Histopathology of the upper small intestines in typhoid fever

Sprinz, Helmuth; Gangarosa, Eugene J.; Williams, M. J.; Hornick, Richard B.; Woodward, Theodore E.

doi:10.1007/bf02233509

Cited by 81 publications

(51 citation statements)

References 2 publications

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“…We suggest that penetration by S. enteritidis occurs in the upper half of the gastrointestinal tract, which possibly indicates sites that are more easily penetrated by S. enteritidis. This finding is compatible with results obtained in previous studies, which showed that S. enteritidis has a rapid transit time through the normal mouse intestine; a small proportion of the inoculum establishes itself within the walls of the small intestine, before a systemic infection can be demonstrated [4,5,19] . However, these studies were unable to precisely establish the primary site of bacterial invasion in these animals.…”

Section: Wwwwjgnetcomsupporting

confidence: 93%

Gastrointestinal tract distribution of Salmonella enteritidis in orally infected mice with a species-specifi c fl uorescent quantitative polymerase chain reaction

Shu-xuan¹,

Deng²,

Anchun³

et al. 2007

WJG

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cecum, without causing apparent symptoms. By 5 d post inoculation, the cecum had significantly higher numbers of S. enteritidis than any of the other areas (P < 0.01), and this appeared to reflect its function as a repository for S. enteritidis. CONCLUSION:The results provided significant data for clarifying the pathogenic mechanism of S. enteritidis in the gastrointestinal tract, and showed that the jejunum, ileum and cecum are the primary sites of invasion in normal mice after oral infection. This study will help to further understanding of the mechanisms of action of S. INTRODUCTIONSalmonella is an enteric pathogen that colonizes the intestinal tract of a variety of animals, especially humans and poultry, and accounts for millions of cases of gastroenteritis and food-borne illness each year [1,2] . Salmonella enteritidis (S. enteritidis) can be transmitted to humans through the food production chain, and undercooked or raw eggs and poultry meat are a particularly high risk for humans [3] . In the last few decades, S. enteritidis has emerged as a major cause of food-borne illness worldwide. As a result of the increased prevalence of S. enteritidis and its complex life cycle, identifying the regular distribution pattern of S. enteritidis in the gastrointestinal tract will help to understand its mechanism of action.Previous studies have shown that orally introduced S. enteritidis has a rapid transit time through the intestine, and a small proportion of the inoculum establishes itself within the walls of the small intestine and cecum several enteritidis. We used this assay to detect genomic DNA of S. enteritidis in the gastrointestinal tract, including duodenum, jejunum, ileum, cecum, colon, rectum, esophagus and stomach, from mice after oral infection. RESULTS

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Section: Wwwwjgnetcomsupporting

confidence: 93%

Gastrointestinal tract distribution of Salmonella enteritidis in orally infected mice with a species-specifi c fl uorescent quantitative polymerase chain reaction

Shu-xuan¹,

Deng²,

Anchun³

et al. 2007

WJG

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“…Gastroenteritis and typhoid fever differ dramatically with regard to symptoms and pathological changes, including the cellular composition of inflammatory infiltrates in the intestine (Santos et al, 2001;Zhang et al, 2003). While gastroenteritis is characterized by intestinal infiltrates that are dominated by neutrophils, this cell type is scarce in infiltrates of typhoid fever patients (Sprinz et al, 1966;Day et al, 1978;Mukawi, 1978;McGovern and Slavutin, 1979;Kraus et al, 1999;Nguyen et al, 2004). The genetic differences between non-typhoidal and typhoidal Salmonella serotypes that account for the different intestinal responses are poorly understood.…”

Section: Discussionmentioning

confidence: 99%

“…S. Typhi is the causative agent of typhoid fever, a severe systemic infection in which neutrophils are scarce in intestinal infiltrates (Sprinz et al, 1966;Mukawi, 1978;Kraus et al, 1999;Nguyen et al, 2004) and fecal leucocyte populations (Harris et al, 1972;Alvarado, 1983;Guyot et al, 1984). Infection of human colonic tissue explants with a nontyphoidal Salmonella serotype, S. Typhimurium, results in expression of the neutrophil chemoattractant interleukin (IL)-8, but this response is not observed during infection with S. Typhi (Raffatellu et al, 2005).…”

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confidence: 99%

The Salmonella enterica serotype Typhi regulator TviA reduces interleukin-8 production in intestinal epithelial cells by repressing flagellin secretion

et al. 2007

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“…which helps explain the scarcity of neutrophils in intestinal infiltrates [28][29][30][31][32] and the long incubation period of typhoid fever. 27 A viaB-mediated inhibition of pyroptosis might also reduce exposure of S. typhi to neutrophil attack.…”

Section: Do Not Distributementioning

confidence: 99%

“…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. These clinical observations raise the question of how pathogens that are so similar in their basic repertoire of virulence factors can cause so different host responses and disease manifestations in humans.…”

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confidence: 99%