Summary Salmonella enterica serotypes (Salmonella sp.) are the second cause of bacterial foodborne zoonoses in humans after campylobacteriosis. Pork is the third most important cause for outbreak‐associated salmonellosis, and colibacillosis is the most important disease in piglets and swine. Attachment to host cells, translocation of effector proteins into host cells, invasion and replication in tissues are the vital virulence steps of these pathogens that help them to thrive in the intestinal environment and invade tissues. Feed contamination is an important source for Salmonella infection in pig production. Many on‐farm feeding strategies intervene to avoid the introduction of pathogens onto the farm by contaminated feeds or to reduce infection pressure when pathogens are present. Among the latter, prebiotics could be effective at protecting against these enteric bacterial pathogens. Nowadays, a wide range of molecules can potentially serve as prebiotics. Here, we summarize the prevalence of Salmonella sp. and Escherichia coli in pigs, understanding of the mechanisms by which pathogens can cause disease, the feed related to pathogen contamination in pigs and detail the mechanisms on which prebiotics are likely to act in order to fulfil their protective action against these pathogens in pig production. Many different mechanisms involve the inhibition of Salmonella and E. coli by prebiotics such as coating the host surface, modulation of intestinal ecology, downregulating the expression of adhesin factors or virulence genes, reinforcing the host immune system.

Adding mucus to in vitro fermentation models of the large intestine shows that some genera, namely lactobacilli, are dependent on host-microbiota interactions and that they rely on mucosal layers to increase their activity. This study investigated whether this dependence on mucus is substrate dependent and to what extent other genera are impacted by the presence of mucus. Inulin and cellulose were fermented in vitro by a fecal inoculum from pig in the presence or not of mucin beads in order to compare fermentation patterns and bacterial communities. Mucins increased final gas production with inulin and shifted short-chain fatty acid molar ratios (P < 0.001). Quantitative real-time PCR analyses revealed that Lactobacillus spp. and Bifidobacterium spp. decreased with mucins, but Bacteroides spp. increased when inulin was fermented. A more in-depth community analysis indicated that the mucins increased Proteobacteria (0.55 vs 0.25%, P = 0.013), Verrucomicrobia (5.25 vs 0.03%, P = 0.032), Ruminococcaceae, Bacteroidaceae and Akkermansia spp. Proteobacteria (5.67 vs 0.55%, P < 0.001) and Lachnospiraceae (33 vs 10.4%) were promoted in the mucus compared with the broth, while Ruminococcaceae decreased. The introduction of mucins affected many microbial genera and fermentation patterns, but from PCA results, the impact of mucus was independent of the fermentation substrate.