Abstract
Background
Group B Streptococcus (GBS) colonization is one of the major causes of severe neonatal infections. The study was intended to identify GBS colonization in pregnant women, explore its potential risk factors, and analyze the impact of GBS on outcomes for both mothers and newborns.
Material and Methods
A retrospective research was carried out on pregnant women who had undergone GBS screening and delivered from June 2020 to December 2022. Pregnant women between 35 and 37 weeks of gestation had GBS screening using real-time polymerase chain reaction (RT-PCR). The clinical characteristics and outcomes of mothers and newborns were collected. The risk factors linked to maternal GBS colonization and its impact on adverse outcomes for mothers and neonates were assessed using chi-square and logistic regression analyses. The composite neonatal adverse outcomes included low Apgar scores, neonatal pneumonia, neonatal hyperbilirubinemia, neonatal sepsis, or low birth weight.
Results
Overall, the rate of GBS positivity was 10.63% (551/5183), and the rate of maternal GBS screening was 88.4%. Diabetic pregnant women were more likely to become colonized with GBS. Our research revealed that GBS carriers experienced higher rates of fetal distress and neonatal adverse outcomes than non-GBS carriers. Fetal distress (OR, 1.940; 95% CI, 1.355 to 2.778, P < 0.001), neonatal sepsis (OR, 5.063; 95% CI, 2.536–10.109, P < 0.001), low Apgar scores (OR, 2.097; 95% CI, 1.184–3.715, P = 0.011), neonatal pneumonia (OR, 1.638; 95% CI, 1.039 to 2.582, P = 0.034) and neonatal hyperbilirubinemia (OR, 1.438; 95% CI, 1.080 to 1.915, P = 0.013) were significantly related to maternal GBS colonization. When we used the composite adverse neonatal outcomes as the dependent variable and analyzed the influencing factors, the logistic regression analysis revealed that GBS colonization was still significantly related to an elevated risk of adverse neonatal outcomes (OR = 1.752, 95% CI, 1.389–2.208; P < 0.001).
Conclusions
Diabetes may be a risk factor for maternal GBS colonization. Moreover, in this study, GBS colonization correlated with neonatal adverse outcomes but not with maternal outcomes.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12879-025-10510-8.
Keywords: Group B Streptococcus, Risk factors, Neonatal outcomes
Introduction
Group B Streptococcus (GBS), or Streptococcus agalactiae, is the most common cause of newborn infectious morbidity and mortality worldwide. GBS can colonize the human gastrointestinal tract or lower genital tract asymptomatically, but in other hosts, it is highly pathogenic [1]. The frequency of maternal GBS colonization varies significantly across countries and regions. It was found that the overall rate of maternal GBS colonization worldwide in 85 countries was estimated to be 18%, with regional variation from 11 to 35% [2]. In mainland China, the rate of GBS carriers in pregnant women ranged from 3.7 to 14.52%, the prevalence of invasive neonatal GBS disease was 0.55 to 1.79 per 1000 live births, and the case fatality rate ranged from 6.45 to 7.1% [3]. These studies highlight the high global burden of GBS-related disease and the fact that maternal GBS colonization is common worldwide. Earlier reports have identified a number of risk factors for GBS colonization, such as maternal age, gestational age, the presence of meconium-stained amniotic fluid, a history of preterm delivery, and diabetes mellitus [4–6].
GBS infection mostly occurs through vertical transmission during labor or after membrane rupture, and it can lead to invasive neonatal infections such as pneumonia, septicemia, and meningitis [7]. In addition, GBS colonization can also result in stillbirth and preterm birth but rarely causes maternal sepsis [8–10]. According to the Centers for Disease Control and Prevention (CDC) guidelines [11], all pregnant women are recommended to receive the screening of GBS at 35–37 weeks of gestation, and all GBS-positive pregnant women should be given intrapartum antibiotic prophylaxis (IAP) at the onset of labor or after rupture of membranes. After implementing IAP, the incidence of early-onset GBS disease(EOD) in newborns declined from 1.8 to 0.23 per 1,000 live births from 1990 to 2015 in the United States [12]. Globally, there is still a high burden of GBS-related diseases despite screening and the application of IAP in some countries [1].
In this study, we aimed to retrospectively analyze the risk factors associated with GBS colonization and study the effect of GBS on maternal and neonatal outcomes in women screened for GBS at 35 – 37 weeks of gestation. In addition, we also analyzed the factors that influenced the composite neonatal adverse outcomes to determine whether GBS colonization was associated with it.
