The main disease syndromes caused by Salmonella serovars in immunocompetent individuals are gastroenteritis and typhoid fever. These syndromes differ with regard to the host niches in which Salmonella serovars grow and survive to ensure their transmission. During gastroenteritis, non-typhoidal Salmonella serovars such as Salmonella enterica serovar Typhimurium (S. Typhimurium) use their virulence factors to elicit acute intestinal inflammation, thereby creating a novel luminal niche. Reactive oxygen species produced by phagocytes in the intestinal lumen oxidize endogenous sulfur compounds to produce a new respiratory electron acceptor, tetrathionate. Respiration of tetrathionate confers a growth advantage to S. Typhimurium over competing microbes. This growth advantage ensures transmission of the pathogen by the faecal-oral route. In typhoid fever, S. enterica serovar Typhi (S. Typhi) establishes a chronic infection in the gall bladder, and perhaps in additional niches. Studies using the mouse model of typhoid fever suggest that survival and proliferation in the gall bladder may involve several strategies. Invasion of the gallbladder epithelium and formation of biofilms on gallstones may protect the pathogen from the bactericidal activities of bile salts. In the gallbladder lumen, activation of bile defence responses may permit survival of planktonic Salmonella cells. Individuals developing chronic carriage after an episode of typhoid fever can transmit the disease for the remainder of their lives by shedding the pathogen through the cystic duct. Shedding promotes S. Typhi transmission to new susceptible hosts. Here we review Salmonella virulence strategies for growth and survival in host niches that represent reservoirs for transmission.
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