites) typically do not produce chronic or long-lasting intestinal inflammation and have not been found in the intestines or stools of patients with IBD. They usually do not recur once the microbe is cleared by the immune system, unless a person is exposed again to the microbe in question.

 

 

Although it appears unlikely that a disease causing (pathogenic) bacterium is the cause of IBD, the thousands of billions of bacteria normally present in the intestine may somehow contribute to the inflammatory process. No single bacterial species or strain is solely responsible for the inflammatory effect; it requires a particular combination of strains to induce inflammation in someone who is genetically susceptible.

 

 

One particular bacterial infection, called Clostridium difficile, is found in the stool of IBD patients from time to time, particularly during a flare of the disease. However, Clostridium difficile is not known to cause IBD; rather, IBD likely provides suitable conditions for the growth of this bacterial species.

 

 

Other bacteria that do not cause infection may contribute to the cause of IBD. Researchers have experimented with bacteria that were missing their cell wall as a possible cause. It was thought that these bacteria, called L-forms, could produce chronic infection that is indistinguishable from IBD. Subsequent studies have shown that these bacterial forms are not involved in IBD.

 

 

Another species of mycobacterium, called Mycobacterium paratuberculosis, produces Johne's disease in cattle. Johne's disease looks somewhat like Crohn's disease in humans. Prevalent in dairy herds and excreted in milk, this bacterium is not completely killed by the pasteurization of milk and is, therefore, potentially present in the milk supply. Some experts have suggested that Mycobacterium paratuberculosis may be able to infect humans and that this chronic infection may be the cause of Crohn's disease, in at least some patients.

 

In some studies, researchers have been able to detect antibodies against specific segments of mycobacterial proteins in the blood of human Crohn's disease patients, and in other studies, they have been able to detect genetic sequences specific to mycobacteria in inflamed intestinal tissues of Crohn's disease patients.

 

Some investigators have apparently had success in treating Crohn's disease using multiple antibiotic treatment regimens that are active against Mycobacterium paratuberculosis. However, the number of patients treated has been relatively small, and most researchers have not been able to reproduce the findings of mycobacteria in the intestinal tissues or the response to therapy against mycobacteria.

 

 

Microbes other than bacteria can cause intestinal inflammation and have, therefore, also been considered as possible causes of IBD. Viruses, in particular, may be very difficult to detect in the intestinal lining or in stool samples, and it has been speculated that a virus that has eluded detection may be the cause of IBD.

 

 

Paramyxoviruses, of which the measles virus is the best known, has received considerable attention. By using blood testing to detect antibodies directed against paramyxovirus or by using very powerful electron microscopy on biopsy and surgical resection specimens from Crohn's disease patients, some investigators have found what they believe is evidence of a paramyxovirus infection in Crohn's disease patients. However, in more recent studies, very sensitive genetic probes for paramyxovirus have not been able to detect this evidence of measles virus.

 

Subsequently, the proponents of the "measles theory" have suggested that it is not necessarily an actual infection by measles virus that produces Crohn's disease, but rather the late effects of early childhood infection or exposure of one's mother to measles virus during pregnancy. They have also suggested that Crohn's disease may be a result of childhood immunization against measles using the live measles vaccine, in which the virus is still alive but cannot produce the usual measles infection. There is some indirect evidence supporting this theory, but it consists mainly of the apparent increase in the incidence of Crohn's disease following the institution of universal measles vaccination programs in developed countries in the 1960s.