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A database of blood group correlations to common diseases



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SIDS (Sudden infant death syndrome)


Description:One study examining the susceptibility of infants to other infections, suggested that the following might be factors leading to colonisation of infants by toxin producing S aureus: The Lewis blood group antigen appears to act as a receptor for some micro-organisms. Epithelial cells expressing high concentrations of Lewis bound appreciably more toxin producing S aureus than cells expressing low concentrations of the antigen. Lewis is expressed in secretions of nearly 90% of infants aged 3 months, the peak age for SIDS. RSV infects about 50% of infants by the first year of life and it is often isolated from infants with SIDS. Studies in our laboratory indicate that RSV infected HEp-2 cells bind more toxin producing S aureus than uninfected controls. (1)

They conclude that S. aureus fits the mathematical model for SIDS. Both staphylococci and/or their toxins were identified in a significant proportion of SIDS cases. Isolation of staphylococci from healthy infants was associated with the 2-4-month age range, a risk factor consistently found in all epidemiological studies of SIDS. This might reflect the developmental stage in which 80-90% of infants express the Lewis(a) antigen which we have shown to be one of the receptors for S. aureus. (2)

The significance of this work is discussed with reference to expression of Lewis a antigen in infants and the proposed role of toxigenic strains of staphylococci in some cases of sudden infant death syndrome. (4)
In persons with anti-Lewis antibodies, erythrocyte agglutination might take place during breathing of odors from secretors of Lewis antigens. The agglutinates occlude capillary vessels, increasing resistance to blood flow. This might lead to the sudden death of adults, sudden infant death syndrome or to diseases accompanied by tissue ischemia, such as migraine, glaucoma, epilepsy, etc. 3.)
References:1. Blackwell CC, Saadi AT, Raza MW, Stewart J, Weir DM. Susceptibility to infection in relation to SIDS. J Clin Pathol. 1992 Nov;45(11 Suppl):20-4.

2. Blackwell CC, MacKenzie DA, James VS, Elton RA, Zorgani AA, Weir DM, Busuttil A. Toxigenic bacteria and sudden infant death syndrome (SIDS): nasopharyngeal flora during the first year of life. FEMS Immunol Med Microbiol. 1999 Aug 1;25(1-2):51-8.

3. Grzeszczuk J. Lewis antigens as a possible cause of sudden death of previously healthy adults and infants and of diseases and phenomena linked to tissue ischemia. Med Hypotheses. 1997 Dec;49(6):525-7.

4.Saadi AT, Weir DM, Poxton IR, Stewart J, Essery SD, Blackwell CC, Raza MW, Busuttil A. Isolation of an adhesin from Staphylococcus aureus that binds Lewis a blood group antigen and its relevance to sudden infant death syndrome. FEMS Immunol Med Microbiol. 1994 May;8(4):315-20.





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