Understanding the new group B streptococcal guidelines


On November 19, 2010, the Centers for Disease Control and Prevention released updated guidelines for the prevention of neonatal group B streptococcal GBS infections, which replace the 2002 CDC guidelines.

Background: Limitations of the 2002 guidelines

For the most part, national screening for maternal GBS colonization and the use of intrapartum chemoprophylaxis has been an obstetrical success story but there are limitations to current prevention strategies.

However, success has not been universal. Only 63% of women delivering preterm with unknown GBS status receive prophylaxis.1,5 Moreover, between 2003 and 2006 GBS EOD rates increased significantly among term African American infants from 0.53 to 0.86 per 1,000 (P=.005) compared with Caucasian infants whose rates remained unchanged (0.26 to 0.29 per 1,000; P=.64).6 The cause of this racial disparity remains largely unexplained.

Another concern is that only 14% of penicillin-allergic women receive the appropriate alternative agent, cefazolin. In 1 study, 70% of penicillin allergic women at low risk for anaphylaxis inappropriately received clindamycin.5 This is a major concern because the CDC estimates that resistance among invasive GBS isolates ranges from 25% to 32% for erythromycin and from 13% to 20% for clindamycin.1 Worse, clindamycin and erythromycin susceptibility testing is rarely performed at all despite recommendations that such testing be conducted on all isolates from penicillin-allergic women.1 Moreover, when susceptibility testing is performed, labs often do not use the correct method (ie, D-zone testing) despite the fact that inducible clindamycin resistance can occur when routine susceptibility tests indicate sensitivity.1

The 2002 CDC guidelines did not specify a colony-count threshold for defining GBS bacteriuria.4 They also did not address the utility of PCR-based nucleic acid amplification tests (NAAT) that appear to have nearly comparable sensitivity to culture-based methods and are being increasingly employed.

Another unknown is the optimal duration of intrapartum chemoprophylaxis. EOD is thought to arise from in utero aspiration of GBS-contaminated amniotic fluid, while fetal exposure during passage through the vagina more often results in benign colonization.1

This raises the question of whether therapeutic levels of penicillin are needed in fetal serum or amniotic fluid to confer protection against EOD. Assuming the latter, in 1992 the American Academy of Pediatrics (AAP) made a recommendation for at least 4 hours of intrapartum antibiotic prophylaxis despite a lack of evidence.7

More recent studies have shown therapeutic levels of ampicillin are achieved in amniotic fluid within 5 minutes after maternal infusion8; thus, it is likely that penicillin achieves comparable results. Moreover, this arbitrary threshold has meant that infants of women delivered within 4 hours of initial treatment were subject to potentially invasive diagnostic testing.

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