Abstract
Introduction
Group B Streptococcus (GBS) is a leading cause of invasive infections in infants under 3 months of age. While late-onset GBS disease (LOD) typically presents as bacteremia or meningitis, focal skin infections such as cellulitis are less common.
Presentation of case
A 52-day-old full-term female infant presented with fever and localized erythema in the lumbar region on the day of symptom onset. Her mother had tested positive for GBS during pregnancy and received intrapartum antibiotic prophylaxis. On admission, her vital signs were as follows: temperature, 37.8 °C; heart rate, 124 bpm; respiratory rate, 28 breaths/min; and blood pressure, 100/62 mmHg. Physical examination revealed no other signs of skin infection. Blood and throat cultures were positive for GBS (serotype Ib), and magnetic resonance imaging ruled out osteomyelitis or abscess. Lumbar puncture was deferred because of the location of the inflammation. The patient received intravenous ampicillin for 21 days. The fever and erythema alleviated rapidly by day 2 of hospitalization.
Conclusion
Lumbar cellulitis is an unusual manifestation of LOD. Although breast milk has been implicated in recurrent GBS infections, current evidence does not support the routine cessation of breastfeeding after a single episode. The findings from this case highlight the importance of recognizing the atypical presentations of GBS. Individualized decisions regarding breastfeeding, supported by close follow-up, may be appropriate after LOD without recurrence.
Introduction
Group B Streptococcus (GBS, Streptococcus agalactiae) is the leading cause of invasive infections in neonates and young infants, including sepsis and meningitis, during the first 3 months of life. It commonly presents as early-onset disease (EOD, birth to 6 days) or late-onset disease (LOD, 7–89 days of age). LOD is classically characterized by bacteremia with sepsis or meningitis; localized infections such as cellulitis are less frequent. When cellulitis occurs in young infants, typical sites include the face, submandibular region, and extremities, often as part of a cellulitis–adenitis syndrome. Lumbar cellulitis in infants is exceedingly rare; to the best of our knowledge, only sporadic cases have been documented [1], [2]. Here we report a case of late-onset GBS bacteremia presenting with lumbar cellulitis in a 52-day-old infant. This case provides a unique opportunity to discuss the clinical recognition of atypical GBS infection sites and review management considerations, particularly the role of breastfeeding in relation to GBS recurrence.
Case
A 52-day-old female infant presented to the hospital with fever and localized swelling in the lower back. She was born at 40 weeks of gestation via uncomplicated vaginal delivery (birth weight 3120 g). Her mother had tested positive for GBS in vaginal/rectal culture at 36 weeks of gestation and received intrapartum antibiotic prophylaxis (penicillin) during labor. The infant had been healthy since birth and was exclusively breastfed at home.
On admission at 52 days of life, the infant was febrile (subjective fever noted by parents; temperature on presentation, 37.8 °C) and irritable with reduced feeding. Physical examination revealed a well-nourished infant who appeared irritable but had no acute distress. Over the lumbar region on her back, there was an area of erythema and induration measuring approximately 5–6 cm in diameter, which was tender on palpation and warm, consistent with cellulitis (Fig. 1). There was no visible wound, abrasion, or abscess at the site or any surrounding diaper rash or dermatitis. No skin dimples, sinus tracts, or other congenital anomalies were observed in the lumbosacral area. Examination of other common infection sites in infants showed no signs of cellulitis or inflammation. The infant did not exhibit respiratory distress or gastrointestinal symptoms. Other systemic findings were unremarkable.
Fig. 1.
Findings in the lumbar and dorsal region. There was no visible wound, abrasion, or abscess at the site or any surrounding diaper rash or dermatitis.
A throat swab was also obtained, given the possibility of GBS colonization. Magnetic resonance imaging (MRI) of the spine and soft tissues was performed to evaluate the extent of infection and rule out deeper involvement. The findings demonstrated subcutaneous tissue inflammation in the lumbar area, with no evidence of paraspinal abscess, vertebral osteomyelitis, or diskitis. A lumbar puncture was considered for the assessment of meningitis; however, because the cellulitis was located over the lower back (typical site for lumbar puncture), the procedure was deferred to avoid potential iatrogenic introduction of bacteria into the cerebrospinal fluid through the infected skin. After 36 h of incubation, her blood culture tested positive for gram-positive cocci, which were identified as GBS. All isolates were serotyped using the ImmuLex™ Strep-B Kit (SSI Diagnostica, Denmark), a GBS latex agglutination test kit, according to the manufacturer’s instructions. The isolate was identified as Group B Streptococcus serotype Ib. In addition, the infant’s throat culture showed GBS, indicating colonization of the oropharynx. No other focal source of infection was identified.
