Responses

PDF

Infection: the neglected paradigm in SIDS research
Compose Response

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g. higgs-boson@gmail.com
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests

PLEASE NOTE:

  • Responses are moderated before posting and publication is at the absolute discretion of BMJ, however they are not peer-reviewed
  • Once published, you will not have the right to remove or edit your response. Removal or editing of responses is at BMJ's absolute discretion
  • If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patient's written consent to publication and send them to the editorial office before submitting your response [Patient consent forms]
  • By submitting this response you are agreeing to our full [Response terms and requirements]

Vertical Tabs

Other responses

Jump to comment:

  • Published on:
    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...

    Show More
    Conflict of Interest:
    None declared.
  • Published on:
    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...

    Show More
    Conflict of Interest:
    None declared.
  • Published on:
    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.