Beige mice have been used in several studies to test the effect of dietary calcium on the persistence of MAP infection.

I’m proposing that MAP causes disease by penetrating the mucosal layer, attaching itself to a host's intestinal lining and, if a colony or colonies of MAP eventually become large enough, fermenting a wide-range of sugars to produce enough organic acid(s) at low ph to burn the gut lining, leading to various levels of low-grade intestinal inflammation and, potentially, intestinal lesions and ulceration.

To test this hypothesis a study could be conducted over a six-month period to observe the effect of dietary sugars on intestinal disease expression in MAP-infected Beige mice.

Mice should be randomly assigned one of perhaps 5 diets. The diets should vary in sugar composition from exceptionally low to very high. Sugars that could be used in the diets include: sucrose, fructose, lactose, and starch.

Additionally, administering antibiotics before MAP inoculation may facilitate intestinal MAP infection.

If my hypothesis is correct and MAP successfully infects the mice intestines, various levels of Johne’s disease should be observed in the mice on autopsy: from virtually no signs of intestinal disease (very low carb diet) to pathological lesions and ulceration (very high carb diet).

(During this study, starch should be considered a fermentable sugar. Also, dried vegetables may contain a greater amount of starch than fresh vegetables; this may be an important factor when devising an exceptionally low-sugar diet.)