Submitted to: Veterinary Immunology and Immunopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/21/1998
Publication Date: N/A
Citation: N/A Interpretive Summary: Johne's disease is a chronic, debilitating, intestinal disorder in cattle characterized by diarrhea, reduced feed intake, weight loss, and death. Cattle usually become infected as young calves by ingesting feces containing the causative bacteria. However, symptoms of disease do not usually present themselves until the animals reach 3 to 5 years of age or even older. During this time the animal is infected and may be shedding the organism in its feces without showing any clinical signs of disease. In addition to reduced production by these animals through reduced milk production, they also present a potential infective threat to the rest of the herd. The disease often shifts to a clinical state after the animal is stressed. Examples of stressors which may invoke clinical disease are parturition and early lactation. During parturition and lactation, body calcium stores are rapidly mobilized to fulfill the needs of the dam and her calf. Factors that influence mobilization of body calcium may be associated with the shift in the disease state of animals infected with paratuberculosis. Low available calcium may influence the ability of the infected dam to control the disease. This study demonstrates that feeding low dietary levels of calcium significantly increased the infection level in tissues of mice infected with M. paratuberculosis. It is our conclusion that altering available calcium in infected animals may increase the severity of the disease.
Technical Abstract: A 6-month study was conducted to evaluate the effects of feeding different levels of dietary calcium (Ca) on the persistence of Mycobacterium paratuberculosis infection using a mouse model. Beige mice, averaging 8 weeks of age, were randomly assigned to one of the following dietary treatments: 1) 0.02% Ca, 2) 0.15% Ca, 3) 0.45% Ca, and 4) 1.0% Ca. Mice were infected intraperitoneally with 108 CFU viable M. paratuberculosis fo 1, 3, and 6 month periods. Plasma Ca was unaffected by dietary Ca (x = 7.3 mg/dl). Plasma 1, 25(OH)2D3 was elevated significantly in 0.02% and 0.15% Ca groups compared to other treatments at the end of each period, with the highest levels observed for 0.02% Ca mice and intermediate values for 0.15% Ca mice. One month after infection, numbers of viable M. paratuberculosis cultured from the spleen were significantly reduced for 0.15% Ca mice, whereas the number of bacteria isolated from the liver and mesenteric lymph hnode (MLN) were higher for the 0.02% Ca group. There were no differences in bacterial numbers in the ileum although they tended to be higher for the 0.02% Ca group. Three months after infection, bacterial numbers in the spleen, ileum, and MLN did not differ across treatments, however, significantly lower numbers were found in the liver of 1.0% Ca mice. Reduced bacterial counts were also observed in the liver of 0.15%, 0.45%, and 1.0% Ca mice after a 6-month infection period compared to the 0.02% Ca group, with the lowest numbers isolated from the 1.0% Ca mice. Numbers of viable bacteria cultured from the ileum and MLN after 6 months of infection were also significantly reduced in 1.0% Ca mice. These results suggest that Ca metabolism is an important modulator of M. paratuberculosis infection.