Isogenic Group B Streptococci Devoid of Capsular Polysaccharide or β-Hemolysin: Pulmonary Hemodynamic and Gas Exchange Effects during Bacteremia in Piglets

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Abstract
Group B β-hemolytic streptococcus (GBS) causes thromboxane (Tx)-associated pulmonary hypertension and hypoxemia in neonatal animals and human infants. The components of GBS that induce these features of sepsis are incompletely characterized. The capsular polysaccharide has been implicated based on the effects of GBS extracts. We used isogenic mutants of a parent GBS strain (COH 31 r/s) devoid of capsular polysaccharide or β- hemolysin to determine if these components caused the acute features of GBS bacteremia. In neonatal piglets, we observed a similar increase in pulmonary vascular resistance (PVR, mm Hg/L/min) during a 1 h infusion at 5 × 108 colony-forming unit/kg/h of COH 31 r/s (n = 5, 11.6 ± 1.4 to 67.1 ± 17.9), an isogenic GBS mutant devoid of type III CP (n = 5, 12.5 ± 1.4 to 56.9 ± 5.0), and an isogenic GBS mutant devoid of β-hemolysin (n = 4, 11.0 ± 1.9 to 51.9 ± 7.9). All three GBS strains caused increases in blood TxB2 levels, mild arterial hypoxemia, mild reduction in mixed venous PO2 and a 30-40% reduction in cardiac output after a 1 h infusion. The Tx-synthase inhibitor, dazmegrel, completely reversed pulmonary hypertension, and partially reversed arterial hypoxemia and TxB2 levels to baseline values for all GBS strains. In six additional piglets, infusion of polystyrene beads of similar size to GBS at a dose of 5 × 108 beads/kg/h caused no changes in gas exchange or blood TxB2 levels, but a mild increase in PVR (13.3 ± 2.0 to 17.7 ± 3.5). This suggests a nonspecific response to circulating particulates is not the major cause of the acute features of GBS bacteremia in piglets. We conclude that type III capsular polysaccharide and β-hemolysin are not essential for type III GBS to cause acute Tx-associated pulmonary hypertension and hypoxemia in piglets.