If you search for an answer to what causes Crohn’s disease, you will find results that mostly say there is no known cause. However, studies from the last 10 years point to a variety of microbes as the culprits. Certain microbes are associated with Crohn’s disease. This information may lead to new treatments, which target those microbes. In addition, the information may also lead to preventative measures.
The cause of inflammatory bowel disease, especially Crohn’s disease, is thought to involve an inappropriate, persistent inflammatory response to commensal gut microbes in genetically susceptible individuals. This is an important element. Many microbial infections or imbalances can result in an inflammatory response.
Once Crohn’s disease has begun, an altered immune response causes gut inflammation and loss of tolerance to intestinal antigens. The loss of tolerance stimulates the T-helper cells to produce proinflammatory cytokines that cause considerable damage. It becomes a continuous cycle that damages healthy tissue. Still, the genetic component is crucial because, without the susceptibility, those individuals are unlikely to develop Crohn’s from the microbes.
Which microbes can trigger Crohn’s in a person with a genetic susceptibility? Scientists are just beginning to pinpoint the specific agents. For now, let’s look at three potential microbial triggers, a bacterium, a fungus, and a virus.
Mycobacterium avium subspecies paratuberculosis (MAP)
Mycobacterium avium subspecies paratuberculosis or MAP for short is a bacteria known for its ability to cause a disease in the stomach of cattle called Johne’s disease. Johne’s disease looks similar to Crohn’s disease, which is why scientists suspected the bacterium for Crohn’s. Some strains of MAP can survive pasteurization, which has prompted concerns that milk may be a frequent source of MAP.
MAP can hide in white blood cells thereby eluding the immune system. It can also cause immune system dysregulation, which is the mechanism MAP uses to trigger Crohn’s disease. The drugs that are frequently successful against Crohn’s, clarithromycin and rifabutin, target MAP.
MAP is emerging as a causative factor of Crohn’s disease. Research also shows that MAP can trigger an array of gastrointestinal issues. One research report in 2011 stated, “If we accept that both ulcerative colitis and Crohn’s disease are caused by specific microorganisms, MAP, a long-overdue transformation will take place in the prevention and treatment of these diseases.”
Candida tropicalis
A 2016 study that came out in the journal American Society for Microbiology found a significantly higher prevalence of Candida tropicalis in the stool of Crohn’s disease patients. High rates of this fungus were also found in conjunction with anti-Saccharomyces cerevisiae antibodies, which is one way to differentiate Crohn’s disease from ulcerative colitis.
This fungus is typically found existing with two bacteria: E. coli and S. marcescens. They work together to create a triple-species biofilm that is thick and larger than normal. These biofilms contributed to dysbiosis in Crohn’s disease.
Learning more about how fungi, bacteria, and other microbes have evolved to interact with one another within our bodies is only going to expose future insights and novel approaches to treatments. This particular fungus is the first to be suspected as a causative agent in Crohn’s disease, rather than only bacteria and viruses.
Epstein-Barr Virus
Epstein-Barr virus was only discovered 50 years ago. Since its discovery, scientists have found that it is so common, up to 90% of adults have the virus, and for many years, scientists believed it was benign. However, it is now linked to many digestive conditions including:
- Crohn’s disease
- Ulcerative colitis
- Peptic ulcer disease
- Acute appendicitis
- Gastric cancers
Epstein-Barr virus is common in many health conditions in which gastrointestinal inflammation is a key characteristic, specifically Crohn’s disease. One study found that while there was no Epstein-Barr virus in normal gastrointestinal mucosa, 55 percent of those with Crohn’s disease had Epstein-Barr virus. Another study found this rate to be 63 percent in Crohn’s patients.
Researchers have shown that the Epstein-Barr virus can remain dormant until activated by immunosuppressant medications like steroids. In addition, immunosuppressant medications can worsen Crohn’s disease. This goes against conventional thinking. Because Crohn’s disease is an autoimmune disorder in which the immune system attacks the healthy gut lining, it would seem that an immunosuppressant drug would be helpful. The opposite occurs.
Thus, the vicious cycle begins. The drugs activate the Epstein-Barr virus, causing Crohn’s. Then, the patient is prescribed more immunosuppressant drugs, which only makes it worse. If doctors were more apt to test their patients on immunosuppressive drugs for Epstein-Barr virus and activity, they could catch the development of gut conditions early, possibly even prevent them.