Paucity of mycobacteria in mucosal bowel biopsies from adults and children with early inflammatory bowel disease
Received 30 January 2010; received in revised form 14 May 2010; accepted 14 May 2010. published online 21 June 2010. Corrected Proof
Abstract
Background
The presence of Mycobacterium avium subspecies paratuberculosis (MAP) has previously been inferred in the genesis of Crohn's disease (CD), and a higher incidence of MAP PCR positivity has been demonstrated in the gut and peripheral blood of CD patients than in healthy individuals. The objective of this prospective study was to assess the potential etiological role of MAP in the pathogenesis of CD.
Methods
The presence of mycobacteria was assessed in bowel biopsies from newly diagnosed, treatment naïve Norwegian patients with IBD, including CD and ulcerative colitis (UC), as compared to a hospital-based cohort of CD and UC patients. Biopsies were collected from the small and large bowel in 354 individuals with suspected IBD. Detection of mycobacteria was performed by long-term cultivation in combination with direct detection by MAP IS900-specific PCR.
Results
Among the specimens included from the patients with early IBD, samples from only two of the patients with CD (2.7%) and two of the non-IBD controls (1.5%) exhibited a positive growth signal. None of the CD patients and only one of the non-IBD controls was MAP PCR positive. Only the single PCR positive non-IBD control was also mycobacterial culture positive with Mycobacterium avium subsp. hominissuis. In the referral patients with long-term IBD, the prevalence of growth signal and MAP PCR positivity was higher (52 and 9%, respectively).
Conclusions
These findings demonstrate the paucity of MAP in the gut of treatment naïve CD patients. This study does not provide evidence for a role of MAP in early IBD.
aCentre for Molecular Biology and Neuroscience and Institute of Microbiology, Oslo University Hospital (Rikshospitalet), Oslo, Norway
bDepartment of Gastroenterology, Akershus University Hospital, Lørenskog, Norway
cEpiGen-Institute, University of Oslo, Faculty Division Akershus University Hospital, Lørenskog, Norway
dDepartment of Pediatrics, Akershus University Hospital, Lørenskog and Oslo University Hospital (Ullevål), Oslo, Norway
eDepartment of Medicine, Oslo University Hospital (Rikshospitalet), Oslo, Norway
fUniversity of Oslo, Faculty Division Akershus University Hospital, Lørenskog, Norway
gCentre for Molecular Biology and Neuroscience and Institute of Microbiology, University of Oslo, Oslo, Norway
Corresponding author. Centre for Molecular Biology and Neuroscience and Institute of Microbiology, Oslo University Hospital (Rikshospitalet), Sognsvannsveien 20, NO-0027 Oslo, Norway. Tel.: +47 23074065; fax: +47 23074061.
ABSTRACT