Abstract

It has long been thought that bacterial superantigens invariably cause pathology by causing the powerful stimulation of large numbers of T cells, a phenomenon seen in several models, which leads to high levels of cytokine release. Clinically this scenario manifests as toxic shock syndrome following burns, trauma, or in relation to menstruation. More limited local T-cell stimulation, probably caused by superantigens, has been described in atopic dermatitis, food poisoning and psoriasis. The implication of studies so far has been that antibodies provide protection against these molecules; the most vulnerable group should therefore be infants. However, careful prospective observation of a group of 49 healthy Swedish infants over their first year challenges this disease model 1 Lindberg E et al. Long-time persistence of superantigen-producing Staphylococcus aureus strains in the intestinal microflora of healthy infants. Pediatr. Res. 2000; 48: 741-747 Crossref PubMed Scopus (76) Google Scholar . These healthy infants had fecal flora sampled and tested at intervals; it was observed that Staphylococcus aureus colonization rates rose from 16% on the third day of life to 73% by six months of age. The organisms resembled those known to colonize the skin. Strains of S. aureus were identified using their characteristic polymorphic DNA patterns. It was found that individual strains frequently persisted for several months in stool samples. Following culture, Staphylococci in 23 infants were capable of producing superantigens (over a quarter synthesized more than one superantigen). Some 25% of toxin-producing strains were found in numbers of >108 per gram of feces. Levels of colonization or toxin production did not correspond to any obvious clinical symptom in the infants.

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