Determinants of persistent Salmonella infections

Gram-negative Salmonella bacteria are ingested with contaminated food or transmitted via the fecal-oral route. Pathogenic serovars cause a broad range of diseases, including enterocolitis, enteric fever, and bacteremia [1]. Infections with typhoidal serovars (TS), including S. Typhi and S. Paratyphi, are restricted to humans and can lead to a life-threatening, systemic disease called enteric or typhoid/paratyphoid fever [2]. Nontyphoidal Salmonella serovars (NTS), including S. Typhimurium and S. Enteritidis, can infect a broad range of hosts. In immunocompetent adults, NTS usually cause self-limiting gastroenteritis with occasional secondary bacteremia [3].

Salmonella infections can result in either acute infections with subsequent clearance of the pathogen, persistent infections or death of the host. Persistent infections can follow asymptomatic or symptomatic acute infections that are not fully cleared by the host immune system resulting in continuous shedding of the bacteria with the feces as a source for transmission. In persistent infections, the pathogen is able to colonize the host for long periods of time. Salmonella manipulates the host immune system to its own benefit and can alter its metabolism to withstand antimicrobial drug treatment. Salmonella resides intracellularly or extracellularly in the intestinal or gall bladder lumen which may result in persistent or periodic fecal shedding 2•, 4.

In this review, we highlight the recent progress in our understanding of persistence mechanisms of typhoidal and nontyphoidal Salmonella enterica serovars, their sites of persistence as well as the different lifestyles promoting long-term survival and describe the modulation of the immune response facilitating persistent infection.

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