The Rockefeller University

Clostridium perfringens enterotoxin and Rotaviral gastroenteritis as novel candidate triggers for Sudden Infant Death Syndrome

Purpose

Sudden Infant Death Syndrome (SIDS) is the leading cause of death in children less than one year of age (one death for every 1250 births). Surely the impact of SIDS on parents and families is tragic. However the cause of this disease remains unknown. Our current understanding of SIDS involves unexplained abnormalities in the region of the brain that controls our automatic desire to breathe. In SIDS the nerve cells that comprise this brain region are decreased in number. Furthermore there is evidence of brain injury suggesting that some form of damage has previously occurred. Typically children who die from SIDS are laid down to sleep for the night and find themselves in sleeping positions that cause them to rebreathe spent air (e.g. face down). Without this automatic respiratory drive these infants fail to reposition themselves such that they can breathe fresh well-oxygenated air and they die of suffocation. The leading hypothesis for how SIDS related brain damage occurs is that there is a defect during brain development; however I will suggest that other mechanisms may be play. Bacteria release a substance called a toxin that causes damage to human cells. These bacterial toxins have also drawn attention in SIDS research. One toxin in particular made by the bacteria called Clostridium perfringens has been previously implicated. Interestingly researchers have found that Clostridium can be identified in the intestines of up to 81% children who died from SIDS compared to just 20% healthy infants. Furthermore damage to the intestine has been identified in 84% SIDS cases and can be recreated in an animal studies. Comparison of magnified images shows striking similarities between the intestinal damage present in children who died from SIDS and the intestinal damage found in experimental animals that have been exposed to toxin. How toxin may weaken the automatic desire to breathe in children who died from SIDS remains unknown. Data from our laboratory has identified that the cells responsible for our desire to breathe are susceptible to Clostridium toxin. Similarly our data also show that a virus called Rotavirus which causes infant diarrhea may also be involved. Briefly the brain cells involved in the automatic desire to breathe also express receptors for Rotavirus and one scientific study has shown evidence for Rotavirus infection in children who died from SIDS. These findings may explain how the brain damage in SIDS occurs. In light of our recent findings we wish to collect stool samples from healthy infants and compare them to children who died fromSIDS . We will assess and compare the presence of the Clostridium toxin and Rotavirus between SIDS and healthy infants. (Please note that frozen fecal samples from infants with SIDS were previously collected under the PIs protocol "Identification of Clostridium perfringens enterotoxin as a novel candidate trigger for SIDS" deemed as Not Human Subjects Research in Decemebr 2015.)

Condition

• Sudden Infant Death Syndrome