Pathogenesis

The ingested bacteria enter the intestinal wall through the small intestinal mucosa. The point of entry in experimentally infected goats has been shown to be through M cells found in the follicle-associated epithelium lining the domes of the Peyer's patches and also through enterocytes in areas without Peyer's patches (SigurSardottir et al., 2001, 2005).

Infection with MAP is usually characterized by an initial clinically silent period. Eventually, macrophages may lyse and facilitate spread of MAP (Koets et al., 2015). Granulomatous arteri­tis has been detected in the intestine of goats and might contribute to the spread of MAP (Kruger et al., 2015b). New infectious foci could also de­velop following dissemination from, for example, areas of caseous necrosis (Kruger et al., 2015a, b; Lybeck et al., 2013).

Most animals infected with MAP are able to control the infection. However, subclinically infected animals will probably remain infected for the rest of their life, and some may intermit­tently shed the bacteria in faeces, contributing to spread of the infection. Whether infected animals can clear the infection or not remains unclear. The bacteria could not be cultured from tissue lesions of goats that previously had been faecal shedders and IFN-γ positive, and a reduc­tion in lesions and bacterial load was seen at 6-12 months compared with 3 months of age in some animals (Kohler et al., 2015). In other stud­ies, some individuals of experimentally infected goats where a cell-mediated immune response had been detected were found not to display le­sions or harbour MAP bacteria (SigurSardottir et al., 1999; Storset et al., 2001). Still, it cannot be excluded that these animals were infected, but that the numbers of bacteria were too low to be detected.

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