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Medical Rounds

Pediatrics: Preventing Neonatal Dysbiosis

Necrotizing enterocolitis (NEC) is a leading cause of death in infants. Doctors know that premature babies are more vulnerable to NEC than full-term infants, but the reasons are not altogether clear. Preventing and treating the condition is particularly challenging.

Akhil Maheshwari, director of neonatology at the Johns Hopkins Children’s Center, notes that NEC and other serious conditions in infancy, such as sepsis and even developmental delays, are related to an unhealthy imbalance of bacteria in infants’ digestive tracts, a condition known as dysbiosis. “It starts in the gut when bad bacteria take control,” he says.

Dysbiosis is a concern because the microbial imbalance is tipped in favor of a class of microbes known as gammaproteobacteria, which includes the pathogens that cause typhoid, gonorrhea, plague, cholera and other well-known infectious diseases, as well as E. coli, which can cause deadly food poisoning in children.

Prevailing wisdom has been that premature infants are more prone to dysbiosis because they spend a great deal of time in the hospital after birth, where they contract the harmful bacteria from other infants. But a new study by Maheshwari, published last September in Microbiome, has flipped that understanding on its head.

Maheshwari set out to determine how these unwanted bacteria come to thrive in premature infants, who have a higher rate of developing full-blown dysbiosis. His study shows that preterm babies who develop dysbiosis fall into two categories: Half begin life with low levels of gammaproteobacteria in their intestines and are colonized in the first few weeks after birth; the other half of babies have extremely high levels of these bacteria as soon as they are born. Maheshwari’s study is the first to demonstrate this dual-track dichotomy in the progression of dysbiosis.

More critical, however, is what the study says about how the infants acquired the bacteria. Both groups are born with gammaproteobacteria. “It suggests the bad bacteria come directly from the mother to the child, not from other infants,” Maheshwari says.

Doctors also know that mothers who carry babies for a full term do not have the gammaproteobacteria in their blood, milk, feces or other bodily fluids. “If full-term moms don’t have them and preterm moms do, where did they come from?” Maheshwari asks rhetorically.

The answer is in the data. He now believes that the bad bacteria are acquired by the mothers during lengthy and sometimes numerous hospital stays intended to stave off preterm delivery. Sixty percent of mothers in preterm labor are admitted to the hospital three or four times, he says, and many more have at least two admissions.

Transmission from mother to child would also explain another fact about dysbiosis: Vaginal birth, in which infants are more likely to come in contact with blood, feces and other bodily fluids from the mother, leads to greater likelihood of developing the condition among preterm babies whose mothers were hospitalized prior to their birth.

“Colonization in mothers happens long before birth, and the mothers are passing it on,” Maheshwari says. Based on these findings, Maheshwari has begun a broad collaboration with his obstetrics colleagues to implement new admission policies and procedures at the Johns Hopkins Children’s Center to counteract dysbiosis.

Rather than attacking microbial imbalances after the fact—in already colonized newborns, by disinfecting neonatal ICUs or administering antibiotics—the fight needs to begin much sooner, ideally from the moment the mother goes into preterm labor, he says. Maheshwari believes that potential risks of hospital stays for preterm labor should be more carefully considered, and such stays should be avoided or limited to the greatest extent possible.

“Doctors need to start prevention before delivery,” he says. “If we wait until birth, it’s already too late.”