Methods
Study population
We conducted a retrospective chart audit of pregnant mothers who gave birth at Taixing People’s Hospital, Jiangsu Province, China, from June 2020 to December 2022. The inclusion criteria were (1) Chinese, (2) complete clinical data, (3) single pregnancy, and (4) no antibiotic treatment within the last three weeks before specimen collection. The exclusion criteria were (1) stillbirths, (2) twins or multiple births, (3) GBS colonization results were unavailable, (4) the screened woman who delivered outside our hospital, and (5) gestational age below 35 weeks.
Sample collection and GBS detection
A combination of the lower vaginal and rectal specimens for GBS colonization status is screened for all women at 35 to 37 weeks of gestation [11]. A sterile cotton swab was used to collect vaginal secretions below one-third of the vagina and rectal secretions from 2–3 cm above the anal sphincter. Then, the swab was placed in a sterile tube and tested within 24 h.
The real-time polymerase chain reaction (RT‒PCR) method was used for the detection of GBS, and the testing was done directly on the specimen collected. GBS DNA was extracted by the GBS DNA Diagnostic Kit (Triplex International Biosciences (China) Co., Ltd.) following the producers’ instructions. Primers and probes used were described in a previous study [13]. PCR was performed on a SLAN-965 PCR system for amplification.
IAP administration
According to the CDC guidelines [11], all pregnant women who tested positive for GBS colonization received IAP at the time of labor onset or after the rupture of membranes during the study period. Most GBS prophylaxis was completed ≥ 4 h before delivery, except for a few GBS-positive pregnant women with a short total stage of labor. IAP agents and dosing were also administered according to the guidelines. GBS-positive women received an initial dose of 5 million units of penicillin intravenously at the time of labor onset, then 2.5 million units intravenously every 4 h until delivery. Cefazolin or clindamycin was administered for penicillin-allergic women. Cefazolin, 2 g initial dose intravenously, 1 g every 8 h until delivery; clindamycin, 900 mg intravenously every 8 h until delivery.
Data collection
Mothers and newborns were followed throughout the entire delivery hospitalization. The medical records were reviewed for maternal age, parity, gestational age, miscarriage, GBS status, mode of delivery, comorbidities, and clinical events during pregnancy, including diabetes ( pregestational diabetes (PGDM) and gestational diabetes mellitus (GDM)), hypertensive disorders of pregnancy (HDP), hypothyroidism, obesity (body mass index ≥ 28 kg/m2), anemia, Hepatitis B virus (HBV) infection and infants born after in vitro fertilization (IVF) procedures. Basic neonatal information, including fetal sex and body weight, was collected. Small for gestational age (SGA) and Large for gestational age (LGA) were divided according to the Chinese neonatal growth reference [14].
The maternal outcomes of the study included premature rupture of membranes (PROM), preterm delivery, chorioamnionitis, meconium-stained amniotic fluid (MSAF), postpartum hemorrhage (PPH). Adverse neonatal outcomes included fetal distress, low Apgar scores, neonatal pneumonia, neonatal hyperbilirubinemia, neonatal sepsis, and low birth weight (LBW), the composite adverse neonatal outcomes are defined as including any of these five items (including low Apgar scores, neonatal pneumonia, neonatal hyperbilirubinemia, neonatal sepsis, or LBW). Adverse neonatal outcomes were followed up within one week after birth.
Important definitions
Diabetes includes PGDM and GDM. All pregnant women who had not yet been diagnosed with diabetes were performing a 75 g oral glucose tolerance test (OGTT) at 24 ∼ 28 weeks of gestation. GDM was diagnosed with a plasma glucose concentration ≥ 5.1 mmol/L (fasting), ≥ 10.0 mmol/L (1 h after glucose intake), or ≥ 8.5 mmol/L (2 h after glucose intake). PGDM was diagnosed with fasting plasma glucose [FPG] > 7.0 mmol/l or 2-h plasma glucose > 11.1 mmol [15].
PROM was defined as spontaneous rupture of membranes before the onset of labor.
Preterm delivery was defined as the range of delivery at > 35 weeks of gestation but < 37 weeks of gestation in this study.
Chorioamnionitis was defined as confirmed by pathological examination of placental tissue after delivery.
Fetal distress was defined as a syndrome that the health and life of the fetus is threatened due to acute or chronic hypoxia, based on abnormal cardiotocograph (CTG).
Low Apgar scores were defined as Apgar score ≤ 7 at 1 min or 5 min.
Neonatal hyperbilirubinemia was defined as total bilirubin levels exceeding the 95th percentile [16].
