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Infection: the neglected paradigm in SIDS research
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  • Published on: 12 October 2017
    Response to Edward J O’Hagan: Tertium non datur

    Response to Edward J O’Hagan: Tertium non datur

    I thank Mr O’Hagan for his insightful comments. Indeed it is implicit in the ideas put forward in my paper that a specific infection is not the “cause” of SIDS but, rather, it is the immunological response to the infection (bacterial or viral) in the predisposed infant that results in SIDS as proposed by Dr Korsch with his suggested “immunological burst.”

    As mentioned in my response to Dr Korsch, I have extended the infection paradigm to take into account the as yet unexplained risk factor of prone sleep position. (See my paper accepted for publication in Frontiers in Pediatrics.1) The presence of infection is a requirement for the effect of prone sleep position to prevail and suggests a role for the Vagus in unfavourably tipping the homeostatic balance through neuroimmunological pathways.

    Paul N. Goldwater

    Reference:

    1. Goldwater PN. SIDS, infection, prone sleep position & Vagal neuroimmunology. Front Pediatr 2017; doi:10.3389/fped.2017.00223

    Conflict of interest

    None declared.

    Conflict of Interest:
    None declared.
  • Published on: 12 October 2017
    Response to Dr Eckhard Korsch’s letter: SIDS as the consequence of an immunological burst

    Response to Dr Eckhard Korsch’s letter: SIDS as the consequence of an immunological burst

    I thank Dr Korsch for his supportive and helpful comments with which I fully concur. I remain concerned by the general lack of appreciation by mainstream SIDS researchers of the essential requirement of congruency between risk factors (male gender, prone sleep position, contaminated sleeping surfaces, smoke exposure, lack of breast feeding, high birth order, etc.) and various staining findings of brainstem nuclei or other pathological findings such as intrathoracic petechiae. The silence from the mainstream sector in relation to my ideas is also of concern. Funding of mainstream SIDS research will continue unimpeded as long as facts set out in my papers are not publicised and addressed. Such funding is an unconscionable waste.

    In a new paper accepted for publication in Frontiers in Pediatrics1 I have extended the infection paradigm to take into account the as yet unexplained risk factor of prone sleep position. It seems that only in the presence of infection does prone sleep position achieve significance. My thinking suggests a role for the Vagus in unfavourably tipping the homeostatic balance through neuroimmunological pathways.

    Paul N. Goldwater

    Reference:

    1. Goldwater PN. SIDS, infection, prone sleep position & Vagal neuroimmunology. Front Pediatr 2017; doi:10.3389/fped.2017.00223

    Conflict of interest

    None declared.

    Conflict of Interest:
    None declared.
  • Published on: 10 September 2017
    Tertium non datur

    Dr. Goldwater's review once again reflects a suberb understanding of SIDS and related phenomena. He consistently presents information to his readers in a most interesting and objectively accurate and well-written set of steps, which are typically precise, factual, and to the point. For example, he ends the review by observing as follows:
    " If multiple causes were involved, then it would be reasonable to expect a variety of pathological findings. This demonstrably is not the case. There is a fixed pattern to the vast majority of cases. The crux of the argument against broad polycausality of SIDS is the consistent pathological picture (usually in more than 90% of cases) "
    " In moving forward, SIDS researchers should be asking the following questions: (1) Does my hypothesis take into account the key pathological findings in SIDS? (2) Is my hypothesis congruent with the key epidemiological risk factors? (3) Does the hypothesis link questions (1) and (2) This review has shown that infection meets these questions appropriately and researchers in this area deserve acknowledgement and funding support. There remain gaps in our knowledge with regard to the infection model, but it is clear that other lines of research are not making the grade ...."
    Note that while Dr. Goldwater has provided a formidable case on behalf of supporting and funding infection related SIDS research, and also given that there unquestionably is a relationshi...

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    Conflict of Interest:
    None declared.
  • Published on: 5 September 2017
    SIDS as the consequence of an immunological burst
    • Eckhard Korsch, Pediatrician, Neonatologist Childrens Hospital of the City of Colonge, Germany

    In his recent review “Infection: the neglected paradigm in SIDS research” Goldwater (2017) demonstrated that the infection model is the key pathological finding and the key epidemiological risk factor in SIDS. He reasoned that future research regarding the process how the microbiome shapes the immune system in infancy, will close remaining gaps in the knowledge about these tragic events. The well-known and worldwide similar distribution of age of SIDS-death with a clear peak between the 2nd and 4th month (AAP 2005, 2016) likewise supports this infection hypothesis. In this time slot the battle between microbial colonizing of the dermal and the mucosal tissue, including pathogens as well as microbiome building bacteria (Gensollen 2016) and the proceeding of the infant’s immature to a mature immune system (Basha 2014, Elahi 2013), potentially complicated by viral infections, opens a wide window for an immunological burst. In the neonate with little immunological memory the innate and adaptive immune system (immune cells, cytokines, antibodies, etc.) starts to mature rapidly in the first three months of his life (Basha 2014). Additionally CD71+ erythroid cells, which are enriched in the newborn period and which have actively immunosuppressive and immunomodulatory properties, vanish during the first months, leaving the infant exceedingly susceptible to infections (Elahi 2014).
    At the same time the passive protection by transplacentally transferred maternal antibodies, w...

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    Conflict of Interest:
    None declared.
  • Published on: 17 August 2017
    Support for Dr. Goldwater's proposal that an acute respiratory infection may be a causative factor in SIDS
    • David T. Mage, Health Scientist World Health Organization (retired)
    • Other Contributors:
      • E. Maria Donner, Genetic Toxicologist

    I agree with Dr. Goldwater that an undetected prodromal respiratory infection can suddenly fulminate and cause acute anoxic encephalopathy. In such an instance, there may not be time for visible pulmonary histological pathology to form. Then if a lung culture is not performed or gives sepsis-negative results, the cause may be coded as SIDS rather than an ARI. See Farber S. Fulminating streptococcus infections in infancy as a cause of sudden death. N Engl J Med 211:154-158, 1934 and Mage et al. .Front Neurol. 2016 Aug 23;7:129. doi: 10.3389/fneur.2016.00129. eCollection 2016. PubMed ID 27602017

    Conflict of Interest:
    None declared.