Late-onset Group B Streptococcus Research Articles

Burden of Invasive Group B Streptococcus Infection Among Omani Infants Less Than 90 Days Old: A Multicenter Study.

Group B Streptococcus (GBS) infection is the leading cause of neonatal morbidity and mortality worldwide. This study aims to investigate the incidence of invasive GBS disease among infants less than 90 days old in Oman and to describe their risk factors, clinical presentations and clinical outcomes. We retrospectively collected the data of less than 90-day-old Omani infants with culture-positive GBS from sterile samples. This study was conducted in 3 tertiary hospitals in Oman from 2009 to 2018. Over 10 years, we identified 92 cases of culture-confirmed invasive GBS infection from 178,285 live births in the 3 hospitals, giving an overall incidence of 0.53 per 1000 live births [95% confidence interval (CI): 0.4-0.7)]. Of those, 59 (64.1%) had early-onset neonatal GBS disease and 33 (35.9%) had late-onset neonatal GBS disease. The incidence of invasive GBS disease was significantly higher in the last 5 years from 2014 to 2018 (0.69 per 1000 live births, 95% CI: 0.5-0.9) compared to the previous years from 2009 to 2013 (0.36 per 1000 live births, 95% CI: 0.2‒0.5), (P = 0.004). Infants with late-onset neonatal GBS disease had a higher risk of meningitis compared to infants with early-onset neonatal GBS disease (30.3% vs. 10.2%, P = 0.021). The mortality rate was 13.5%. The incidence of invasive GBS disease in Oman is similar to what was reported worldwide, however, the burden of the disease in terms of mortality is high. In addition, a significant increase in the annual incidence of invasive GBS disease in Omani infants was found over the study period.

Early-onset group B streptococcal infections in five Nordic countries with different prevention policies, 1995 to 2019.

BackgroundNeonatal early-onset disease caused by group B Streptococcus (GBS) is a leading cause of infant morbidity. Intrapartum antibiotic prophylaxis (IAP) is effective in preventing early-onset GBS disease, but there is no agreement on the optimal strategy for identifying the pregnant women requiring this treatment, and both risk-based prophylaxis (RBP) and GBS screening-based prophylaxis (SBP) are used.AimThe aim of this study was to evaluate the effect of SBP as a public health intervention on the epidemiology of early-onset GBS infections.MethodsIn 2012, Finland started the universal SBP, while Denmark, Iceland, Norway and Sweden continued with RBP. We conducted an interrupted time series analysis taking 2012 as the intervention point to evaluate the impact of this intervention. The incidences of early- and late-onset GBS infections during Period I (1995-2011) and Period II (2012-2019) were collected from each national register, covering 6,605,564 live births.ResultsIn Finland, a reduction of 58% in the incidence of early-onset GBS disease, corresponding to an incidence rate ratio (IRR) of 0.42 (95% CI: 0.34-0.52), was observed after 2012. At the same time, the pooled IRR of other Nordic countries was 0.89 (95% CI: 0.80-1.0), specifically 0.89 (95% CI: 0.70-1.5) in Denmark, 0.34 (95% CI: 0.15-0.81) in Iceland, 0.72 (95% CI: 0.59-0.88) in Norway and 0.97 (95% CI: 0.85-1.1) in Sweden.ConclusionsIn this ecological study of five Nordic countries, early-onset GBS infections were approximately halved following introduction of the SBP approach as compared with RBP.

Group B Streptococcus and Perinatality in the South of Tunisia: Epidemiology, Serotype Distribution, and Antibiotic Susceptibility

IntroductionIn the lack of updated Tunisian epidemiological data, we sought to describe the epidemiology of Group B Streptococcus (GBS) in pregnant women and newborns.Materials and methodsA retrospective analysis of GBS neonatal invasive infections and a cross-sectional study evaluating the prevalence of maternal GBS colonization were conducted. GBS isolates were tested for antimicrobial susceptibility, serotyped, and assessed for the appurtenance to the hypervirulent ST17 clone.ResultsOf 98 neonates with GBS, early-onset GBS disease (EOD) comprised 83.7 and 16.3% were late-onset GBS disease (LOD). The prevalence of maternal GBS colonization was 27%. All GBS isolates were susceptible to penicillin. Serotype III predominated (42.6%) for neonatal invasive infections. GBS isolates belonging to the ST17 sequence type were found only as serotype III.ConclusionThis study documents the frequency of GBS EOD, the high rate of maternal GBS colonization, and the predominance of the hypervirulent clone type III/ST17 in infants.

