Comparison of early-onset neonatal sepsis caused by Escherichia coli and group B Streptococcus.
ABSTRACT The purpose of this study was to compare maternal characteristics and neonatal morbidity and mortality rates that are associated with early-onset neonatal sepsis that is caused by group B Streptococcus and Escherichia coli.
This was a retrospective review of newborn infants with a positive blood culture (and/or cerebrospinal fluid) that was positive for either E coli or group B Streptococcus during the first week of life. Data were abstracted from maternal and neonatal medical records.
Among 28,659 deliveries during the study period, 102 episodes of early-onset neonatal sepsis were identified, 61 of which were caused by group B Streptococcus and 41 of which were caused by E coli. E coli sepsis cases had a lower birth weight, a higher percentage with 5-minute Apgar score <7, and a longer stay in the hospital neonatal intensive care unit and required mechanical ventilation more frequently. Death after early-onset neonatal sepsis with E coli was also more frequent.
Early-onset sepsis with E coli is associated with more morbidity and a higher mortality rate compared with early-onset group B Streptococcus.
[show abstract] [hide abstract]
ABSTRACT: Despite substantial progress in prevention of perinatal group B streptococcal (GBS) disease since the 1990s, GBS remains the leading cause of early-onset neonatal sepsis in the United States. In 1996, CDC, in collaboration with relevant professional societies, published guidelines for the prevention of perinatal group B streptococcal disease (CDC. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR 1996;45[No. RR-7]); those guidelines were updated and republished in 2002 (CDC. Prevention of perinatal group B streptococcal disease: revised guidelines from CDC. MMWR 2002;51[No. RR-11]). In June 2009, a meeting of clinical and public health representatives was held to reevaluate prevention strategies on the basis of data collected after the issuance of the 2002 guidelines. This report presents CDC's updated guidelines, which have been endorsed by the American College of Obstetricians and Gynecologists, the American Academy of Pediatrics, the American College of Nurse-Midwives, the American Academy of Family Physicians, and the American Society for Microbiology. The recommendations were made on the basis of available evidence when such evidence was sufficient and on expert opinion when available evidence was insufficient. The key changes in the 2010 guidelines include the following: • expanded recommendations on laboratory methods for the identification of GBS, • clarification of the colony-count threshold required for reporting GBS detected in the urine of pregnant women, • updated algorithms for GBS screening and intrapartum chemoprophylaxis for women with preterm labor or preterm premature rupture of membranes, • a change in the recommended dose of penicillin-G for chemoprophylaxis, • updated prophylaxis regimens for women with penicillin allergy, and • a revised algorithm for management of newborns with respect to risk for early-onset GBS disease. Universal screening at 35-37 weeks' gestation for maternal GBS colonization and use of intrapartum antibiotic prophylaxis has resulted in substantial reductions in the burden of early-onset GBS disease among newborns. Although early-onset GBS disease has become relatively uncommon in recent years, the rates of maternal GBS colonization (and therefore the risk for early-onset GBS disease in the absence of intrapartum antibiotic prophylaxis) remain unchanged since the 1970s. Continued efforts are needed to sustain and improve on the progress achieved in the prevention of GBS disease. There also is a need to monitor for potential adverse consequences of intrapartum antibiotic prophylaxis (e.g., emergence of bacterial antimicrobial resistance or increased incidence or severity of non-GBS neonatal pathogens). In the absence of a licensed GBS vaccine, universal screening and intrapartum antibiotic prophylaxis continue to be the cornerstones of early-onset GBS disease prevention.MMWR. Recommendations and reports: Morbidity and mortality weekly report. Recommendations and reports / Centers for Disease Control 11/2010; 59(RR-10):1-36.
