Taxonomic and functional microbiota changes in dysenteric colitis produced by Brachyspira hyodysenteriae in pigs

Background The gut microbiota is essential for maintaining nutritional, physiological and immunological processes, but colonic infections such as swine dysentery, caused by Brachyspira hyodysenteriae ( B. hyo ) disrupt this homeostasis. This study uses shotgun and full-length 16S rRNA sequencing in faeces, colonic contents and mucosa from pigs challenged with B. hyo to provide a high-resolution characterisation of hte taxa, functions and metagenome-assembled genomes (MAGs) of interest, disclose their association with the primary pathogen and how they are affected by the pathological changes of the infection. Results Changes in the microbiota were associated with disease severity. In early infection, no major findings were observed in diversity or abundance analyses, whereas in acute infection, B. hyo load, mucosal neutrophil infiltration, epithelial ulceration and mucosal thickness were clearly associated with changes in microbiota ordination, which were also associated with a decrease in species richness. Changes included a significant increase in Acetivibrio ethanolgignens , Campylobacter hyointestinalis and Roseburia inulinivorans , which, with the exception of C. hyointestinalis , established themselves as part of the core microbiota and shifted the colonic enterotype in acutely infected animals. MAGs analyses revealed that no major virulence genes were detected in the genomes of the species co-interacting with B. hyo in acute infection. Similarly, functional changes were observed only after the onset of clinical signs, with an increase in functions related to inflammation and toxic effects on the colonic epithelium. Conclusions Our study shows that in colitis caused by B. hyo , changes in the microbiota are mainly a consequence of the lesions that occur in the intestine, with no differences observed in early infection. Similarly, the bacterial species that are increased at the onset of clinical signs may promote intestinal inflammation caused by B. hyo infection, but the analysis of their genomes rule out their participation in the primary infection.