Common bacterial toxins and physiological vulnerability to sudden infant death: the role of deleterious genetic mutations.
The common bacterial toxin hypothesis of sudden infant death syndrome (SIDS) is consistent with the epidemiological features of the condition including the age distribution, seasonal incidence, association with prone sleeping and with exposure to tobacco smoke. The hypothesis is supported by experimental evidence but there are two barriers to its acceptance: the speed of onset does not fit with conventional concepts of an infective process; furthermore, the hypothesis appears to offer a single explanation for what is regarded as a multifactorial disease. Concepts from information theory are used to explore these objections. Complex physiological systems process information and need a high level of redundancy to minimise error. Models show that deleterious mutations in such a system will interact synergistically. Environmental perturbations are most likely to cause failure (sudden death) in systems with several mutations. Models also indicate that mutation rates will pose a limit to the size of the functioning genome and, therefore, increased complexity in evolution depends on using old genes in new combinations rather than the chance appearance of new genes. The idea that we share our genes with the rest of creation (same genes but different combinations) leads to the following conjecture: for every receptor controlling the flow of information across a cell membrane there will be a bacterially coded molecule that can switch it off or on. Based on this premise, bacterial toxaemia could cause sudden death, merely the time it takes for a molecule to associate with or dissociate from its receptor. Regardless of the number of physiological systems involved in SIDS, the age distribution will have a unimodal peak corresponding to the age range during which infant serum IgG reaches its nadir. In this way, the two barriers to the common bacterial toxin hypothesis can be overcome: one explanation but multiple bacteria and toxins acting with variable speed on multiple target systems.
Morris
J A
JA
Royal Lancaster Infirmary, Lancaster LA1 4RP, UK. jim.a.orris@rli.mbht.nhs.uk
D001419:Bacteria / Q000378:metabolism; D001424:Bacterial Infections / Q000150:complications* / Q000235:genetics; D001427:Bacterial Toxins / Q000633:toxicity*; D020022:Genetic Predisposition to Disease; D006801:Humans; D007223:Infant; D009154:Mutation; D013398:Sudden Infant Death / Q000209:etiology / Q000235:genetics*
D001427:Bacterial Toxins