++
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CONGENITAL INFECTIONS
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Congenital infections acquired in utero are a significant cause of neonatal mortality and childhood morbidity. The original concept of the TORCH acronym was to group five infections with similar presentations: toxoplasmosis, “other” (traditionally referring to syphilis), rubella, cytomegalovirus (CMV), and herpesvirus. However, recent additions have expanded the scope of this term to include infections such as human immunodeficiency virus (HIV), enteroviruses, parvovirus B19, and varicella. The incidence of TORCH infections in the United States is variable, ranging from 0.7% for CMV, the most common congenital viral infection, to ≤1 in 10,000 for rare infections such as rubella and toxoplasmosis. A high index of suspicion for congenital infection and awareness of the prominent features of the most common etiologies will help to facilitate early diagnosis and management.
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Transplacental spread and invasion of the bloodstream after maternal infection is the primary route for intrauterine infection, though it is also possible for the fetus to be infected by extension from adjacent infections of the peritoneum and the genitalia during the birth process or during invasive procedures such as fetal monitoring and intrauterine transfusion.1
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In order for the maternal immune system to tolerate pregnancy, the placenta serves as a protective barrier that shields the fetus from maternal humoral and cell-mediated immune activity. Without immunologic mechanisms necessary to eradicate an infecting organism, the fetus is susceptible to infection, and a state of immunologic tolerance is often established. The fetus is particularly vulnerable during the first trimester of pregnancy, when the most complex events in embryogenesis occur, including development of sensory organs such as the eyes and ears.
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The outcome of fetal infection depends on several factors, including gestational age at the time of infection, organism virulence, degree of associated placental damage, and maternal disease severity.1 Primary infection is also likely to have more significant effects on the fetus than recurrent infection. Infection during the first few weeks of gestation may cause embryonal death and resorption, prior to recognition of pregnancy. Spontaneous abortion and stillbirth are among the earliest recognizable effects of fetal infection after 6 to 8 weeks of pregnancy. In infants who are live-born, effects of fetal infection may present as preterm birth, intrauterine growth restriction (IUGR), congenital anomalies, or local or systemic signs of infection. Alternatively, fetal infection may present in live-born infants as the complete absence of any clinical signs of disease, with abnormalities becoming obvious only as the child develops and fails to reach appropriate physiologic or developmental milestones.
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CLINICAL PRESENTATION
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Intrauterine infection with CMV, herpes simplex virus (HSV), syphilis, rubella, toxoplasmosis, and enterovirus may present in the neonatal period with signs of widely disseminated disease caused by microbial invasion and proliferation over weeks or months prior to delivery.1 In such infants it can be difficult to determine whether infection was acquired in utero, intrapartum, or postpartum. However, if the onset of clinical symptoms after birth occurs within the minimal incubation period for the disease, it is likely that infection was acquired before delivery.
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Congenital CMV infection may present at birth with generalized petechiae, direct hyperbilirubinemia, hepatosplenomegaly, purpuric rash, microcephaly, seizures, focal or general neurologic deficits, retinitis, and intracranial calcifications (usually periventricular) (Figure 128-1A). However, 90% of infants with congenital CMV infection are asymptomatic at birth, and most cases are undetected prior to discharge from the birth hospital. Infants who are symptomatic at birth are at highest risk of long-term neurological sequelae, including sensorineural hearing loss, mental retardation, cerebral palsy, and vision impairment. However, approximately 10% to 15% of asymptomatic, infected infants will also experience later, long-term adverse neurological outcomes.2
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Intrauterine infection with HSV is rare (approximately 1 in 300,000 deliveries), compared with the vast majority of neonatal HSV infections which result from exposure during delivery. Intrauterine HSV transmission is highest during the first 20 weeks of pregnancy, resulting in abortion, stillbirth, and congenital anomalies in infants who survive.3 Perinatal mortality is high, and infected infants usually have clinical abnormalities identified at birth. Typical presentation is a triad of clinical findings: cutaneous manifestations (i.e. scarring, active lesions, hypo- and hyperpigmentation, aplasia cutis, and/or an erythematous macular exanthem), ophthalmologic findings (i.e. micro-opthalmia, retinal dysplasia, optic atrophy, and/or chorioretinitis), and neurologic involvement (i.e. microcephaly, encephalomalacia, hydranencephaly, and/or intracranial calcification).3
