There is a growing body of evidence that infectious agents or their products contribute to events leading to unexpected infant deaths. This issue summarizes the current information on the interactions between genetic background of the infant, environmental and developmental risk factors, and the microbial flora of the infant that could trigger lethal responses to common infections.
The evidence for the role of infection and inflammation in these deaths comes from a variety of sources. When the risk factors for Sudden Infant Death Syndrome (SIDS) were compared to those of susceptibility to infections, there was a remarkable parallel. The peak incidence of Sudden Infant Death Syndrome (SIDS) (2-4 months) occurs when specific immunity to infections is at its lowest. Maternal antibodies acquired passively prior to birth are waning and infant immunisation is incomplete. The protective effect of immunisation in relation to SIDS indicates that microorganisms commonly encountered in infancy might be involved in triggering these deaths. During the period in which infants are at greatest risk of SIDS, they are dependent on their innate inflammatory responses to deal with new infections encountered in their environment. This period also coincides with developmental changes that affect control of inflammatory responses. Histological evidence of inflammation in SIDS infants has been reported by a number of groups and molecular evidence of inflammatory responses reflected in high interleukin-6 levels in many of these infants.
Bacterial infections have been implicated in Sudden Unexpected Death in Infancy (SUDI). The presence of toxigenic bacteria, bacterial toxins or isolation of normal flora from normally sterile sites has been reported among infants and older children. The need for screening for bacterial toxins which are not normally assessed in relation to these deaths is reviewed.
Because a variety of microbes has been implicated in sudden death in infancy, it is difficult to apply Koch’s postulates to investigation of the underlying mechanisms. The common elements are inflammatory responses elicited by infectious agents. While there is no universally accepted animal model that reflects the genetic, developmental and environmental risk factors for these deaths, those available are compared in this issue.
Sudden death in infancy is a complex problem; this issue is an update on the latest approaches to investigation of the role of infection and inflammatory responses in triggering the physiological events leading to death. It examines the evidence for interactions among genetic, environmental and developmental risk factors identified in epidemiological studies for effects on dysregulation of the inflammatory responses. Recommendations are made for additional screening at autopsy for evidence of infection and inflammation or predisposing genetic factors. Recommendations are also made for applying the findings and techniques used to investigate SIDS and SUDI to investigation of the role of infection and inflammation in stillbirths.
There is a growing body of evidence that infectious agents or their products contribute to events leading to unexpected infant deaths. This issue summarizes the current information on the interactions between genetic background of the infant, environmental and developmental risk factors, and the microbial flora of the infant that could trigger lethal responses to common infections.
The evidence for the role of infection and inflammation in these deaths comes from a variety of sources. When the risk factors for Sudden Infant Death Syndrome (SIDS) were compared to those of susceptibility to infections, there was a remarkable parallel. The peak incidence of Sudden Infant Death Syndrome (SIDS) (2-4 months) occurs when specific immunity to infections is at its lowest. Maternal antibodies acquired passively prior to birth are waning and infant immunisation is incomplete. The protective effect of immunisation in relation to SIDS indicates that microorganisms commonly encountered in infancy might be involved in triggering these deaths. During the period in which infants are at greatest risk of SIDS, they are dependent on their innate inflammatory responses to deal with new infections encountered in their environment. This period also coincides with developmental changes that affect control of inflammatory responses. Histological evidence of inflammation in SIDS infants has been reported by a number of groups and molecular evidence of inflammatory responses reflected in high interleukin-6 levels in many of these infants.
Bacterial infections have been implicated in Sudden Unexpected Death in Infancy (SUDI). The presence of toxigenic bacteria, bacterial toxins or isolation of normal flora from normally sterile sites has been reported among infants and older children. The need for screening for bacterial toxins which are not normally assessed in relation to these deaths is reviewed.
Because a variety of microbes has been implicated in sudden death in infancy, it is difficult to apply Koch’s postulates to investigation of the underlying mechanisms. The common elements are inflammatory responses elicited by infectious agents. While there is no universally accepted animal model that reflects the genetic, developmental and environmental risk factors for these deaths, those available are compared in this issue.
Sudden death in infancy is a complex problem; this issue is an update on the latest approaches to investigation of the role of infection and inflammatory responses in triggering the physiological events leading to death. It examines the evidence for interactions among genetic, environmental and developmental risk factors identified in epidemiological studies for effects on dysregulation of the inflammatory responses. Recommendations are made for additional screening at autopsy for evidence of infection and inflammation or predisposing genetic factors. Recommendations are also made for applying the findings and techniques used to investigate SIDS and SUDI to investigation of the role of infection and inflammation in stillbirths.