Introduction
ower
gastrointestinal tract is considered as the most likely human reservoir of
group B streptococci (GBS), or Streptococcus
agalactiae with secondary spread to the
genitourinary tract. Pregnant women who are GBS carriers have the potential
to transmit the organism to their newborn infants. There is a spectrum of
maternal and fetal GBS infections ranging from asymptomatic colonization to
sepsis. GBS has been implicated in adverse pregnancy outcomes, including premature
rupture of memb-ranes (ROM), preterm labor, and clinical and sub-clinical
chorioamnionitis.1
Regarding the fact that colonization rates can differ
among ethnic groups and geographic locations,2 this study was
designed to evaluate the incidence of rectovaginal colonization of GBS and its
transmission rate to newborns among pregnant women in Zeinabieh hospital
affiliated to Shiraz University of Medical Sciences in Shiraz, south of Iran.
Maternal and neonatal complications were compared between the GBS carrier and
noncarrier groups.
Materials and Methods
In this study, 2,394 individuals were evaluated for
GBS colonization, which included 1,197 pairs of mothers and newborns.
Rectovaginal cultures were taken from every singleton
pregnant woman with a gestational age greater than 24 weeks who was admitted to
the labor room of Zeinabieh Hospital from April to September 2003. Just after the
delivery, superficial cultures were taken from the skin, ears, mouth, and
throat of every neonate who was born in the study period. The swabs were
incubated in Todd-Hewitt broth media and sub-cultured to blood agar plates
after 18 hours.2 Presence of GBS was confirmed by standard
microbiological studies using catalase, bacitracin, and sodium hippurate
hydrolysis tests.3 Maternal and neonatal complications were compared
between the GBS carrier and noncarrier groups.
The parturients with known GBS colonization received
intrapartum antibiotic prophylaxis (intravenous ampicillin two grams initially,
then one gram every 4 hours until delivery). For those mothers whose culture
results were not ready yet, intrapartum chemoprophylaxis was started on the
basis of clinical risk factors including: preterm labor (labor starting earlier
than 37 weeks of gestation), prolonged ROM (ROM longer than 18 hours), preterm
premature ROM (ROM in a gestational age of less than 37 weeks before labor), having
previous infant with GBS disease, GBS bacteriuria, or intrapartum fever ≥38°C.1
All of the neonates in this study were observed and
evaluated according to the recommendations of Centers for Disease Control and Prevention
(CDC).4 All symptomatic infants had a full diagnostic evaluation,
including complete blood count and differential white cell count, blood
culture, chest radiography, and lumbar puncture. Then, empiric therapy was
initiated with ampicillin and gentamicin according
to the standard protocols.5
The neonates who had a positive blood or cerebrospinal
fluid culture were classified as septic.6 Each case was reviewed by
a neonatologist to confirm the diagnosis.
For statistical analysis, continuous variables were
compared by Student t-test and categorical variables were compared by
Chi-square test and Fisher's exact test. Level of significance was set at P<0.05.
Results
Among the 1197 pregnant women who were screened for
GBS, 110 (9.1%) women had rectovaginal colonization. The mean age of the women
in this study was 24.4±5.4 years ranging from 14 to 45 years. The mean age of
GBS carrier women (group 1), was 24.6±5.2 and for GBS non-carriers (group 2),
it was 24.3±5.4 years (P=0.5). The mean gestational age of neonates at
birth, in group 1 was 32.8±11 weeks compared with 36.2±7.9 in group 2 (P=0.001).
As shown in Table 1 the incidences of preterm labor, prolonged ROM, and preterm
premature ROM were significantly higher among the first group (P=0.001).
|
Table 1. Comparison of
perinatal complications between the GBS carrier (group 1) and non-carrier
(group 2) women.
|
|
Variable
|
Group 1
(n=110)
n (%)
|
Group 2
(n=1087)
n (%)
|
RR (95% CI)
|
P
value
|
|
Preterm labor
|
40
(36.3%)
|
155
(14.3%)
|
2.94 (2.05 – 4.2)
|
0.001
|
|
Preterm
premature ROM (<37 weeks)
|
18
(16.3%)
|
65
(6.0%)
|
2.63 (1.67 – 4.13)
|
0.001
|
|
Prolonged
ROM (>18 hours)
|
7
(6.3%)
|
6
(0.5%)
|
6.19 (3.62 – 10.58)
|
0.001
|
|
Intrapartum
prophylactic antibiotics used
|
34
(30.9%)
|
12
(1.1%)
|
11.19 (8.49 – 14.77)
|
0.001
|
|
Cesarean delivery
|
28 (25.45%)
|
242 (22.26%)
|
1.17 (0.76 – 1.76)
|
0.260
|
|
ROM=rupture
of membranes
|
|
|
|
|
Sixty-six neonates had positive GBS culture, which
showed 60% transmission rate. There was only one out of the 66 neonates with a
positive superficial culture, who was born from a culture negative mother
(0.09%), while the other neonates were born from mothers in group 1 )P=0.001).
