Sudden Infant Death Syndrome

Williams, Alan L.

doi:10.1111/j.1479-828x.1990.tb03235.x

Cited by 19 publications

(10 citation statements)

References 35 publications

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“…Fatty change (for which toxaemia is a cause) is found in the livers of some SIDS babies. 17 77 A second, possibly more important route of curlin/toxin absorption, would be via the lymphatic system and the thoracic duct. Curlin protein/toxin would be delivered via the duct to the innominate vein and thence to the right side of the heart.…”

Section: Prone Sleeping Position and The Changing Prevalence Of Sidsmentioning

confidence: 99%

Sudden infant death syndrome: a critical review of approaches to research

Goldwater

2003

Archives of Disease in Childhood

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Section: Prone Sleeping Position and The Changing Prevalence Of Sidsmentioning

confidence: 99%

Sudden infant death syndrome: a critical review of approaches to research

Goldwater

2003

Archives of Disease in Childhood

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“…This adverse reaction is commonly referred to as endotoxemia, sepsis or septic shock. Endotoxemia is frequently associated with sudden death syndrome observed in feedlot cattle as they near market weight, due to finishing diets high in carbohydrates (Turner, 1971;Williams, 1976 and.…”

Section: Gram-positive Versus Gram-negativementioning

confidence: 99%

Effects of direct-fed microbial supplementation on digestibility and fermentation end-products in horses fed low- and high-starch concentrates1

Swyers

Burk

Hartsock

et al. 2008

Journal of Animal Science

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This research evaluated the viability of lactic acid bacteria (LAB) intended for in vivo application as direct-fed microbial (DFM) supplements in two experiments during feed processing (Exp. 1) and storage (Exp. 2) and determined the efficacy of DFM on the digestibility and hindgut fermentation of horses during and after an abrupt increase in starch (Exp. 3). In Exp. 1, lactobacilli survived feed processing and a commercial enumeration method was validated. In Exp. 2, viable colony forming units of LAB were assessed and remained viable during 12 weeks of storage. Controls in both experiments had high levels of naturally-occurring bacteria present. In Exp. 3, a high-starch concentrate caused fecal pH to decrease, and fecal propionate and digestibility of many nutrients to increase. The DFM induced minimal improvements in digestibility or fermentation parameters and data provided no clear evidence to support the use of a multiple versus a single strain DFM preparation.

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“…A candidate 'toxin' is soluble curlin antigen, CsgA, accompanied (or not) by other toxins absorbed through the gut that may reach the circulation via the portal system which takes it to the liver. Fatty change (of which toxaemia is a cause) is a frequent finding in the livers of SIDS babies [42]. A second route of curlin or toxin absorption would be via the lymphatic system and the thoracic duct.…”

mentioning

confidence: 99%

“…Other pathological findings in SIDS include liquid (unclotted) blood within the chambers of the heart [36,42], and elevated crosslinked fibrin degradation products [43] (seen in toxaemia and sepsis); in this context, curlin protein represents contact-phase bacterial components which can activate the pro-inflammatory pathway [11,44] involving reactions with fibrinogen and fibronectin [45] which can lead to depletion of coagulation factors resulting in a hypocoagulability state [43]. The finding of an empty bladder in most SIDS cases [36,42] suggests decreased renal perfusion (toxaemic shock) during the last sleep. Hypotension could be explained by curlin protein induction of pro-inflammatory cytokines with release of bradykinin or NO, or both [11].…”

mentioning

confidence: 99%