Sudden unexpected infant death (SUID), including Sudden Infant Death Syndrome (SIDS), results in about 3,400 deaths each year in the United States, but despite decades of research the root cause of the SIDS disease remains unknown. Researchers at Rockefeller University in New York have explored the hypothesis that SIDS may be triggered by environmental exposure to Clostridium perfringens enterotoxin (CPE). The toxin can cause gastrointestinal disease, most commonly food poisoning.
In the research supported by the National Institute of Justice, the scientists showed that “the infant brainstem respiratory center is indeed susceptible to damage by bloodborne CPE dissemination” that causes “the inflammatory scarring that has been observed in brain samples harvested from SIDS victims.” Current understanding of SIDS involves unexplained abnormalities in the respiratory center of the medulla oblongata, which is a portion of the brainstem. “The current theory is that selective neuronal loss and/or reduced neurotransmitter binding within [a portion of the medulla oblongata] makes SIDS victims uniquely susceptible to accidental asphyxiation during periods of sleep.”
Clostridium perfingens enterotoxin (CPE), a known human pathogen, has been found in earlier studies to be in the intestinal tracts of up to 80 percent of SIDS infants compared to 20 percent of healthy infants. “How the resulting enterotoxin might result in the lack of respiratory drive present in SIDS has been attributed to its effects as a ‘parasympathomimetic poison,’ which suppresses cardiorespiratory function,” the researchers noted. “However, a definitive mechanism is yet to be identified.”
The research team, led by Vincent Fischetti, head of Rockefeller University’s Laboratory of Bacterial Pathogenesis, found that CPE affects a section of the surface of the medulla oblongata known as the Ventral Medullary Surface (VMS), which controls respiratory drive.
The researcher’s work “suggests that neurons that comprise the VMS are susceptible to enterotoxin-mediated damage. Furthermore, it may provide a mechanism for how enterotoxin might cause brain damage commonly found in SIDS victims on autopsy.”
The brain is protected from many toxins because of the human blood-brain barrier, but Fischetti’s team noted that the barrier does not fully mature until three-to-six months of age,” which suggests “there may be a window of time where small proteins such as enterotoxin may have access to the infant brain.”
The researchers, in collaboration with the Office of the Chief Medical Examiner of New York City, collected and examined fecal samples from 74 infants who died suddenly. Of those 74 samples, 26 (35%) were positive for Clostridium perfingens bacteria. The researchers concluded that their results “suggest a strong association between CPE exposure and SIDS, and perhaps also a relationship to death by respiratory compromise more generally (through respiratory infections).”
That said, however, they noted that their current research “is neither sensitive nor specific enough to be utilized from criminal justice determinations.”
About this Article
The research in this article was funded by National Institute of Justice award 2016-DN-BX-0176, awarded to Vincent Fischetti, The Rockefeller University, New York, NY. This article is based on the grantee report “Identification of Clostridium perfringens enterotoxin as a novel candidate trigger for Sudden Infant Death Syndrome,” by Vincent Fischetti.