Article: No increase in rates of early-onset neonatal sepsis by non-group B Streptococcus or ampicillin-resistant organisms.[show abstract] [hide abstract]
ABSTRACT: We assessed the impact of a risk-based approach to group B Streptococcus (GBS) prophylaxis on the rates of early-onset neonatal sepsis (EONS). A retrospective cohort study of neonates born at a tertiary-care hospital from 1990 to 1996 was performed. Cases of EONS were identified among neonates born in a period without GBS prophylaxis (1990-1992) and compared with those born in a period with GBS prophylaxis (1993-1996). The antibiotic susceptibility data on each organism isolated in the blood culture were obtained. In the period without prophylaxis, 99 cases of EONS were identified among 25,934 neonates for a rate of 3.8 per 1000 births. In the period with prophylaxis, 90 cases of EONS occurred among 34,262 neonates for a rate of 2.6 per 1000. The rate of GBS-EONS significantly decreased between the 2 periods (from 1.9 to 1.1, P =.01). There was a trend toward a decrease in the rate of EONS caused by non-GBS gram-positive organisms (from 1.2 to 0.7, P =.06). There was no significant increase in the rate of EONS caused by gram-negative or ampicillin-resistant organisms. A risk-based approach to GBS prophylaxis reduced the incidence of GBS-EONS at a tertiary-care hospital. This decrease was not accompanied by an increase in the incidence of EONS by non-GBS or ampicillin-resistant organisms.American Journal of Obstetrics and Gynecology 11/2001; 185(4):854-8. · 3.47 Impact Factor
Article: Early-onset sepsis in very low birth weight neonates: A report from the National Institute of Child Health and Human Development Neonatal Research Network[show abstract] [hide abstract]
ABSTRACT: OBJECTIVE: Early-onset sepsis (occurring within 72 hours of birth) is included in the differential diagnosis of most very low birth weight (VLBW) neonates. To determine the current incidence of early-onset sepsis, risk factors for disease, and the impact of early-onset sepsis on subsequent hospital course, we studied a cohort of 7861 VLBW neonates (401 to 1500 gm) admitted to the 12 National Institute of Child Health and Human Development (NICHD) Neonatal Research Network centers during a 32-month period (1991-1993). METHODS: The NICHD Neonatal Research Network maintains a prospectively collected registry on all VLBW neonates born or cared for at participating centers. Data from this registry were analyzed retrospectively. RESULTS: Blood culture-proven early-onset sepsis was uncommon, occurring in only 1.9% of VLBW neonates. Group B streptococcus was the most frequent pathogen associated with early-onset sepsis (31%), followed by Escherichia coli (16%) and Haemophilus influenzae (12%). Decreasing gestational age was associated with increased rates of infection. Antibiotic therapy for suspected sepsis is frequently initiated at birth in VLBW neonates. Almost half of the infants in this cohort were considered to have clinical sepsis and continued to receive antibiotics for 5 or more days, despite a negative blood culture result in 98% of cases. These findings underscore the difficulty of ruling out sepsis in the symptomatic immature neonate and the special concern for culture-negative clinical sepsis in the face of maternal antibiotic use. Neonates with early-onset sepsis were significantly more likely to have subsequent comorbidities, including severe intraventricular hemorrhage, patent ductus arteriosus, and prolonged assisted ventilation. Although 26% of VLBW neonates with early-onset sepsis died, only 4% of the 950 deaths that occurred in the first 72 hours of life were attributed to infection. For those infants discharged alive, early-onset sepsis was associated with a significantly prolonged hospital stay (86 vs 69 days; p <0.02). CONCLUSIONS: Early-onset sepsis remains an important but uncommon problem among VLBW preterm infants. Improved diagnostic strategies are needed to enable the clinician to distinguish between the infected and the uninfected VLBW neonate with symptoms and to target continued antibiotic therapy to those who are truly infected. (J PEDIATR 1996;129:72-80)Journal of Pediatrics 08/1996; · 4.11 Impact Factor
Comparison of early-onset neonatal sepsis caused by
Escherichia coli and group B Streptococcus
Kathleen Mayor-Lynn, MD,aVı ´ctor Hugo Gonza ´lez-Quintero, MD, MPH,a,*
Mary Jo O’Sullivan, MD,aAlan I. Hartstein, MD,b,cSonia Roger, MT,c
Madeline Tamayo, RNc
Department of Obstetrics and Gynecology, Division of Maternal-Fetal Medicine,aand Department of Medicine,
Division of Infectious Diseases,bUniversity of Miami School of Medicine; and Department of Infection Control,
Jackson Health System, Miami, Flac
Received for publication August 31, 2004; revised October 10, 2004; accepted December 7, 2004
Objective: The purpose of this study was to compare maternal characteristics and neonatal
morbidity and mortality rates that are associated with early-onset neonatal sepsis that is caused
by group B Streptococcus and Escherichia coli.
Study design: This was a retrospective review of newborn infants with a positive blood culture
(and/or cerebrospinal fluid) that was positive for either E coli or group B Streptococcus during the
first week of life. Data were abstracted from maternal and neonatal medical records.
