Post-mortems in otherwise unexplained cases of sudden unexpected death in infancy (SUDI) sometimes show high levels of Staphylococcus aureus and Escherichia coli bacteria, indicating that they could be associate with the condition, according to an Article released on May 30, 2008 in The Lancet.

Sudden unexpected infant death, sometimes also known as cot death or sudden infant death syndrome (SIDS), is a common cause of post-neonatal infant death many developed nations. SUDI is defined as the sudden and unexpected death of an infant with an age of less than a year. Its diagnosis is made primarily by exclusion — that is, a detailed autopsy, patient history, and circumstantial investigation must eliminate other causes before it can be attributed to the death. As a result, there is much variance in the cases that are classified as SUDI.

For some time now, underlying infection has been postulated as a potentially important mechanism in SUDI. Additionally, new explanations for SUDI can have important medical as well as legal implications, as shown by the recent United Kingdom high court review of child death investigations.

To examine underlying infection as a cause of SUDI, Neil Sebire, Nigel Klein and Marian Malone, Great Ormond Street Hospital for Children, London, UK and colleagues performed a review of autopsy results of SUDI children. The review was a systematic retrospective case review of the autopsies done at Great Ormond Street Hospital between the years of 1996 and 2005, involving 546 infants between the ages of 7 and 365 days who died suddenly and unexpectedly. Each case was classified as: unexplained, explained with evidence of bacterial infection, or explained by non-infective causes. Any bacterial samples collected post-mortem were classified as: non-pathogens; group 1 pathogens, which are associated with an identifiable locus of infection; or group 2 pathogens, which are known to cause sepsis without an obvious focus of infection, such as S. aureus, or E. coli.

Of the total 546 SUDI cases, 39 autopsies were excluded on teh grounds of viral or bacterial infections contracted during the resuscitation process. In the remaining 507 cases, 470 had bacterial samples for analysis, which yielded 2,871 total isolates from cultures. Group 2 pathogens were identified in all three of the subject groups: of the infants whose deaths were explained by bacterial infection, 24% (78 of 232) were group 2 pathogens; in the deaths from non-infective causes, 19% (440 of 2,306) were group 2 pathogens; and in the deaths that were of non-infective cause, the proportion of group 2 pathogens was 11% (27 out of 243.)

Either S. aureus or E. coli was present in considerably more cultures from the infants whose deaths were unexplained (262/1628, 16% and 93/1628, 6% respectively) than those whose deaths were from non-infective causes (19/211, 9% and 3/211, 1% respectively). This indicates that the unexplained SUDI cases could be associated with these bacteria. Notably, since 11% of the isolates from the non-infective group were also group 2 pathogens, the presence of a positive culture may not be sufficient to imply infection as the cause of death in any given case.

In conclusion, the authors summarize their results, and indicate that this correlation requires further research regarding the mechanism of action. “We found that significantly more organisms that were potentially pathogenic were isolated from infants whose sudden, unexpected death could not be explained than from infants whose death was of non-infective cause. Although the reasons for this are unclear, our findings suggest that microbes or microbial products could be related to the pathogenesis of a proportion of unexplained SUDI. We must now investigate the pathophysiological mechanism involved in these cases.”

Dr James Morris and Dr Linda Harrison, Royal Infirmary, Lancaster, UK, contributed an accompanying Comment in which they note the promise of this sort of research towards the prevention of SUDI in the future. “Recent evidence indicates that death in explained SUDI is often rapid, with transition from being well to death in less than one hour in many cases. If bacteria have a role, this points to direct action of bacterial toxins on cardiorespiratory or neural control. The new science of proteomics offers techniques to recognise bacterial protein products in human body fluids, and this is the obvious next step in investigating sudden infant death.”

Infection and sudden unexpected death in infancy: a systematic retrospective case review
M A Weber, N J Klein, J C Hartley, P E Lock, M Malone, N J Sebire
Lancet 2008; 371: 1848-53
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Sudden unexpected death in infancy: evidence of infection
James A Morris, Linda M Harrison
Lancet 2008; 371: 1815-16
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Written by Anna Sophia McKenney