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Clinical presentation for infants infected with HSV during delivery can be divided into three categories, each associated with different outcomes and manifestations. Neonates with infection confined to the skin, eyes, and mucosa (SEM) comprise about 45% of most case series, most often presenting with cutaneous or mucosal vesicular lesions.4 By definition, infants in this category have no central nervous system (CNS) or visceral organ involvement, although systemic therapy is required to prevent further disease progression. Infants with SEM HSV disease often have recurrent cutaneous outbreaks in early childhood. The second category is HSV infection with CNS involvement, comprising 30% of cases.4 CNS disease can present with lethargy, poor feeding, or seizures, with or without cutaneous lesions. Morbidity with CNS involvement is higher with HSV-2 than HSV-1 infection, with potential long-term sequelae including developmental delay, epilepsy, blindness, and cognitive disabilities. Relapses of CNS infection may also occur during childhood, further increasing morbidity. Disseminated HIV infection is the third category and occurs in 25% of cases. Mortality risk is highest for these infants (approximately 30%), as it is associated with multiorgan dysfunction. Clinical presentation can be indistinguishable from bacterial sepsis.4
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Congenital syphilis results from fetal infection with the spirochete Treponema pallidum via transplacental transmission. In recent years, the rate of congenital syphilis in the United States has increased, now affecting 10 per 100,000 births.5 Untreated syphilis during pregnancy results in fetal or neonatal death in up to 40% of cases. Infected live-born infants are often asymptomatic, with only severe cases clinically apparent at birth. Untreated asymptomatic infants can subsequently develop severe sequelae in the first few weeks, months, or years of life.
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Early presentation of congenital syphilis, manifesting within the first few months to first year of life, can include hepatosplenomegaly, jaundice, lymphadenopathy, meningoencephalitis, chorioretinitis, and mucocutaneous findings such as maculopapular erythema, bullae, and desquamation. Infants may fail to thrive and have a characteristic mucopurulent or blood-stained nasal discharge causing “snuffles.” Osteochondritis of the long bones and ribs may cause pseudoparalysis of the limbs with characteristic radiologic changes. Late presentation of congenital syphilis, manifesting after the first 1 to 2 years of life, can include gummatous ulcers of the nose, septum, or hard palate; periosteal lesions resulting in saber shins and frontal and parietal bossing; juvenile paresis and tabes secondary to neurosyphilis; optic atrophy and interstitial keratitis; and progressive sensorineural deafness. Dental abnormalities include Hutchinson incisors (small, widely spaced, peg-shaped, notched upper incisors with thin discolored enamel), hypoplastic enamel, and mulberry molars. “Hutchinson triad” is a pathognomonic constellation of findings that consist of interstitial keratitis, Hutchinson teeth, and sensorineural hearing loss.
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Toxoplasma gondii is a protozoan parasite transmittable through contact with cat feces or consumption of contaminated foods, such as meat containing infective tissue cysts or unwashed produce from contaminated soil. The risk of transplacental infection is lower (10% to 25%) when maternal infection occurs in the first trimester compared with the third trimester (60% to 90%). However, severe sequelae, including stillbirth and neonatal death, are more likely when infection is acquired in the first trimester. Overall risk of congenital infection from acute prenatal infection ranges from approximately 20% to 50%. Most neonates with congenital toxoplasmosis are asymptomatic; however, clinical presentation can include hepatosplenomegaly, lymphadenopathy, maculopapular rash, jaundice, anemia, and thrombocytopenia. A classic triad of clinical findings associated with this disease is chorioretinitis with intracranial calcifications (typically generalized) (Figure 128-1B) and hydrocephalus.
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Enteroviruses are small, single-stranded RNA viruses belonging to the Picornaviridae family. Congenital enterovirus infection often presents with a maternal history of viral illness including fever, respiratory concerns, or abdominal symptoms preceding or immediately following delivery. There may also be a history of viral symptoms in other family members. Signs of infection in neonates may include temperature instability, irritability, lethargy, jaundice, emesis, abdominal distension, diarrhea, respiratory distress, and macular or maculopapular rash. Most affected neonates have mild disease, however, a small percentage develop severe sequelae including meningoencephalitis, myocarditis, pneumonia, hepatitis, and coagulopathy. Myocarditis in particular confers high-mortality risk for affected infants and has special diagnostic significance for enterovirus infection.
