Hypothesis

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Abstract
Phospholipids from the group B streptococcal (GBS) cell wall cause pulmonary hypertension in experimental animals. When exposed to penicillin, Streptococcus mutans releases phospholipids immediately. We hypothesize that newborns colonized with GBS receive bacterial phospholipids leading to pulmonary hypertension and respiratory distress, especially in the situation of newborns of penicillin-treated mothers. We examined clinical and epidemiologic data on these relations. We used data from a prospective multicenter GBS study conducted from 1995 to 1999 in which 1674 of 17,690 newborns cultured at 4 sites were colonized with GBS. Our analyses included 1610 colonized newborns > or =32 weeks gestation without early-onset disease. Clinical features were compared between 1003 lightly colonized (GBS positive at < or =2 sites) and 607 heavily colonized (positive at 3 or 4 sites) newborns. The rates of respiratory distress were compared between colonized newborns of penicillin-treated mothers and those of untreated mothers. Of the 1610 colonized newborns, 8.8% had signs of respiratory distress within 48 hours after birth (cases). Oxygen supplementation was used in 60% of the cases, mechanical ventilation was required in 5% and persistent pulmonary hypertension was diagnosed in 2%. Compared with light colonization, heavy colonization increased the rate of respiratory distress 1.73-fold (95% CI, 1.26-2.38), a discharge diagnosis of respiratory disorder 2.02-fold (95% CI, 1.16-3.52), a blood/cerebrospinal fluid obtained for culture 1.54-fold (95% CI, 1.24-1.93) and antibiotic administration after birth 1.87-fold (95% CI, 1.34-2.61). Penicillin use during labor was associated with a 2.62-fold (95% CI, 1.79-3.83) increase in respiratory distress in the colonized newborn. Our findings support the association of neonatal respiratory distress with asymptomatic GBS colonization and with penicillin use during labor. These data require confirmation.