Findings and methodology are reported for a study that tested the hypothesis that sudden infant death syndrome (SIDS) may be triggered by environmental exposure to Clostridium perfringens enterotoxin.
SIDS is the leading cause of death in children less than 1 year old; however, the root cause of SIDS is unknown. The current view is that SIDS involves unexplained abnormalities in the respiratory center of the medulla oblongata (a portion of the brainstem), making infants susceptible to accidental asphyxiation during sleep. Having babies sleep in the supine position instead of the prone position has reduced the incidence of SIDS 38 percent. How this region of the brain causes damage has not been determined. The current study found that the infant brainstem respiratory center is susceptible to damage by bloodborne CPE dissemination, which recapitulates the inflammatory scarring observed in brain samples of SIDS victims. In addition to brainstem expression of the CPE receptors claudin3 and claudin 4, the current study discovered brainstem expression of the rotavirus receptor, Junctional Adhesion Molecule 1 (JAM1), which may implicate rotavirus infection as an alternate or coincident SIDS trigger. In addition, the study characterized intestinal carriage of the C. perfringens bacterium and determined the prevalence of CPE gene carriage in fecal samples from infants who died suddenly. Since commensal C. perfringens stratus typically carry the CPE gene at a frequency just under 15 percent, this four-fold CPE gene enrichment in victims of sudden unexpected infant death (SUID) implicates CPE-producing C. perfringens strains in the pathogenesis of sudden infant death syndrome. This report advises, however, that since there were 25 instances where SIDS cases were negative for CPE, the assay in its current form is discouraged for criminal justice purposes. 8 figures, 2 tables, and 44 bibliographic listings