Ethnicity, infection and sudden infant death syndrome

Abstract

Epidemiological studies found the incidence of SIDS among Indigenous groups such as Aboriginal Australians, New Zealand Maoris and Native Americans were significantly higher than those for non-Indigenous groups within the same countries. Among other groups such as Asian families in Britain, the incidence of SIDS has been lower than among groups of European origin. Cultural and childrearing practices as well as socio-economic factors have been proposed to explain the greater risk of SIDS among Indigenous peoples; however, there are no definitive data to account for the differences observed. We addressed the differences among ethnic groups in relation to susceptibility to infection because there is evidence from studies of populations of European origin that infectious agents, particularly toxigenic bacteria might trigger the events leading to SIDS. The risk factors for SIDS parallel those for susceptibility to infections in infants, particularly respiratory tract infections which are also major health problems among Indigenous groups. Many of the risk factors identified in epidemiological studies of SIDS could affect three stages in the infectious process: (1) frequency or density of colonisation by the toxigenic species implicated in SIDS; (2) induction of temperature-sensitive toxins; (3) modulation of the inflammatory responses to infection or toxins. In this review we compare genetic, developmental and environmental risk factors for SIDS in ethnic groups with different incidences of SIDS: low (Asians in Britain); moderate (European/Caucasian); high (Aboriginal Australian). Our findings indicate: (1) the major difference was high levels of exposure to cigarette smoke among infants in the high risk groups; (2) cigarette smoke significantly reduced the anti-inflammatory cytokine interleukin-10 responses which control pro-inflammatory responses implicated in SIDS; (3) the most significant effect of cigarette smoke on reduction of IL-10 responses was observed for donors with a single nucleotide polymorphism for the IL-10 gene that is predominant among both Asian and Aboriginal populations. If genetic makeup were a major factor for susceptibility to SIDS, the incidence of these deaths should be similar for both populations. They are, however, significantly different and most likely reflect differences in maternal smoking which could affect frequency and density of colonisation of infants by potentially pathogenic bacteria and induction and control of inflammatory responses.

Hypoxia Potentiates Endotoxin-Induced Allopregnanolone Concentrations in the Newborn Brain

“…This may be sufficient to raise the threshold for arousal, and blunt responses to challenges such as hypoxia and apnoea [34] and could suppress arousal from sleep. Many sudden infant death syndrome infants have been reported to have respiratory tract infections prior to death (for review see Blackwell et al [35] ). These findings raise the possibility that elevated neurosteroid levels may contribute to the suppression of arousal from sleep in these infants.…”

IL6 G-174C Associated With Sudden Infant Death Syndrome in a Caucasian Australian Cohort

“…Infection and inflammatory responses to infections have been proposed to trigger the physiologic events leading to sudden infant death syndrome (SIDS) [1][2][3]. In a Norwegian study [4], half of the SIDS infants had elevated levels of interleukin (IL)-6 in their cerebrospinal fluid (CSF), comparable to levels found in infants dying of infectious diseases such as meningitis and septicemia.…”

Association of Sudden Infant Death Syndrome With VEGF and IL-6 Gene Polymorphisms

“…Infants in the 2-4 month age range, during which antibody levels are lowest and the peak of SIDS occurs, are dependent on their inflammatory responses to cope with new infectious agents encountered in their environment. It has been suggested that powerful inflammatory responses to common infectious agents or their products precipitate the physiologic events leading to SIDS [5][6][7]. Studies of adults and infants have also demonstrated that sleeping in the prone position increases the number and variety of organisms present in the upper respiratory tract [8,9].…”