Group B Streptococcus Drives Major Transcriptomic Changes in the Colonic Epithelium.

Group B Streptococcus (GBS) is a leading cause of infant sepsis worldwide. Colonization of the gastrointestinal tract is a critical precursor to late-onset disease in exposed newborns. Neonatal susceptibility to GBS intestinal translocation stems from intestinal immaturity; however, the mechanisms by which GBS exploits the immature host remain unclear. β-hemolysin/cytolysin (βH/C) is a highly conserved toxin produced by GBS capable of disrupting epithelial barriers. However, its role in the pathogenesis of late-onset GBS disease is unknown. Our aim was to determine the contribution of βH/C to intestinal colonization and translocation to extraintestinal tissues. Using our established mouse model of late-onset GBS disease, we exposed animals to GBS COH-1 (WT), a βH/C-deficient mutant (KO), or vehicle control (phosphate-buffered saline [PBS]) via gavage. Blood, spleen, brain, and intestines were harvested 4 days post-exposure for determination of bacterial burden and isolation of intestinal epithelial cells. RNA sequencing was used to examine the transcriptomes of host cells followed by gene ontology enrichment and KEGG pathway analysis. A separate cohort of animals was followed longitudinally to compare colonization kinetics and mortality between WT and KO groups. We demonstrate that dissemination to extraintestinal tissues occurred only in the WT exposed animals. We observed major transcriptomic changes in the colons of colonized animals, but not in the small intestines. We noted differential expression of genes that indicated the role of βH/C in altering epithelial barrier structure and immune response signaling. Overall, our results demonstrate an important role of βH/C in the pathogenesis of late-onset GBS disease.

Interspecies Interactions within the Host: the Social Network of Group B Streptococcus.

Group B Streptococcus (GBS) is a pervasive neonatal pathogen accounting for a combined half a million deaths and stillbirths annually. The most common source of fetal or neonatal GBS exposure is the maternal microbiota. GBS asymptomatically colonizes the gastrointestinal and vaginal mucosa of 1 in 5 individuals globally, although its precise role in these niches is not well understood. To prevent vertical transmission, broad-spectrum antibiotics are administered to GBS-positive mothers during labor in many countries. Although antibiotics have significantly reduced GBS early-onset neonatal disease, there are several unintended consequences, including an altered neonatal microbiota and increased risk for other microbial infections. Additionally, the incidence of late-onset GBS neonatal disease remains unaffected and has sparked an emerging hypothesis that GBS-microbe interactions in developing neonatal gut microbiota may be directly involved in this disease process. This review summarizes our current understanding of GBS interactions with other resident microbes at the mucosal surface from multiple angles, including clinical association studies, agriculture and aquaculture observations, and experimental animal model systems. We also include a comprehensive review of in vitro findings of GBS interactions with other bacterial and fungal microbes, both commensal and pathogenic, along with newly established animal models of GBS vaginal colonization and in utero or neonatal infection. Finally, we provide a perspective on emerging areas of research and current strategies to design microbe-targeting prebiotic or probiotic therapeutic intervention strategies to prevent GBS disease in vulnerable populations.

Not Just an Intrapartum Problem: Late-Onset Group B Streptococcus Disease.

Group B streptococcal (GBS) infection is a leading cause of neonatal morbidity and mortality globally. While prevention strategies for early onset GBS disease are well established, methods to prevent late-onset GBS disease do not eliminate disease burden, leaving potential for infection, and devastating consequences for affected neonates. Furthermore, the incidence of late-onset GBS has risen in recent years, with preterm infants at the highest risk of infection and death. Meningitis remains the most common and serious complication associated with late onset disease, occurring in 30 percent of cases. The assessment of risk for neonatal GBS infection should not be limited to the birth process or maternal screening results and intrapartum antibiotic prophylaxis treatment status. Horizontal transmission after birth from mothers, caregivers, and community sources has been observed. Late-onset GBS disease and its sequelae remain a significant risk to neonates, and clinicians should be able to recognize the signs and symptoms to provide timely antibiotic therapy. This article discusses of the pathogenesis, risk factors, clinical manifestations, diagnostics, and treatment of neonatal late-onset GBS infection and identifies implications for practicing clinicians.