Neonatal sepsis was defined as neonates had a positive culture, or dependent on clinical diagnosis regardless of culture results, which had hospitalization with at least 1 laboratory criterion and either respiratory distress or at least 2 other clinical criteria [17].
LBW was defined as the birth weight < 2500 g at delivery.
SGA was defined as birth weight < 10th percentile gestational age.
LGA was defined as birth weight > 90th percentile for gestational age.
Statistical analysis
Statistical analysis was conducted using SPSS 26.0 statistical software. For quantitative variables, the Mann‒Whitney U test and Student’s t-test were utilized. For categorical variables, the Chi-square test was applied. Logistic regression was used to compute odds ratios (OR) with 95% confidence intervals (CI). A p-value < 0.05 was considered statistically significant.
Results
Maternal GBS colonization
During the study period, we identified 6100 pregnant women who delivered at our hospital (Fig. 1). A total of 917 women were excluded; stillbirth accounted for 21 cases, and 5 of the women with stillbirth were tested for GBS colonization (all negative). The GBS colonization status of the remaining 16 women with stillbirth was unknown. A total of 5183 mothers and newborns were eligible for inclusion in the study. Overall, 88.4% of mothers received the screening at 35 to 37 weeks of gestation. Among 5183 women, 551 were confirmed positive for GBS, and 4632 were confirmed negative for GBS, with a 10.63% rate of GBS colonization.
Fig. 1.
Study selection flowchart for pregnant women
Risk factors for maternal GBS colonization
Table 1 shows our analysis of the clinical factor distributions in GBS-colonized and non-colonized pregnant women. There were no significant differences between the two groups concerning age (p = 0.253), number of miscarriages (p = 0.263), parity (p = 0.070), or gestational age (p = 0.325). The proportions of pregnant women with the following diseases such as anemia (p = 0.318), HDP (p = 0.284), IVF (p = 0.377), obesity (p = 0.124), HBV infection (p = 0.167) and hypothyroidism (p = 0.307), also were not significantly different. However, the proportion of diabetes was significantly higher in GBS-colonized pregnant women than in non-colonized (p = 0.001). Among the 1159 pregnant women with diabetes, 1103 (95.2%) were GDM, and 56 (4.8%) cases were PGDM, of which 143 cases of GDM and 10 cases of PGDM were GBS positive. The supplementary Table 1 shows that there was no significant difference in the positive rate of GBS colonization between group PGDM and group GDM (p = 0.29).
Table 1.
Risk Factors for GBS Colonization in Late Pregnancy
| Characteristics | GBS colonization | p | ||
|---|---|---|---|---|
| Negative (n = 4632) | Positive (n = 551) | |||
| Age (years) | 0.253 | |||
| < 35 | 4229(91.3%) | 511 (92.74%) | ||
| ≥ 35 | 403 (8.7%) | 40 (7.26%) | ||
| Parity (times) | 0.070 | |||
| 1 | 2706(58.42%) | 344(62.43%) | ||
| ≥ 2 | 1926 (41.58%) | 207 (37.57%) | ||
| Gestational Age | 39.43(38.86,40.29) | 39.43(38.86,40.14) | 0.325 | |
| Miscarriages | 0.263 | |||
| < 3 | 4434(95.73%) | 433(96.73%) | ||
| ≥ 3 | 198 (4.27%) | 18 (3.27%) | ||
| Hypothyroidism | 0.307 | |||
| Yes | 394 (8.51%) | 54 (9.8%) | ||
| No | 4238(91.49%) | 457(90.2%) | ||
| IVF infants | 0.377 | |||
| Yes | 112 (2.42%) | 10 (1.81%) | ||
| No | 4520(97.58%) | 541(98.19%) | ||
| Diabetes | 0.001 | |||
| Yes | 1006 (21.72%) | 153 (27.77%) | ||
| No | 3626 (78.28%) | 398(72.23%) | ||
| Anemia | 0.318 | |||
| Yes | 430 (9.28%) | 44 (7.99%) | ||
| No | 4202 (90.72) | 507 (92.01%) | ||
| Obesity | 0.124 | |||
| Yes | 239 (5.16%) | 37 (6.72%) | ||
| No | 4393 (94.84%) | 514 (93.28%) | ||
| HBV infection | 0.167 | |||
| Yes | 201(4.34%) | 31(5.63%) | ||
| No | 4431(95.66%) | 520(94.37%) | ||
| HDP | 0.284 | |||
| Yes | 224 (4.84%) | 21 (3.81%) | ||
| No | 4408 (95.16%) | 530 (96.19%) | ||
Abbreviations: GBS Group B Streptococcus, IVF In vitro fertilization, HBV Hepatitis B virus, HDP Hypertensive disorders of pregnancy
The association of maternal and neonatal outcomes with GBS colonization
Table 2 presents the incidence of adverse maternal outcomes. There were no significant differences in terms of maternal outcomes, including delivery modes, preterm delivery, PROM, PPH, chorioamnionitis, or MSAF (p > 0.05).
