Bacterial toxins and sudden unexpected death in infancy

Prtak, Laura; Cohen, Marta C.; Fenton, Paul; Adnani, Mudher Al; Kudesia, Goura

doi:10.1016/s0140-6736(08)61297-0

Cited by 5 publications

(1 citation statement)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The true success of the “back-to-sleep” campaign in reducing SIDS deaths will be seen when further research is able to fully explain the fatal physiological events occurring in vulnerable infants. Infection (particularly with the key players S. aureus and E. coli ) ( 8 , 12 , 13 ) interacting with vagal and/or spinal neural pathways concerned with neuroimmunological and neurochemical physiology and inflammatory responses in predisposed infants should provide a fruitful pathway for research ( 51 ). A complete explanation of SIDS etiopathogenesis should arise from this together with a deeper understanding of fatal perinatal infections.…”

Section: Discussionmentioning

confidence: 99%

Sudden Infant Death Syndrome, Infection, Prone Sleep Position, and Vagal Neuroimmunology

Goldwater

2017

Front. Pediatr.

View full text Add to dashboard Cite

Recent findings suggest that infection (and sepsis) stand alone as the only plausible mechanism of causation of sudden infant death syndrome (SIDS) and accordingly achieves congruence with all clinicopathological and epidemiological findings. This review examines the role of infection in the pathogenesis of SIDS in the context of the major risk factor of prone sleep position. The study explores how sleep position could interact with the immune system and inflammatory response via vagal neural connections, which could play key roles in gut and immune homeostasis. A plausible and congruent clinicopathological and epidemiological paradigm is suggested.

show abstract