Bacteria and Viruses associated with Crohn’s disease

To date no microbe has been identified as the cause of Crohn's Disease (CD). The bacteria living in the intestine are very numerous and there are hundreds of different strains and species. Only two-thirds of these have been fully identified and it is still possible that some previously unknown bug that causes CD or Ulcerative Colitis (UC) may yet be discovered. What is clear is that the normal balance of healthy bacteria is upset in IBD with both a reduction in Lactobacilli and Bifidobacteria and an increase in facultative anaerobes, organisms which are normally oxygen loving, but somehow manage to survive in the colon where oxygen is in short supply. The possibility is that this changes the normal fermentation of the intestinal contents. Whether or not it is this process which leads to disease is currently being investigated.

Certain organisms have been suggested to be important in CD and these are discussed below.

Measles, MMR vaccine

There is no support of a causal role for persistent measles virus infection in Crohn's disease. A suggested link between the development of CD and the measles virus and MMR vaccine was the subject of intense media coverage a few years ago and caused much concern and anxiety amongst sufferers of the disease and their families. Many mothers refused to have their babies immunised.

It has now been shown that there is no link between the MMR vaccination and bowel disease. Therefore, there is no reason for change in the current MMR vaccination policy. Giving the vaccines separately would leave children unnecessarily exposed to preventable infectious diseases along with their often serious consequences.

Mycobacterium paratuberculosis

Mycobacterium paratuberculosis (MAP) is known to cause a disease in cattle (Johne's disease) which is very similar to CD. For many years workers have therefore investigated possible links between MAP and the development of CD in humans, with varying results.

MAP is widely spread in the environment. It can occur in milk supplies (unpasteurised), tap water and soil and it seems possible that it is merely a secondary invader which may enter areas of gut already damaged by CD, possibly influencing histological changes, but not being the primary cause of the disease. However the question is still under investigation.

Professor Hermon Taylor and his colleagues at St George's Hospital in London reported to have found MAP in about 65% of their CD patients. Tissue samples were taken from operation specimens and DNA isolated using sensitive testing methods. However, other researchers were unable to reproduce these positive results despite using the same testing methods and other more specific and sensitive methods. It was suggested that previous positive results were due to laboratory contaminants or other artefacts of testing.

For a disease to be recognised as infectious it must satisfy the four postulates of the great German bacteriologist Robert Koch, i.e.

  1. The organism must be present in all cases of the disease
  2. It must be isolated and grown in pure culture in the laboratory.
  3. It must reproduce the disease in a suitable experimental animal
  4. It must then be transmissible to another animal and be recovered from that animal after it has caused the disease

Professor Taylor was only able to find the organism in 65% of his patients; others were unable to isolate a single organism except in one non-Crohn's patient. Therefore these postulates are not satisfied.

Furthermore, treatment with anti-tubercular therapy is ineffective in the treatment of CD.

Some patients worry that if they find their CD is made worse by milk products, and as MAP is known to occur in unpasteurised milk, that this must mean that MAP is causing their problem. This is not so. Although gastroenterologists accept that bacteria are a possible cause of CD, this may be due, not to infection, but rather to the process of abnormal fermentation of food residues by bacteria in the large intestine. Chemicals are produced from this process which may damage the lining of the intestines causing inflammation, ulceration and bleeding and lead to the body's immune system attacking the healthy bacteria of the bowel. The problem is intolerance to fat, protein or sugar in milk which can lead to the development of the disease when these are fermented, and not due to the possibility that the milk could be contaminated with MAP.

Faecalobacterium prausnitzii (Fp)

Recently there has been considerable excitement because a French group of workers reported that patients with CD had low numbers of this organism living in their intestines. Fp has an anti-inflammatory effect and it was suggested it might be possible to treat CD by giving sufferers this bacterium. Unfortunately it was found that there was no difference in the numbers of Fp in patients with CD, UC, Irritable Bowel Syndrome (IBS) and healthy controls. Furthermore, when patients with CD were treated successfully by elemental diet, the numbers of Fp, far from increasing, fell even lower. If a reduction in numbers is associated with improvement in CD it is difficult to see that lack of Fp can be an important factor in producing this disease.

Sulphate reducing bacteria (SRBs)

These bacteria live in the bowel and produce hydrogen sulphide (H2S) which is a very toxic chemical. It has therefore been suggested SRBs may be important in causing IBD. This suggestion has still to be proved. It seems likely that H2S is rapidly reconverted to sulphate, which is harmless, making it unlikely to be important.


Yersinia may infect the small intestine giving changes which are similar to those of CD. However, there is no convincing evidence to date that this organism is the cause of the disease.