Clinical characteristics and risk factors for imaging abnormalities in pediatric Group B Streptococcus meningitis: a multicenter study

Introduction

Group B Streptococcus (GBS), also known as Streptococcus agalactiae, is a β-hemolytic, gram-positive bacterium. Although it is a commensal organism in the vaginal and intestinal microbiota of healthy adults, it has the potential to transition into a highly invasive pathogen. Vertical perinatal transmission of GBS can result in life-threatening infections, including pneumonia, sepsis, and meningitis (1,2). GBS meningitis primarily affects neonates and young infants. In a nationwide multicenter epidemiological study on pediatric bacterial meningitis (BM), GBS meningitis constituted 21.5% (170/790) of cases, with 85.9% manifesting in neonates aged 0–3 months (3). Due to the young age of onset and atypical clinical presentations, delayed diagnosis and treatment often complicate disease progression. The incidence of cranial imaging abnormalities in pediatric BM patients is high, commonly occurring 1–2 weeks after disease onset. These imaging abnormalities are strongly associated with treatment challenges, long-term neurological sequelae, and poor prognoses (4). Therefore, early prediction of imaging abnormalities is critical for clinical monitoring, therapeutic planning, and prognostic assessment.

Studies on predictors of imaging abnormalities in GBS meningitis patients are rare, and most predictors are derived from single-center studies with limited sample sizes (5). To address this gap, we conducted a multicenter retrospective study. Clinical data were collected from 327 hospitalized children under 15 years of age with confirmed diagnoses of GBS meningitis who were treated between 2019 and 2020 at 12 hospitals in China, and extending through 2024 at Children’s Hospital of Zhejiang University School of Medicine. The aim of this study was to examine the clinical and laboratory parameters associated with imaging abnormalities in patients with GBS meningitis, identify independent risk factors of these imaging abnormalities, and provide an evidence-based framework for the early identification of high-risk patients. We present this article in accordance with the STROBE reporting checklist (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-381/rc).

Methods

Subjects

This retrospective study analyzed children under 15 years of age who were diagnosed with GBS meningitis between 2019 and 2020 at 12 hospitals across China, and extending through 2024 at Children’s Hospital of Zhejiang University School of Medicine. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Ethics Committee of the Children’s Hospital affiliated with Zhejiang University School of Medicine (approval No. 2019-IRB-094), and individual consent for this retrospective analysis was waived. All participating hospitals were informed of and agreed to the study.

Inclusion criteria: all patients met the diagnostic criteria for GBS meningitis—(I) the presence of clinical symptoms/signs of meningitis, including fever or hypothermia, altered mental status or consciousness, feeding difficulties or vomiting, seizures, bulging fontanelle, neck stiffness, or focal neurological deficits; (II) cerebrospinal fluid (CSF) examination showing at least one of the following: turbid appearance, elevated white blood cell (WBC) count (>100 cells/µL), mild elevation in WBC count (10–100 cells/µL) with increased total protein (>1.0 g/L), or decreased glucose (GLU) concentration (<2.2 mmol/L); (III) positive identification of GBS in CSF and/or blood cultures (6,7).

Exclusion criteria: (I) patients with coexisting intracranial infection, such as viral encephalitis, tuberculous meningitis, or cryptococcal meningitis; (II) patients with other central nervous system diseases, such as aseptic meningitis, autoimmune encephalitis, brain tumors, or postcranial surgery conditions.

Data collection

Electronic medical records from all participating hospitals were reviewed for discharge diagnoses of “acute bacterial meningitis”, “central nervous system infection”, “intracranial infection”, or “meningitis”. Patients meeting the diagnostic criteria for GBS meningitis were identified. The data collected included the patient’s age, sex, admission and discharge dates, clinical characteristics, laboratory findings, cranial imaging results, and clinical outcomes at discharge.