Table 2.
The association between GBS colonization and adverse maternal outcomes
| Factors | GBS colonization | p | ||
|---|---|---|---|---|
| Negative (n = 4632) | Positive (n = 551) | |||
| Modes of Delivery | 0.185 | |||
| VD | 2337(50.45%) | 256(46.46%) | ||
| CS | 2264 (48.88%) | 292 (52.99%) | ||
| Forceps | 31 (0.67%) | 3 (0.54%) | ||
| Preterm delivery | 0.571 | |||
| Yes | 92 (1.99%) | 9 (1.63%) | ||
| No | 4540 (98.01%) | 542 (98.37%) | ||
| PROM | 0.555 | |||
| Yes | 827 (17.85%) | 104 (18.87%) | ||
| No | 3805 (82.15%) | 447(81.13%) | ||
| PPH | 0.22 | |||
| Yes | 90 (1.94%) | 15 (2.72%) | ||
| No | 4542(98.06%) | 536(97.28%) | ||
| Chorioamnionitis | 0.873 | |||
| Yes | 54 (1.17%) | 6 (1.09%) | ||
| No | 4578 (98.83%) | 545 (98.91%) | ||
| MSAF | 0.758 | |||
| Yes | 116 (2.5%) | 15 (2.72%) | ||
| No | 4516 (97.5%) | 536(97.28%) |
Abbreviations: VD Spontaneous vaginal delivery, CS Cesarean section, PROM Premature rupture of membranes, PPH Postpartum hemorrhage, MSAF Meconium-stained amniotic fluid
Table 3 presents the incidence of basic information and adverse neonatal outcomes. No significant differences in fetal sex, weight, or LBW rate were detected between the two groups (p > 0.05). However, the rate of fetal distress, low Apgar scores, neonatal pneumonia, neonatal sepsis, and neonatal hyperbilirubinemia in GBS carriers was significantly greater than that in non-GBS carriers (p < 0.05).
Table 3.
The association between GBS colonization and adverse neonatal outcomes
| Factors | GBS colonization | p | ||
|---|---|---|---|---|
| Negative (n = 4632) | Positive (n = 551) | |||
| Fetal sex | 0.333 | |||
| Male | 2438(52.63%) | 278(50.45%) | ||
| Female | 2194 (47.37%) | 273 (49.55%) | ||
| Weight (grams) | 3509.53 ± 473.76 | 3493.59 ± 527.39 | 0.703 | |
| LBW | 0.372 | |||
| Yes | 48 (1.04%) | 8 (1.45%) | ||
| No | 4584(98.96%) | 543(98.55%) | ||
| Fetal distress | < 0.001 | |||
| Yes | 175 (3.78%) | 39 (7.08%) | ||
| No | 4457 (96.22%) | 512 (92.92%) | ||
| Low Apgar scores | 0.009 | |||
| Yes | 61 (1.32%) | 15 (2.72%) | ||
| No | 4571 (98.68%) | 536(97.28%) | ||
| Neonatal sepsis | < 0.001 | |||
| Yes | 22 (0.47%) | 13 (2.36%) | ||
| No | 4610 (99.53%) | 538 (97.64%) | ||
| Neonatal pneumonia | 0.032 | |||
| Yes | 120 (2.59%) | 23 (4.17%) | ||
| No | 4512(97.41%) | 528(95.83%) | ||
| Neonatal hyperbilirubinemia | 0.013 | |||
| Yes | 369 (7.97%) | 61 (11.07%) | ||
| No | 4263(92.03%) | 490(88.93%) |
Abbreviations: LBW Low birth weight
Table 4 presents the logistic analysis of the associations between GBS colonization and adverse neonatal outcomes. Univariate logistic analysis revealed that fetal distress (OR, 1.940; 95% CI, 1.355 to 2.778, p < 0.001), neonatal sepsis (OR, 5.063; 95% CI, 2.536–10.109, p < 0.001), low Apgar scores (OR, 2.097; 95% CI, 1.184–3.715, p = 0.011), neonatal pneumonia (OR, 1.638; 95% CI, 1.039 to 2.582, p = 0.034) and neonatal hyperbilirubinemia (OR, 1.438; 95% CI, 1.080 to 1.915, p = 0.013) were significantly related to maternal GBS colonization. After adjusting for diabetes as a covariate, a significant association between these adverse neonatal outcomes and GBS colonization remained.
