Search
Tobias Strunk MD, PhD, FRACP Head, Neonatal Health tobias.strunk@thekids.org.au Head, Neonatal Health Clinical Professor Tobias Strunk is a
Tobias Strunk MD, PhD, FRACP Head, Neonatal Health tobias.strunk@thekids.org.au Head, Neonatal Health Clinical Professor Tobias Strunk is a
Late-onset sepsis (LOS) with Staphylococcus epidermidis is common in preterm infants, but the immunological mechanisms underlying heightened susceptibility are poorly understood. Our aim is to characterize the ontogeny of cytokine responses to live S. epidermidis in preterm infants with and without subsequent Gram-positive LOS.
Very preterm infants have a marked innate inflammatory response at the time of late-onset sepsis
Impaired oxygen delivery or blood flow to the brain around the time of birth can cause injury. Hypoxic ischaemic encephalopathy is a leading cause of death and disability in term and near-term infants.
Viral infections are associated with significant morbidity and mortality in neonates. The COVID-19 pandemic led to changes in viral epidemiology in Western Australia. The impact on patients in neonatal intensive care is uncertain.
Sepsis is one of the leading causes of neonatal mortality. There is heterogeneity in the outcomes measured and reported in studies of neonatal sepsis. To address this challenge, a core outcome set (COS) for research on neonatal sepsis was needed.
The abundant skin commensal, Staphylococcus epidermidis, is the leading cause of late-onset sepsis (LOS) in preterm infants but rarely causes infections in term infants and adults. Staphylococcal virulence mechanisms and the role of the preterm immune responses in driving these life-threatening infections remain poorly understood.
Antibiotic exposure in neonatal intensive care units (NICU) is high. This study describes antibiotic use in very preterm infants and examines the association between duration of exposure and outcomes in blood culture negative (CN) infants.
The neonatal skin is central to early survival and immune development. Far from being a passive mechanical barrier, it integrates physical, chemical, and microbial defences that together protect the infant in the immediate postnatal period. In preterm infants, structural immaturity, reduced antimicrobial capacity, and altered microbial colonisation confer heightened vulnerability to infection and inflammation.