Review on the effects of potential prebiotics on controlling intestinal enteropathogens Salmonella and Escherichia coli in pig production. Issue 1 (27th December 2016)

• Record Type: Journal Article
• Authors: Tran, T. H. T.; Everaert, N.; Bindelle, J.
• Is Part Of: Journal of animal physiology and animal nutrition. Volume 102:Issue 1(2018)
• Page Start: 17
• Page End: 32
• Publication Date: 2016-12-27
• Subjects: Salmonella enterica -- Escherichia coli -- prebiotics -- pigs; Animal nutrition -- Periodicals; Feeds -- Periodicals; 636.085
• DOI: 10.1111/jpn.12666
• Languages: English
• ISSNs: 0931-2439

Abstract

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.