Background and aims Complement and IgG are humoral opsonins. We theorised platelets might be opsonins in neonates. We proposed that persistent neonatal bloodstream infections and thrombocytopenia might provide proof of the concept if there was high rather than low mean platelet volumes [MPVs] during infections (i.e., platelets consumed during phagocytosis).

Methods From 2008 to 2013, all neonates >3 days of age and that had positive blood cultures underwent a record review. Infants were included if they had ≥ 2 positive blood cultures and had platelet counts <10⁵ per mm³. Exclusion criteria were necrotizing enterocolitis, coagulopathy, organ or catheter-related thrombosis or endocarditis.

Results Among 77 positive blood cultures, two methicillin-resistant Staphylococcus aureus [MRSA] and two Candida bloodstream infections persisted and had thrombocytopenia. The four infants had initial elevated MPVs that declined to normal only with the resolution of infection. Blood smears had no aggregates of platelet, microbes and phagocytes. One MRSA and two Candida infections with associated thrombocytopenia occurred in extremely preterm infants; they had no elevation in MPVs and expired quickly. A review of all 77 infants with late-onset sepsis revealed the infecting microbe and extreme prematurity modulated the kinetics of MPVs during infection.

Conclusions Two pathogens that likely resisted opsonization with complement and IgG were associated with continuing neonatal sepsis and thrombocytopenia. High MPVs suggests defective platelet production was not responsible for thrombocytopenia, but macrophages and neutrophils likely removed platelet-microbe-aggregates from the blood. These findings offer indirect proof that platelets may act as opsonins during neonatal phagocytosis.