Results: Among 28,659 deliveries during the study period, 102 episodes of early-onset neonatal
sepsis were identified, 61 of which were caused by group B Streptococcus and 41 of which were
caused by E coli. E coli sepsis cases had a lower birth weight, a higher percentage with 5-minute
Apgar score !7, and a longer stay in the hospital neonatal intensive care unit and required
mechanical ventilation more frequently. Death after early-onset neonatal sepsis with E coli was
also more frequent.
Conclusion: Early-onset sepsis with E coli is associated with more morbidity and a higher
mortality rate compared with early-onset group B Streptococcus.
? 2005 Elsevier Inc. All rights reserved.
Among very low birth weight infants, the greatest
lethal risk is extreme prematurity. Early-onset sepsis
(during the first week of life) fortunately is an infrequent
complication, which in the past was most frequently
caused by group B Streptococcus (GBS).
After the development and implementation of con-
sensus guidelines for GBS prophylaxis in 1996,1both the
frequency of and death from early-onset sepsis that is
caused by this bacteria has decreased markedly. The
initial guidelines recommended both a screen and a risk-
based approach for intrapartum antibiotic prophylaxis.
The modified 2002 guidelines recommend universal
screening by vaginal and rectal GBS cultures for all
pregnant women at 35 to 37 weeks of gestation.2In
Presented at the 52nd Annual Clinical Meeting of the American
College of Obstetricians and Gynecologists, Philadelphia, Pa, May 2-5,
* Reprint requests: Vı´ctor H. Gonza ´ lez-Quintero, MD, MPH,
University of Miami, PO Box 016960 (R-136), Miami, FL 33101.
0002-9378/$ - see front matter ? 2005 Elsevier Inc. All rights reserved.
American Journal of Obstetrics and Gynecology (2005) 192, 1437–9
2003, the overall disease incidence was 0.32, which
represented a 34% decline in incidence since 2000 to
Intrapartum antibiotic prophylaxis has been shown
to be most effective to prevent GBS early-onset sepsis,
regardless of which of the aforementioned strategies is
used to prevent this disease. The widespread use of
antibiotics has led to concern over the possible selection
for other organisms and/or increased antibiotic resis-
tance. There is a concern that early-onset sepsis could be
caused by other more virulent organisms in the future.4,5
Although Gram-positive organisms (most commonly
GBS) were responsible most infections between 1991
and 1993, Gram-negative organisms (most commonly
Escherichia coli) became the most frequent cause of
early-onset sepsis between 1998 and 2000.5,6The objec-
tives of this study were to compare maternal character-
istics and neonatal morbidity and mortality rates that
were associated with early-onset neonatal sepsis caused
by E coli and GBS.
This was a retrospective study of early-onset neonatal
sepsis cases caused by either E coli or GBS at Jackson
Memorial Hospital between January 1, 1998, and June
30, 2002. Approval from the University of Miami’s
Institutional Review Board was obtained. Early-onset
sepsis was defined as a positive blood or cerebrospinal
fluid culture that was obtained between birth and the
end of day 6 of life. Analyzed maternal variables
included demographics, the number of vaginal exami-
nations, the duration of rupture of membranes, the use
of fetal scalp electrodes and/or intrauterine pressure
catheters, the development of chorioamnionitis, and
the gestational age at delivery. Neonatal variables
included birth weight, Apgar scores at 5 minutes,
length of stay, number of days in the neonatal intensive
care unit, and neonatal morbidities (specifically septi-
cemia, pneumonia, intraventricular hemorrhage, sei-
Statistical analyses were performed with SPSS for
Windows (version 10.0; SPSS Inc, Chicago, Ill). De-
scriptive statistics were obtained for all variables.
Continuous variables were analyzed with 2- sample
t-test, and dichotomous variables were analyzed by
There were 28,659 live births during the study period.
One hundred two cases of early-onset neonatal sepsis
were caused by GBS (61 cases) or E coli (41 cases). No
significant differences were noted with respect to mater-
nal demographics. There was no perceptible increase in
the number of cases of E coli–induced early-onset sepsis
during the era of risk-based GBS prophylaxis. A
comparison of intrapartum factors between cases of
early-onset GBS and E coli sepsis in the neonate is
shown in the Table I.