Patients grouping

All patients with suspected BM should undergo early cranial imaging examination, including cranial ultrasound/computed tomography (CT)/magnetic resonance imaging (MRI). If the patient exhibits persistent fever, altered consciousness, increased intracranial pressure, or unexplained neurological symptoms/signs despite appropriate antibiotic therapy and intracranial pressure-lowering treatment, repeat cranial imaging should be promptly performed. And a final imaging evaluation was conducted before discharge. Cranial imaging abnormalities are defined as the presence of at least one of the following findings on cranial ultrasound/CT/MRI reports: subdural effusion/empyema, intracranial hemorrhage, ventricular dilatation/fullness/hydrocephalus, cerebral softening, abnormal parenchymal signals, ventriculitis, cerebral infarction, cerebral atrophy, or brain abscess. Patients were stratified into two groups based on cranial imaging findings: the imaging abnormalities group and the non-imaging abnormalities group. Patients were divided into three groups based on discharge outcomes. (I) Clinically cured group: complete resolution of symptoms and signs, normalization of peripheral blood counts, and CSF parameters (leucocyte count <20 cells/µL, predominantly mononuclear, protein <1 g/L, GLU >2.0 mmol/L) with no imaging abnormalities or sequelae. (II) Improvement group: resolution of clinical symptoms and signs, negative CSF cultures, normalization of blood infection markers, mild abnormalities in CSF parameters, and no progression of cranial imaging findings at discharge. (III) Adverse outcome group: patients with neurological sequelae, treatment withdrawal, discharge against medical advice, and mortality (3,7).

Statistical analysis

The data were analyzed via SPSS 23.0. Nonnormally distributed quantitative data were expressed as medians (P25, P75) and were compared via the Mann-Whitney U test. Categorical data were expressed as cases (%) and were compared via the χ² test or Fisher’s exact test. Missing values were handled using complete-case analysis (listwise deletion) to eliminate potential bias from missing data. We compared demographic characteristics (age, sex, season of onset), clinical features (preceding/concurrent infections, underlying diseases, length of hospital stay, hospitalization costs), laboratory parameters (initial and final CSF results, CSF and blood culture results), and outcome measures (neurological sequelae, disease outcomes) between the two groups. Variables showing P<0.05 in univariate analysis were all included in the subsequent multivariate logistic regression model to calculate odds ratios with 95% confidence intervals. Statistical significance was set at P<0.05.

Results

General information and clinical characteristics

Among the 327 children with GBS meningitis, 48.9% (160 patients) were male. The median age was 29 days [interquartile range (IQR): 15–57 days]. The age distribution was as follows: <1 month (51.1%, n=167), 1–3 months (39.4%, n=129), and >3 months (9.5%, n=31). Among 132 patients at the Children’s Hospital of Zhejiang University School of Medicine, 11 (8.3%) were preterm infants. Based on the age at disease onset, cases were categorized as early-onset disease (EOD) (<7 days; 18.2%, 24/132), late-onset disease (LOD) (7 days to 3 months; 73.5%, 97/132), and very LOD (VLOD) (>3 months; 8.3%, 11/132). Preceding or concurrent infections were present in 83.4% (273/327) of the patients, with sepsis without a clear infection site (defined as cases meeting sepsis diagnostic criteria without an identifiable primary infection focus) being the most common (51.9%, n=170). Underlying diseases were identified in 29.7% (97/327) of the patients, predominantly chronic/congenital heart disease (15%, n=49) (Table 1 provides additional details).

Laboratory findings

Initial CSF examination revealed the following: median WBC count was 1,072×10⁶/L (IQR: 220–3,453.5 ×10⁶/L), with 76% (246/324) of cases exceeding 100×10⁶/L and 46.6% (151/324) surpassing 1,000×10⁶/L. Median GLU concentration was 1.56 mmol/L (IQR: 0.61–2.46 mmol/L), with 29.5% (91/308) of patients showing critically low levels (<1 mmol/L). Median protein was 2,200 mg/L (IQR: 1,281.5–3,333.33 mg/L), and 28.1% (85/302) had levels >3,000 mg/L. However, 4% (13/324) of patients had normal WBC counts (<10×10⁶/L), 27.2% (84/308) showed no significant decrease in GLU concentration (>2.2 mmol/L), and 22.8% (69/302) exhibited no marked elevation in protein levels (<1,000 mg/L).

Before discharge, CSF parameters improved significantly: The final WBC count had a median of 18 (IQR: 6–36.25) ×10⁶/L, with 51% (156/306) having counts <20×10⁶/L and 6.9% (21/306) having counts >100×10⁶/L. The final GLU concentration had a median of 2.24 (IQR: 1.97–2.49) mmol/L, with all patients achieving ≥1 mmol/L and 25% (77/308) having levels <2 mmol/L. The final protein concentration had a median of 780 (IQR: 511–1,140) mg/L, with 30.6% (94/307) having levels >1,000 mg/L.

Culture findings

A total of 34.9% (114/327) had positive CSF cultures only, 29.1% (95/327) had positive blood cultures only, and 36.1% (118/327) had both CSF and blood cultures positive. Before discharge, both blood and CSF cultures were negative.

