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Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome

Published online by Cambridge University Press:  15 May 2009

A. T. Saadi
Affiliation:
Department of Medical Microbiology, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
C. C. Blackwell
Affiliation:
Department of Medical Microbiology, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
M. W. Raza
Affiliation:
Department of Medical Microbiology, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
V. S. James
Affiliation:
Department of Medical Microbiology, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
J. Stewart
Affiliation:
Department of Medical Microbiology, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
R. A. Elton
Affiliation:
Medical Statistics Unit, Department of Public Health Sciences, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
D. M. Weir
Affiliation:
Department of Medical Microbiology, University of Edinburgh, Medical School, Teviot Place, Edinburgh EH8 9AG
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Toxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewisa antigen and infection with respiratory syncytial virus (RSV). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from non-secretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewisa or anti-type-1 precursor significantly reduced bacterial binding (P < 0·01); however, attachment of the bacteria correlated only with the amount of Lewisa antigen detected on the cells (P < 0·01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context of factors previously associated with SIDS (mother's smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1993

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