Table 4.
Impact of GBS colonization on different neonatal outcomes
| Crude | Adjust Diabetes | |||||
|---|---|---|---|---|---|---|
| Variable | OR | 95% CI | P-value | OR | 95% CI | P-value |
| Fetal distress | 1.940 | 1.355–2.778 | < 0.001 | 1.963 | 1.370–2.812 | < 0.001 |
| Low Apgar scores | 2.097 | 1.184–3.715 | 0.011 | 2.063 | 1.163–3.659 | 0.013 |
| Neonatal sepsis | 5.063 | 2.536–10.109 | < 0.001 | 5.133 | 2.567–10.264 | < 0.001 |
| Neonatal hyperbilirubinemia | 1.438 | 1.080–1.915 | 0.013 | 1.435 | 1.077–1.911 | 0.014 |
| Neonatal pneumonia | 1.638 | 1.039–2.582 | 0.034 | 1.652 | 1.047–2.606 | 0.031 |
In Table 4, diabetes was the only variable adjusted in the logistic regression
Supplement Tables 2 and 3 show a subgroup analysis of the association between IAP completion or the types of antibiotics used and adverse neonatal outcomes in GBS colonized pregnancies. Among 259 GBS-positive vaginal delivery women, IAP was completed ≥ 4 h before delivery in 207 cases and < 4 h before delivery in 52 cases. The types of antibiotics used in 259 GBS-positive vaginal deliveries were as follows: 237 cases of penicillin (91.51%), 13 cases of cefazolin (5.02%), and 9 cases of clindamycin (3.47%).
Risk factors for adverse neonatal outcomes
This finding prompted us to reanalyze the data, we used the composite adverse neonatal outcomes as the dependent variable and analyzed the influencing factors. As shown in Table 5, there were 693 cases in the group with composite adverse neonatal outcomes and 4490 cases in the group without composite adverse neonatal outcomes. There were statistical differences in GBS colonization (p < 0.001), gestational age (p < 0.001), preterm delivery (p < 0.001), parity (p = 0.012), PROM (p = 0.002), chorioamnionitis (p = 0.001), MSAF (p = 0.006), fetal distress (p < 0.001), abruptio placentae (p < 0.001), SGA (p < 0.001), modes of delivery (p = 0.002), and HDP (p = 0.011). However, no significant differences were found in age (P = 0.062), number of miscarriages (p = 0.16), diabetes (p = 0.491), anemia (p = 0.184), IVF infants (p = 0.321), obesity (p = 0.573), HBV infection (p = 0.997), LGA (p = 0.507) or hypothyroidism (p = 0.477).
Table 5.
Risk factors for the composite adverse neonatal outcomes
| Characteristics | Composite adverse neonatal outcomes | p | ||
|---|---|---|---|---|
| No (n = 4490) | Yes (n = 693) | |||
| GBS colonization | < 0.001 | |||
| Positive | 440 (9.8%) | 111 (16.02%) | ||
| Negative | 4050 (90.2%) | 582 (83.98%) | ||
| Age (years) | 0.062 | |||
| < 35 | 4119 (91.74%) | 621 (89.61%) | ||
| ≥ 35 | 371 (8.26%) | 72 (10.39%) | ||
| Gestational Age | 39.43 (38.86,40.29) | 39.29 (38.43,40) | < 0.001 | |
| Parity (times) | 0.012 | |||
| 1 | 2612 (58.17%) | 438 (63.2%) | ||
| ≥ 2 | 1878 (41.83%) | 255 (36.8%) | ||
| Miscarriages | 0.16 | |||
| < 3 | 4296 (95.68%) | 671 (96.83%) | ||
| ≥ 3 | 194 (4.32%) | 22 (3.17%) | ||
| Preterm delivery | < 0.001 | |||
| Yes | 63 (1.4%) | 38 (5.48%) | ||
| No | 4427 (98.6%) | 655 (94.52%) | ||
