Hiie Soeorg will defend her doctoral thesis titled „Coagulase-negative staphylococci in gut of preterm neonates and in breast milk of their mothers“ on Tuesday, 24. October 2017 at 15.00.
Professor Irja Lutsar, University of Tartu, Institute of Biomedicine and Translational Medicine
Associate Professor Micael Widerström, PhD, University of Umeå (Sweden)
Coagulase-negative staphylococci (CoNS), mostly Staphylococcus epidermidis, are common colonizers of gut and skin, but also the commonest causative agents of late-onset sepsis (LOS) in preterm neonates. Invasive strains carry virulence-related genes and are considered to enter the bloodstream from skin through intravascular catheters; translocation from gut has been proposed, but not yet confirmed. Mother’s own breast milk (BM) reduces the risk of LOS, hypothetically due to being a source of less virulent CoNS compared with those causing LOS. The aim of this thesis was to assess the relationship between colonization with CoNS of gut and skin of preterm neonates, BM of their mothers and development of LOS. In two studies, CoNS from rectal swabs of 276 neonates hospitalized in neonatal intensive care unit and stool and skin swabs of 49 preterm neonates and 20 healthy non-hospitalized term neonates and BM of their mothers were genotyped and the presence of genes contributing to virulence was determined. S. epidermidis colonized nearly all preterm neonates and all term neonates and mothers. In the first week of life, nearly all term neonates, but less than a quarter of preterm neonates harboured in gut and on skin S. epidermidis strains genetically similar to those in mother’s BM. Compared with healthy term neonates, preterm neonates were colonized with more virulent S. epidermidis strains. More than half of preterm neonates with LOS caused by CoNS were colonized with invasive strain in gut and half on skin prior to the onset of LOS. None of the mothers had LOS-causing strain in BM. BM of mothers of preterm compared with term neonates contained more often virulent S. epidermidis, whereas the odds of colonization increased with increasing duration of mother’s hospitalization during the first month after delivery. Still, strains in BM of mothers of preterm neonates were less virulent compared with those colonizing their neonates and by the end of the first month of life colonized gut of the majority of preterm neonates. In conclusion, gut can be the source of invasive CoNS strains in preterm neonates. Initially colonizing virulent strains in gut are gradually replaced by less virulent strains present in mother’s BM.