Of the most common morbidities that are associated
with both E coli and GBS early-onset neonatal sepsis,
only septicemia and mechanical ventilation were signif-
icantly higher in the E coli group (Table II). Most
importantly, the neonatal mortality rate was increased
Maternal and neonatal variables among cases with early-onset GBS and E coli sepsis
VariableGBS cases (n = 61) E coli cases (n = 41)P value
Vaginal examination (n)*
Duration of rupture of membranes (hr)*
Chorioamnionitis (% affected)
Fetal scalp electrode (% used)
Gestational age at delivery (wk)*
Birth weight (g)
5-Minute Apgar score !7 (%)
Length of stay (d)*
Neonatal intensive care unit (d)*
4.8 G 31
17.5 G 59.6
37.0 G 4.7
3151.7 G 1032.5
18.2 G 24.4
8.8 G 25.4
1.7 G 1.4
1.3 G 5.2
32.6 G 6.2
2055.9 G 1163.3
43.0 G 53.5
32.0 G 52.9
NS, Not significant.
* Data are given as mean G SD.
early-onset sepsis caused by E coli and GBS
Selected neonatal morbidities among cases with
E coli cases
NS, Not significant.
1438Mayor-Lynn et al
among neonates who were diagnosed with E coli sepsis
compared with GBS sepsis (19% vs 7%; P ! .007).
Early-onset sepsis is a rare, but potentially lethal
problem, that affects primarily neonates of low birth
weight.1Vertical transmission of GBS during labor or
delivery may result in an invasive infection in the
newborn infant during the first week of life, which
results in approximately 1600 cases and 80 deaths
annually, according to the latest report from the Centers
for Disease Control.3The incidence of invasive GBS
infections among pregnant women in the United States
decreased by 21% from 1993 to 1998 to an incidence of
0.23 per 1000 live births,7with a further decrease in
2003.3The emergence of other pathogens and an
increase in the incidence of early-onset sepsis caused
by E coli during or after this interval have been
reported.4However, we found no increase in the number
of cases of early-onset E coli sepsis at our institution.
There were a number of differences that were noted
between cases of E coli– and GBS-induced early-onset
sepsis, which were related mostly to intrapartum events
in the GBS cases. Infants who received a diagnosis of
E coli sepsis were born at an earlier gestational age and
of lower birth weights and had a higher percentage of
Apgar scores of !7 at 5 minutes than those with GBS
sepsis. It follows then that these infants had a longer
length of stay and a greater number of days spent in the
neonatal intensive care unit. The 2 morbidities that were
significantly higher in the E coli group were septicemia
and a need for mechanical ventilation. More impor-
tantly, the neonatal mortality rate was significantly
higher with E coli sepsis, compared with GBS sepsis.
The increased mortality rate in the E coli sepsis group
may be confounded by the higher prematurity rate
among the affected neonates in our study group.
In conclusion, E coli sepsis occurred in a more
premature patient population in comparison to GBS
and was associated with higher morbidity and mortality
rates. On-going surveillance of infecting organisms and
antimicrobial prophylaxis that is directed at GBS must
1. Centers for Disease Control and Prevention. Prevention of perinatal
group B streptococcal disease: a public health perspective. MMWR
Recomm Rep 1996;45:1-24.
2. Schrag S, Gorwitz R, Fultz-Butts K, Schuchat A. Prevention of
perinatal group B streptococcal disease: revised guidelines from
CDC. MMWR Recomm Rep 2002;51:1-22.
3. Centers for Disease Control and Prevention. Diminishing racial
disparities in early-onset neonatal group B streptococcal disease:
United States, 2000-2003. Morb Mortal Wkly Rep MMWR
4. Stoll BJ, Hansen N, Fanaroff A, Wright LL, Carlo W, Ehrenkranz
RA, et al. Changes in pathogens causing early-onset sepsis in very-
low-birth-weight infants. N Engl J Med 2002;347:240-7.
5. Chen KT, Tuomala RE, Cohen AP, Eichenwald EC, Lieberman E.
No increase in rates of early-onset neonatal sepsis by non-group
B Streptococcus or ampicillin-resistant organisms. Am J Obstet
6. Stoll BJ, Gordon T, Korones SB, Shankaran S, Tyson JE, Bauer
CR, et al. Early-onset sepsis in very-low-birth-weight neonates:
a report from the National Institute of Child Health and Human
Development Neonatal Research Network. J Pediatr 1996;129:
7. Schrag SJ, Zywicki S, Farley MM, Reingold AL, Harrison LH,
Lefkowitz LB, et al. Group B streptococcal disease in the era of
intrapartum antibiotic prophylaxis. N Engl J Med 2000;342:15-20.
Mayor-Lynn et al 1439