Study found higher levels of staph, E. coli in babies who died from unexplained causes
THURSDAY, May 29 (HealthDay News) -- Could common bacterial infections cause some cases of sudden infant death syndrome, or SIDS?
According to the British authors of a study in this week's issue of The Lancet, the answer is a qualified yes. The researchers found high levels of Staphylococcus aureus and Escherichia coli (E. coli) bacteria in children who had died of SIDS.
But in no way does this mean that parents should be demanding antibiotics for their newborns, cautioned Dr. Jim Greenberg, director of the division of neonatology at Cincinnati Children's Hospital. "This still falls under the category of preliminary research and doesn't have any direct application to how we think about patient care," he said.
"As yet, we do not understand the true significance of the findings," added Dr. Nigel Klein, co-author of the study and professor of infectious disease and immunology and head of the department of infection at the University of London and Great Ormond Street Hospital for Children in the United Kingdom. "At present, a causal link has not been established. As such, there are no direct clinical implications."
According to the American SIDS Institute, the rate of SIDS has dropped dramatically since 1983, thanks to concerted prevention efforts on the part of a number of organizations. However, about 2,500 infants still die of SIDS every year in the United States.
The causes largely remain a mystery, although putting a baby to sleep on his or her back and avoiding smoking near the child are known to be protective.
Klein and his colleagues conducted autopsies on 546 infants who had died suddenly between the ages of 7 and 365 days. Samples of bacteria were taken from 470 of the infants.
Many more potentially harmful organisms were isolated from children whose sudden death could not be explained than from infants whose deaths were explained by non-infectious causes. In particular, S. aureus ("staph") and E. coli had a greater presence in unexplained deaths than in those explained by non-infectious causes.
As an accompanying editorial pointed out, the number of SIDS cases peaks at 8 weeks to 10 weeks of age. That's a time-frame coinciding with blood concentrations of immunoglobulin that protect newborns against bacterial infections.
"This is just at the point that antibodies that go across the placenta -- from mom to baby -- to protect them are starting to disappear, and babies haven't made a lot of their own antibodies yet," noted Dr. Cheryl Cipriani, an associate professor of pediatrics at Texas A&M Health Science Center College of Medicine and a neonatologist with Scott & White. "This is a particular point in time where babies seem to be vulnerable," she said.
Also, both S. aureus and E. coli are bacteria that make toxins, Cipriani explained, "and a toxin might not necessarily cause all the histological changes that you see with infections."
"This is another building block in our knowledge about these kinds of deaths, but association doesn't mean cause," Cipriani cautioned. "But it's a large enough group of babies where you think the findings need to be paid attention to."
Until precise causes for SIDS are uncovered, parents should be aware that putting infants to sleep on their back ("Back to Sleep") reduces the risk of SIDS by 40 percent to 60 percent, Greenberg said. Avoiding your child's exposure to cigarette smoke also reduces this risk.
Using a pacifier might also lower risk, but this is controversial, Greenberg added.
There's more on SIDS at the National Institute of Child Health and Human Development.
SOURCES: Nigel Klein, MBBS, Ph.D., professor of infectious disease and immunology, and head, department of infection, University of London and Great Ormond Street Hospital for Children, London, U.K.; Jim Greenberg, M.D., director, division of neonatology, Cincinnati Children's Hospital; Cheryl Cipriani, M.D., associate professor of pediatrics, Texas A&M Health Science Center College of Medicine, and neonatologist, Scott & White, Temple, Texas; May 31, 2008, The Lancet
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