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Editor,—At present, we do not understand the pathogenesis of sudden infant death syndrome (SIDS), however, it is accepted to be a multifactorial disease for which certain risk factors have been identified. Various theories have been developed to explain the existence of these risk factors.
Blackwell reminds us of the accepted fact that PCR detects DNA from both live and dead organisms, but her phrase “transient contamination of the infant with DNA from non-viable bacteria” seems inappropriate. The detection of H pylori DNA in the trachea and lung of such babies is a finding of particular importance both for our understanding of the pathogenesis of SIDS and for our understanding of the pathogenesis and epidemiology of H pylori infection in infants.
The study by Kerr et al 1 showedH pylori DNA in the stomach, trachea, and lung tissues of SIDS cases, but did not visualise bacteria at these sites. As stated in the paper and by several other authors, the study used haematoxylin and eosin staining, a suboptimal methodology for visualisation of gastric bacteria. Other studies have shown inflammatory changes in both antrum and trachea ofH pylori-PCR positive SIDS cases.2
Genetic subtyping would be valuable as suggested, but not essential, as the PCR-ELISA utilised was specific, tests were performed in duplicate and positive and negative controls consistently gave expected results.1
Our hypothesis is that H pylori infection accounts …
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