NEONATAL GROUP B STREPTOCOCCAL DISEASE IN A NEONATAL INTENSIVE CARE UNIT: A TWELVE-YEAR STUDY

Introduction: Group B Streptococcus (GBS) is a gram-positive coccus, that frequently colonizes the human genital and gastrointestinal tract, and is the most common cause of invasive infections in neonates. The high clinical suspicion and early treatment are essential to prevent devastating sequelae and improve the prognosis of these patients. Materials and Methods: A retrospective descriptive study made with children younger than 3 months of age, admitted to a neonatal intensive care unit of a level II hospital, from January 1, 2010 to December 31, 2021, with early (EOI) or late-onset (LOI) neonatal GBS infection. Reviewed obstetric history, risk factors, intrapartum chemoprophylaxis (IPA), clinical manifestations, antibiotic therapy, supportive care, recurrent infection, morbidities and deaths. Results: There were 6 cases registered during 12-year period with GBS infection, 3(50%) had EOI, 3(50%) had LOI and 1 case with recurrent infection (more 2 episodes). Most cases were prematures (4/6; 67%)with average gestational age of 29weeks. Eight GBS infections were documented. In EOI, prematurity and prolonged rupture of membranes without chemoprophylaxis were identified as risk factors. The most common clinical diagnosis was meningitis (62,5%, 5/8) and sepsis/bacteriemia without a focus (37,5%, 3/8). The most used empirical therapy was ampicillin, gentamicin and cefotaxime (50%, 4/8) and the most frequent definitive therapy was Penicillin G. 4 patients needed ventilatory support and 1 needed shock and seizures treatment. In one case hydrocephalus and delayed psychomotor development (DPD) were reported and in another case DPD and eyelid ptosis were also reported. 1 death occurred. Conclusion: In our study, maternal colonization wasn’t a risk factor for EIO, because the 4 mothers who performed GBS culture (2 mothers of term newborns and 2 mothers of preterms, one with invasive disease and other with recurrent infection) were negative. We obtained a higher percentage of meningitis than previously described (62.5% vs 5-10%), probably because most patients were premature and immunosuppressed.

Neuropathology Evaluation of in Utero Correction of Myelomeningocele and Complications of Late-Onset GBS Infection

Background: Myelomeningocele (MMC) causes significant morbidity and mortality. Efforts have been directed to correct this defect in utero. The neuropathology literature on antenatally repaired MMC and associated complications in humans is limited. Case report: A 12-day-old female, who underwent prenatal MMC repair via a two-layer closure (dural replacement patch, primary skin closure), was born at 34 weeks’ gestation. Her group B streptococcus positive mother received appropriate antepartum prophylactic antibiotics. She remained stable until day 11 of life when she underwent rapid clinical deterioration. Despite aggressive intervention, she expired on day 12. Review of placental pathology showed maternal and fetal inflammatory response. Autopsy revealed Gram-positive cocci and inflammation within the basilar leptomeninges and lumbosacral region. Neural and dermal elements were present within the MMC repair. Conclusion: This case documents integration of the dermal matrix patch to neural elements, adhering the spinal cord to scar tissue, the clinical implications of which remain unclear.

Late-Onset Sepsis in a Premature Infant Mediated by Breast Milk: Mother-to-Infant Transmission of Group B Streptococcus Detected by Whole-Genome Sequencing.

