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Crohn's disease happens in clusters, and no one knows why.


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Clustering of Crohn's disease within affected sibships

Jean-Pierre Hugot, Jean-Pierre Cézard, Jean-Frédéric Colombel, Sven Almer, Curt Tysk, Sean Montague, Miquel Gassull, Steen Christensen, Yigael Finkel, Corinne Gower-Rousseau, R Modigliani, Habib Zouali, Suzanne Lesage, Mathias Chamaillard, Jeanne Macry, Gilles Thomas, Jean-Marc Victor & J Belaiche on behalf of and the GETAID

Crohn's disease (CD) is a complex genetic disorder for which aetiology is unknown. Recently, genetic factors for susceptibility have been described. Several genetic loci have been mapped and partially explain the familial aggregations of the disease. However, environmental factors may also contribute to these aggregations. We considered that if the role of non-genetic factors was negligible, CD patients would be randomly distributed in sibships with multiple affected siblings. On the other hand if there was a significant environmental contribution, the siblings would be affected non-randomly over exposure status. In order to test this hypothesis, we studied 102 sibships with two or more affected siblings. A statistical test, named Cluster of Affected Sibling Test or CAST, was developed, based on the exact calculation of the probability of observing a given number of clusters of affected siblings in multiplex families. The null hypothesis of a random distribution of affected siblings was rejected (P=0.005). The observed excess of affected sibling clusters indicates that birth order influences the disease status. Considering that an adjacent order of birth is a global estimate of environmental sharing, this observation strongly suggests that environmental factors contribute to the observed familial aggregations of the disease. This observation provides evidence that familial CD is a relevant tool for further studies of environmental factors and gene-environment interaction. More generally, the CAST statistics may be widely applicable to estimate the involvement of environmental factors in the aetiology of other binary traits which may be observed in multiple members of the same sibship.

A clustering of Crohn's disease in Mankato, Minnesota

H J Van Kruiningen, B J Freda

Infrequently, clusterings of Crohn's disease (CD) occur that suggest it is transmissible. We studied such a clustering. Graduates of the Mankato West High School Class of 1980 were contacted by mail and asked to respond, by self-addressed postcard, to a six-item questionnaire about inflammatory bowel disease and CD. Responses were followed-up by telephone contact and additional mailings. Two visits were made to Mankato, Minnesota, to interview individuals with CD, to obtain medical records, radiographs, and sera, and to study environmental risk factors. Of the 320 graduates of the class of 1980, 285 were contacted. Seven cases of CD were identified, the equivalent of a prevalence of 2,400/100,000. Concerns were discovered that CD may have emanated from recreational swimming. Fecal coliform counts in excess of 200/dL, the standard above which water is regarded as unsafe for recreational use, had been recorded year after year for the Blue Earth River at Mankato and for the Minnesota River. Recent fecal coliform counts (1993-1995) of Lake Washington, Lake German/Jefferson, and Lake Shetek were greater than 200/dL in 57%, 65%, and 62% of water samples. This clustering, in unrelated individuals, argues against a genetic cause for CD and suggests that environmental transmission occurred.

An in-depth study of Crohn's disease in two French families

H J Van Kruiningen 1 , J F Colombel, R W Cartun, R H Whitlock, M Koopmans, H O Kangro, J A Hoogkamp-Korstanje, M Lecomte-Houcke, M Devred, J C Paris, et al.


Background: Two French families were investigated. In the first a husband, wife, and 4 children had Crohn's disease; in the second 7 of 11 children had the disease. There was no history of Crohn's disease in antecedent generations and no linkage to HLA haplotypes.

Methods: Methods included family interviews; review of medical records, radiographs, and pathology slides; serology; selective stool culture; enzyme-linked immunosorbent assay for fecal viral detection; and immunocytochemistry.

Results: In both families multiple cases occurred among siblings in 7-13-month periods. There appeared to be a 4-8-year recurrence of new disease in both families. Radiographs showed a remarkable similarity in the pattern of disease, confined to distal ileum and cecum, in the members of family 1. Examination for pathology showed granulomas in all 8 patients for whom tissues were available. Acid-fast organisms or Campylobacter-like organisms were not found in tissue sections, and immunocytochemistry was negative for mycobacteria and Yersinia. Stool cultures were negative for mycobacteria, Yersinia, and Mycoplasma. Torovirus and coronavirus antigens were not found in stool. Serology was negative for antibodies to Brucella, Yersinia, influenza, and three enteropathogenic viruses of animals.

