This bacterium, along with others, has seen a lot of study. A viable theory for the origin of Crohn's is an over-response to some bacteria or virus, but no clear smoking guns found yet. Still, this seems to be the basis of antibiotic therapies, including triple-antibiotic therapy. Broady had published a paper on triple-antibiotic and Crohn's about 10 years ago.
There is a 2012 review of gastrointestinal infection and IBD, which says that it is still unclear whether MAP leads to Crohns (for some people) or IBD allows MAP infestation. One study in particular, did not find much MAP in new/early Crohn's patients; but did find a lot of it in long-term Crohn's patients - this suggested Crohn's came 1st. This is also consistent with theories that draw on unbalanced gut flora. MAP would be one of the bad flora that gets to bloom when the good flora get wiped out.
Below is what the 2012 review said about MAP:
Gastrointestinal infection as a trigger for inflammatory bowel disease
Mann, Elizabeth A.; Saeed, Shehzad A.
Current Opinion in Gastroenterology
Issue: Volume 28(1), January 2012, p 24–29
from the review said...
Mycobacterium avium subspecies paratuberculosis (MAP) causes epidemic chronic inflammatory bowel disease (Johne's disease) in animals, including nonhuman primates, and was one of the first micro-organisms suggested as a causative agent of IBD [17]. Meta-analysis has demonstrated a strong relationship between the presence of MAP DNA and Crohn's disease [18,19] although the source of DNA varied across studies, and methods for both DNA isolation and the MAP-specific PCR assay were not standardized. Recently, a strong association was shown between Crohn's disease and MAP [6] detected by long-term culture from blood samples (Table 1). However, MAP PCR was positive in DNA from all blood samples, including healthy controls and the authors conclude that MAP is endemic to the area (Spain). In a prospective study conducted in Norway, Ricanek et al. (Table 1) found a very different result in patients either concurrently diagnosed with IBD or categorized as non-IBD. Both groups exhibited a similar low level of MAP detected by long-term cultivation of biopsy specimens. This was in contrast to a strong association of positive MAP cultures from biopsies obtained from a cohort of established IBD patients versus non-IBD controls. Again PCR results did not correlate with culture results. On the basis of this study, MAP infection may not be a factor in initiation but rather may occur secondary to the disease state. An independent method of evaluating MAP exposure confirmed its association with Crohn's disease [20]. Peripheral blood mononuclear cells (PBMCs) from patients with Crohn's disease demonstrated increased proliferation of T cells and altered cytokine response, including increased TNF[alpha], in response to MAP compared to PBMC from ulcerative colitis patients and healthy controls. The response was specific to MAP, as responses to other bacteria were similar among the groups. The authors propose a role for repeated MAP exposure via the food chain as a modifying factor in the inflammatory response in Crohn's disease patients.