BackgroundLate-onset group B Streptococcus (LOGBS) sepsis is a cause of infection and death in infants. Infected breast milk has been considered a source of neonatal GBS infection and invasive infection. However, mother-to-infant transmission of GBS detected by the high-resolution diagnostic method is rarely reported.MethodsThis study describes a low-weight premature infant who developed late-onset GBS septicemia 21 days after birth. GBS strains isolated from the mother’s cervical secretion, the mother’s milk, and the baby’s blood were cultured to identify the source of GBS infection. We further confirmed the GBS isolates through matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF-MS). Finally, we performed whole-genome sequencing (WGS) and phylogenetic analyses on the GBS strains recovered.ResultsGBS isolates were cultured from the bloodstream of the premature infant and the mother’s milk, respectively. Subsequently, WGS and phylogenetic analyses on three GBS isolates demonstrated that the GBS strain from the infant’s bloodstream was 100% homologous to that from the mother’s breast milk, which had some different gene fragments from the GBS strain from the mother’s cervical secretion. It provided evidence that this infant’s late-onset GBS septicemia originated from his mother’s breast milk instead of the vertical mother-to-infant transmission.ConclusionThrough WGS and phylogenetic analysis of the GBS strains, we proved in this study that the late-onset GBS sepsis in a premature infant was derived from his mother’s breast milk. It indicated that WGS diagnosis is an effective tool for infection tracing. Furthermore, this report provides direction for preventing late-onset GBS infection.

Colonization of pregnant women with group B streptococcus: current view at the problem

The relevance of the problem of group B streptococcus (GBS) in obstetric practice casts no doubt. Attracting the close attention of leading experts, introducing new solutions and based on practical experience gained, it is still not possible to prevent all cases of neonatal infections associated with GBS. The review article demonstrates the current view of the problem. According to the literature, African-American race in combination with sexually transmitted infections are predisposing risk factors for GBS colonization. A direct relationship between obesity and the percentage of GBS carriers was revealed. GBS-colonized primigravidas have a 50 % increased chance of detecting the pathogen in subsequent pregnancies. Absolute factors for massive GBS colonization of the birth tract include GBS-associated asymptomatic bacteriuria and a history of GBS-colonized children. It is assumed that such virulence factors as hemolytic pigment and hyaluronidase contribute to the GBS pathogenic potential. The protective function in the immune system is performed by Kaschenko–Gofbauer cells, but their role is ambiguous. Early neonatal GBS infection realized in 90 % of newborns that manifested by sepsis, pneumonia and purulent meningitis. Implemented measures to prevent early neonatal GBS infection have a number of disadvantages. False-negative results of culture screening for GBS antigen at gestational age of 35–37 weeks increase a risk of vertical transmission, whereas false-positive results underlie a reason for prescribing irrational intranatal antibiotic prophylaxis. Moreover, antenatal GBS microbiological screening and antibiotic prophylaxis at birth do not prevent the risks of late-onset neonatal GBS infection.

Epidemiology and Trends of Infective Meningitis in Neonates and Infants Less than 3 Months Old in Hong Kong

ObjectivesMeningitis in neonates and young infants leads to significant morbidity and mortality worldwide. This study aimed to investigate pathogens, antibiotic resistance and secular change of incidence in Hong Kong. MethodsA retrospective search was performed on meningitis in neonates and infants aged <3 months in three Hong Kong public hospitals from 2004 to 2019. Medical charts were reviewed, with focus on the identification and antibiotic resistance of the pathogens. ResultsA total of 200 cases of meningitis were identified (67% were bacterial). Group B Streptococcus (GBS) and Escherichia coli (E. coli) were the commonest bacterial pathogens. The annual rates of early-onset GBS meningitis decreased after the implementation of universal GBS screening and intrapartum antibiotic prophylaxis (IAP) in 2012, while that of late-onset GBS meningitis remained similar. A significant portion of E. coli isolates were resistant to ampicillin and/or gentamicin. ConclusionGBS and E. coli were the most common bacteria for meningitis in this age group. The annual rate of bacterial meningitis in Hong Kong has declined in recent years, which has been attributed to the decline in early-onset GBS meningitis due to universal GBS screening and IAP. Antimicrobial-resistant bacterial strains that cause meningitis require further clinical and public health attention.

