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27 Group B Streptococcal Infections inChildren andHearing Loss
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rifampin treatment subsequently to completing the parenteral therapy to eliminate mucosal colonization [7]; however, the last is not recommended for routine use [46]. Nevertheless, the recommendation to continue treatment 1 week more than the ordinary course for recurrent GBS disease has little data support [4].
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27.9 Outcome
The outcome in newborns, infants, and children varies according to the infant’s gestational age, the onset time (EOD, LOD, late-LOD), the localization, and the severity of the infection. Mortality is 2–3% in EOD and 1–3% in LOD.Mortality is higher in preterm infants: 20–30% in EOD and 5–8% in LOD [4, 28, 32]. A study examining 15,429 infants younger than 90days in England reported that GBS­attributable mortality per 1000 live births decreased from 0.044in 2001 to 0.014in 2017 [47]. Factors affecting mortality in EOD consist of preterm birth, low birth weight (<2500g), hypotension, shock, apnea, seizures, neutropenia, and thrombo­cytopenia [41, 48, 49].
In 20–30% of patients followed up for early- or late-onset meningitis investi­gated for long-term sequelae, permanent severe neurologic impairment such as cerebral palsy, motor decits, bilateral sensorineural hearing loss (SNHL), cortical blindness, or signicantly delayed development and learning disorders were diag­nosed [1, 2, 4, 7]. Approximately one-quarter of patients develop hydrocephalus requiring VPS, seizure controllable with medication, or mild delayed learning and development. Although the incidence of GBS infection is low in Europe, the inci­dences of mortality and cerebral palsy were high in a cohort study from Norway [50]. The study concluded that preterm birth and low Apgar scores moderately increased the development of cerebral palsy. In another study comparing 2258 patients with invasive GBS disease and 22,462 controls without a history of GBS infection in Denmark and the Netherlands, there was an association between GBS meningitis and increased mortality at 5years of age detected [51]. In addition, any invasive GBS disease was correlated to an increase in the risk of neurodevelopmen­tal impairment at the age of 10years.
GBS infections also create a serious disease and patient burden. The invasive GBS disease was correlated to more common outpatient clinic visits and admissions to the hospital in children aged 5years or younger [51]. The hearing loss (HL) inci­dence throughout the GBS infection is unknown, but all GBS meningitis patients should have diagnostic auditory brainstem response (ABR) testing.
27.10 Group B Streptococcal Infections inChildren
andHearing Loss
Hearing loss within the rst years of life, generally preventable, may result in delays in speech, language, and cognitive development [52–54]. Therefore, early identi­cation of whether a temporary or permanent HL is vital in the child’s communica­tion and development [55–58].
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In GBS invasive infection, an inammatory response may occur in the host dur­ing bacteria’s ongoing replication and digestion, damaging some tissues [59]. Immune complexes circulate long in newborns with GBS disease and cause end­organ damage [60]. In addition, immune complexes containing GBS components cause the release of cytokines such as leukotriene B4 and IL-6. The IL-6 release from monocytes is induced by group B and type III capsular polysaccharides, and group B antigen stimulates TNF-α release [61]. Like other gram-positive agents, GBS cell walls have peptidoglycan and lipoteichoic acid. Various proinammatory cytokines, including TNF-α, IL-1, IL-6, and G-CSF, are elicited by gram-positive agents’ peptidoglycan [62, 63]. Moreover, lipoteichoic acid stimulates IL-1β, IL-6, and TNF-α releases [64, 65].
The cytokine responses, especially proinammatory cytokines, are important in morbidities such as HL caused by bacterial meningitis, otitis media, and labyrin­thitis ossication [66]. Tumor necrosing factor-alpha is essential in HL’s pathogen­esis. Aminpour etal. [67] revealed that TNF-α blockade via anti-TNF-α antibody caused a remarkable improvement of postmeningitic HL and cochlear damage induced by Streptococcus pneumoniae meningitis. In contrast, the exposition of non-infected animals to the intrathecal ow of TNF-α caused HL, like in bacterial meningitis. The mechanisms of HL in pneumococci have been demonstrated, and it can be thought that similar mechanisms play a role in GBS infections.
The frequency of HL and the mechanism behind GBS meningitis are still unknown; more studies are needed to determine efcient treatments of GBS meningitis- related HL processes, including regulating cytokines and antioxidants and promoting cochlear implants in patients with permanent, profound HL.
E. Karadağ Öncel et al.
27.11 Prevention
As with many infectious diseases, it is critical to prevent GBS infections, given the serious mortality and morbidity in early infancy. There are several different preven­tive approaches to reduce GBS infection, mainly maternal prophylaxis to reduce transmission, infant prophylaxis to minimalize colonization, and immunoprophy­laxis to enhance protection against the disease. However, infant prophylaxis is not recommended because it is not yet effective, according to studies [1, 68].