| Chorioamnionitis | 0.001 | |||
| Yes | 43 (4.32%) | 17 (4.32%) | ||
| No | 4447 (95.68%) | 676 (95.68%) | ||
| MSAF | 0.006 | |||
| Yes | 103 (2.29%) | 28 (4.04%) | ||
| No | 4387 (97.71%) | 665 (95.96%) | ||
| PROM | 0.002 | |||
| Yes | 777 (17.31%) | 154 (22.22%) | ||
| No | 3713 (82.69%) | 539 (77.78%) | ||
| Modes of Delivery | 0.002 | |||
| VD | 2253 (50.18%) | 340 (49.06%) | ||
| CS | 2215 (49.33%) | 341 (49.21%) | ||
| Forceps | 22 (0.49%) | 12 (1.73%) | ||
| SGA | < 0.001 | |||
| Yes | 113 (2.52%) | 50 (7.22%) | ||
| No | 4377 (97.48%) | 643 (92.78% | ||
| LGA | 0.507 | |||
| Yes | 581 (12.94%) | 96 (13.85%) | ||
| No | 3909 (87.06%) | 597 (86.15%) | ||
| abruptio placentae | < 0.001 | |||
| Yes | 9 (0.2%) | 7 (1.01%) | ||
| No | 4481 (99.8%) | 686 (98.99%) | ||
| Fetal distress | < 0.001 | |||
| Yes | 168 (3.74%) | 46 (6.64%) | ||
| No | 4322 (96.26%) | 647 (93.36%) | ||
| Hypothyroidism | 0.477 | |||
| Yes | 393 (8.75%) | 55 (7.94%) | ||
| No | 4097 (91.25%) | 638 (92.06%) | ||
| IVF infants | 0.321 | |||
| Yes | 102 (2.27%) | 20 (2.89%) | ||
| No | 4388 (97.73%) | 673 (97.11%) | ||
| Diabetes | 0.491 | |||
| Yes | 997 (22.2%) | 162 (23.38%) | ||
| No | 3493 (77.8%) | 531 (76.62%) | ||
| Anemia | 0.184 | |||
| Yes | 420 (9.35%) | 54 (7.79%) | ||
| No | 4070 (90.65%) | 639 (92.21%) | ||
| Obesity | 0.573 | |||
| Yes | 236 (5.26%) | 40 (5.77%) | ||
| No | 4254 (94.74%) | 653 (94.23%) | ||
| HBV infection | ||||
| Positive | 201 (4.48%) | 31 (4.47%) | 0.997 | |
| Negative | 4289 (95.52%) | 662 (95.53%) | ||
| HDP | 0.011 | |||
| Yes | 199 (4.43%) | 46 (6.64%) | ||
| No | 4291 (95.57%) | 647 (93.36%) | ||
Abbreviations: GBS Group B Streptococcus, MSAF Meconium-stained amniotic fluid, PROM Premature rupture of membranes, VD Spontaneous vaginal delivery, CS Cesarean section, IVF In vitro fertilization, HBV Hepatitis B virus, HDP Hypertensive disorders of pregnancy, SGA Small for gestational age, LGA Large for gestational age
Then, we analyzed the risk factors of the composite adverse neonatal outcomes by using a logistic regression model. In Table 6, multivariate logistic regression analysis indicated that the risk of adverse neonatal outcomes increased with decreasing gestational age (OR = 0.745, 95% CI, 0.682–0.813, p < 0.001) and with the occurrence of GBS colonization (OR = 1.752, 95% CI, 1.389–2.208, p < 0.001), chorioamnionitis (OR = 2.281, 95% CI, 1.243–4.185, p = 0.008), MSAF (OR = 1.910, 95% CI, 1.218–2.995, p = 0.005), fetal distress (OR = 1.507, 95% CI, 1.038–2.186, p = 0.031), SGA (OR = 2.962, 95% CI, 2.074–4.230, p < 0.001), abruptio placentae (OR = 3.263, 95% CI, 1.130–9.423, p = 0.029) and forceps delivery (OR = 3.877, 95% CI, 1.867–8.052, p < 0.001) and multiparity decreased the risk of adverse neonatal outcomes (OR = 0.808, 95% CI, 0.676–0.965, p = 0.019). The effects of other factors, including PROM, preterm delivery, cesarean section, and HDP, on neonatal adverse outcomes were not significant (p > 0.05).
Table 6.