Conclusions: The circumstances and data suggest that an infectious microorganism is responsible for these clusterings of Crohn's disease.

Clustering of Crohn's disease in a Cotswold village


The first large cluster of patients with Crohn's disease, identified in the parish of Blockley, Gloucestershire is reported. Twelve patients with Crohn's disease have been identified of whom only two (a father and daughter) are known to be related. The age and sex distribution and macroscopic site of disease at diagnosis is similar to that expected in an unselected series. The identification of such a cluster suggests that environmental factors may be important in pathogenesis.


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Some explanations so far have been.

-bacterial infection from the same food source
-zoonotic infection from an animal living within the cluster
-viral infection from a norovirus, which would make crohn's disease an infectious and transmittable disease

Acute gastroenteritis is followed by an increased risk of inflammatory bowel disease

Background & aims: Bacterial intestinal infections have been implicated as a possible cause of exacerbation of inflammatory bowel disease (IBD). We explored the relationship between infectious gastroenteritis and the occurrence of IBD using data from the General Practice Research Database.

Methods: A cohort of patients aged 20-74 years with an episode of acute infectious gastroenteritis (n = 43,013) was identified. From the same source population, an age-, sex-, and calendar time-matched control group free of gastroenteritis was sampled (n = 50,000). Both cohorts were followed up for a mean duration of 3.5 years.

Results: The estimated incidence rate of IBD was 68.4 per 100,000 person-years after an episode of gastroenteritis and 29.7 per 100,000 person-years in the control cohort. The hazard ratio of IBD was 2.4 (95% confidence interval [CI], 1.7-3.3) in the gastroenteritis cohort compared with the control cohort, and the excess risk was greater during the first year after the infective episode (hazard ratio, 4.1; 95% CI, 2.2-7.4). The relative risk of developing Crohn's disease in the gastroenteritis cohort was greater than that of ulcerative colitis, especially during the first year after the infective episode (hazard ratio, 6.6; 95% CI, 1.9-22.4).

Conclusions: Our results are compatible with the hypothesis that infectious agents causing an episode of infectious gastroenteritis could play a role in the initiation and/or exacerbation of IBD.

Decoding norovirus infection in Crohn's disease

Although a causing viral infectious agent remains untraceable in Crohn's disease, most recent genome-wide association studies have linked the FUT2 W143X mutation (resulting in asymptomatic norovirus infection) with the pathogenesis of Crohn's ileitis and with vitamin B12 deficiency (i.e., a known risk factor for Crohn's disease with ileal involvement). In line with these findings, host variations in additional genes involved in host response to norovirus infection (such as ATG16L1 and NOD2) predispose humans to Crohn's ileitis. One may therefore presume that asymptomatic norovirus infection may contribute to disruption of the stability of the gut microbiota leading to Crohn's ileitis. These paradigms highlight not only the need to revisit the potential transmissibility of Crohn's disease, but also potential safety issues of forthcoming clinical trials on human probiotic infusions in Crohn's ileitis by rigorous donors screening program.
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Infection is definitely a possibility for starting Crohn's, but I wouldn't rule out the possibility some non-infectious toxin starting the inflammation cycle. The mouse model in which they induce colitis with DSS may be more similar than you would expect.
The map bacterium hypothesis is that the clusters are linked to excess map levels in particular rivers, I believe this is why Cardiff in Wales is thought to have high case numbers as the rivers flowing from the valleys get contaminated with map from the farms.
As I understand it the initial feedback from the early phase anti-map vaccine trials are due in April 23 so we may get a steer soon on whether this theory is gathering speed or not
The map bacterium hypothesis is that the clusters are linked to excess map levels in particular rivers, I believe this is why Cardiff in Wales is thought to have high case numbers as the rivers flowing from the valleys get contaminated with map from the farms.
As I understand it the initial feedback from the early phase anti-map vaccine trials are due in April 23 so we may get a steer soon on whether this theory is gathering speed or not
Yeah a lot of people are so excited about the trial result release date. I dont know why I am not holding my breath? There has been no update and not even a preview of what's to come. I tend to interpret no communication to be things are not going well. I hope I am wrong.