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Despite the continued development of new antibiotics with increased ranges of activity and spiralling prices, sepsis-either acquired from the mother intrapartum or acquired nosocomially from invasive procedures-remains a serious problem in preterm infants. All neonatologists must have witnessed infants dying of septicaemia despite treatment with an antibiotic to which the organism was sensitive in vitro. The problem is largely one of host defence. Infants born before 32 weeks' gestation are seriously immunodeficient with cord blood concentrations of IgG being less than half those found in babies born at full term. Concentrations of IgA and IgM are negligible in cord blood. In addition, very preterm infants have reduced complement factors, opsonic activity, polymorphonuclear chemotaxis, and are liable to exhaust their neutrophil storage pools. ' As IgG is acquired across the placenta, and the infant produces virtually none of its own for months, serum IgG concentrations decline from birth for six to eight weeks reaching 1-2 g/l between 2 and 4 months of age; these low concentrations must be of functional importances. Opsonisation of important capsulated perinatal pathogens such as group B streptococi, Escherichia coli and Staphylococcus epidermidis is facilitated by specific antibody.2 Release of marrow neutrophils is accelerated by type specific antibody,3 which also speeds up migration of neutrophils into the infected tissue.4 Accepting that infants born at less than 32 weeks' gestation have clinically important immmunoglobulin deficiency, can they be effectively and safely treated with replacements? What preparations are suitable? What size of dose and number of doses are required? What is the evidence of efficacy?

Treatment of sepsis with IgG in very low birthweight infants.