Hypervirulent Streptococcus agalactiae septicemia in twin ex-premature infants transmitted by breast milk: report of source detection and isolate characterization using commonly available molecular diagnostic methods

BackgroundGroup B Streptococcus (GBS) infections caused by Streptococcus agalactiae is a leading cause of meningitis and sepsis in neonates, with early-onset GBS symptoms emerging during the first week of life and late-onset occurring thereafter. Perinatal transmission of GBS to the neonate through the birth canal is the main factor associated with early-onset neonate infections, while less is understood about the source of late-onset infections.MethodsIn this report we describe a case of twin ex-premature infants who presented one month after birth with GBS septicemia. The mother had been appropriately screened at gestational age 35–37 weeks and laboratory methods failed to detect GBS colonization by culture or clinical molecular methods. In attempts to identify and isolate the source of GBS infection, additional surveillance swabs were collected from the mother at the time of neonate admission. Culture and a commercially available, FDA-cleared molecular PCR assay were performed.ResultsNo GBS was detected from swabs collected from the perianal, thigh/groin or axillary areas. However, expressed breast milk and swabs from the breastmilk pump were positive by both methods. Since simultaneous culture and molecular methods which used breastmilk as a source were performed, investigators ascertained the limit of detection for GBS in breastmilk. The limit of detection was determined to be tenfold lower than that of LIM-broth enriched cultures—the FDA-approved source. Subsequent whole genome sequencing (WGS) analysis of isolates recovered from breastmilk and blood cultures from the infants demonstrated all strains were related and characterized as ST-452. Both infants responded very well to treatment and continued to have no related events or concerns at the two-year follow up appointment.ConclusionsStrain type 452 (capsular type IV) has recently emerged as a hypervirulent strain and has previously been documented as causing GBS infections in elderly populations. Antibiotic therapy resolved both mother and infant infections. Subsequent testing for the presence of GBS in breastmilk samples also showed an absence of bacteria. This is the first report of infant twins late-onset GBS infections caused by the hypervirulent S. agalactiae ST-452 with breastmilk as the source.

The Impact of Circulating Antibody on Group B Streptococcus Intestinal Colonization and Invasive Disease.

Gastrointestinal (GI) colonization with group B Streptococcus (GBS) is an important precursor to late-onset (LO) disease in infants. The host-pathogen interactions that mediate progression to invasive disease remain unknown due, in part, to a paucity of robust model systems. Passively acquired maternal GBS-specific antibodies protect newborns from early-onset disease, yet their impact on GI colonization and LO disease is unexplored. Using murine models of both perinatal and postnatal GBS acquisition, we assessed the kinetics of GBS GI colonization, progression to invasive disease, and the role of GBS-specific IgG production in exposed offspring and juvenile mice at age 12 and 14 days, respectively. We defined LO disease as >7 days of life in the perinatal model. We studied the impact of maternal immunization using a whole-cell GBS vaccine on the duration of intestinal colonization and progression to invasive disease after postnatal GBS exposure in offspring. Animals exhibit sustained GI colonization following both perinatal and postnatal exposure to GBS, with 21% and 27%, respectively, developing invasive disease. Intestinal colonization with GBS induces an endogenous IgG response within 20 days of exposure. Maternal vaccination with whole-cell GBS induces production of GBS-specific IgG in dams that is vertically transmitted to their offspring but does not decrease the duration of GBS intestinal colonization or reduce LO mortality following postnatal GBS exposure. Both perinatal and postnatal murine models of GBS acquisition closely recapitulate the human disease state, in which GBS colonizes the intestine and causes LO disease. We demonstrate both endogenous production of anti-GBS IgG in juvenile mice and vertical transfer of antibodies to offspring following maternal vaccination. These models serve as a platform to study critical host-pathogen interactions that mediate LO GBS disease.

