Young Investigator Award 2008

Abstract

Bacterial Toxins and Genetic Variations in Sudden Infant Death Syndrome (SIDS)

Amanda Highet
PhD candidate, Discipline of Paediatrics, University of Adelaide and Department of Microbiology and Infectious Diseases, Children, Youth and Women’s Health Service/SA Pathology

SIDS follows a pattern similar to viral or bacterial infections suggesting that one or both of these types of infectious agents may play a role in SIDS. SIDS infants have been shown to carry more viruses and toxin-producing bacteria than comparison infants. Furthermore, post-mortem findings are similar to those observed in cases of shock caused by infection or toxin. We seek bacterial toxins in SIDS infants that could explain these observations. Diarrhoea and intestinal damage observed in SIDS indicate bacteria from the intestinal tract are candidates. Additionally, variations in genes that regulate the immune system can influence how the body responds to these toxins. Material from SIDS infants previously studied for bacterial toxins is now being screened for gene variations that may predispose infants to develop a shock-like condition when exposed to toxin.

We looked directly for toxin DNA in bacteria grown from the intestine or faeces. Toxin genes included those that 1) Have the potential to cause sudden death in infants, e.g infant botulism toxin, 2) Have the ability to cause toxic shock, e.g. Staphylococcus aureus toxic shock syndrome toxin, and 3) Genes that give the common bacterium Escherichia coli extra ability to cause toxin-mediated disease. We also looked for variations in the infant’s DNA regulating the immune system that may make the infant more susceptible to the effects of S. aureus toxins.

We showed that S. aureus toxins are found in 64% of SIDS babies; giving a 4.5 times increased risk compared to healthy babies.

 

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