Stereotypic immune response in <i>Mycobacterium avium</i> ssp. <i>paratuberculosis</i> infection among different Swiss caprine genotypes

Paratuberculosis is an infection with <i>Mycobacterium avium</i> ssp. <i>paratuberculosis</i> (MAP) causing chronic enteritis in domestic and wild ruminants worldwide. In goats, the infection is caused by C (cattle)-type and S (sheep)-type strains. In this study, the correlation between different MAP strains and histomorphological lesions in the small and large intestines, as well as the mesenteric lymph nodes, in Swiss goats (<i>Caprae aegagrus hircus</i>) was investigated. Ten Swiss caprine MAP isolates were characterized using polymerase chain reaction (PCR) and enzymatic restriction-based single nucleotide polymorphism (SNP) analysis. In addition, mycobacterial interspersed repetitive units and variable-number tandem repeats (MIRU-VNTR) profiling was performed, and the correlation with histologic lesions, scored as previously described for goats, was analyzed. Furthermore, immunohistochemical expression of CD3, CD79a, Iba1, cleaved caspase 3, and interleukin (IL)-17 was evaluated, and a morphometric analysis was conducted to quantify the different inflammatory cells. Diffuse multibacillary lesions were found in C-type/L'Institut national de recherche pour l'agriculture, l'alimentation et l'environnement (INRAE) Nouzilly MIRU-VNTR (INMV)1 (2/10) and S-type/INMV220 (1/10) animals. Diffuse lymphocytic lesions occurred in C-type/INMV1 (2/10) animals, while diffuse mixed lesions were observed in S-type/INMV218 (3/10) and S-type/INMV220 (2/10) animals. No significant differences in intestinal histological lesion scores were detected between S- and C-type INMV strains. Morphometrical analysis revealed similar inflammatory and apoptotic cell numbers in the intestinal mucosa of C- and S-type animals; however, S-type animals exhibited significantly more Iba1- and cleaved caspase 3-positive cells in mesenteric lymph nodes. Lesions in mesenteric lymph nodes might indicate a differentially regulated course in MAP pathogenesis.