Death from Staphylococci in Mice

Smith, Ian M.; Wilson, A.P.R.; Hazard, Elia Ch.; Hummer, William K.; Dewey, Mary E.

doi:10.1093/infdis/107.3.369

Cited by 28 publications

(6 citation statements)

References 5 publications

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“…Bacteria were rapidly cleared from blood and tissues following intravenous challenge. These findings are consistent with earlier experimental animal studies, in which rapid clearance of infected bacteria was observed in mice infected with S. aureus (25,26). However, the relationships among bacterial clearance, tissue damage, and cytokine expression was not examined.…”

Section: Discussionsupporting

confidence: 90%

Correlation of histopathologic and bacteriologic changes with cytokine expression in an experimental murine model of bacteremic Staphylococcus aureus infection

et al. 1997

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Staphylococcus aureus infections are often life threatening. Relatively little is known about the host response to these infections, in particular, the role played by cytokines. We established a mouse model of bacteremic S. aureus infection to correlate bacteriologic findings and pathologic changes with cytokine gene expression. Bacterial density in blood and tissue was highest at 1 h and minimal by 48 h. Despite the rapid clearance of bacteria, pathologic abnormalities and inflammatory cytokines were detected after clearance of the bacteria. The number of infiltrating inflammatory cells, as well as the size of inflammatory foci, increased with time. Interstitial accumulation of inflammatory cells and tissue damage, such as microabscesses, edema, and necrosis progressed following clearance of bacteria from the tissues. Levels of tumor necrosis factor and interleukin-1 protein in serum were detectable at 1 h and peaked at 4 h. Interleukin-6 protein expression showed different kinetics, with low levels detected at 1 h and increasing levels at 72 h postinfection. Tumor necrosis factor and the interleukins were expressed in inflammatory and noninflammatory cells in lung, liver, and heart tissues. Leukocytes in the infected tissues were highly reactive with antibodies to the three cytokines, suggesting that activated leukocytes are a major source of inflammatory cytokines after staphylococcal infection. Expression of interleukin-1 and interleukin-6 in tissue-specific cells and endothelial cells was also detected in infected tissues, indicating that cells other than leukocytes contribute to the elevated cytokine levels in this model. Once initiated, expression of inflammatory cytokines contributes to the pathogenesis of S. aureus disease.

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Section: Discussionsupporting

confidence: 90%

Correlation of histopathologic and bacteriologic changes with cytokine expression in an experimental murine model of bacteremic Staphylococcus aureus infection

et al. 1997

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“…This difference in virulence has been shown with spontaneous nonmucoid variant strains (13,56,76,98,101) as well as with isogenic strains that have been derived by genetic methods (62,71). Mucoid isolates are not effectively phagocytosed within the peritoneal cavity, and thus these highly encapsulated S. aureus are free to replicate extracellularly.…”

Section: Role Of Serotype 1 and 2 Capsules In Virulencementioning

confidence: 88%

Staphylococcus aureusCapsular Polysaccharides

2004

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Serotype 5 and 8 capsular polysaccharides predominate among clinical isolates of Staphylococcus aureus. The results of experiments in animal models of infection have revealed that staphylococcal capsules are important in the pathogenesis of S. aureus infections. The capsule enhances staphylococcal virulence by impeding phagocytosis, resulting in bacterial persistence in the bloodstream of infected hosts. S. aureus capsules also promote abscess formation in rats. Although the capsule has been shown to modulate S. aureus adherence to endothelial surfaces in vitro, animal studies suggest that it also promotes bacterial colonization and persistence on mucosal surfaces. S. aureus capsular antigens are surface associated, limited in antigenic specificity, and highly conserved among clinical isolates. With the emergence of vancomycin-resistant S. aureus in the United States in 2002, new strategies are needed to combat staphylococcal infections. Purified serotype 5 and 8 capsular polysaccharides offer promise as target antigens for a vaccine to prevent staphylococcal infections, although the inclusion of other antigens is likely to be essential in the development of an effective S. aureus vaccine. The genetics and mechanisms of capsule biosynthesis are complex, and much work remains to enhance our understanding of capsule biosynthesis and its regulation

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“…Thus, evidence is conflicting with regard to the role alpha hemolysin plays in staphylococcal disease. A number of investigators have argued for the importance of alpha hemolysin as a virulence factor (59,60,104,179,184) and others have refuted it (6,58). Kapral (107) has reviewed his work in which mice and rabbits were used in the study of experimental infections.…”

Section: Role Of the Hemolysins In Pathogenicity Andmentioning

confidence: 99%

The hemolysins of Staphylococcus aureus.

Wiseman¹

1975

Bacteriological Reviews

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Death from Staphylococci in Mice

Cited by 28 publications

References 5 publications

Correlation of histopathologic and bacteriologic changes with cytokine expression in an experimental murine model of bacteremic Staphylococcus aureus infection

Correlation of histopathologic and bacteriologic changes with cytokine expression in an experimental murine model of bacteremic Staphylococcus aureus infection

Staphylococcus aureusCapsular Polysaccharides

The hemolysins of Staphylococcus aureus.

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