Initial antibiotic therapy was initiated with cefazolin, targeting the superficial skin flora. Once GBS was identified, antibiotic therapy was streamlined to ampicillin alone. The infant continued to receive ampicillin for 21 days for adequate treatment of possible meningitis in the absence of cerebrospinal fluid examination, following standard recommendations for invasive GBS disease. The lumbar cellulitis did not require any surgical intervention or drainage, as there was no abscess formation.
The patient demonstrated rapid clinical improvement within the second day of therapy, and her fever resolved by the second hospital day. She was discharged home after completion of 21 days of antibiotic treatment, appearing well and feeding normally. At discharge, the possibility of recurrent GBS infection was discussed with the parents, given the persistent colonization. In particular, the role of ongoing breastfeeding was considered; we explained that some reports recommend culturing the mother’s breast milk or even temporarily stopping breastfeeding in cases of LOD to prevent recurrence. The mother submitted a breast milk sample for culture, which yielded no growth. However, she had received prior antibiotic treatment for mastitis before the sample was obtained, which may have influenced the culture result. She opted to continue exclusive breastfeeding, given the known benefits of breast milk and her desire to continue. The medical team supported this decision and emphasized vigilant follow-up. The family was informed of the signs of potential GBS reinfection and scheduled for regular follow-up visits. At the pediatric follow-up visit 4 months after discharge, the infant remained in good health with normal growth and development. A surveillance throat swab culture at that visit revealed GBS, indicating that colonization persisted despite clearance of the infection. Nonetheless, the infant showed no symptoms, and no antibiotics were administered because there was no clinical illness. By 12 months of age, she had not experienced a recurrence of GBS infection. Breastfeeding was continued throughout this period without any signs of relapse. The outcome at 6 months post-treatment was excellent, with the infant meeting developmental milestones and showing no chronic sequelae of the infection.
Discussion
This case highlights an atypical presentation of late-onset GBS infection. Most GBS cellulitis in infants involves the submandibular or facial regions as part of the classic cellulitis–adenitis syndrome [3]. In addition, several reports have described similar infections in the diaper or inguinal region, where mucosal colonization and minor skin barrier disruption are presumed routes of entry [4], [5], [6]. Although our patient’s lesion occurred in the lumbar area, a comparable pathogenesis is plausible, involving local invasion or hematogenous seeding from colonized mucosal surfaces. Clinicians should be aware that GBS infection in infants can occasionally present with localized soft tissue inflammation in atypical locations; when a young infant has localized cellulitis with fever or systemic signs, GBS should be included in the differential diagnosis, even if the location is uncommon.
According to previous studies, serotype III is the most common cause of GBS cellulitis in infants, accounting for approximately 64 % of reported cases [4]. In contrast, serotype Ib, as identified in our patient, was reported in only 8 % (2 of 25 cases) and both cases occurred in preterm infants [4]. The presence of serotype Ib in our full-term infant therefore represents an uncommon etiology and expands the recognized spectrum of late-onset invasive GBS disease associated with focal skin and soft tissue infection.
Another aspect underscored in this case was the pathogenesis of GBS skin infection in infants. Neonatal skin is delicate and immunologically immature. Minor trauma or irritation can disrupt the skin barrier, potentially allowing colonizing bacteria to invade. GBS is frequently a part of the maternal vaginal and rectal flora and can colonize the infant’s mucous membranes postpartum, even if intrapartum prophylaxis is administered [1]. We found that the infant’s throat was colonized with GBS, and this indicated an environmental or caregiver source, possibly breast milk or close contact with the colonized mother. It is plausible that GBS from the infant’s pharynx or other sites may was transferred to the skin, followed by local invasion through a microscopic break in the skin. Alternatively, the sequence may have involved transient bacteremia from mucosal colonization, leading to the seeding of lumbar subcutaneous tissues. Indeed, GBS cellulitis in infants is often accompanied by positive blood cultures, suggesting that bacteremia is a part of the disease process in many cases [2]. In the present case, the blood culture was positive, confirming an invasive infection. MRI helped ensure that the infection had not spread to deeper structures such as the bone or central nervous system.
