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H pylori DNA may not imply infection
  1. C P DOHERTY,
  2. W G MACKAY,
  3. L T WEAVER
  1. Department of Child Health
  2. University of Glasgow, UK
  3. cd1c{at}clinmed.gla.ac.uk
  4. Department of Nursing and Midwifery
  5. Stirling University, UK
  6. Department of Microbiology
  7. Royal Alexandra Hospital, Paisley, UK
    1. A J SHEPHERD
    1. Department of Child Health
    2. University of Glasgow, UK
    3. cd1c{at}clinmed.gla.ac.uk
    4. Department of Nursing and Midwifery
    5. Stirling University, UK
    6. Department of Microbiology
    7. Royal Alexandra Hospital, Paisley, UK
      1. C L WILLIAMS
      1. Department of Child Health
      2. University of Glasgow, UK
      3. cd1c{at}clinmed.gla.ac.uk
      4. Department of Nursing and Midwifery
      5. Stirling University, UK
      6. Department of Microbiology
      7. Royal Alexandra Hospital, Paisley, UK

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        Editor,—Kerr et alreport an association between SIDS and H pylori infection. In 32 SIDS cases aged up to 28 weeks old, the H pylori ureC gene was amplified from the stomachs of 15, from the trachea of 19, and from the lungs of 16. The H pylori cagA gene was amplified from the stomachs of 13 (of which seven were positive for the ureC gene), from the trachea of 20, and the lungs of 20 (of which 14 were positive for the ureC gene). Amplified DNA was detected semiquantatively using an ELISA, with a cut off value calculated from the mean of eight controls. The authors offered little explanation for the discordant detection ofH pylori DNA between the two PCR assays used. It may be appropriate to compare the prevalence ofH pylori in SIDS and controls, but inappropriate to make these two groups the basis for defining cutoffs for an H pylori assay.

        The presence of H pylori DNA does not itself imply infection and no visible bacteria were observed in any tissue sections. H pylori can be acquired early in life1 probably from other members of the family. Infection has only previously been detected in the microenvironment of the gastric mucosa and its presence is closely related to socioeconomic status,2 as is SIDS. No details of the socioeconomic status of the infants from whom tissues were obtained, nor details of familial contact were given. Four of the controls died under eight weeks of age from what could possibly be neonatal complications and no details of whether they had been discharged home were provided.

        The authors propose that primary gastric infection and subsequent aspiration into the lungs led to lethal production of ammonia in infants as young as two weeks of age. It is difficult to imagine that an organism specifically adapted to the microaerophilic and acidic conditions of the gastric mucosa thriving well enough in the lungs to produce toxic amounts of ammonia in infants that presumably had normal livers, particularly when no organisms were visible on histology.

        This interesting report could well describe a proxy for the already widely known association between H pyloriand poor socioeconomic status. Arguing that the discordant presence ofH pylori DNA in various organs of SIDS cases represents causation is premature, but warrants further investigation.

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