Infection, inflammation and sleep: more pieces to the puzzle of sudden infant death syndrome (SIDS)

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Risk factors for sudden infant death syndrome (SIDS) parallel those for respiratory tract infections; however, infectious agents suggested to be involved in SIDS do not fulfil Koch's postulates. No single agent has been identified in all cases and there is no suitable animal model for SIDS which could be used to test the candidate organisms. Based on epidemiological and experimental work by our group and others, we suggested some SIDS deaths are due to pathophysiological responses elicited by combinations of microbial products and/or cigarette smoke during a developmental stage when infants' endocrine responses are less able to "damp down" the effects of inflammatory mediators. Here we review evidence from studies on interactions between developmental and environmental risk factors that could affect 1) mucosal colonization of infants by potentially pathogenic bacteria, and 2) induction and control of infants', inflammatory responses to infectious agents. New evidence suggests that there are genetic factors involved in the induction of inflammatory responses to some bacterial antigens implicated in SIDS. Further investigation of the role of infection, exposure to cigarette smoke and inflammation in infants, particularly differences in ethnic groups at increased risk of SIDS, could lead to new insights into the events leading to a fatal outcome and perhaps to new intervention schemes to reduce further the incidence of these deaths.

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