27.11.1 Intrapartum Antibiotic Prophylaxis (IAP)
Following the reports of Boyer and Gotoff [69], stating that the incidence of GBS­induced neonatal sepsis decreased signicantly with intrapartum intravenous (IV) ampicillin administration to females with preterm labor or preterm premature rup­ture of membranes, obstetric and pediatric professional organizations have initiated studies to nd the most effective approach in terms of both clinical and cost­effectiveness. Intrapartum antibiotic prophylaxis for EOD was implemented in 1996 with a consensus recommended by the AAFP, the AAP, the ACNM, the ACOG,
27 Group B Streptococcal Infections inChildren andHearing Loss
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and other stakeholder organizations [18]. This consensus includes risk- or culture­based approaches. The risk-based approach recommends giving IAP in one of the following risk factors; premature labor <37weeks, GBS bacteriuria, body tempera­ture≥100.4°F (38°C) at birth, prolonged premature rupture of membranes over 18 h, or a history of GBS infection in a previous infant. In the culture-based approach, IAP is recommended for all females having GBS isolated in vaginal and rectal cultures at 35–37th gestational weeks, disregarding risk factors. With these approaches, there has been a reduction of approximately 70% in EOD incidence [24, 68].
In a population-based study conducted in 2002 comparing these two approaches, the culture-based approach was 50% more efcient in preventing EOD [70]. It has also been shown that the mothers of 62% of infants who develop EOD have no identied risk factors. Therefore, in 2002, the Centers for Disease Control and Prevention (CDC) recommended universal vaginal and rectal culture screening for all women between 35 and 37weeks of pregnancy and recommended giving intra­partum prophylaxis to GBS carriers [21]. Table27.4 shows the indications and the non-indication conditions of IAP use in EOD.A beta-lactam antibiotic (penicillin is preferred) is effective in prophylaxis against GBS-induced EOD when given four doses or longer before birth [71]. The risk-based approach should be chosen only in patients whose culture results are unknown at birth [7].
Table 27.4 Indications and non-indication conditions for maternal intrapartum prophylaxis to prevent early-onset group B streptococcal (GBS) infection
Intrapartum GBS prophylaxis indicated Intrapartum GBS prophylaxis not indicated Previous infant with invasive GBS disease Colonization with GBS during a previous
pregnancy
GBS bacteriuria during any trimester of current pregnancy
Positive GBS vaginal–rectal screening culture within the preceding 5 weeks
Unknown GBS status at the onset of labor and any of the following:
• Delivery at <37weeks’ gestation
• Prolonged rupture of membranes for ≥18h
• Intrapartum temperature≥100.4°F (38°C)
• Intrapartum nucleic acid amplication test (NAAT) positive for GBS
a
Adapted and modied from Ref. [68]
b
Intrapartum chemoprophylaxis is not indicated in this circumstance if a cesarean delivery is per-
formed before the onset of labor on a woman with intact membranes
c
If amnionitis is suspected, broad-spectrum antibiotic therapy that includes an agent active against
GBS should replace GBS prophylaxis
d
GBS nucleic acid amplication tests (NAATs) are optional and may not be available in all set­tings. If intrapartum NAAT is negative for GBS, but any other above intrapartum risk factor is present, then intrapartum GBS prophylaxis is indicated
b
b
c
d
GBS bacteriuria during previous pregnancy
Negative vaginal–rectal screening culture, regardless of intrapartum risk factors
Cesarean delivery is performed before the onset of labor on a woman with intact amniotic membranes, regardless of GBS colonization status or gestational age
a
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The CDC renewed its guidelines to include approaches and algorithms in 2010 [68]. These new recommendations included descriptive laboratory methods for demonstrating GBS colonization in pregnancy, screening and IAP administration algorithms for females with preterm labor and premature rupture of membranes, prophylaxis approaches in penicillin allergy, and a revised algorithm for neonatal care. Empirical management of a newborn for secondary prevention of EOD is shown in Fig.27.2.
Signs of neonatal sepsis?
No
Maternal
chorioamnionitis?
3
No
Maternal intrapartum antibiotic prophylaxis (IAP) indicated?