Logistic regression models of the risk factors for the composite adverse neonatal outcomes
| Univariate logistic analysis | Multivariate logistic analysis | |||||
|---|---|---|---|---|---|---|
| Variable | OR | 95% CI | P-value | m_ OR | m_95% CI | m_ P-value |
| GBS | 1.756 | 1.401–2.200 | < 0.001 | 1.752 | 1.389–2.208 | < 0.001 |
| Gestational age | 0.735 | 0.683–0.790 | < 0.001 | 0.745 | 0.682–0.813 | < 0.001 |
| Parity (times ≥ 2) | 0.810 | 0.686–0.955 | 0.012 | 0.808 | 0.676–0.965 | 0.019 |
| Preterm delivery | 4.077 | 2.703–6.148 | < 0.001 | 1.620 | 0.991–2.648 | 0.055 |
| Chorioamnionitis | 2.601 | 1.475–4.587 | 0.001 | 2.281 | 1.243–4.185 | 0.008 |
| MSAF | 1.793 | 1.172–2.745 | 0.007 | 1.910 | 1.218–2.995 | 0.005 |
| Fetal distress | 1.829 | 1.306–2.561 | < 0.001 | 1.507 | 1.038–2.186 | 0.031 |
| PROM | 1.365 | 1.123–1.659 | 0.002 | 1.109 | 0.898–1.368 | 0.337 |
| HDP | 1.533 | 1.101–2.135 | 0.011 | 1.197 | 0.840–1.707 | 0.319 |
| SGA | 3.012 | 2.137–4.245 | < 0.001 | 2.962 | 2.074–4.230 | < 0.001 |
| Abruptio placentae | 5.080 | 1.886–13.686 | < 0.001 | 3.263 | 1.130–9.423 | 0.029 |
| CS | 1.020 | 0.868–1.199 | 0.808 | 0.930 | 0.780–1.108 | 0.416 |
| Forceps | 3.614 | 1.722–7.371 | < 0.001 | 3.877 | 1.867–8.052 | < 0.001 |
Adjusted variables consisted of GBS, gestational age, parity, preterm delivery, Chorioamnionitis, MSAF, fetal distress, PROM, HDP, SGA, abruptio placentae, CS, and forceps delivery
Abbreviations: GBS Group B Streptococcus, MSAF Meconium-stained amniotic fluid, PROM Premature rupture of membranes, HDP Hypertensive disorders of pregnancy, SGA Small for gestational age, LGA Large for gestational age
Discussion
Our study revealed a relatively high GBS screening rate (88.4%) for pregnant women in Taixing, East China. Unexpected preterm delivery was the main reason for not undergoing GBS screening. In this study, the rate of GBS carriers was 10.63%, which was greater than the 8.1% overall rate of maternal GBS colonization in China reported [18], and greater than that reported in a previous study in Jiangsu, which used two detection methods (8.7% by PCR vs 3.5% by culture) [19]. In our study, RT-PCR was used for GBS screening. PCR has the advantages of being rapid, simple, and low-cost, and higher sensitivity and repeatability than culture [20]. Our study revealed that the rate of GBS positivity is relatively high, so it is necessary to conduct universal GBS screening for pregnant women.
We found that pregnant diabetic women were more likely to have GBS colonization than nondiabetic pregnant women, which was consistent with some previous findings [21, 22]. Further analysis showed that there was no statistical difference in the positive rate of GBS between the PGDM group and the GDM group, which suggested that there was no significant difference in susceptibility to GBS colonization between the two groups. However, another study showed that diabetes does not change the incidence of GBS colonization during pregnancy [23]. Glucose is the main carbon source for GBS [24], so the diabetic environment could promote GBS metabolism and proliferation and may enhance GBS virulence factor production [25]. A recent study in a murine pregnancy model confirmed that gestational diabetes had enhanced fetal GBS infection and worsened neonatal outcomes by disrupting immunity system and the vaginal microbiota [26], which supports our observations. These findings suggest that obstetricians should pay attention to GBS screening in diabetic pregnant women, since it may reduce the occurrence of GBS colonization by monitoring blood glucose in diabetic women. In addition, diabetic mothers may benefit from a vaccine to reduce GBS-related pregnancy complications [27]. In contrast, there was no significant association between maternal age, gestational age, parity, miscarriages, obesity or anemia, and GBS carriers in late pregnancy (P > 0.05), which is inconsistent with previous reports [22, 28].
Previous studies have presented that maternal GBS carriers can result in a variety of adverse pregnancy outcomes. For instance, Dai Wei et al. reported that GBS colonization was correlated with intrauterine infection, fetal distress, PPH, PROM, and postpartum infection [29]. Liu YX et al. indicated that GBS colonization was related to premature birth, fetal distress, PROM and LBW[30]. Jie Ren et al. revealed that pregnant women with GBS carriers had a greater rate of PROM and histological chorioamnionitis[31]. Tano Sho et al. reported that vaginal GBS colonization was closely associated with preterm birth[32]. However, Mavenyengwa RT et al. did not find a statistical difference between GBS colonization and adverse perinatal outcomes[33]. Our study shows that fetal distress was observed to be significantly associated with maternal GBS colonization, the reason for this is not clear. GBS colonization may lead to poor fetal environment in utero, may cause infection, and so on. GBS colonization might be an indirect factor but not a direct factor of fetal distress.