Imaging findings

Among 327 patients, cranial imaging results (ultrasound, CT, and MRI) were available for 322 patients. Four patients died from rapid disease progression before imaging, and imaging data for one patient were unavailable. Cranial imaging abnormalities were observed in 65.2% (210/322) of the patient, primarily subdural effusion and/or empyema (30.4%, 98/322), followed by intracranial hemorrhage (22.0%, 71/322), ventricular dilation/fullness/hydrocephalus (21.1%, 68/322), cerebral softening (13.4%, 43/322), abnormal parenchymal signals (11.2%, 36/322), ventriculitis (2.8%, 9/322), cerebral infarction (2.5%, 8/322), cerebral atrophy (1.9%, 6/322), and brain abscess (1.2%, 4/322). Multiple abnormalities were present in 27.6% of the patients (89/322).

Univariate analysis revealed that patients with imaging abnormalities exhibited lower CSF-GLU concentrations, higher initial protein levels, higher rates of simultaneous positive CSF and blood cultures, longer hospital stays, and higher hospitalization costs (all P<0.05; Table 2).

Multivariate logistic regression identified two independent risk factors for cranial imaging abnormalities (Table 3): initial CSF-GLU concentration [odds ratio (OR) =0.7, 95% confidence interval (CI): 0.557–0.880], concurrent positivity of CSF and blood cultures (OR =1.945, 95% CI: 1.131–3.346).

The receiver operating characteristic (ROC) curve analysis of initial CSF-GLU for predicting imaging abnormalities yielded an area under the curve (AUC) of 0.626, with a cutoff value of 1.57 mmol/L, sensitivity of 64.5%, and specificity of 58.2% (Figure 1).

Figure 1 ROC curve of initial CSF glucose for predicting imaging abnormalities in GBS meningitis. ROC curve analysis showing the predictive performance of initial CSF glucose level for the occurrence of imaging abnormalities. The AUC is 0.626, with an optimal cutoff value of 1.57 mmol/L (sensitivity: 0.645; specificity: 0.582). AUC, area under the curve; CSF, cerebrospinal fluid; GBS, Group B Streptococcus; GLU, glucose; ROC, receiver operating characteristic.

Treatment and outcomes

Patients with GBS meningitis have prolonged hospital stays and high medical costs. Among 327 GBS meningitis patients, the median hospital stay was 32 days (IQR: 22–47 days) with a median hospitalization cost of 42,121.5 CNY (IQR: 25,120–65,423.3 CNY), and patients with imaging abnormalities demonstrated significantly longer stays (35 vs. 29, P<0.05) and higher expenses (50,541.1 vs. 31476.8, P<0.05).

Clinical outcomes included 15.6% (n=51) achieving clinical cure, 71.6% (n=234) showing improvement, and 12.8% (n=42) experiencing adverse outcomes, including mortality (1.8%, n=6), discharge against medical advice (2.4%, n=8), epilepsy (3.4%, 11/320), motor dysfunction (1.9%, 6/320), and hearing impairment (4.0%, 13/325). Patients with imaging abnormalities demonstrated significantly lower cure rates (0% vs. 44.6%, P<0.05), higher incidence of adverse outcomes (16.2% vs. 3.6%, P<0.05), and increased rates of neurological sequelae (7.6% vs. 0.9%, P<0.05).

Discussion

In this study, 90.5% of the children were under 3 months of age at admission, a demographic characteristic consistent with previous studies, suggesting that GBS meningitis is more prevalent in infants under 90 days of age (8). GBS-EOD typically presents as sepsis or pneumonia, with meningitis being relatively rare, whereas LOD commonly manifests as bacteremia and meningitis (9). Our findings demonstrate a predominance of LOD cases (73.5%, 97/132). The higher LOD incidence results from multiple factors, including horizontal transmission through hospital exposure or non-maternal caregivers, in addition to vertical transmission. Although prenatal GBS screening and intrapartum antibiotic prophylaxis (IAP) effectively reduce EOD incidence, they minimally impact LOD, highlighting the need for alternative prevention strategies. Maternal GBS vaccination may prevent GBS infections in mothers and neonates by transferring protective antibodies through the placenta, reducing risks of EOD and LOD disease. Despite evidence of safety and efficacy, no GBS vaccine has been licensed, indicating key barriers to clinical development (10,11).

