At the present time, there is no convincing indication that Crohn's disease
is a bacterial disease, although an association with mycobacteria has been
hypothesised for many years. The hypothesis that bacteria could be the cau
se, or at least an important concause of Crohn's disease is supported by se
veral experimental and clinical observations: animals kept in a germ-free e
nvironment fail to develop intestinal inflammation; bacteria are the cause
of human and animal intestinal diseases similar to Crohn's disease: luminal
content is necessary for causing gut lesions; and, more-over antibiotics a
re successfully risen in the treatment of Crohn's disease. Bradford Hill cr
iteria recently used to assess a causal relationship for Helicobacter pylor
i and peptic ulcer can be applied for establishing or excluding a causality
between mycobacteria and Crohn's disease. Of these criteria, only biologic
al plausibility coherence and analogy are satisfied. However, failure To id
entity a specific pathogen does not exclude a possible role for bacteria in
causing Crohn's disease lesions and symptoms. Pathogenic or commensal ente
ric bacteria could overinfect the primary lesions, leading to chronic intes
tinal inflammation in generically susceptible hosts. Another possibility is
that components of the normal intestinal flora could acquire pathogenic ch
aracteristics.