Abstract
The risk factors for sudden infant death syndrome (SIDS) parallel those associated with susceptibility to or severity of infectious diseases. There is no evidence that a single infectious agent is associated with SIDS; the common thread appears to be induction of inflammatory responses to infections. In this review, interactions between genetic and environmental risk factors for SIDS are assessed in relation to the hypothesis that many infant deaths result from dysregulation of inflammatory responses to “minor” infections. Risk factors are assessed in relation to three important stages of infection: (1) bacterial colonization (frequency or density); (2) induction of temperature-dependent toxins; (3) induction or control of inflammatory responses. In this article, we review the interactions among risk factors for SIDS for their effects on induction or control of inflammatory responses. The risk factors studied are genetic factors (sex, cytokine gene polymorphisms among ethnic groups at high or low risk of SIDS); developmental stage (changes in cortisol and testosterone levels associated with 2- to 4-month age range); environmental factors (virus infection, exposure to cigarette smoke). These interactions help to explain differences in the incidences of SIDS observed between ethnic groups prior to public health campaigns to reduce these infant deaths.
Highlights
Sudden infant death syndrome (SIDS) is still the major cause of death between 1 month to 1 year of age among infants in industrialized countries
The original definition was “. . . the sudden death of any infant or young child, which is unexpected by history, and in which a thorough post mortem examination fails to demonstrate an adequate cause of death” [1].The definition was revised in 1989 to “the sudden death of an infant under one year of age, which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history” [2] Comparison of epidemiological data from different countries found that infants of some ethnic groups had an increased risk of SIDS (Table 1)
There is a wealth of knowledge about the risk factors for sudden death in infancy; it is important, to attempt to explain how these risk factors could result in death
Summary
Sudden infant death syndrome (SIDS) is still the major cause of death between 1 month to 1 year of age among infants in industrialized countries. The objective of this review was to assess how the risk factors identified in epidemiological studies of SIDS affect susceptibility to infection and/or alter inflammatory responses to infections It addresses the interactions between these identified risk factors and the three key stages of infection: [1] increased frequency or density of bacterial colonization; [2] induction of temperaturedependent toxins; [3] induction or control of inflammatory responses (Table 5). In an in vitro study of first degree relatives of SIDS infants or infants who had suffered an acute life threatening episode (ALTE), there was evidence of increased mast cell hyper-releasability and degranulation [84] This could be mediated by some of the pyrogenic staphylococcal toxins through non-antibody activation of mast cells. Evidence of mast cell tryptase and other products of mast cells have been published [15] (Walls, this volume)
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