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Since licensure of live attenuated rubella vaccines in the late 1960s, the number of reported US cases of congenital rubella infection has declined dramatically to <1 case per year. Risk of infection and associated defects is highest during the first 12 weeks of gestation. Severe sequelae including spontaneous abortion and stillbirth are possible outcomes of infection early in pregnancy. Infection in the first trimester is considered to be uniformly teratogenic, while birth defects are very rare among infants infected after 20 weeks of gestation.6 Common congenital manifestations include cataracts, congenital heart disease (most commonly patent ductus arteriosus or peripheral pulmonary artery stenosis), hearing impairment, and developmental delay. Affected infants usually present with more than one sign or symptom, however, they may present with a single defect. Eye findings including glaucoma, chorioretinitis, retinopathy, and cataracts have special diagnostic significance for this infection. In some cases, congenital rubella may only be identified years after birth due to isolated hearing defects.
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Human Immunodeficiency Virus
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Although the transmission rate of HIV from an untreated mother to the fetus is estimated to be about 25%, this risk can be reduced to <2% with use of antiretroviral regimens and obstetrical intervention (i.e. zidovudine or nevirapine and elective cesarean section at 38 weeks of pregnancy), and by avoiding breastfeeding. Infants with congenital HIV infection are usually asymptomatic at birth and through the first few months of life. The median age of onset for clinical signs is approximately 3 years, but many children remain asymptomatic for more than 5 years. Clinical presentation of congenital HIV infection can include failure to thrive, persistent diarrhea, recurrent suppurative infections, and opportunistic infections that occur weeks to months or years after birth.
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Varicella-zoster virus (VZV) is one of eight herpes viruses known to cause human infection; primary infection during pregnancy carries significant implications for both maternal and fetal health. Congenital varicella syndrome due to transplacental infection is rare and mostly occurs with infection between 8 and 20 weeks gestation. Characteristic findings in affected neonates may include: low birth weight; cutaneous scars in a dermatomal distribution; eye findings of cataracts, chorioretinitis, microphthalmos, or nystagmus; hypoplastic limbs; gastrointestinal abnormalities including bowel stenosis; and neurological findings of cortical atrophy or seizures. Varicella is not generally associated with spontaneous fetal loss, preterm birth, or stillbirth.
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Parvovirus B19 is a single-stranded, DNA virus that preferentially infects rapidly dividing cells and is cytotoxic for erythroid progenitor cells. The risk for transplacental transmission from an infected mother to the fetus is between 10% to 35%, and is highest in the first and second trimesters of pregnancy. Infection prior to 20 weeks gestation is associated with a higher fetal mortality rate (14.8%) compared with infection after 20 weeks (2.3%). Presentation is typically related to severe anemia, high-output cardiac failure, and extramedullary hematopoiesis, resulting in nonimmune hydrops fetalis, ascites, pleural effusion, and pericardial effusions. Persistent anemia due to hematopoietic suppression can also persist for months after birth.
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DIFFERENTIAL DIAGNOSIS
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As shown in Table 128-1, clinical presentations for infections acquired in utero share many features, including but not limited to IUGR, microcephaly, cataracts, hearing loss, hepatosplenomegaly, cutaneous findings, and thrombocytopenia. Consequently, in the absence of maternal history or prenatal laboratory results that suggest a specific infection (e.g. positive syphilis serology), the differential diagnosis for each TORCH infection includes all of the other TORCH or TORCH-like infections. It is also important to note that neonates with suspected or confirmed congenital HIV or syphilis infection should also be considered at risk for other sexually transmitted infections including gonorrhea and Chlamydia trachomatis.
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Noninfectious diseases in the differential include genetic disorders (e.g. pseudo-TORCH syndrome), inborn errors of metabolism, ABO or Rh incompatibility, neoplastic disorders, and prenatal teratogen or drug exposure.