Rapid initiation of appropriate therapy was crucial for our patient. GBS is known for its high virulence. Factors such as its polysaccharide capsule and beta-hemolysins contribute to immune evasion and tissue destruction, allowing the infection to progress quickly if untreated [7]. Empirical antibiotic coverage for neonatal sepsis was initiated as soon as a bacterial infection was suspected, and these likely prevented further complications. The decision to treat the patient for 21 days with ampicillin at 300 mg/kg/day, the recommended dose for meningitis, was influenced by the inability to perform lumbar puncture; thus, we presumptively treated the patient for possible GBS meningitis. This approach is supported by standard guidelines for invasive neonatal GBS disease, which recommend a full course for meningitis if CNS infection cannot be definitively excluded [8]. During treatment, no abscess developed, and the infant’s health improved without any surgical intervention. Notably, we did not attempt a needle aspiration of the cellulitis area for culture. In general, in young infants with suspected GBS cellulitis, direct culture from skin lesions is often not necessary to confirm the pathogen if blood cultures are positive, because GBS is predictable as the causative agent in this clinical setting [2], [3]. Invasive procedures such as aspiration from the lesion should be avoided when classic signs (e.g., erythema, induration, warmth, tenderness, rapid clinical progression) indicate GBS, and prompt empirical therapy should be administered, as followed in the present case [1], [2]. The outcome in our patient demonstrates that early recognition and aggressive antibiotic treatment of GBS infection, even in unusual forms such as lumbar cellulitis, can lead to complete recovery without sequelae.
Recurrent late-onset GBS infection occurs in approximately 1–4 % of infants, often involving the same strain as in the initial episode, suggesting a persistent reservoir. Breast milk has been implicated as one possible source of reinfection, as identical strains have been detected in both maternal milk and infant blood [9]. However, recent systematic evidence indicates that recurrence can still occur even after breastfeeding cessation, suggesting that breast milk is not the only source of relapse [10].
Table 1 summarizes the main findings of a recent systematic review [10], which analyzed 140 reported cases of recurrent GBS infection in infants. Notably, two-thirds of tested breast milk samples were GBS-positive, but recurrence occurred in about one-fourth of infants even after breastfeeding was stopped. These findings imply that discontinuing breastfeeding does not necessarily prevent recurrence.
Table 1.
Summary of recurrent group B streptococcal (GBS) infections (n = 146) in infants based on a systematic review [10].
| Variables | Number of infants (percentages) |
|---|---|
| Median time to recurrence (days) | 10 [range 2–98] |
| Preterm infants | 87/138 (63.0 %) |
| Initial antibiotic duration (median, days) | 13 [IQR 10–14] |
| Breast milk tested for GBS | 62/146 (42.5 %) |
| Positive GBS in breast milk | 41/62 (66.1 %) |
| Stopped breastfeeding after first recurrence | 19/32 (59.4 %) |
| Further recurrence despite breastfeeding cessation | 5/19 (26.3 %) |
| Mortality rate from recurrence | 5/136 (3.7 %) |
This table summarizes key findings from a systematic review of 146 cases of recurrent GBS infections in infants. The denominator is shown except for missing cases. The data include demographic characteristics, timing of recurrence, breastfeeding practices, and clinical outcomes. IQR; Interquartile Range.
In our case, the mother’s breast milk culture was negative, although she had recently received antibiotic therapy for mastitis, which may have affected the culture result. Taking this into consideration, breastfeeding was continued under close observation. The infant remained colonized with GBS but experienced no recurrence during a one-year follow-up. Therefore, for healthy term infants, continued breastfeeding with careful monitoring may represent an appropriate and safe management strategy, given its nutritional and immunological benefits.
