AIMS: To investigate the hypothesis that commonly occurring bacterial toxins cause sudden infant death syndrome (SIDS) by (1), determining in which tissues bacterial toxins are concentrated after intravenous injection in rats; and (2), seeing if the same tissues contain detectable toxins in cases of SIDS. METHODS: The tissue distribution of intravenously injected staphylococcal enterotoxin A (SEA), enterotoxin B (SEB), enterotoxin C (SEC), enterotoxin D (SED), toxic shock syndrome toxin (TSST-1), and alpha-haemolysin was studied in rats using immunohistology and polyacrylamide gel electrophoresis with immunoblotting. Immunostaining was also carried out on formalin fixed kidneys from cases of SIDS and a comparison series of necropsy cases using anti-SEA, anti-SEB, anti-SEC2 and anti-SED. RESULTS: Immunohistology showed that SEB, SEC, SED and TSST-1 were all concentrated in the proximal convoluted tubular cells of the kidney. The presence of these toxins was confirmed in kidney homogenates using electrophoresis and immunoblotting. There was positive granular staining in the proximal convoluted tubular cells of the kidney in 36% of SIDS cases and 12% of the comparison series with anti SEC2 (chi 2 = 6; p < 0.025). CONCLUSION: SEC, or a bacterial toxin with epitopes in common, could have a pathogenic role in SIDS.
AIMS: To investigate the hypothesis that commonly occurring bacterial toxins cause sudden infant death syndrome (SIDS) by (1), determining in which tissues bacterial toxins are concentrated after intravenous injection in rats; and (2), seeing if the same tissues contain detectable toxins in cases of SIDS. METHODS: The tissue distribution of intravenously injected staphylococcal enterotoxin A (SEA), enterotoxin B (SEB), enterotoxin C (SEC), enterotoxin D (SED), toxic shock syndrome toxin (TSST-1), and alpha-haemolysin was studied in rats using immunohistology and polyacrylamide gel electrophoresis with immunoblotting. Immunostaining was also carried out on formalin fixed kidneys from cases of SIDS and a comparison series of necropsy cases using anti-SEA, anti-SEB, anti-SEC2 and anti-SED. RESULTS: Immunohistology showed that SEB, SEC, SED and TSST-1 were all concentrated in the proximal convoluted tubular cells of the kidney. The presence of these toxins was confirmed in kidney homogenates using electrophoresis and immunoblotting. There was positive granular staining in the proximal convoluted tubular cells of the kidney in 36% of SIDS cases and 12% of the comparison series with anti SEC2 (chi 2 = 6; p < 0.025). CONCLUSION: SEC, or a bacterial toxin with epitopes in common, could have a pathogenic role in SIDS.