title: The protective effect of breast feeding in relation to sudden infant death syndrome (SIDS): III. Detection of IgA antibodies in human milk that bind to bacterial toxins implicated in SIDS.
abstract: Two toxin-producing bacteria implicated in sudden infant death syndrome (SIDS) are Staphylococcus aureus and Clostridium perfringens. Epidemiological studies have shown that breast feeding reduces an infant's risk of SIDS. This protective effect could be due partly to IgA antibodies to these toxins in human milk. The aim of this work was to use a quantitative ELISA to determine levels of IgA antibodies that bound to toxic shock syndrome toxin (TSST-1), staphylococcal enterotoxin C (SEC) and C. perfringens enterotoxin A (CEA) in individual samples of human milk. All samples of milk tested contained IgA antibodies that bound to the bacterial toxins. For individual samples, IgA bound to TSST-1, SEC and CEA were in the range of 900-3100 ng ml(-1), 1000-3600 ng ml(-1) and 1000-4300 ng ml(-1) respectively. Isolation of S. aureus from mothers donating breast milk samples was used to determine if the presence of bacteria affected IgA levels which bound TSST-1 and SEC. For 3/5 samples with levels above the upper limit of the standard deviation (2375 ng ml(-1)) for IgA bound to TSST-1, S. aureus was isolated from the mother whilst 4/5 samples found to contain levels above the upper limit of the standard deviation (2627 ng ml(-1)) for IgA bound to SEC, had S. aureus isolated from the mother. In conclusion, if bacterial toxins do play a role in precipitating a SIDS death, the presence of IgA antibodies to toxins in breast milk, but not in infant formula, might contribute to the protective effect of breast feeding in relation to SIDS.
authors.affiliation: Department of Medical Microbiology, The Medical School, University of Edinburgh, UK. gordon@srv1.med.ed.ac.uk
authors.forename: A E
authors.initials: AE
authors.lastname: Gordon
authors.forename: A T
authors.initials: AT
authors.lastname: Saadi
authors.forename: D A
authors.initials: DA
authors.lastname: MacKenzie
authors.forename: N
authors.initials: N
authors.lastname: Molony
authors.forename: V S
authors.initials: VS
authors.lastname: James
authors.forename: D M
authors.initials: DM
authors.lastname: Weir
authors.forename: A
authors.initials: A
authors.lastname: Busuttil
authors.forename: C C
authors.initials: CC
authors.lastname: Blackwell
mesh_terms: D000328:Adult; D000818:Animals; D000907:Antibodies, Bacterial / Q000032:analysis / Q000276:immunology; D001427:Bacterial Toxins; D001942:Breast Feeding; D003016:Clostridium perfringens / Q000276:immunology / Q000378:metabolism; D004768:Enterotoxins / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D007070:Immunoglobulin A / Q000032:analysis* / Q000276:immunology; D007223:Infant; D007225:Infant Food; D007231:Infant, Newborn; D008895:Milk, Human / Q000276:immunology*; D009666:Nose / Q000382:microbiology; D010614:Pharynx / Q000382:microbiology; D013211:Staphylococcus aureus / Q000276:immunology / Q000302:isolation & purification / Q000378:metabolism; D013398:Sudden Infant Death / Q000517:prevention & control*; D018089:Superantigens
chemical_list: D000907:Antibodies, Bacterial; D001427:Bacterial Toxins; D004768:Enterotoxins; D007070:Immunoglobulin A; D018089:Superantigens; C030107:enterotoxin F, Staphylococcal; C035598:enterotoxin, Clostridium; C034959:enterotoxin C, staphylococcal