Gut microbiome in sudden infant death syndrome (SIDS) differs from that in healthy comparison babies and offers an explanation for the risk factor of prone position

Highet, Amanda R.; Berry, Anne M.; Bettelheim, K. A.; Goldwater, Paul N.

doi:10.1016/j.ijmm.2014.05.007

Cited by 43 publications

(39 citation statements)

References 40 publications

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“…The clinical background and manifestations were similar to C. difficileeassociated diarrhoea [1,2,16]. Severe C. innocuum infections have been described [17]. In a previous study, we found that C. innocuum was the second most common aetiologic agent for extraintestinal clostridial infection [18].…”

Section: Discussionsupporting

confidence: 60%

Clostridium innocuum is a vancomycin-resistant pathogen that may cause antibiotic-associated diarrhoea

Chia

et al. 2018

Clinical Microbiology and Infection

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Section: Discussionsupporting

confidence: 60%

Clostridium innocuum is a vancomycin-resistant pathogen that may cause antibiotic-associated diarrhoea

Chia

et al. 2018

Clinical Microbiology and Infection

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“…Prone sleep position has been associated with Staphylococcus aureus gut colonization in SIDS. The increased risk of ingestion/inhalation of bacteria contaminating the sleeping surface during prone position, with resultant gut dysbiosis, could account for the increased risk of SIDS in such infants (22). …”

Section: New Hypothesismentioning

confidence: 99%

Microbiome–Gut–Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS—A Novel Hypothesis

Vijayakumar

Praveen

2017

Front. Pediatr.

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Sudden infant death syndrome (SIDS) continues to be a major public health issue. Following its major decline since the “Back to Sleep” campaign, the incidence of SIDS has plateaued, with an annual incidence of about 1,500 SIDS-related deaths in the United States and thousands more throughout the world. The etiology of SIDS, the major cause of postneonatal mortality in the western world, is still poorly understood. Although sleeping in prone position is a major risk factor, SIDS continues to occur even in the supine sleeping position. The triple-risk model of Filiano and Kinney emphasizes the interaction between a susceptible infant during a critical developmental period and stressor/s in the pathogenesis of SIDS. Recent evidence ranges from dysregulated autonomic control to findings of altered neurochemistry, especially the serotonergic system that plays an important role in brainstem cardiorespiratory/thermoregulatory centers. Brainstem serotonin (5-HT) and tryptophan hydroxylase-2 (TPH-2) levels have been shown to be lower in SIDS, supporting the evidence that defects in the medullary serotonergic system play a significant role in SIDS. Pathogenic bacteria and their enterotoxins have been associated with SIDS, although no direct evidence has been established. We present a new hypothesis that the infant’s gut microbiome, and/or its metabolites, by its direct effects on the gut enterochromaffin cells, stimulates the afferent gut vagal endings by releasing serotonin (paracrine effect), optimizing autoresuscitation by modulating brainstem 5-HT levels through the microbiome–gut–brain axis, thus playing a significant role in SIDS during the critical period of gut flora development and vulnerability to SIDS. The shared similarities between various risk factors for SIDS and their relationship with the infant gut microbiome support our hypothesis. Comprehensive gut-microbiome studies are required to test our hypothesis.

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“…The results were inconclusive that H. pylori are a primary cause of SIDS; however, this model is consistent with infectious challenge ( 77 – 79 ). Recent work by Highet and colleagues on samples from SIDS infants show that the gut microbiome are significantly different than found in control infants and should be explored further as a cause of inflammation ( 80 ).…”

Section: Reflux and Infectionmentioning

confidence: 99%

Animal Models for Assessment of Infection and Inflammation: Contributions to Elucidating the Pathophysiology of Sudden Infant Death Syndrome

Blood‐Siegfried

2015

Front. Immunol.

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Sudden infant death syndrome (SIDS) is still not well understood. It is defined as the sudden and unexpected death of an infant without a definitive cause. There are numerous hypotheses about the etiology of SIDS but the exact cause or causes have never been pinpointed. Examination of theoretical pathologies might only be possible in animal models. Development of these models requires consideration of the environmental and/or developmental risk factors often associated with SIDS, as they need to explain how the risk factors could contribute to the cause of death. These models were initially developed in common laboratory animals to test various hypotheses to explain these infant deaths – guinea pig, piglet, mouse, neonatal rabbit, and neonatal rat. Currently, there are growing numbers of researchers using genetically altered animals to examine specific areas of interest. This review describes the different systems and models developed to examine the diverse hypotheses for the cause of SIDS and their potential for defining a causal mechanism or mechanisms.

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Gut microbiome in sudden infant death syndrome (SIDS) differs from that in healthy comparison babies and offers an explanation for the risk factor of prone position

Cited by 43 publications

References 40 publications

Clostridium innocuum is a vancomycin-resistant pathogen that may cause antibiotic-associated diarrhoea

Clostridium innocuum is a vancomycin-resistant pathogen that may cause antibiotic-associated diarrhoea

Microbiome–Gut–Brain Axis: A Pathway for Improving Brainstem Serotonin Homeostasis and Successful Autoresuscitation in SIDS—A Novel Hypothesis

Animal Models for Assessment of Infection and Inflammation: Contributions to Elucidating the Pathophysiology of Sudden Infant Death Syndrome

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