The present study showed that the incidence of the adverse neonatal outcomes, including low Apgar scores, neonatal sepsis, neonatal hyperbilirubinemia, and neonatal pneumonia, were significantly increased by maternal GBS colonization. Multivariate logistic analysis revealed that GBS colonization was still significantly related to an increased risk of the composite adverse neonatal outcomes. Our results were consistent with those in previous study. Dai Wei et al. reported that the GBS colonization was positively related to neonatal pneumonia and sepsis [29]. Ren et al. reported that GBS colonization was significantly correlated with neonatal pathological jaundice and low birth weight infants [31]. But no significant differences in LBW rate was detected in our study, this may be influenced by the range of preterm delivery in this study. The inhalation and swallowing of vaginal secretions cause GBS bacteria to adhere to the mucous membranes of the respiratory and gastrointestinal tract of newborns. Subsequently, bacteria invade the bloodstream and usually lead to pneumonia or sepsis at birth or shortly after birth [34]. Physiological hyperbilirubinemia may inhibit the growth of pathogenic GBS, and elevated serum bilirubin may have a protective effect on early-onset neonatal sepsis [35]. Despite all GBS-positive pregnant women were applied with IAP in this study, GBS colonization remains a risk factor for adverse neonatal outcomes. However, there were no serious infection complications or deaths in this study. Supplementary Table 2 shows no significant difference in the rates of adverse neonatal outcomes between treated ≥ 4 h and treated < 4 h before delivery. In this study, the insignificant results between fully and incompletely treated patients were due to the small number of incompletely treated patients. So, IAP is still the most effective treatment strategy in the prevention of early-onset GBS infection.
Our research has several limitations that should be taken into account. First, the range of GBS screening in this study was 35–37 weeks of gestation and was not conducted for pregnant women under 35 weeks. Therefore, it is not fully clear whether preterm delivery and low birth weight are associated with maternal GBS colonization. Figure 1 shows that most pregnant women with stillbirths were not tested for GBS colonization. This may create a bias in whether GBS colonization is associated with preterm delivery and stillbirths. Second, we used PCR for GBS screening but did not pre-enriched beforehand, so the rate of GBS carriers in the study may introduce some bias concerning its actual value. Although PCR has a greater sensitivity than traditional culture, it cannot evaluate antibiotic sensitivity in GBS-colonized women. Finally, the lack of neonatal cord blood gas analysis data is regrettable. There are some possible factors of adverse neonatal outcomes that we have not considered, such as the length of labor, the prolonged rupture of membranes, and so on. This was a single-center study, and we lacked long-term follow-up results for newborns.
Conclusions
Our data have revealed that the rate of GBS positivity was 10.63%, and the GBS screening rate was 88.4%. Diabetes may be a risk factor for maternal GBS colonization, and obstetricians should pay attention to GBS screening in diabetic pregnant women. In this study, GBS colonization may have adverse effects on fetal and neonatal outcomes but not on maternal outcomes.
Supplementary Information
Acknowledgements
Not applicable.
Abbreviations
- GBS
Group B Streptococcus
- IAP
Intrapartum antibiotic prophylaxis
- RT-PCR
Real-time polymerase chain reaction
- CDC
Centers for Disease Control and Prevention
- PROM
Premature rupture of membranes
- HDP
Hypertensive disorders of pregnancy
- HBV
Hepatitis B virus
- IVF
In vitro fertilization
- PPH
Postpartum hemorrhage
- LBW
Low birth weight
- MSAF
Meconium-stained amniotic fluid
- SGA
Small for gestational age
- LGA
Large for gestational age
Authors’ contributions
GXJ contributed to the conception of the study, data's collection and analysis, drafting and editing of paper. JLF: data analysis. LHL, XLW, ZLZ, ZYJ and ML took part in the design of the work, data analysis and interpretation, and revising of the article.
Funding
This study was supported by The Research Fund Project of Taixing People’s Hospital (try2116).
Data availability
The datasets used during the current study are available from the corresponding author on reasonable request.
Declarations
Ethics approval and consent to participate
The study was approved by the Ethical Board of Taixing People’s Hospital. As this is an observational retrospective study, no interventions were done to these women.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Change history
2/6/2025
The order of the corresponding email addresses was swapped.
Contributor Information
Ziyan Jiang, Email: zyjiangchm@163.com.
Min Liu, Email: 15052883356@163.com.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The datasets used during the current study are available from the corresponding author on reasonable request.