PEDIATRICS Vol. 105 No. 1 January 2000, pp. 21-26
Risk Factors and Opportunities for Prevention of Early-onset Neonatal Sepsis: A Multicenter Case-Control Study
Received Apr 20, 1999; accepted Jun 8, 1999.
,
,,
From the * Centers for Disease Control and Prevention, Atlanta,
Georgia; Medical College of Virginia of Virginia Commonwealth
University, Richmond, Virginia; § University of Tennessee at Memphis,
Regional Medical Center, Memphis, Tennessee; University of Puerto
Rico, San Juan, Puerto Rico; ¶ University of Miami Medical
Center-Jackson Memorial Hospital, Miami, Florida; # University of
Mississippi Medical Center, Jackson, Mississippi; ** Broward General
Medical Center, Fort Lauderdale, Florida; and the Department of
Pediatrics, Emory University School of Medicine, Atlanta, Georgia.
Background. Early-onset group B streptococcal (GBS) prevention efforts are based on targeted use of intrapartum antibiotic prophylaxis (IAP); applicability of these prevention efforts to infections caused by other organisms is not clear.
Methods. Multicenter surveillance during 1995 to 1996 for culture-confirmed, early-onset sepsis in an aggregate of 52 406 births; matched case-control study of risk factors for GBS and other sepsis.
Results. Early-onset disease occurred in 188 infants (3.5 cases per 1000 live births). GBS (1.4 cases per 1000 births) and
Escherichia coli (0.6 cases per 1000 births) caused most
infections. GBS sepsis less often occurred in preterm deliveries
compared with other sepsis. Compared with gestation-matched
controls without documented sepsis, GBS disease was associated with
intrapartum fever (matched OR, 4.1; CI, 1.2-13.4) and frequent vaginal
exams (matched OR, 2.9; CI, 1.1-8.0). An obstetric risk
factor
preterm delivery, intrapartum fever, or membrane rupture 
18
hourswas found in 49% of GBS cases and 79% of other sepsis. IAP had
an adjusted efficacy of 68.2% against any early-onset sepsis.
Ampicillin resistance was evident in 69% of E coli
infections. No deaths occurred among susceptible E coli
infections, whereas 41% of ampicillin-resistant E coli
infections were fatal. Ninety-one percent of infants who developed
ampicillin-resistant E coli infections were preterm, and
59% of these infants were born to mothers who had received IAP.
Conclusions. Either prenatal GBS screening or a risk-based strategy could potentially prevent a substantial portion of GBS cases. Sepsis caused by other organisms is more often a disease of prematurity. IAP seemed efficacious against early-onset sepsis. However, the severity of ampicillin-resistant E coli sepsis and its occurrence after maternal antibiotics suggest caution regarding use of ampicillin instead of penicillin for GBS prophylaxis. Key words: group B streptococcal, neonatal, sepsis, meningitis, Escherichia coli, antibiotic resistance, streptococcal, risk factors.
CiteULike 
Connotea 
Del.icio.us 
Digg 
Facebook 
Reddit 
Technorati 
Twitter What's this?
This article has been cited by other articles:
|
|
 |
|
  P T Heath, G F Balfour, H Tighe, N Q Verlander, T L Lamagni, A Efstratiou, and on behalf of the HPA GBS Working Group Group B streptococcal disease in infants: a case control study Arch. Dis. Child., September 1, 2009; 94(9): 674 - 680. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. J. Bizzarro, L.-M. Dembry, R. S. Baltimore, and P. G. Gallagher Changing Patterns in Neonatal Escherichia coli Sepsis and Ampicillin Resistance in the Era of Intrapartum Antibiotic Prophylaxis Pediatrics, April 1, 2008; 121(4): 689 - 696. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. J. Schrag, J. L. Hadler, K. E. Arnold, P. Martell-Cleary, A. Reingold, and A. Schuchat Risk Factors for Invasive, Early-Onset Escherichia coli Infections in the Era of Widespread Intrapartum Antibiotic Use Pediatrics, August 1, 2006; 118(2): 570 - 576. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S Vergnano, M Sharland, P Kazembe, C Mwansambo, and P T Heath Neonatal sepsis: an international perspective Arch. Dis. Child. Fetal Neonatal Ed., May 1, 2005; 90(3): F220 - f224. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Seepersaud, S. B. Hanniffy, P. Mayne, P. Sizer, R. Le Page, and J. M. Wells Characterization of a Novel Leucine-Rich Repeat Protein Antigen from Group B Streptococci That Elicits Protective Immunity Infect. Immun., March 1, 2005; 73(3): 1671 - 1683. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. E. Adair, L. Kowalsky, H. Quon, D. Ma, J. Stoffman, A. McGeer, S. Robertson, M. Mucenski, and H. D. Davies Risk factors for early-onset group B streptococcal disease in neonates: a population-based case-control study Can. Med. Assoc. J., August 5, 2003; 169(3): 198 - 203. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Velaphi, J. D. Siegel, G. D. Wendel Jr, N. Cushion, W. M. Eid, and P. J. Sanchez Early-Onset Group B Streptococcal Infection After a Combined Maternal and Neonatal Group B Streptococcal Chemoprophylaxis Strategy Pediatrics, March 1, 2003; 111(3): 541 - 547. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Facklam What Happened to the Streptococci: Overview of Taxonomic and Nomenclature Changes Clin. Microbiol. Rev., October 1, 2002; 15(4): 613 - 630. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. B. Hyde, T. M. Hilger, A. Reingold, M. M. Farley, K. L. O'Brien, and A. Schuchat Trends in Incidence and Antimicrobial Resistance of Early-Onset Sepsis: Population-Based Surveillance in San Francisco and Atlanta Pediatrics, October 1, 2002; 110(4): 690 - 695. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. Stoll, N. Hansen, A. A. Fanaroff, L. L. Wright, W. A. Carlo, R. A. Ehrenkranz, J. A. Lemons, E. F. Donovan, A. R. Stark, J. E. Tyson, et al. Changes in Pathogens Causing Early-Onset Sepsis in Very-Low-Birth-Weight Infants N. Engl. J. Med., July 25, 2002; 347(4): 240 - 247. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Berner, B. Furll, F. Stelter, J. Drose, H.-P. Muller, and C. Schutt Elevated Levels of Lipopolysaccharide-Binding Protein and Soluble CD14 in Plasma in Neonatal Early-Onset Sepsis Clin. Vaccine Immunol., March 1, 2002; 9(2): 440 - 445. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Intrapartum Antibiotic Prophylaxis: Less Disease, But More Resistance Journal Watch Infectious Diseases, March 1, 2000; 2000(301): 4 - 4. [Full Text]
|
|
