Capsular type-specific
polysaccharide is thought to be an important pathogenetic factor in Group B streptococcus (GBS)
sepsis. To determine the effects of capsular type-specific
polysaccharide on GBS-induced hemodynamic 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 the larger
capsule strain by transposon insertion mutagenesis. The smaller
capsule strain and
capsule-deficient mutant caused similar elevations in mean pulmonary artery pressure and pulmonary vascular resistance index and reductions in cardiac index. The larger
capsule strain caused moderate
pulmonary hypertension, but this response was smaller than for the other two GBS strains. Further comparisons in responses between the large
capsule strain and its
capsule-deficient mutant were then performed using unanesthetized piglets. The mutant caused significantly greater
pulmonary hypertension and arterial plasma
thromboxane B2 levels than the large
capsule strain. The
pulmonary hypertension induced by both strains was reversed by
dazmegrel, a
thromboxane A2 synthase inhibitor. These results suggest that (1) capsular type-specific
polysaccharide is not an essential component in the generation of acute hemodynamic responses; (2) expression of large amounts of capsular type-specific
polysaccharide on the organism surface partially inhibits GBS-induced
pulmonary hypertension; and (3) the inhibition of the pulmonary responses is due to reduced
thromboxane A2 release.(ABSTRACT TRUNCATED AT 250 WORDS)