Outbreaks of typhoid fever in the United States, 1960–99

Olsen, Sonja J.; Bleasdale, Susan C; Magnano, Anna Rosa; Landrigan, Christopher P.; Holland, Ben; Tauxe, Robert V.; Mintz, Eric D.; Luby, Stephen P.

doi:10.1017/s0950268802007598

Cited by 69 publications

(45 citation statements)

References 19 publications

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“…In contrast, ingestion of the human-restricted pathogen Salmonella enterica serovar Typhi results in typhoid fever, a severe febrile illness due to the dissemination of S. Typhi to systemic sites (19,20). After a median incubation period of 2 weeks, only a fraction of patients develop intestinal complications, with the infiltrates being dominated by mononuclear cells (21). The absence of an initial severe inflammatory response in the mucosa suggests that unlike Salmonella serovars associated with gastroenteritis, S. Typhi evades detection by innate PRRs in the gut (19,20).…”

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confidence: 99%

The Flagellar Regulator TviA Reduces Pyroptosis by Salmonella enterica Serovar Typhi

Winter

Atluri

et al. 2015

Infect Immun

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To discern virulent from innocuous microbes, the innate immune system senses events associated with bacterial access to immunoprivileged sites such as the host cell cytosol. One such pathway is triggered by the cytosolic delivery of flagellin, the major subunit of the flagellum, by bacterial secretion systems. This leads to inflammasome activation and subsequent proinflammatory cell death (pyroptosis) of the infected phagocyte. In this study, we demonstrate that the causative agent of typhoid fever, Salmonella enterica serovar Typhi, can partially subvert this critical innate immune recognition event. The transcriptional regulator TviA, which is absent from Salmonella serovars associated with human gastroenteritis, repressed the expression of flagellin during infection of human macrophage-like (THP-1) cells. This mechanism allowed S. Typhi to dampen inflammasome activation, leading to reduced interleukin-1␤ (IL-1␤) secretion and diminished cell death. Likewise, the introduction of the tviA gene in nontyphoidal Salmonella enterica serovar Typhimurium reduced flagellin-induced pyroptosis. These data suggest that gene regulation of virulence factors enables S. Typhi to evade innate immune recognition by concealing a pathogen-induced process from being sensed by the inflammasome. To distinguish between self and nonself, the host employs a multitude of innate pattern recognition receptors (PRRs) to initiate adequate host responses aimed at eradicating invading microbes. Activation of PRRs can be achieved by two conceptually different types of events: recognition of conserved microbial structures (pathogen-associated molecular patterns [PAMPs]) (1) and recognition of virulence-associated strategies aimed at manipulating host cells (patterns of pathogenesis) (2, 3). PAMPs are specific for certain groups of microbes regardless of their pathogenic potential, while host cell manipulation is a trait found exclusively in pathogens (2, 3).PAMPs are typically detected by Toll-like receptors (TLRs), resulting in the activation of the NF-B pathway (4). For example, flagellin, the major component of the flagellum, is recognized by TLR5, which enables the innate immune system to detect flagellated bacteria, regardless of their pathogenic potential (5, 6). In contrast, detection of host cell manipulation events allows the host to discern virulent from commensal microbes and scale the host defenses commensurate with the threat (2, 3). A prime example is the translocation of bacterial flagellin into the host cell cytosol through virulence-associated type III secretion system or type IV secretion system, which triggers a proinflammatory form of cell death termed pyroptosis (7-9). Pyroptotic cell death is characterized by the assembly and activation of the inflammasome (10, 11). In the center of this multiprotein complex, active caspase-1 processes pro-interleukin-1␤ (IL-1␤) as well as pro-IL-18 into the biologically active forms by proteolytic cleavage. IL-1␤ and IL-18 are highly proinflammatory cytokines that are critical for coordi...

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confidence: 99%

The Flagellar Regulator TviA Reduces Pyroptosis by Salmonella enterica Serovar Typhi

Winter

Atluri

et al. 2015

Infect Immun

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“…For example, S. Typhimurium-induced gastroenteritis manifests as diarrhoea and vomiting within 48 hours of infection 3 . By contrast, the median incubation period for typhoid fever is 2 weeks, which is similar to the 2-4 week incubation period for brucellosis 4,5 .…”

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confidence: 63%

Is Brucella an enteric pathogen? Reply from Tsolis, Solnick and Baümler

2009

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“…27 A viaB-mediated inhibition of pyroptosis might also reduce exposure of S. typhi to neutrophil attack. 52 Furthermore, inhibition of C3b deposition on the bacterial surface prevents phagocytosis of S. typhi through complement receptor (CR) 3, 53,54 a process coupled to a respiratory burst in neutrophils.…”

Section: Do Not Distributementioning

confidence: 99%

“…While rapid recruitment of neutrophils leads to symptoms of gastroenteritis within 24 h after ingestion of non-typhoidal Salmonella serovars, 26 S. typhi does not evoke overt responses during the initial invasion of the intestinal mucosa, as indicated by an average incubation period of two weeks. 27 Although S. typhi causes intestinal inflammation, the inflammatory infiltrates are dominated by mononuclear cells and neutrophils are scarce. [28][29][30][31][32] Finally, S. typhi causes a disseminated bloodstream infection in immunocompetent individuals, while non-typhoidal Salmonella serovars are associated with a localized gastroenteritis.…”

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confidence: 99%