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Susceptibility to infection in relation to SIDS
C C Blackwell1, A T Saadi, M W Raza
1Department of Medical Microbiology, University of Edinburgh Medical School.
Abstract:
Because there is little evidence that invasive bacterial diseases contribute to cot deaths, most studies on infectious causes of SIDS have focused on viruses or toxin producing bacteria. Although epidemiological studies found marginally significant associations between influenza virus and SIDS, respiratory syncytial virus (RSV) was isolated from 90% of older infants with SIDS. There are conflicting reports that some toxigenic bacteria (Clostridium botulinum, Clostridium difficle, enterotoxigenic Escherichia coli and Staphylococcus aureus) might be implicated in cot deaths. S aureus are common micro-organisms and their toxins are very powerful. As the pyrogenic toxic shock syndrome toxin of S aureus can kill a previously healthy adult, it might easily kill a small infant. Based on our studies on susceptibility of infants to other infections, we suggest the following might be factors leading to colonisation of infants by toxin producing S aureus: The Lewis blood group antigen appears to act as a receptor for some micro-organisms. Epithelial cells expressing high concentrations of Lewis bound appreciably more toxin producing S aureus than cells expressing low concentrations of the antigen. Lewis is expressed in secretions of nearly 90% of infants aged 3 months, the peak age for SIDS. RSV infects about 50% of infants by the first year of life and it is often isolated from infants with SIDS. Studies in our laboratory indicate that RSV infected HEp-2 cells bind more toxin producing S aureus than uninfected controls.
Insights
Respiratory syncytial virus (RSV) and toxin-producing Staphylococcus aureus may contribute to Sudden Infant Death Syndrome (SIDS). Lewis blood group antigen may increase infant susceptibility to S. aureus colonization, especially when coinfected with RSV.
Area of Science:
- Microbiology
- Immunology
- Pediatrics
Background:
- Sudden Infant Death Syndrome (SIDS) is multifactorial, with infectious agents being a focus of research.
- While viruses like influenza and respiratory syncytial virus (RSV) have been implicated, the role of toxigenic bacteria in SIDS remains debated.
- Staphylococcus aureus (S. aureus) produces potent toxins capable of causing severe illness.
Purpose of the Study:
- To investigate the potential role of toxin-producing S. aureus in SIDS.
- To explore factors influencing infant susceptibility to S. aureus colonization.
- To examine the interaction between RSV infection and S. aureus binding.
Main Methods:
- Analysis of existing epidemiological data on SIDS and infectious agents.
- In vitro studies examining the binding of S. aureus to epithelial cells expressing Lewis blood group antigens.
- Investigation of S. aureus binding to HEp-2 cells infected with RSV.
Main Results:
- RSV was isolated from a high percentage of infants with SIDS.
- Epithelial cells with high concentrations of Lewis blood group antigen showed increased binding of S. aureus.
- RSV-infected cells demonstrated enhanced binding of S. aureus compared to uninfected cells.
Conclusions:
- Toxin-producing S. aureus, potentially facilitated by Lewis blood group antigen expression, may contribute to SIDS.
- RSV infection might increase infant susceptibility to S. aureus colonization and toxin exposure.
- Further research is warranted to elucidate the precise mechanisms linking these factors to SIDS.