The role of bacterial toxins in Sudden Infant Death Syndrome (SIDS)
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Cited by (60)
A mouse zoonotic virus (LCMV): A possible candidate in the causation of SIDS
2022, Medical HypothesesCitation Excerpt :These all support the infection model for SIDS. Interaction between viral respiratory tract infection, prone sleeping and secondary bacterial changes in the nasopharynx offered a simple and convincing explanation of how sepsis could cause death [20,21]. In addition to the epidemiology, there are features from pathological findings that also support the infection model, such as low grade inflammation within the lungs[22] and/or myocardium[22], raised fibrin degradation products (d-dimer)[23], actual detection of bacterial toxins in SIDS tissues[24,25], raised proinflammatory cytokines in SIDS tissues[26], isolation of bacterial pathogens (e.g. Staphylococcus aureus and Escherichia coli) from normally sterile sites[27,28], shock-like diaphragmatic muscular degeneration[29,30] and cardiac changes[31] consistent with haematogenous shock and neuropathological features such as neuronal apoptosis, [32] and microglial activation [33].
SIDS, prone sleep position and infection: An overlooked epidemiological link in current SIDS research? Key evidence for the “Infection Hypothesis”
2020, Medical HypothesesCitation Excerpt :The cytokines TNF, IFN-α, and IL-6 appear to be involved in the pathogenetic process as suggested by Lundemose et al 1993 [30]. The involvement of bacterial toxins and cytokine responses has now been well described in studies that support such a toxigenic shock pathogenetic mechanism in SIDS/SUDI [5–8,37]. Highet et al. [38] showed staphylococcal enterotoxins of several groups were highly likely to have been involved in SIDS pathogenesis.
Forensic microbiology applications: A systematic review
2019, Legal MedicineA systematic review exploring the relationship between infection and sudden unexpected death between 2000 and 2016: A forensic perspective
2018, Forensic Science InternationalProteomic MALDI-TOF/TOF-IMS examination of peptide expression in the formalin fixed brainstem and changes in sudden infant death syndrome infants
2016, Journal of ProteomicsCitation Excerpt :Increases in GAPDH expression have been shown in animal models of both intermittent and acute hypoxia exposure or due to LPS injections [69]. Both intermittent hypoxia (associated with the prone sleeping position [2]) and bacterial endotoxins [70] are considered modifiable risk factors for SIDS [71], and these two risk factors could mediate increased GAPDH expression such as we found in the RVRG, Rpa and XII. In neurological disorders, increased GAPDH is seen as a precursor to apoptosis due to its colocalisation with terminal deoxynucleotidyl transferase-mediated dUTP nick-end (marker for DNA fragmentation) and caspase 3 [72].