Sudden infant death syndrome and cardiac arrhythmias.
- ISSN: 1744-8298
- ISBN: 1744-8298 (Electronic)
- DOI: http://dx.doi.org/10.2217/147966184.108.40.206
- PubMed: 19371193
There is a considerable body of evidence that common bacterial toxins, absorbed from the mucosal surface or delivered as part of a transient bacteremia, have a pathogenic role in sudden infant death syndrome (SIDS). The candidate organisms are Staphylococcus aureus and Escherichia coli. Death in SIDS is rapid, with infants progressing from well, or only mildly unwell, to death in less than 20 min. This mode of death is not typical of infection but it is consistent with toxin action on cardiovascular or respiratory control. Both S. aureus and E. coli secrete toxins (cytolysins and colicins) that create channels in cell membranes and disturb ion currents. Recent evidence indicates that between 5 and 15% of SIDS cases carry potentially lethal loss-of-function mutations in cardiac channelopathy genes. However, only a minority of individuals with these mutations die of SIDS and the hypothesis proposed is that toxin-gene interaction could explain the deaths. Furthermore, channelopathy mutations predispose to sudden death at all ages and since episodes of transient bacteremia occur throughout life the idea of toxin-gene interaction could have wider applicability. These ideas can be investigated and answered in the near future using the new science of proteomics.