5
Yes
Mother received intravenous
penicillin, ampicillin,
or cefazolin
≥4 hours before delivery
No
≥37 weeks’ gestation and
rupture of
membranes <18 hours
Yes
Yes
No
Yes
Yes
Full diagnostic evaluation Antibiotic therapy
Limited evaluation
Antibiotic therapy
Routine clinical care
2
4
2
6
Observation for ≥48 hours
Observation for ≥48 hours
1
6,7
6,8
No
Either <37 weeks’ gestation
or rupture of
membranes ≥18 hours
Fig. 27.2 Empirical management of a newborn for secondary prevention of early-onset group B streptococcal infection. (Adapted and modied from Ref. [68])
Yes
Limited evaluation
4
Observation for ≥48 hours
6
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In maternal chemoprophylaxis, IV penicillin G (initial dose, 5 million units; fol­lowing doses, 2.5–3 million units every 4h until delivery) is preferred [68, 70]. As an alternative to penicillin, ampicillin (initial dose, 2g; following doses, 1g every 4h) can be administered for prophylaxis. Clindamycin and erythromycin resistance rates should be considered when choosing prophylaxis in women with penicillin allergy [72, 73]. If the anaphylaxis risk is low, cefazolin (initial dose, 2g; following doses, 1g every 8h) may also be used for prophylaxis. Clindamycin (900mg every 8 h) may be used if the organism is susceptible based on susceptibility testing. Erythromycin is not an acceptable alternative [68]. When there is no susceptibility test, the results are unknown, or if there is clindamycin resistance, vancomycin (1g every 12h) may be administered as an alternative therapy. However, the vancomy­cin efciency is not known.
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27.11.2 Immunoprophylaxis
Although IAP is an effective approach, about 30% of women use antibiotics; there is still a possibility of antimicrobial resistance development, the inability to prevent late-onset GBS infections, and the inability to avoid miscarriage and fetal death caused by GBS disease. Vaccine studies to prevent GBS infection and disease are ongoing. Maternal immunization can improve the drawbacks of IAP and decrease the invasive GBS infection global burden in pregnant women and newborns. Monovalent, divalent, and trivalent GBS vaccines against serotypes Ia, Ib, II, III, and V were previously studied in non-pregnant and pregnant women. These vac­cines have been proven safe and cause increased GBS antibodies after vaccination in newborns [74, 75]. A recent phase 1/2 study about the safety and immunogenicity of a novel hexavalent group B streptococcus conjugate vaccine (GBS6), including serotypes Ia, Ib, II, III, IV, and VI, determined that GBS6 was well tolerated and caused robust immune responses in women during 6 months [76]. Hopefully, with new studies and a valid and effective vaccine, GBS infections will decrease, and infants can be protected from GBS disease soon.
27.12 Conclusion
The most critical risk in neonatal GBS disease is morbidity, including cerebral palsy, intellectual disorder, seizures, visual disturbances, and HL, which are long term. Neurologic sequelae are more common, especially in infants with GBS men­ingitis. There are insufcient data on the frequency of HL in GBS meningitis. However, HL is one of the most critical sequelae after bacterial meningitis. Prompt diagnosis and treatment are crucial, and infants with GBS disease or meningitis should have a rapid and complete hearing assessment. These infants need regular follow-ups for HL and, once identied, referred for early cochlear implantation.
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Pneumococcal Meningitis inChildren
https://t.me/medicina_free
andHearing Loss
AyşeTekin Yılmaz, EnerÇağrıDinleyici, EminSamiArısoy, TinaQ.Tan, andSheldonL.Kaplan
28.1 Introduction
Streptococcus pneumoniae, rst isolated in 1881 by two scientists separately, remains a signicant pathogen in public health today. Louis Pasteur identied the bacterium in France and named it “microbe septicemique de la salive.” George
A. Tekin Yılmaz (*) Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine, Sakarya University, Sakarya, Türkiye e-mail: aaysetekin@gmail.com
E. Ç. Dinleyici Division of Pediatric Intensive Care, Department of Pediatrics, Faculty of Medicine, Eskişehir Osmangazi University, Eskişehir, Türkiye e-mail: enercagri@gmail.com
E. S. Arısoy Division of Pediatric Infectious Diseases, Department of Pediatrics, Faculty of Medicine, Kocaeli University, Kocaeli, Türkiye e-mail: emin.sami.arisoy@gmail.com
T. Q. Tan Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA
Division of Infectious Diseases, Ann and Robert H. Lurie Children’s Hospital of Chicago, Chicago, IL, USA e-mail: titan@luriechildrens.org
S. L. Kaplan Division of Infectious Diseases, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA
Infectious Disease Service, Texas Children’s Hospital, Houston, TX, USA e-mail: slkaplan@texaschildrens.org
28
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023 A. E. Arısoy et al. (eds.), Hearing Loss in Congenital, Neonatal and Childhood Infections, Comprehensive ENT, https://doi.org/10.1007/978-3-031-38495-0_28
421
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