Recurrent Late-Onset GBS Sepsis in the NICU

Recurrent Late-Onset GBS Sepsis in the NICU

Recurrent neonatal group B streptococcus cellulitis and adenitis syndrome with late-onset sepsis

Abstract Objectives Group-B streptococcus (GBS) continues to be a significant cause of late-onset neonatal illness. Rarely does it present as cellulitis-adenitis syndrome, and rarely does the infection recur in the same infant after complete recovery. Case presentation Here we report a case of recurrent late-onset cellulitis-adenitis GBS syndrome in a term 12-day-old neonate. The infant presented with fever and cellulitis of the right neck. Full sepsis workup was normal and the infant recovered completely with antibiotics. Three days after the completion of antibiotics the patient returned to the emergency department due to fever, toxic appearance and rapidly spreading cellulitis, and adenitis on the left side of the neck. Blood culture revealed GBS. The patient was re-admitted to the hospital and successfully treated with a prolonged course of antibiotics. Conclusions This case highlights the importance of treating neonatal cellulitis with fever as bacteremia, and reminds us of the rare possibility of recurrent invasive GBS disease. Moreover, this case illustrates that GBS cellulitis-adenitis syndrome is possibly underdiagnosed in mild cases. Physicians should be aware that neonatal cellulitis can precede the appearance of severe sepsis. Neonates with fever and cellulitis without a clear external port of entry should undergo a complete sepsis workup and receive antibiotic treatment appropriate for bacteremia, even if the blood cultures are negative. Although the recurrence of GBS sepsis is rare, physicians should be aware of this possibility in order to treat the infection early.

Late onset group B streptococcus disease manifesting as acute suppurative parotitis

Few patients with acute suppurative parotitis (ASP) due to group B streptococcus (GBS) have been documented. Limited data on clinical and microbiological features and infectious route are available. We present a 21-day-old boy with invasive GBS disease manifesting as ASP. The patient was admitted because of irritability, fever, and erythematous swelling over the right parotid area. No purulent material exuded from the Stensen's duct. Ultrasonography and computed tomography of the neck showed findings indicative of ASP. On the day after admission, blood culture yielded GBS. The isolate was determined as GBS serotype Ia and sequence type-23, and the patient was successfully treated with intravenous ampicillin for 10 days. A review of the literature revealed 11 GBS ASP infants including ours with age at onset between 13 days and 12 weeks. All infants had bacteremia while pus from the Stensen's duct was detected in only one case. This finding remarkably contrasts with ASP caused by pathogens other than GBS, where the infection usually spreads via a retrograde route from Stensen's duct. The present case and literature review indicate GBS ASP primarily arises from bloodstream infection, and that ASP should be included in an infectious focus as late onset GBS disease.

To screen or not to screen women for Group B Streptococcus (Streptococcus agalactiae) to prevent early onset sepsis in newborns: recent advances in the unresolved debate.

Streptococcus agalactiae, also known as Group B streptococcus (GBS) is the commonest cause of early onset sepsis in newborns in developed high-income countries. Intrapartum antimicrobial (antibiotic) prophylaxis (IAP) is recognized to be highly effective in preventing early onset Group B sepsis (EOGBS) in newborns. The key controversy is about the strategy that should be used to identify mothers who should receive IAP. There are two strategies that are followed in developed countries: screening-based or risk-factor-based identification of women requiring IAP. The debate regarding which of the two approaches is better has intensified in the recent years with concerns about antimicrobial resistance, effect on newborn’s microbiome and other adverse effects. In this review, we have discussed some of the key research papers published in the period 2015–2019 that have addressed the relative merits and disadvantages of screening versus risk-factor-based identification of women requiring IAP. Although screening-based IAP appears to be more efficacious than risk-based IAP, IAP-based prevention has several limitations including ineffectiveness in prevention of late-onset GBS infection in babies, premature and still births, impact of IAP on neonatal microbiota, emergence of antimicrobial resistance and difficulties in implementing IAP-based strategies in middle and low income countries. Alternative strategies, principally maternal immunization against GBS would circumvent use of IAP. However, no licensed vaccines are currently available for use.

The Febrile Infant: Where Art Meets Science to Prevent Harm.

