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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.

Rates of anaphylaxis in early childhood are rising, yet there remains a paucity of data on age-specific presentations and outcomes. While prompt treatment is essential, symptoms can differ from older children. Observation after stabilization is routinely used; however, no infant and toddler-specific data guide the duration of monitoring. Identifying predictors of biphasic anaphylaxis could help guide observation times.

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.

Appropriate use of antibiotics is life-saving in neonatal early-onset sepsis (EOS), but overuse of antibiotics is associated with antimicrobial resistance and long-term adverse outcomes.

Tick-borne diseases are a growing global health concern. Despite extensive studies, ill-defined tick-associated pathologies remain with unknown aetiologies. Human immunological responses after tick bite, and inter-individual variations of immune-response phenotypes, are not well characterised.

Rotifers are used as the first feed for marine fish larvae and are grown in large cultures that have high loads of organic matter and heterotrophic bacteria; these bacteria are passed on to the developing fish larvae and can potentially lead to bacterial infections.

Polymicrobial sepsis is associated with worse patient outcomes than monomicrobial sepsis. Routinely used culture-dependent microbiological diagnostic techniques have low sensitivity, often leading to missed identification of all causative organisms.

Preterm infants are at increased risk for invasive neonatal bacterial infections. S. epidermidis, a ubiquitous skin commensal, is a major cause of late-onset neonatal sepsis, particularly in high-resource settings. The vulnerability of preterm infants to serious bacterial infections is commonly attributed to their distinct and developing immune system.

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