CSF analysis and culture are essential for diagnosing suspected BM in children. CSF culture positivity remains the diagnostic gold standard, although positivity rates are low due to early antibiotic use or low bacterial counts. In this study, the initial CSF findings were consistent with those of previous studies (12): elevated WBC counts, protein levels, and decreased GLU concentrations. However, 4.0% of the patients had WBC counts <10×10⁶/L, 27.2% had GLU concentrations ≥2.2 mmol/L, and 22.8% had protein levels ≤1,000 mg/L without significant abnormalities, which may be attributed to early CSF testing or prior antibiotic use. The vast majority of patients demonstrated significant improvement in final CSF inflammatory markers before discharge. However, mild abnormalities were commonly observed prior to antimicrobial discontinuation: 49.0% had WBC counts ≥20×10⁶/L, 25% showed GLU concentrations <2 mmol/L, and 30.6% exhibited protein levels >1,000 mg/L. Notably, the recurrence rate remained low (3.1%), potentially attributable to the gradual resolution of inflammation and persistent host immune responses. Significant differences were observed between patients with and without imaging abnormalities in terms of simultaneous positive CSF and blood cultures, lower CSF GLU concentrations, and higher initial micro total protein concentration (P<0.05). Elevated CSF protein concentrations correlate with more severe immune and inflammatory responses, indicating greater parenchymal damage to the brain (13). Therefore, pathogen culture and CSF testing should be promptly conducted prior to antibiotic use. These factors are significantly associated with neuroimaging abnormalities in children with GBS meningitis. Normal early culture and CSF cell results do not completely exclude BM.

The high incidence of imaging abnormalities in GBS meningitis patients highlights the importance of timely diagnostic evaluation. In this study, 65.2% of patients had imaging abnormalities, primarily subdural effusion/abscess (30.4%, 98/322) and intracranial hemorrhage (22.0%, 71/322), which is consistent with the findings of Zhang et al. (14). The young age of the patients may have contributed to the greater incidence. The formation of subdural effusion could result from inflammatory changes in vascular permeability, allowing proteins and cells to enter the subdural space and obstruct CSF reabsorption (15). Arfi et al. suggested that, unlike pneumococcal meningitis, GBS meningitis is characterized mainly by thin exudates and a propensity to involve intracranial blood vessels (16). Kralik et al. reported that neonates with GBS meningitis are more likely to develop cerebral infarction (17). In this study, 24.5% patients (79/322) developed cerebrovascular abnormalities, with intracranial hemorrhage predominating (n=71) over cerebral infarction (n=8), potentially attributable to GBS-specific virulence factors and the distinct cerebrovascular vulnerability of neonates (18,19).

Multivariate binary logistic regression analysis revealed that an initial CSF GLU concentration <1.57 mmol/L and simultaneous positive CSF and blood cultures were independent risk factors for imaging abnormalities. Previous studies have shown that a decreased CSF GLU concentration is an independent risk factor for poor outcomes in children with BM (20). Lower CSF GLU concentrations reflect bacterial proliferation and active metabolism, consuming GLU and producing metabolites that inhibit GLU transport (21). The detection of GBS in both CSF and blood suggests more severe systemic and intracranial infections, thus increasing the risk of imaging complications. Therefore, close attention to the initial CSF GLU level and pathogen culture results is crucial for predicting imaging abnormalities in GBS meningitis patients. In this study, an AUC of 0.626 (sensitivity 64.5%, specificity 58.2%) for initial CSF GLU indicates limited predictive utility as a standalone marker for individualized risk assessment of imaging abnormalities in GBS meningitis. A comprehensive assessment should incorporate both blood and CSF culture positivity for GBS. Additionally, other statistically significant factors (P<0.05), particularly elevated initial CSF protein levels, should be considered in the clinical evaluation. Despite the low AUC, these identified risk factors (initial CSF-GLU <1.57 mmol/L with concurrent CSF/blood culture positivity) retain clinical value for risk stratification. They enable targeted identification of high-risk subsets requiring intensified monitoring and prompt neuroimaging, thereby avoiding unnecessary universal imaging in all GBS meningitis patients solely based on overall imaging abnormalities rates.

Prompt antibiotic treatment is essential for treating BM. The intravenous administration of adequate doses of antimicrobials with bactericidal properties that readily cross the blood-brain barrier is recommended within 1 hour of admission (5). A combination of penicillin and aminoglycosides is the standard therapy for neonatal GBS meningitis, with ceftriaxone, meropenem, vancomycin, and linezolid added if necessary (22). The course of treatment for uncomplicated GBS meningitis is 14 days, whereas complicated cases (subdural effusion, cerebral ventricular meningitis, etc.) should be treated for at least 21 days (23). Therefore, the length of hospitalization and hospitalization costs were significantly greater in children with imaging complications in the present study than in those without imaging abnormalities (P=0.006).

