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Fifty calves inoculated at either 2 weeks or at 3, 6, 9, or 12 months of age with either a low or high dose of Mycobacterium avium subspecies paratuberculosis (MAP) were on average 32 and 39 kg lower in body weight, respectively, compared to negative controls at 17 months of age.

Part I of this 2-part review examined the clinical stages, pathophysiology, diagnosis, and epidemiology of Johne's disease, providing information relevant to Canada, where available. In Part II, a critical review of the economic impacts of the disease, risk factors, and important control measures are presented to enable Canadian bovine practitioners to successfully implement control strategies and participate in control programs. In cattle positive by enzyme-linked immunosorbant assay, there is a 2.4 times increase in the risk of their being culled, and their lactational 305-day milk production is decreased by at least 370 kg. Reduced slaughter value and premature culling account for losses of CDN dollars 1330 per year per infected 50-cow herd. Research has failed to show a consistent association between Mycobacterium avium subsp. paratuberculosis test status and reduced fertility or risk of clinical or subclinical mastitis. Host level factors include age and level of exposure, along with source of exposure, such as manure, colostrum, or milk. Agent factors involve the dose of infectious agent and strains of bacteria. Environmental management factors influence the persistence of the bacteria and the level of contamination in the environment. Emphasizing a risk factor approach, various control strategies are reviewed, including a number of national control programs currently in place throughout the world, specifically Australia, The Netherlands, and the United States. By reviewing the scientific literature about Johne's disease, control of the disease could be pursued through informed implementation of rational biosecurity efforts and the strategic use of testing and culling.

A paired feeding experiment was conducted to investigate if reduced food intake is a reason for the body weight loss previously observed in severe combined immunodeficient beige (SCID bg) mice infected with Mycobacterium paratuberculosis. Mice were paired on the basis of age, litter and sex. One of each pair was injected intraperitoneally with 10(5) viable M. paratuberculosis organisms. The remainder served as uninfected pairfed mates. Each uninfected mouse was restricted to the amount of food (per gram body weight) that its infected paired mate ate in the previous 24 hour period starting at four weeks postinfection until 12 weeks postinfection when the mice were necropsied. The mean body weights of the two groups were not significantly different (p < 0.05) at the start of the experiment (infected 27.6 +/- 2.1 g, pairfed 27.3 +/- 3.4 g) but the pairfed group weighed less after 12 weeks of restricted food intake. Mycobacterium paratuberculosis was isolated from the spleen, liver, gut and fecal pellets of the infected but not the uninfected mice. Acid-fast bacilli were seen histologically in the liver, spleen and intestines of the infected mice only. Analysis of carcass compositions indicated that both infected and pairfed mice lost dry matter. Despite the loss in dry matter, the infected mice appeared to have maintained their body weights due to an increased retention of body water (presumably due to edema of inflammation). These results suggest that infection of SCID bg mice with M. paratuberculosis causes a reduction in their food intake (presumably due to reduced appetite) which, in turn, contributes to a loss in dry matter. We suggest that this loss in dry matter is one of the initial events that eventually lead to cachexia, and that it precedes the body weight loss that inevitably occurs in SCID bg mice chronically affected with M. paratuberculosis.