1. Mobeen H. Rathore, MD, CPE* 1. *Editorial Board Member, Pediatrics in Review > With a nod (tongue in cheek) to the author’s previously published title (1) > One consistent thought continues to hold true when it comes to assessing the febrile infant. Be suspicious. > > —JZ, HDA Perhaps Dr Arnold Smith put it most eloquently: “Sorting out the child at risk, from those with illness that is not a threat to their health, is a fundamental goal of pediatrics” (Fig 1). (2) What Dr Smith wrote 40 years ago is true even today. Fever continues to be one of the most common ailments in children. Although fever is a friend of the patient, infection is a foe. Identifying the foe is a complicated task for the evaluating physician. This is even more challenging in infants and especially neonates because of less-than-optimal history, mostly unreliable examination, and more specific signs of infection in the neonates often appearing later in the disease course. Even a thorough laboratory evaluation is not always helpful. Ultimately it is the selection of optimum broad spectrum empirical antibiotic drug therapy that is really the most important decision to protect neonates from the serious morbidity and mortality of neonatal sepsis. Fortunately, most infections in children, including in neonates, are viral and self-limited, causing no serious morbidity. Unfortunately, rarely, bacterial infections can be serious and sometimes life-threatening. Herein lies the challenge even for the most experienced and knowledgeable …

Clinical characteristics and antibiotic susceptibility features of different types of invasive infections caused by group B Streptococcus: a multicenter prospective study

Objective To study the clinical manifestations and antibiotic sensitivity features of early- and late-onset invasive infections caused by group B Streptococcus (GBS). Methods A total of 96 infants with invasive GBS infections were enrolled prospectively from seven tertiary hospitals of GBS Infection Research Cooperative Group in southwest Fujian, such as Xiamen Maternal and Child Care Hospital, etc., from January 2016 to June 2018. According to the onset time of infection after birth, they were divided into early-onset GBS disease (GBS-EOD) group (<7 d, n=67) and the late-onset GBS disease (GBS-LOD) group (7-89 d, n=29). Clinical manifestations, disease spectrum, complications and outcomes of the two groups were compared. Drug sensitivity test was carried out using disk diffusion test. Chi-square or Fisher's exact test, two independent sample t-test or Mann-Whitney U tests were used for statistical analysis. Results (1) The average ages at onset in GBS-EOD and GBS-LOD groups were (15.8±6.7) h (0.5-142.0 h) and (25.0±8.1) d (9-89 d), respectively. The incidence of tachypnea, pallor, fever and convulsion were noted in 68.7% (46/67) vs 44.8% (13/29), 52.2% (35/67) vs 17.2% (5/29), 23.9% (16/67) vs 65.5% (19/29) and 7.5% (5/67) vs 48.3% (14/29) of GBS-EOD and GBS-LOD groups with χ2 values of 6.282, 10.199, 15.146 and 21.237 (all P<0.05). The main clinical manifestations of GBS-EOD were tachypnea and pallor, while most of the patients in the GBS-LOD group developed fever and convulsions. (2) The incidence of pneumonia, sepsis, meningitis, sepsis complicated by septic joints, pneumonia complicated by sepsis, sepsis complicated by meningitis and pneumonia complicated by sepsis and meningitis were noted in 43.3% (29/67) vs 20.7% (6/29), 9.0% (6/67) vs 17.2% (5/29), 0.0% (0/67) vs 3.4% (1/29), 0.0% (0/67) vs 6.9% (2/29), 31.3% (21/67) vs 13.8% (4/29), 6.0% (4/67) vs 31.0% (9/29) and 10.4% (7/67) vs 6.9% (2/29) of GBS-EOD and GBS-LOD groups. There was a statistically significant difference in the disease spectrum between the two groups (Fisher's exact test, all P<0.001). Compared with the GBS-LOD group, the GBS-EOD group had a higher incidence of pneumonia [85.1% (57/67) vs 41.4% (12/29), χ2=19.116, P<0.001] and a lower incidence of meningitis [16.4% (11/67) vs 41.4% (12/29), χ2=6.922, P=0.009]. Complications such as acute respiratory distress syndrome (ARDS), pulmonary hemorrhage, shock and persistent pulmonary hypertension of the newborn (PPHN) occurred much more in the GBS-EOD group than the GBS-LOD group [28.4% (19/67) vs 6.9% (2/29), 13.4% (9/67) vs 0.0% (0/29), 11.9% (8/67) vs 10.3% (3/29), 4.5% (3/67) vs 0.0% (0/29), χ2=13.683, P<0.001]. (3) Among the 96 patients, 23 (24.0%) had meningitis and 73 (76.0%) developed pneumonia and sepsis. Meningitis resulted in a higher fatality rate [17.4% (4/23) vs 4.1% (3/73), χ2=4.564, P=0.035] and longer average hospital stay [(37.2±12.6) vs (14.1±5.3) d, t=7.831, P<0.001] than pneumonia and sepsis. Seven out of the 19 meningitis survivors developed intracranial complications. (4) The overall fatality rate in this study was 7.3% (7/96) and no significant difference was found between GBS-EOD and GBS-LOD group [7.5% (5/67) vs 6.9% (2/29), χ2=0.010, P=0.982]. Among the 67 GBS-EOD infants, 58 (86.6%) occurred within 24 h and five of them died, but no death was reported in the other nine cases occurred after 24 h. (5) Totally 96 strains of GBS were isolated with 100% sensitivity to penicillin, ampicillin, cefazolin and meropenem, and 97% to vancomycin. Around 79.3%-91.0% of GBS isolates were resistant to clindamycin and erythromycin. Conclusions Clinial features vary greatly in GBS-LOD and GBS-EOD cases. Infants with meningitis have poor prognosis. The drug resistance rate of GBS to erythromycin and clindamycin are relatively high. Key words: Streptococcus agalactiae; Streptococcal infections; Drug resistance, bacterial; Microbial sensitivity tests; Multicenter study

