The effect of group B streptococcal meningitis on cerebral prostanoid levels and blood flow regulation in the newborn

The effect of a heat-killed, unencapsulated strain of type III group B streptococcus (GBS), COH 1-13, on cerebral blood flow (CBF) and prostanoid production was investigated in two separate piglet models. In the first model, we examined the temporal profile of changes in CBF and cerebrospinal fluid cytochemistry in response to GBS challenge during a 6 hour study period. Despite marked leukocytosis at 6 hours, GBS did not significantly affect CBF and other cardiovascular parameters, hematology and cerebral prostanoid production. In the second model, we evaluated the early effect of GBS on CBF autoregulatory function and subsequently employed pharmacologic agents to inhibit the effect of GBS. Cerebral perfusion pressure (CPP) was altered by inflating balloon-tipped catheters placed at the aortic root to produce cerebral hypotension and at the descending aorta to produce cerebral hypertension. Piglets inoculated with GBS exhibited a narrow range of CBF autoregulation due to an impairment at the upper limit of CPP, which was prevented by treatment with dexamethasone or ibuprofen. Cerebral prostanoid production did not change significantly with adjustments in CPP between the various treatment groups. We conclude that GBS may impair CBF control without affecting cerebral prostanoid production and may increase the risk of brain damage in neonates with bacterial meningitis