Survivors of GBS meningitis face a high risk of neurological or psychological sequelae. Approximately 20% of children with GBS meningitis exhibit moderate to severe neurological damage at follow-up (median of 18 months) (24). This study demonstrated a remarkably low cure rate (15.6%) and high adverse outcome rate (12.8%, comprising 3.4% epilepsy, 1.9% motor dysfunction, and 4.0% hearing impairment). Children with imaging abnormalities presented a lower cure rate and a greater rate of adverse outcomes and were more likely to have neurological sequelae (P<0.05). The observed 0% cure rate in patients with imaging abnormalities may reflect an overly stringent definition of “clinical cure” in our study. Clinically, cases demonstrating gradual resolution of imaging abnormalities without neurological sequelae should reasonably be considered cured. While the reported low cure rate effectively underscores the severity of GBS meningitis and heightens clinical vigilance toward imaging abnormalities, future investigations should incorporate long-term follow-up to assess neurological outcomes and reevaluate cure rates more comprehensively. Abnormal cranial imaging at the end of treatment was significantly associated with sequelae, with abnormal cranial ultrasound findings, extensive bilateral deep gray matter lesions, and white matter lesions associated with abnormal motor outcomes, whereas extensive bilateral deep gray matter lesions were associated with abnormal cognitive outcomes (25). Therefore, children with GBS meningitis, especially those with persistent abnormal cranial imaging at the end of treatment, should be regularly evaluated for neurologic development, leading to timely intervention and functional exercises to improve prognosis.

Limitations

A key limitation of this study is the lack of data collection on critical time intervals, including symptom onset to hospital admission, admission to diagnosis, and treatment initiation, as well as detailed antibiotic regimens (drug selection and treatment duration) and gestational age, all of which may be associated with imaging abnormalities. In the participating medical centers of this study, CSF polymerase chain reaction (PCR) testing was not yet implemented, which may have led to the exclusion of PCR-positive but culture-negative cases. This multicenter retrospective study demonstrates associations rather than causation, necessitating validation through prospective studies. Missing data for certain variables at some centers and heterogeneity in medical equipment across sites may introduce bias. The generalizability of findings from this exclusively Chinese cohort should be interpreted with caution, particularly given China’s lack of universal late-pregnancy GBS screening and potential variations in IAP implementation compared to other regions (26).

Conclusions

In summary, GBS meningitis primarily affects infants under 3 months of age. The incidence of cranial imaging abnormalities is substantial. Compared to the imaging abnormalities-free group, patients with imaging abnormalities exhibited more severe biological markers (simultaneous CSF-blood culture positivity, lower GLU, higher protein) and worse clinical outcomes (longer stays, greater costs, lower cure rates, higher incidence of neurological sequelae). A CSF GLU concentration <1.57 mmol/L on initial analysis, along with positive results from both CSF and blood cultures, are independent risk factors for imaging abnormalities in children with GBS meningitis. The cure rate for GBS meningitis is low, and some children may experience varying degrees of neurological sequelae. Close monitoring of clinical manifestations, CSF analysis, and pathogen culture results throughout the course of the disease is essential to facilitate early identification and management of imaging abnormalities for improved prognostic outcomes.

Acknowledgments

Thanks to the collaborating hospitals of Chinese Pediatric Bacterial Meningitis Surveillance (CPBMS) Study Group: Anhui Provincial Children’s Hospital, The First Affiliated Hospital of Zhengzhou University, Xinhua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Jiangxi Provincial Children’s Hospital, Shanghai Children’s Medical Center Affiliated to Shanghai Jiao Tong University School of Medicine, Hainan Maternal and Child Health Hospital, Shanxi Provincial Children’s Hospital, Qilu Children’s Hospital of Shandong University, The Affiliated Hospital of Qingdao University, Xiamen University Affiliated Women’s and Children’s Hospital, Taiyuan Maternal and Child Health Hospital.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-381/rc

Data Sharing Statement: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-381/dss

Peer Review File: Available at https://tp.amegroups.com/article/view/10.21037/tp-2025-381/prf

Funding: This work was supported by a grant from the National Science Foundation of China (No. 82371829).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tp.amegroups.com/article/view/10.21037/tp-2025-381/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the Ethics Committee of the Children’s Hospital affiliated with Zhejiang University School of Medicine (approval No. 2019-IRB-094), and individual consent for this retrospective analysis was waived. All participating hospitals were informed of and agreed to the study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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