Original Contribution
The American Journal of Gastroenterology (2008) 103, 1168–1172; doi:10.1111/j.1572-0241.2007.01742.x
Incidence of Mycobacterium avium Subspecies paratuberculosis in a Population-Based Cohort of Patients With Crohn's Disease and Control Subjects
Robert W Bentley PhD1, Jacqui I Keenan PhD3, Richard B Gearry MBChB, PhD2, Martin A Kennedy PhD1, Murray L Barclay MBChB, MD2 and Rebecca L Roberts PhD1
- 1Departments of Pathology, University of Otago, Christchurch, New Zealand
- 2Departments of Gastroenterology, University of Otago, Christchurch, New Zealand
- 3Departments of Surgery, University of Otago, Christchurch, New Zealand
Correspondence: Robert W Bentley, PhD, Department of Pathology, Christchurch School of Medicine & Health Sciences, P.O. Box 4345, Christchurch 8140, New Zealand.
Received 4 September 2007; Accepted 15 November 2007.
Abstract
OBJECTIVE:
To define the incidence of Mycobacterium avium subspecies paratuberculosis (MAP) in patients with Crohn's disease (CD) and in control subjects.
METHODS:
Blood samples from 361 CD patients from a previously described population-based inflammatory bowel disease (IBD) cohort and 200 blood donor controls, of known NOD2 genotype, were screened by PCR for MAP-specific IS900 DNA. These results were correlated with NOD2 genotype.
RESULTS:
The PCR assay was capable of detecting 20 fg of purified MAP DNA, equivalent to roughly 100 MAP cells/mL of blood. MAP-specific IS900 DNA was detected in 33.8% of CD cases and 21.5% of controls (OR 1.86, 95% CI 1.247–2.785, P = 0.002). All study participants were genotyped for the NOD2 mutations 2104C>T (R702W), 2722G>C (G908R), and 3020insC (1007fs). Carriage of one or two NOD2 mutations was not associated with a significantly higher risk of CD (OR 0.75, 95% CI 0.465–1.207, P = 0.234). No significant association was seen in the CD cohort for carriage of one or two NOD2 mutations and MAP status (OR 0.883, 95% CI 0.494–1.579, P = 0.675).
CONCLUSIONS:
Screening peripheral blood using IS900 PCR indicated that MAP DNA could be detected in a significant proportion of CD cases from a large population-based cohort, and also, in control subjects. The over-representation of MAP DNA in CD suggests either a role or a probable role for MAP in the etiology of CD.
