Abstract
Human infections by the bacterial pathogen Salmonella enterica represent major disease burdens worldwide. This highly ubiquitous species consists of more than 2600 different serovars that can be divided into typhoidal and non-typhoidal Salmonella (NTS) serovars. Despite their genetic similarity, these two groups elicit very different diseases and distinct immune responses in humans. Comparative analyses of the genomes of multiple Salmonella serovars have begun to explain the basis of the variation in disease manifestations. Recent advances in modeling both enteric fever and intestinal gastroenteritis in mice will facilitate investigation into both the bacterial- and host-mediated mechanisms involved in salmonelloses. Understanding the genetic and molecular mechanisms responsible for differences in disease outcome will augment our understanding of Salmonella pathogenesis, host immunity, and the molecular basis of host specificity. This review outlines the differences in epidemiology, clinical manifestations, and the human immune response to typhoidal and NTS infections and summarizes the current thinking on why these differences might exist.
Highlights
Salmonella enterica is a highly diverse Gram negative bacterial species containing more than 2600 different serovars differentiated by their antigenic presentation
Human infections by the bacterial pathogen Salmonella enterica represent major disease burdens worldwide. This highly ubiquitous species consists of more than 2600 different serovars that can be divided into typhoidal and non-typhoidal Salmonella (NTS) serovars
Most S. enterica serovars associated with diseases in humans and other warm blooded animals belong to subspecies I consisting of both typhoidal and non-typhoidal serovars
Summary
Salmonella enterica is a highly diverse Gram negative bacterial species containing more than 2600 different serovars differentiated by their antigenic presentation. Given that typhoidal serovars do not typically illicit septic shock, in contrast to many other Gram-negative pathogens that induce bacteremia and leukopenia (Pohan, 2004; Tsolis et al, 2008; Gal-Mor et al, 2012), suggests a restrained immune response mediated by these pathogens in the human host This view is consistent with the clinical observation that serum levels of pyrogenic cytokines IL-1β and TNF-α are relatively low in patients with typhoid fever compared to the levels found in patients with sepsis caused by other Gram-negative pathogens. A substantial degree of metabolic and virulence gene degradation exists in the genomes of typhoidal serovars which may explain the restricted host-tropism of these pathogens and may provide at least a partial explanation as to why typhoidal and NTS-infections induce such different clinical presentations and immune responses in humans
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