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Group B Streptococcus and Escherichia coli Infections in the Intensive Care Nursery in the Era of Intrapartum Antibiotic Prophylaxis

Bauserman, Melissa S. MD*; Laughon, Matthew M. MD, MPH*; Hornik, Christoph P. MD, MPH†‡; Smith, P. Brian MD, MPH, MHS†‡; Benjamin, Daniel K. Jr. MD, PhD, MPH†‡; Clark, Reese H. MD§; Engmann, Cyril MD*; Cohen-Wolkowiez, Michael MD†‡

Pediatric Infectious Disease Journal: March 2013 - Volume 32 - Issue 3 - p 208–212
doi: 10.1097/INF.0b013e318275058a
Original Studies

Background: Group B Streptococcus (GBS) and Escherichia coli cause serious bacterial infections (SBIs) and are associated with morbidity and mortality in newborn infants. Intrapartum antibiotic prophylaxis reduces early-onset SBIs caused by GBS. The effect of intrapartum antibiotic prophylaxis on late-onset SBIs caused by these organisms is unknown.

Methods: We examined all blood, urine and cerebrospinal fluid culture results from infants admitted from 1997 to 2010 to 322 neonatal intensive care units managed by the Pediatrix Medical Group. We identified infants with positive cultures for GBS or E. coli and compared the incidence of early- and late-onset SBI for each organism in the time period before (1997 to 2001) and after (2002 to 2010) universal intrapartum antibiotic prophylaxis recommendations.

Results: We identified 716,407 infants with cultures, 2520 (0.4%) with cultures positive for GBS and 2476 (0.3%) with cultures positive for E. coli. The incidence of GBS early-onset SBI decreased between 1997 to 2001 and 2002 to 2010 from 3.5 to 2.6 per 1000 admissions, and the incidence for E. coli early-onset SBI remained stable (1.4/1000 admissions in both time periods). Over the same time period, the incidence of GBS late-onset SBI increased from 0.8 to 1.1 per 1000 admissions, and incidence of E. coli late-onset SBI increased from 2.2 to 2.5 per 1000 admissions.

Conclusions: In our cohort, the incidence of GBS early-onset SBI decreased, whereas the incidence of late-onset SBI for E. coli and GBS increased.

From the *School of Medicine, Division of Neonatal-Perinatal Medicine, University of North Carolina, Chapel Hill; Department of Pediatrics, Duke University; Duke Clinical Research Institute, Durham, NC; and §Pediatrix-Obstetrix Center for Research and Education, Sunrise, FL.

Accepted for publication September 18, 2012.

M.M.L. receives support from the US government for his work in pediatric and neonatal clinical pharmacology (Government Contract HHSN267200700051C [PI: D.K.B.] under the Best Pharmaceuticals for Children Act and 1K23HL092225-01). D.K.B. receives support from the US government for his work in pediatric and neonatal clinical pharmacology (1R01HD057956-02, 1R01FD003519-01, 1U10-HD45962-06, 1K24HD058735-01 and Government Contract HHSN267200700051C under the Best Pharmaceuticals for Children Act), the nonprofit organization Thrasher Research Foundation for his work in neonatal candidiasis and from industry for neonatal and pediatric drug development (http://www.dcri.duke.edu/research/coi.jsp). P.B.S. receives support from the US government for his work in pediatric and neonatal pharmacology (NICHD 1K23HD060040-01) and epidemiology (DHHS-1R18AE000028-01). M.C.-W. receives support from the US government for his work in pediatric and neonatal pharmacology (NICHD 1K23HD064814-01) and from industry for neonatal and pediatric drug development (http://www.dcri.duke.edu/research/coi.jsp). The authors have no other funding or conflicts of interest to disclose.

Address for correspondence: P. Brian Smith, MD, MPH, MHS, Department of Pediatrics, Duke Clinical Research Institute, Duke University, PO Box 17969, Durham, NC 27715. E-mail: brian.smith@duke.edu.

© 2013 Lippincott Williams & Wilkins, Inc.