title: Three different strains of heat-killed group B beta-hemolytic streptococcus cause different pulmonary and systemic hemodynamic responses in conscious neonatal lambs.
abstract: Although group B beta-hemolytic streptococcus (GBS) causes pathologic hemodynamic alterations in both human neonates and neonatal animal models of sepsis, little is known about strain-dependent differences in hemodynamic responses to GBS. This study compared pulmonary and systemic hemodynamic dose-response profiles in conscious neonatal lambs with three different strains of heat-killed GBS originally isolated from infected human neonates (group 1: serotype Ib, early-onset sepsis; group 2: serotype Ib, necrotizing enterocolitis; and group 3: serotype III, meningitis). Regression models of hemodynamic responses were characterized after lambs were injected with heat-killed GBS (dose range 0.1-6.0 x 10(9) colony-forming units, i.v.). All three GBS strains caused dose-dependent increases in mean pulmonary arterial pressure and pulmonary and systemic vascular resistances and decreases in cardiac output and heart rate. The GBS strain used in group 1 caused a greater effect on mean pulmonary arterial pressure and systemic vascular resistance than those used in groups 2 and 3 and was the only strain to cause an increase in mean systemic arterial pressure. The GBS strains used in groups 1 and 2 had a greater effect on pulmonary vascular resistance than that used in group 3. No group differences were observed in cardiac output and heart rate responses, which were, however, influenced by age, gender, and duration of postoperative recovery of the lambs. No attenuation or augmentation of hemodynamic effect was observed after sequential doses of 10(9) colony-forming units of GBS given in a single day. This study demonstrates strain-dependent quantitative differences in pulmonary vascular response and qualitative differences in systemic vascular response to heat-killed GBS.
authors: Department of Pediatrics, Wyler Children's Hospital, Pritzker School of Medicine, University of Chicago, Illinois 60637.
authors: R F
authors: RF
authors: Covert
authors: M D
authors: MD
authors: Schreiber
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002302:Cardiac Output; D005260:Female; D006339:Heart Rate; D006439:Hemodynamics; D006976:Hypertension, Pulmonary / Q000209:etiology; D008297:Male; D011652:Pulmonary Circulation; D012756:Sheep; D013045:Species Specificity; D013290:Streptococcal Infections / Q000150:complications / Q000209:etiology / Q000503:physiopathology*; D013292:Streptococcus agalactiae / Q000145:classification / Q000472:pathogenicity