Respiratory viruses and cot death.

Scott, DE; Gardner, P. S.; McQuillin, Joyce; Stanton, A N; Downham, M. A. P. S.

doi:10.1136/bmj.2.6129.12

Cited by 58 publications

(17 citation statements)

References 4 publications

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“…Frequent apnoic pauses associated with rapid onset of severe hypoxaemia, possibly due to mismatch between ventilation and perfusion of the lungs among infected young infants have been reported [24]. In addition, characteristic findings of the inflammatory response to BP, such as inflammation of the mucosal lining of the respiratory tract and peribronchial lymphoid hyperplasia, have been observed in a proportion of SID victims [5,23]. To our knowledge, the first paper that addressed the question of whether respiratory tract infections could be involved in the pathophysiology of SID was published by Adelson and Kinney in 1956 [1].…”

Section: Discussionmentioning

confidence: 95%

“…The notion of a temporal association between infection and sudden death is also supported by findings of marginal inflammatory changes in the upper airways among some SID victims [5,23]. Following the cessation of the immunisation programme against Bordetella pertussis (BP) in Sweden in 1979, an increasing trend in whooping cough (WC) prevalence, as well as a rise in sudden infant death (SID) mortality rate, have been reported [15,22].…”

Section: Introductionmentioning

confidence: 93%

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Sudden infant death and prevalence of whooping cough in the Swedish and Norwegian communities

Lindgren

Milerad

Lagercrantz

1997

European Journal of Pediatrics

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 93%

Sudden infant death and prevalence of whooping cough in the Swedish and Norwegian communities

Lindgren

Milerad

Lagercrantz

1997

European Journal of Pediatrics

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“…There are conflicting results on the role of viruses [9,10] and toxigenic intestinal bacteria in SIDS [11][12][13][14][15]. Recently, it has been suggested that nasopharyngeal colonization by toxigenic strains of Staphylococcus aureus, particularly those producing the toxic shock syndrome toxin 1 (TSST-1), might be involved in some of these infant deaths [16].…”

Section: Introductionmentioning

confidence: 99%

Factors enhancing adherence of toxigenicStaphylococcus aureusto epithelial cells and their possible role in sudden infant death syndrome

et al. 1993

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SUMMARYToxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewisa antigen and infection with respiratory syncytial virus (RSVT). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from nonsecretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewisa or anti-type-I precursor significantly reduced bacterial binding (P < 0 01); however, attachment of the bacteria correlated only with the amount of Lewisa antigen detected on the cells (P < 0 01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context, of factors previously associated with SIDS (mother's smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

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“…Several findings have suggested respiratory or other viruses such as echovirus, respiratory syncytial virus, adenovirus, influenza A and B, and other enteroviruses [1,13] may also be involved. It has been postulated that viruses, particularly pneumotrophic species, may trigger an increase in sensitivity to bacteria [3], but few have postulated a direct role for bacteria.…”

Section: Introductionmentioning

confidence: 99%

Bacterial flora of Tasmanian SIDS infants with special reference to pathogenic strains ofEscherichia coli

et al. 1994

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SUMMARYThe general bacterial flora of 38 Tasmanian SIDS infants was examined together with faecal flora of 134 comparison infants ranging in age from birth to 6 months. The microflora of all specimens received was investigated with special emphasis on the toxigenic Escherichia coli (TEC). Samples were examined for verocytotoxigenic E. coli, free faecal verocytotoxin (FVT), heat labile toxin (LT) and heat stable toxin (ST) producers with the use of a Vero cell assay and commercial kits. The findings of this study revealed a high isolation rate (39 %) of TEC from SIDS infants as compared to 15 % from the healthy comparison infants. Atypical E. coli strains were also identified during the study, including E. coli A-D. An analysis of the same specimens for rotaviral and adenoviral antigens indicated that 30% of the SIDS cases were positive as compared to 20% in the comparison group.

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Respiratory viruses and cot death.

Cited by 58 publications

References 4 publications

Sudden infant death and prevalence of whooping cough in the Swedish and Norwegian communities

Sudden infant death and prevalence of whooping cough in the Swedish and Norwegian communities

Factors enhancing adherence of toxigenicStaphylococcus aureusto epithelial cells and their possible role in sudden infant death syndrome

Bacterial flora of Tasmanian SIDS infants with special reference to pathogenic strains ofEscherichia coli

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