No obvious link between intestinal microbiota and sudden infant death syndrome
Several paths have been suggested to explain sudden infant death syndrome (SIDS) through disruptions of the intestinal microbiota. Australian researchers therefore tried to establish a link between dysbiosis and SIDS, without noticeable success.
Sudden infant death syndrome is poorly understood but is still the major cause of mortality in babies under one year of age. Its etiology is thought to be multifactorial (environmental and pathophysiological factors). According to previous studies, this syndrome could be explained, in part, by an impairment of the intestinal microbiota. Several hypotheses have been formulated: the intestinal microbiota is believed to be necessary for the correct development of the hypothalamo-pituitary-adrenal axis in order to respond appropriately to stress (such as hypoxia in a baby sleeping on its stomach); the harmful presence of enteropathogenic E.coli could exacerbate this stress response whilst the presence of Bifidobacterium infantis could be protective; a toxic or septic shock which could trigger an inflammatory cascade, a modulation of serotonin levels in the brain stem, amongst others.
No anomaly to report
An Australian team therefore conducted a case-control study in 44 infants who died between 1989 and 1994 by comparing their preserved stools with those of babies matched for age, sex, and diet. Various bacterial alpha (within each sample) and beta (between samples) diversity indices were analyzed. Enterohemorrhagic (EHEC) and enteropathogenic (EPEC) C. difficile, S. aureus, and E.coli bacteria were investigated, and Bifidobacterium levels were measured. No difference was detected between healthy infants and SIDS infants, for any parameter, regardless of sex or diet type. The intestinal microbiota of the deceased babies did not display any anomaly: it was dominated by Clostridiales, Bacteroidales, Lactobacillales, Enterobacteriales and Bifidobacteriales, with a diversity which increased during the first year of life.
All studies have their limits and this study is no exception to the rule: the team emphasizes that a larger cohort could perhaps allow a link to be detected, although their study—conducted over six years—covered an entire Australian state where the prevalence of SIDS was still high before decreasing markedly thanks to the introduction of recommended practices. The researchers wonder whether the microbiota should be compared at very precise moments in the first year of life, a period when the intestinal microbiota changes rapidly. A challenge in terms of coordination and resources. In any event, the Australian team could only conclude here that there is no link between SIDS and dysbiosis or bacterial infection, and calls for research into the causes of SIDS to be continued in order to improve preventive methods.
Lex Leong et al. Intestinal Microbiota Composition in Sudden Infant Death Syndrome and Age-Matched Controls. J Pediatr 2017; 191:63-68.e1