NEONATAL GROUP B STREPTOCOCCAL (GBS) PNEUMONIA: AN IMMUNE COMPLEX DISEASE?

Abstract

GBS pneumonia in the newborn is often fatal despite early treatment. Three infants with GBS pneumonia and sepsis were studied to define the role of immunoglobulins (Ig) and complement (C) in the development of this disease. Cord blood samples from 2 of the 3 infants had been obtained and were found to contain antibodies to GBS, but normal C levels. Serum C levels were obtained from all 3 infants during illness, at which time C3, C4 and Factor B (B) were depressed. Necropsy lung specimens from the 3 infants were studied by light microscopy. PAS positive hyaline membranes were observed in alveoli and gram stains showed gram positive cocci. Lung specimens were also snap-frozen for immunofluorescence (IF) with antisera to Ig, C and fibrin. Deposits of IgG, C3, C4 and fibrin were observed in the alveolar hyaline membranes. IF staining for GBS organisms and B was distributed throughout the lung parenchyma. IF for igM was negative in all patients. Specimens taken from three infants who died from other causes did not show these patterns of staining. C3, C4 and B IF staining in lungs associated with serum C depression in patients with GBS pneumonia suggests activation of classical and alternative C pathways in this illness. In addition, the presence of IgG, C3 and C4 in the alveolar membranes suggests that maternal IgG may contribute to immune complex deposition as part of the pathogenesis of this disease, and further suggests that treatment other than antibiotics should be considered.