Is cardiorespiratory failure induced by bacterial toxins the cause of sudden infant death syndrome? Studies with an animal model (the rabbit).

Recent studies have implicated various toxigenic bacteria and their toxins in the aetiology of sudden infant death syndrome (SIDS). Therefore the effect of six bacterial toxins on the cardiorespiratory system of the rabbit was studied as a model for SIDS. The toxins' effect on the heart rate, arterial blood pressure, and breathing of anaesthetized rabbits was determined and their action compared to that of endotoxin. Intravenous injection of Clostridium perfringens enterotoxin and alpha-toxin, Staphylococcus enterotoxin B, Escherichia coli heat-stable toxin (STa), Clostridium difficile toxin A and B reduced heart rate, blood pressure, respiration and increased, slowed and prolonged thorax expansion, and at higher concentrations caused sudden death without visible stress or trauma. A combination of a low concentration of enterotoxins caused a greater reduction of these activities and sudden death. These effects were generally similar to those produced by endotoxin. In non-anaesthetized rabbits, the toxins slowed metabolism until death occurred without agitation, spasms, visible distress or prolonged illness. Intestinal production of these toxins by toxigenic strains, when conditions are suitable, and their systemic absorption, could therefore cause SIDS by an endotoxin-like shock mechanism.