Forty-six (3.8%) out of the 1197 women received intrapartum chemoprophylaxis. Of
them 34 women (30.9%) were from group 1 and 12 (1.1%) from group 2 (P=0.001).
Intrapartum antibiotics were started for six women in group 1 due to positive
rectovaginal culture and 40 mothers were treated following the risk-based
strategy.
Seventeen patients from group 1 and 169 women from
group 2 left the study after delivery. So, 93 women in group 1, 918 women in
group 2 and their neonates remained for further evaluations. Early GBS sepsis
developed in one neonate (1.07%) in group 1 whose mother had no risk factor and
did not receive intrapartum chemoprophylaxis. Early-neonatal sepsis developed
in four neonates (0.43%) in group 2. The rate of early-neonatal sepsis was not
statistically different between the two groups (P=0.3).
Postpartum fever developed in two (2.15%) and eight
(0.87%) of the mothers in group 1 and 2, respectively (P=0.2). No mother
with postpartum wound infection was seen in group 1. However, there were seven
cases (0.76%) of postpartum wound infection in group 2 (P=0.5).
Discussion
This study showed that 9.1% of pregnant women who
delivered in this center had rectovaginal colonization with GBS. In most
population based studies, a rate of 10 – 30% has been estimated for GBS
carriage during pregnancy.4 The effect of race and geographical area
on the incidence of GBS may be related to the differences in nutrition,
socioeconomic status, sexually transmitted diseases, or host immunity.5
Transmission of organism to the neonates can occur
vertically or, rarely, by hematogenous dissemination. A neonatal transmission
rate of 60% was calculated in this study. More than 98% of the cases of
early-onset GBS sepsis are the consequence of vertical transmission from the
genital tract of the mother to the infant.7
With an increase in prevention implementation measures
since the mid-1990s, a 70% decline in the rate of early-onset neonatal GBS
disease has been achieved. The screening approach is stated to be 50% more
effective than the risk based approach,8 because, about 30 – 50% of
the cases with early-onset GBS sepsis develop in infants born to women without
risk factors. In this study, there was one neonate who developed early GBS
sepsis and was born from a risk-free mother. These data confirm the advantages
of universal antenatal culture-based screening.
Microbial pathogens have been recovered from the
amniotic cavity in 10 – 15% of the cases with spontaneous preterm labor and in
32 – 35% of women with preterm premature ROM.9,10 This study showed
a strong association between maternal GBS colonization with preterm birth,
prolonged ROM, and preterm premature ROM.
Although universal culture-based screening at 35 to 37
weeks of gestation and intrapartum antibiotic prescriptions have decreased the
rate of early-neonatal GBS sepsis, we believe that prevention of preterm birth
and preterm premature ROM, which are important clinical issues, necessitate the
promotion of new strategies for eradication of GBS carrier states earlier
during pregnancy. Ideally, establishing immunization strategies against GBS
would enable us to prevent the adverse maternal and neonatal effects of GBS
colonization and antimicrobial resistance.
References
1
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FG, Leveno KJ, Bloom SL, Hauth JC, Gilstrap L, Wenstrom KD. Williams
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Campbell JR, Hillier SL, Krohn MA, Ferrieri P, Zaleznik DF,
Baker CJ. Group B streptococcal colonization and serotype-specific immunity in
pregnant women at delivery. Obstet Gynecol. 2000; 96: 498 – 503.
3
ACOG
Committee Opinion. Prevention of early-onset group B streptococcal disease in
newborns. Int J Gynecol Obstet. 2003; 81: 115 – 122.
4
Centers
for Disease Control and Prevention. Prevention of perinatal group B streptococcal
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1 – 22.
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Kenyon SL, Taylor DJ,
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AIM
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