{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,7]],"date-time":"2025-07-07T17:27:54Z","timestamp":1751909274069},"reference-count":24,"publisher":"Microbiology Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2009,3,1]]},"abstract":"<jats:p>Consistent pathological findings in sudden infant death syndrome (SIDS) are seen which display similarities to the pathogenesis of toxaemic shock and\/or sepsis. A key candidate infectious agent that is possibly involved is <jats:italic>Escherichia coli<\/jats:italic>, given its universal early colonization of the intestinal tract of infants and an increased frequency of toxigenic and mouse-lethal isolates from SIDS compared with comparison infants. An explanation for these findings has yet to be identified. Using PCR, we screened <jats:italic>E. coli<\/jats:italic> isolates from 145 SIDS and 101 dead control and healthy infants for three new candidate pathogenicity-related genes: <jats:italic>clyA<\/jats:italic> (cytolysin A), <jats:italic>irp2<\/jats:italic> [high-pathogenicity island (HPI)-specific gene] and <jats:italic>cdt<\/jats:italic> (cytolethal distending toxin). The results failed to show a positive correlation with SIDS, instead proving that <jats:italic>clyA<\/jats:italic> and <jats:italic>irp2<\/jats:italic> genes were common to the infant intestinal <jats:italic>E. coli<\/jats:italic>. Interestingly we observed a high rate of carriage of these two potentially pathogenic genes in <jats:italic>E. coli<\/jats:italic> from healthy infants in the absence of diarrhoeal disease, and we report that in a number of cases, the detection of HPI-specific genes was predictable by serotype. Despite the lack of associations defined so far, there remains the likelihood that genetic determinants influence the interactions between <jats:italic>E. coli<\/jats:italic> and the host, so these factors may be part of the multi-factorial aspect of SIDS.<\/jats:p>","DOI":"10.1099\/jmm.0.005322-0","type":"journal-article","created":{"date-parts":[[2009,2,10]],"date-time":"2009-02-10T19:51:08Z","timestamp":1234295468000},"page":"285-289","source":"Crossref","is-referenced-by-count":11,"title":["The frequency of molecular detection of virulence genes encoding cytolysin A, high-pathogenicity island and cytolethal distending toxin of Escherichia coli in cases of sudden infant death syndrome does not differ from that in other infant deaths and healthy infants"],"prefix":"10.1099","volume":"58","author":[{"given":"Amanda R.","family":"Highet","sequence":"first","affiliation":[{"name":"University of Adelaide Discipline of Paediatrics, North Adelaide, South Australia, Australia"},{"name":"Department of Microbiology and Infectious Diseases, SA Pathology, Women's and Children's Hospital, 72 King William Road, North Adelaide, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Anne M.","family":"Berry","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Infectious Diseases, SA Pathology, Women's and Children's Hospital, 72 King William Road, North Adelaide, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Karl A.","family":"Bettelheim","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Infectious Diseases, SA Pathology, Women's and Children's Hospital, 72 King William Road, North Adelaide, South Australia, Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paul N.","family":"Goldwater","sequence":"additional","affiliation":[{"name":"University of Adelaide Discipline of Paediatrics, North 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