Abstract
Johne’s disease (JD) is a chronic enteric infection of cattle caused by Mycobacterium avium subsp. paratuberculosis (MAP). The high economic cost and potential zoonotic threat of JD have driven efforts to develop tools and approaches to effectively manage this disease within livestock herds. Efforts to control JD through traditional animal management practices are complicated by MAP’s ability to cause long-term environmental contamination as well as difficulties associated with diagnosis of JD in the pre-clinical stages. As such, there is particular emphasis on the development of an effective vaccine. This is a daunting challenge, in large part due to MAP’s ability to subvert protective host immune responses. Accordingly, there is a priority to understand MAP’s interaction with the bovine host: this may inform rational targets and approaches for therapeutic intervention. Here we review the early host defenses encountered by MAP and the strategies employed by the pathogen to avert or subvert these responses, during the critical period between ingestion and the establishment of persistent infection in macrophages.
Highlights
Johne’s disease (JD) is a chronic enteric infection of cattle caused by Mycobacterium avium subsp. paratuberculosis (MAP)
MAP is a pathogen of clear concern for animal health and it results in a significant economic cost to dairy and other livestock producers
The losses incurred by the dairy industry due to infected animals, and the ongoing concerns of a zoonotic disease threat through contaminated dairy products, suggest that a successful vaccine against MAP infection would be a valuable and welcome development
Summary
MAP invasion of the intestinal barrier 7.1.1 Tissue uptake of MAP MAPs' efforts to establish infection are not limited to considerations of the conditions that exist within a single animal; they extend to changes in conditions that exist across hosts. Oral challenge models suggest MAP may invade the host as early as the oral mucosa in the tonsils. There are marked age-dependent changes in the structure and function of this lymphoid tissue [28] which may be consistent with an age-dependent susceptibility to MAP infection This information may be critical for the design and delivery of a protective vaccine if immune effector cells must localize to a specific region of the small intestine. The MAP invasion of this first host cell barrier occurs very quickly, within 30 min of contact [34]. These cells translocate MAP from the intestinal lumen to the submucosa [35]. MAP translocation from the intestinal lumen into submucosal macrophages occurs in a matter of minutes to hours [35] (Figure 1)
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