CRediT authorship contribution statement
Akimichi Shibata: Writing – review & editing. Ryutaro Koga: Writing – original draft. Munehiro Furuichi: Writing – review & editing. Satoshi Nakano: Writing – review & editing. Masayoshi Shinjoh: Writing – review & editing.
Ethical approval
This case study was in accordance with the ethical standards of the Institutional Review Board of the Japanese Red Cross Ashikaga Hospital. The infant’s parents provided informed consent for publication of this case report and any accompanying data. All identifying details have been removed or anonymized to protect patient privacy, in compliance with journal and institutional guidelines.
Consent
Written informed consent was obtained from the patient’s legal guardian for publication of this case report and accompanying clinical data and images. A copy of the signed consent is available for review by the Editor-in-Chief of this journal upon request.
Funding
This work was supported by grants from the Japan Agency for Medical Research and Development (AMED) [Grant nos. JP22fk0108612, JP22fk0108540, and 24wm0225048] to S.N.
Conflict of Interest
The authors declare no conflicts of interest relevant to this publication.
Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgements
We thank the medical and nursing staff of the Japanese Red Cross Ashikaga Hospital for their excellent care of the patient and support with this case. We also acknowledge the assistance of the Antimicrobial Resistance Research Center at the National Institute of Infectious Diseases and the Department of Pediatrics at Keio University School of Medicine for their valuable insights and laboratory support. The authors are grateful to the patient’s family for their cooperation and permission to share the details of this case for educational purposes.
References
- 1.Mittal M.K., Shah S.S., Friedlaender E.Y. Group B streptococcal cellulitis in infancy. Pediatr Emerg Care. 2007;23:324–325. doi: 10.1097/01.pec.0000270168.70615.be. [DOI] [PubMed] [Google Scholar]
- 2.Rand T.H. Group B streptococcal cellulitis in infants: a disease modified by prior antibiotic therapy or hospitalization? Pediatrics. 1988;81:63–65. doi: 10.1542/peds.81.1.63. [DOI] [PubMed] [Google Scholar]
- 3.Baker C.J. Group B streptococcal cellulitis-adenitis in infants. Am J Dis Child. 1982;136:631–633. doi: 10.1001/archpedi.1982.03970430063018. [DOI] [PubMed] [Google Scholar]
- 4.Penella A. Group B streptococcal cellulitis-adenitis syndrome in infants: insights from 24 years of experience. J Pediatr Infect Dis Soc. 2022;11(8):375–378. doi: 10.1093/jpids/piac033. [DOI] [PubMed] [Google Scholar]
- 5.Strunk T., Burgner D. Late-onset group B streptococcal cellulitis. Arch Dis Child Fetal Neonatal Ed. 2015;100(3):F215. doi: 10.1136/archdischild-2014-307388. [DOI] [PubMed] [Google Scholar]
- 6.Wirth J., Raymond J., Lapillonne A. Unusual report of diaper rash in a premature infant with group B streptococcal infection. Pediatr Infect Dis J. 2006;25(8):750–751. doi: 10.1097/01.inf.0000227826.83386.9d. [DOI] [PubMed] [Google Scholar]
- 7.Salleo E., MacKay C.I., Cannon J., King B., Bowen A.C. Cellulitis in children: a retrospective single centre study from Australia. BMJ Paediatr Open. 2021;5 doi: 10.1136/bmjpo-2021-001130. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Verani J.R., McGee L., Schrag S.J., Division of Bacterial Diseases, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention (CDC) Prevention of perinatal group B streptococcal disease: revised guidelines from CDC, 2010. MMWR Recomm Rep. 2010;59(59):1–36. [PubMed] [Google Scholar]
- 9.Zimmermann P., Gwee A., Curtis N. The controversial role of breast milk in GBS late-onset disease. J Infect. 2017;74(1):S34–S40. doi: 10.1016/S0163-4453(17)30189-5. [DOI] [PubMed] [Google Scholar]
- 10.Miselli F., Boncompagni A., Cuoghi Costantini R., Zini T., Bedetti L., Buttera M., et al. Recurrence of group B streptococcal infections in infants: a systematic review. Expert Rev Anti-Infect Ther. 2025;23:305–314. doi: 10.1080/14787210.2025.2474569. [DOI] [PubMed] [Google Scholar]

