Affiliations: Queensland Health, Gold Coast Population Health Unit,
Southport, Gold Coast, Queensland, Australia | Faculty of Health Science and Medicine, Population
Health and Neuroimmunology Unit, Bond University, Robina, Queensland,
Australia
Note: [] Correspondence: Dr. Donald R. Staines, Gold Coast Population
Health Unit, 10–12 Young Street, Southport 4215, Queensland, Australia. Tel.:
+61 7 5509 7222; Fax: +61 7 5561 1851; E-mail: [email protected]
Abstract: Sudden infant death syndrome (SIDS) has been extensively
investigated in the context of infection as a contributing factor in the death
of otherwise apparently healthy infants. A number of infectious agents have
been implicated suggesting the causal pathomechanism is related to infection,
but not necessarily solely attributable to any one type of infection. An
alternative provocative hypothesis is that of post-infection autoimmunity
affecting critical novel neurotransmitters of the vasoactive neuropeptide
family. Their role in respiratory and cardiac functioning together with novel
hypotheses postulating their autoimmune compromise may suggest a role in SIDS
etiology following infection. Animal models demonstrate their vital role in
neonatal survival and the neuronal control of breathing. Autoimmune compromise
of vasoactive neuropeptide receptors through molecular mimicry following
infection or idiopathic autoimmunity is postulated as a cause of SIDS.