Phenotypic and genetic differences among group B Streptococcus recovered from neonates and pregnant women in Shenzhen, China: 8-year study

BackgroundGroup B Streptococcus (GBS) is a leading cause of early-onset disease (EOD) and late-onset disease (LOD) in infants. We sought to investigate the antibiotic susceptibility profiles, resistance genes, virulence-related genes, serotype distribution and genotypic characteristics of GBS recovered from infected or colonized neonates and pregnant women in a tertiary teaching hospital in Shenzhen, China, from 2008 to 2015.ResultsHigh resistance rates of erythromycin (66.7–100%) were detected among early-onset GBS (EOGBS), late-onset GBS (LOGBS), neonatal colonizing GBS (NCGBS) and maternal colonizing GBS (MCGBS). 89.5–100% of four groups of GBS isolates showed resistance to tetracycline. More than 90 % of erythromycin resistant isolates of EOGBS (8/8, 100%), LOGBS (16/17, 94.1%) and NCGBS (10/11, 90.9%) harbored ermB, while only 9.1–17.6% harbored mefA/E. By contrast, 55.8% (24/43) and 62.8% (27/43) of erythromycin resistant MCGBS isolates carried ermB and mefA/E genes, respectively. The tetO gene was more common in tetracycline resistant EOGBS (10/11, 90.9%), LOGBS (17/17, 100%) and NCGBS (10/11, 90.9%), compared to tetracycline resistant MCGBS (12/51, 23.5%). Additionally, the tetM gene accounted for 90.9% (10/11), 76.5% (13/17), 45.5% (5/11) and 80.4% (41/51) of four groups of isolates, respectively. Serotype III was the most predominant in EOGBS (8/12, 66.7%) and LOGBS (15/17, 88.2%), while serotype Ib accounted for 50.0% (6/12) of NCGBS, and serotype Ia and III accounted for 45.6% (26/57) and 33.3% (19/57) of MCGBS, respectively. Sequence type 17 (ST17) was the most common in EOGBS (6/12, 50%) and LOGBS (12/17, 70.6%), while ST12 was predominant in NCGBS (5/12, 41.7%), and five STs (ST19, ST23, ST12, ST103 and ST485) accounted for 66.7% (38/57) of the MCGBS. All serotype III-ST17 isolates recovered from neonates were associated with invasive infections.ConclusionsThis study shows the meaningful differences in molecular mechanisms of resistance to erythromycin and tetracycline, and the prevalence of serotypes and STs among GBS recovered from neonates and pregnant women. ST17 is predominant in neonatal invasive GBS, but rare in NCGBS and MCGBS.