1887

Abstract

Consistent pathological findings in sudden infant death syndrome (SIDS) are seen which display similarities to the pathogenesis of toxaemic shock and/or sepsis. A key candidate infectious agent that is possibly involved is , given its universal early colonization of the intestinal tract of infants and an increased frequency of toxigenic and mouse-lethal isolates from SIDS compared with comparison infants. An explanation for these findings has yet to be identified. Using PCR, we screened isolates from 145 SIDS and 101 dead control and healthy infants for three new candidate pathogenicity-related genes: (cytolysin A), [high-pathogenicity island (HPI)-specific gene] and (cytolethal distending toxin). The results failed to show a positive correlation with SIDS, instead proving that and genes were common to the infant intestinal . Interestingly we observed a high rate of carriage of these two potentially pathogenic genes in from healthy infants in the absence of diarrhoeal disease, and we report that in a number of cases, the detection of HPI-specific genes was predictable by serotype. Despite the lack of associations defined so far, there remains the likelihood that genetic determinants influence the interactions between and the host, so these factors may be part of the multi-factorial aspect of SIDS.

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2009-03-01
2019-10-18
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