B. infantis EVC001 is well-tolerated and improves human milk oligosaccharide utilization in preterm infants in the NICU

Sarah Bajorek, DO

High Levels of B. infantis Correlated with Less Excreted Fecal HMOs

Human Milk Oligosaccharide Utilization

The infant gut microbiome provides protection against enteric infection and is critical for proper immune system development. Interventions such as caesarean sections and antibiotics can disrupt the formation of the microbiome. The bacterial family Bifidobacterium is a core component of the infant’s microbial community, and yet, colonization with beneficial bifidobacteria is delayed in preterm infants. 1 Instead, preterm infants in the neonatal intensive care unit (NICU) are colonized by potential pathogens linked to adverse outcomes, including high-mortality conditions such as late onset sepsis (LOS) and necrotizing enterocolitis (NEC). 2 Thus, strategies to promote overall gut health by increasing populations of beneficial Bifidobacterium in the preterm gut warrant attention.

Prior studies have shown that activated B. infantis EVC001, an infant-adapted microbe, has profound effects on the gut microbiome of term and preterm infants, specifically by increasing the abundance of beneficial bifidobacteria and reducing taxa capable of eliciting pathogenicity.3 The formation of a Bifidobacterium-dominant gut microbiome in neonates is attributed to the presence of human milk oligosaccharides (HMOs) in the diet.3 B. infantis is an infant gut symbiont uniquely equipped to utilize these HMOs.4

To continue to improve quality of care and patient outcomes at Orlando Health Winnie Palmer Hospital for Women & Babies, a small, prospective, open-label study was conducted to evaluate the tolerability, HMO utilization capacity, and effects on the fecal microbiota of feeding activated B. infantis EVC001 to preterm infants in the NICU.

B. infantis EVC001 feeding resulted in significantly higher relative abundance of Bifidobacterium in the gut microbiome due to a significant improvement in HMO utilization. The Control infants excreted significant quantities of unutilized HMO, which would otherwise support growth and development of the infant. Higher levels of Bifidobacterium in infants fed B. infantis EVC001 was also significantly associated with reduced Enterobacteriaceae, a family that includes species such as E. coli and Klebsiella, often implicated with NEC and LOS.

Safety and Tolerability

This study adds to a growing body of evidence supporting the use of B. infantis EVC001 as a high-quality nutritional product to preterm infants in the NICU. In this study, feeding B. infantis EVC001 was safely fed and well-tolerated in this population.

Health care providers seeking to reduce risk associated with the neonatal gut should consider increasing Bifidobacterium and improving HMO utilization by adding B. infantis EVC001 to standard feeding protocols in the NICU.

High Levels of B. infantis Correlated with Less Excreted Fecal HMOs ​

References

  1. Henderickx JGE, Zwittink RD, Lingen RA van, Knol J, Belzer C. The Preterm Gut Microbiota: An Inconspicuous Challenge in Nutritional Neonatal Care. Front Cell Infect Mi. 2019;9:85.doi:10.3389/fcimb.2019.00085
  2. Masi AC, Stewart CJ. The role of the preterm intestinal microbiome in sepsis and necrotising enterocolitis. Early Hum Dev. 2019;138:104854. doi:10.1016/j.earlhumdev.2019.104854
  3. Frese SA, Hutton AA, Contreras LN, et al. Persistence of Supplemented Bifidobacterium
    longum subsp. infantis EVC001 in Breastfed Infants. Msphere. 2017;2(6):e00501-17.
    doi:10.1128/msphere.00501-17
    4. Sela DA, Chapman J, Adeuya A, et al. The genome sequence of Bifidobacterium longum subsp. infantis reveals adaptations for milk utilization within the infant microbiome. Proc National Acad Sci. 2008;105(48):18964-18969. doi:10.1073/pnas.0809584105

Learn more about Evivo (activated B. infantis EVC001)

The first and only infant probiotic clinically demonstrated to functionally metabolize human milk oligosaccharides to improve the biochemistry of the infant gut.