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Group B streptococci (GBS) are the leading cause of bacterial meningitis in newborns, resulting in significant mortality and a high incidence of major neurological sequelae. Although GBS are presumed to gain access to the central nervous system following bacteremic spread, the mechanism(s) by which the organisms enter the subarachnoid space is unknown. Using human brain microvascular endothelial cells (BMEC), which alone constitute the blood-brain barrier, we have developed an in vitro model system to study early stages in the pathogenesis of GBS meningitis. Three GBS strains belonging to serotype III, the predominant meningeal isolate, were shown to enter(“invade”) BMEC, as demonstrated by protection from killing with antibiotics restricted to the extracellular media. Using a bacterial inoculum of 105 cfu per tissue culture well (≈5 GBS per BMEC), 1-5% of GBS had invaded the endothelial monolayer by 2 hrs. GBS were shown to survive intracellularly, without appreciable replication, for up to 20 hrs. Electron microscopy revealed intracellular GBS within membrane bound vacuoles, suggesting GBS entered BMEC by stimulating their own endocytic uptake. Dose-dependent inhibition of GBS invasion by cytochalasin D shows this process requires actin microfilaments of the host cytoskeleton. An isogenic nonencapsulated transposon mutant invaded BMEC twice as efficiently as the parent strain, suggesting the polysaccharide capsule masks GBS surface molecules involved in promoting cell entry. We hypothesize that GBS invasion of human BMEC is a primary event in translocation of the organism across the blood-brain barrier to produce meningitis. We are using our in vitro model to screen for GBS mutants deficinet in BMEC invasion, so that we may begin to characterize virulence factors required for penetration of the bacteria into the central nervous system.

INVASION OF BRAIN MICROVASCULAR ENDOTHELIAL CELLS BY GROUP B STREPTOCOCCI• 1332