Group B Streptococcus impairs erythrocyte deformability in neonates more than in adults.

Group B beta-haemolytic Streptococcus (GBS) may cause severe septic shock and death in neonates, whereas this is rarely the case in adults. As impaired red blood cell (RBC) deformability might disturb microcirculation in septic shock, the in vitro effects of GBS (1.7 x 10(8) cfu/ml) on RBC deformation (rheoscope) and haemolysis were studied in blood from preterm infants, term neonates, and adults. Furthermore, RBC deformation was studied in term neonates with GBS sepsis. RBC deformation at a shear stress of 4 Pa decreased significantly within 5 minutes of GBS incubation in preterm infants (-13%) and term neonates (-9%). In adults RBC deformation did not change during the first 15 minutes, but decreased significantly after 30 (-10%) and 60 minutes (-13%). In the term infants there was little further decrease in RBC deformation between 5 and 60 minutes of GBS incubation; RBC deformation in preterm infants decreased by 19% after 60 minutes compared with the preincubation values. RBC deformation in septic neonates was significantly decreased at shear stresses of 1, 2, and 3 Pa (-19%, -18%, and -9%). Sixty minutes of incubation of RBC from adults and neonates with GBS and without GBS resulted in haemolysis below 4%. It is concluded that neither neonatal nor adult RBC are haemolysed by GBS. In vitro, neonatal RBC deformability is more impaired than that in adults. This may contribute to the high risk of neonates for compromised microcirculation and circulatory shock as a result of GBS sepsis.

Lipid A binding to neonatal and adult red blood cells.

Lipid A is responsible for the endotoxic activities of gram-negative bacteria. Binding of lipid A (50 micrograms/ml) to RBC was studied using a passive hemolysis test. RBC from adults, cord and venous RBC from full-term infants and RBC from preterm infants were studied. Lipid A sensitized RBC were hemolysed with anti-lipid A and guinea pig complement. Hemolysis was expressed as hemoglobin concentration (absorbance at 546 nm) in the supernatant after centrifugation. 50 micrograms/ml lipid A did not increase spontaneous hemolysis (< 3%) after 60 min of incubation in any of the four groups. The passive hemolysis test did not result in additional hemolysis (5%) of umbilical cord RBC. RBC of preterm infants showed a significant increase in hemolysis (24%) after 60 min of incubation. In RBC of full-term neonates, increased hemolysis (14 and 46%) was detected after 30 and 60 min of incubation. Adult RBC hemolysed stronger (26 and 64%) after 30 and 60 min than neonatal RBC. We conclude that lipid A binds less to neonatal RBC compared to adults.

Effects of group-A streptolysin O on neonatal and adult red blood cell deformability and haemolysis.

Neonates are more susceptible than adults to many Gram-positive and Gram-negative bacterial infections. Whereas group B streptococcus causes life-threatening infections in neonates, group A beta-haemolytic streptococcus infections rarely occur in neonates. To test the hypothesis that group A streptococcus may have different effects on neonatal and adult red blood cells (RBCs), haemolysis and deformability (rheoscope) of RBCs from adults, full-term and pre-term neonates were studied during 60 min incubation with 1 haemolytic unit (HU) mL-1 group A streptolysin O (SLO). SLO incubation of adult RBCs resulted in almost linearly increasing time-dependent haemolysis reaching 82%, whereas haemolysis of neonatal RBCs was below 60% after 1 h. After 60 min SLO incubation, RBC deformation was significantly (P < 0.05) more reduced in adults than in full-term and preterm neonates. An inverse overall relationship (r = 0.68) between SLO-induced haemolysis and RBC deformation was found after 60 min of SLO incubation. We conclude that SLO causes less haemolysis and less impairment of RBC deformation in neonates than in adults. The decreased RBC deformation of unhaemolysed RBC indicates that, before lysis, mechanical RBC membrane properties are altered by SLO.