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Enteric pathogens are transmitted to humans through direct contact with infected hosts or by exposure to environments contaminated with feces (1)
Exposure to animals has recently attracted attention as a risk factor for enteric infections in low- and middle-income countries. There have been reports of strain-sharing between humans and domestic or wild animals that are in close proximity (2, 3).
Enteric pathogens, like Salmonella enterica serovar Typhimurium, have developed mechanisms to bypass microbiota-mediated colonization resistance by triggering intestinal inflammation (colitis) (4, 5, 6, 7, 8, 9).
Inflammation significantly alters the gut's metabolic environment, resulting in the accumulation of new nutrients that both Salmonella Enterica Serovar Typhimurium (S. Tm) and resident microbiota compete for, including amino acids. Commensal Bacteria / Commensalism can decrease amino acid availability in the gut lumen, which restricts early intestinal colonization by enteric pathogens. To thrive in the gastrointestinal tract, a pathogen must interfere with the microbiota-mediated sequestration of amino acids (10, 11, 12, 13).
The most prevalent enteric pathogens include Shigella spp., Escherichia coli, Clostridium difficile, and Salmonella spp., which can cause a range of intestinal diseases and complications by disrupting intestinal homeostasis (14, 15).
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see also:
Aspartate / Aspartic acid
Bacterial enteric infections
Pathogens / Pathobionts / Pathogenic Bacteria
Urbanization