CAPSULAR TYPE-SPECIFIC POLYSACCHARIDE PARTIALLY INHIBITS GROUP-B STREPTOCOCCUS-INDUCED PULMONARY-HYPERTENSION

Capsular type-specific polysaccharide is thought to be an important pa thogenetic factor in Group B streptococcus (GBS) sepsis. To determine the effects of capsular type-specific polysaccharide on GBS-induced he modynamic responses, anesthetized infant piglets were infused for 3 h With three related GBS Type lb strains that express different amounts of capsular type-specific polysaccharide. A larger capsule strain and a smaller capsule strain were isolated from an infected infant and its mother, respectively. A capsule-deficient mutant was then made from t he larger capsule strain by transposon insertion mutagenesis. The smal ler capsule strain and capsule-deficient mutant caused similar elevati ons in mean pulmonary artery pressure and pulmonary vascular resistanc e index and reductions in cardiac index. The larger capsule strain cau sed moderate pulmonary hypertension, but this response was smaller tha n for the other two GBS strains. Further comparisons in responses betw een the large capsule strain and its capsule-deficient mutant were the n performed using unanesthetized piglets. The mutant caused significan tly greater pulmonary hypertension and arterial plasma thromboxane B2 levels than the large capsule strain. The pulmonary hypertension induc ed by both strains was reversed by dazmegrel, a thromboxane A2 synthas e inhibitor. These results suggest that (1) capsular type-specific pol ysaccharide is not an essential component in the generation of acute h emodynamic responses; (2) expression of large amounts of capsular type -specific polysaccharide on the organism surface partially inhibits GB S-induced pulmonary hypertension; and (3) the inhibition of the pulmon ary responses is due to reduced thromboxane A2 release. Variations in capsular type-specific polysaccharide expression may play a role in th e manifestations and severity of GBS sepsis in infants.