The literature of human infection with Salmonella choleraesuis in China was fully reviewed with special reference to those written in Chinese language which are inaccessible to many readers. Compared with other regions of the world the ratio of S. choleraesuis to other salmonella infection in Hong Kong is high and is parallel to that in China. Dietetic habits of the local population apparently contribute to the high incidence. The clinical manifestations of 47 cases were outlined and details of the biochemical reactions and in vitro drug sensitivities of these strains were described. Two diphasic H2S-positive strains were encountered.

Colonization resistance (CR), defined as the ability of intestinal microbiota and host defenses to protect against pathogens, is the first line defense against intestinal infection. In our studies of innate immune recognition of intestinal Salmonella, we discovered Naip5−/− and Rag1−/− mice harbor microbiota that protect mice against Salmonella infection, which is associated with intestinal colonization by Tritrichomonas muris (Tm). Tm is a protozoon commonly found in laboratory, pet shop and wild mice, which has no definitive disease association. Recent studies have demonstrated Tm and other intestinal parasites are sensed by tastant receptors expressed by specialized intestinal tuft cells, which enhances intestinal barrier by tuft cell and goblet cell hyperlasia. Helminths and protozoa have been associated with changes in the intestinal microbiota, suggesting that intestinal protozoa may produce biologically significant alterations in the composition of gut bacteria. We demonstrate that Tm colonization of mice is associated with decreased inflammation in the intestine during Salmonella infection of streptomycin pretreated mice. Tm colonization is also associated with increased resistance to Salmonella infection and CR. Finally, we demonstrate that Tm colonized mice have an altered gut microbiome, suggesting that Tm cultivates a protective microbiome that helps prevent Salmonella colonization and infection. Our studies indicate that intestinal protozoa may influence the complex environment within the gut to help limit Salmonella invasion of the gut ecosystem and Salmonella induced intestinal inflammation, and provide insight into novel strategies that may help prevent Salmonella infection and transmission.

Salmonella is the causative agent in Salmonellosis and is a leading cause of gastrointestinal bacterial infections worldwide. During mucosal Salmonella infection Salmonella must first establish a niche in the gastrointestinal tract in order to initiate infection. Colonization resistance (CR), defined as the ability of intestinal microbiota and host defenses to protect against pathogens, is the first line defense against intestinal infection. The mechanism for commensal bacteria mediated CR has been studied for a long time; however, only a few studies have explored how microbiota can induce CR against Salmonella infection. Herein we demonstrate that a mouse commensal E. coli strain mediates CR against mucosal Salmonella Typhimurium infection, and that this CR is independent of the inflammasome, TLR5, MyD88, adaptive immunity, and a complex microbiome. The commensal E. coli strain does not directly compete with Salmonella growth in vitro, and is only capable of inducing colonization resistance in vivo. Gene expression analysis demonstrates that colonization of mice by commensal E. coli induces a large number of host defense genes involved in the regulation of mucosal barriers, innate immune cells and arachidonic acid metabolism. Our studies demonstrate that commensal E. coli interacts with the host through a novel pathway to induce CR against mucosal Salmonella infection and illuminate the complex interactions between microbiota and the host that shape defenses and defend against enteric infections.