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DIAGNOSTIC EVALUATION
++
Initial evaluation of a neonate with suspected intrauterine infection should begin with a thorough review of maternal history, including routine prenatal laboratory studies, history of HSV, HIV, and other diseases, and potential exposures including contact with cats and persons infected with VZV. A head-to-toe assessment should be performed to identify physical findings that may be more prominent features of a particular congenital infection. Additional helpful studies for initial evaluation are a complete blood count (CBC) with differential and platelet count, liver function tests, long bone radiography, ophthalmologic and audiologic evaluation, neuroimaging, and lumbar puncture.7,8 Based on initial results, further tailored evaluation for a specific infection or group of infections may follow. Table 128-2 depicts specific fetal and neonatal laboratory studies to guide antenatal and postnatal diagnosis for each infection.
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Care of the HIV-Exposed Infant
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Because treatment recommendations change over time, consultation with a pediatric HIV expert is recommended in the care of HIV-exposed and infected infants. Care of the HIV-exposed infant is addressed in Chapter 108. Current treatment recommendations are available online at http://aidsinfo.nih.gov. The National Perinatal HIV Hotline (1-888-448-8765) also provides free clinical consultation for providers.
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Currently, it is recommended that for HIV-exposed infants, virologic testing should be performed within the first 2 to 3 weeks of life, at 1 to 2 months, and at 4 to 6 months of age. Additionally, some experts recommend virologic testing at birth, particularly in women who have not had good virologic control during pregnancy or if adequate follow-up of the infant is uncertain.9 A 6-week regimen of zidovudine chemoprophylaxis is recommended for all HIV-exposed neonates; this should be initiated as close to the time of birth as possible and preferably within 6 to 12 hours of life. HIV-exposed infants who did not receive antepartum antiretroviral (ARV) drugs should receive 6 weeks of zidovudine as well as nevirapine. To prevent opportunistic infection with Pneumocystis jirovecii, all HIV-exposed infants should begin trimethoprim-sulfamethoxazole prophylaxis at 4 to 6 weeks, after completion of ARV prophylaxis. Because of the risk of HIV transmission through breast milk, infants in the United States should not breastfeed. If the infant’s virologic testing is positive at any time, chemoprophylaxis should be discontinued and the infant should be promptly seen by a pediatric HIV specialist for treatment with standard combination ARV therapy.
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Congenital Toxoplasmosis
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For congenital toxoplasmosis infections, initial therapy is pyrimethamine combined with sulfadiazine (supplemented with folinic acid).10 Dosage and duration of therapy should be determined in consultation with an infectious disease specialist.
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HSV Exposure and Infection
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Management of the asymptomatic, HSV-exposed neonate is complex, as risk of infection varies significantly based on whether maternal infection is primary or recurrent. For infants born vaginally or by cesarean to mothers with active genital HSV lesions at delivery, surface cultures should be obtained at 12 to 24 hours of life from the nasopharynx, mouth, urine, and stool or rectum.11 These asymptomatic, exposed infants should be kept in contact isolation and closely observed. Most experts would not administer empiric antiviral therapy, although parents or caregivers should be educated about the signs and symptoms of neonatal HSV infection during the first 6 weeks of life.
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For infants with known maternal, recurrent genital HSV infection but no genital lesions at delivery, close observation without contact isolation or surface cultures is indicated.11 As above, parents or caregivers should be educated about the signs and symptoms of neonatal HSV infection at discharge.
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Any neonate with a vesicular rash should be evaluated for HSV. Disseminated HSV infection should also be considered in neonates with signs of sepsis, particularly those with negative bacteriologic culture results and/or severe liver dysfunction. For infants with suspected or confirmed HSV infection, parenteral acyclovir is the treatment of choice regardless of manifestations and clinical findings.11 Treatment for infants with CNS involvement or disseminated disease is a minimum of 21 days. Use of oral acyclovir for 6 months following treatment of acute disease has been shown to improve neurodevelopmental outcomes and to prevent skin recurrences. In addition to parental acyclovir, infants with ocular involvement should also receive topical ophthalmic medication (1% trifluridine, 0.1% iododeoxyuridine, or 3% vidarabine).
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Evaluation and Treatment of Congenital Syphilis
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Parenteral penicillin remains the standard treatment for congenital syphilis. Factors to consider in treatment include adequacy of maternal treatment and response to treatment, infant serologic titers compared with maternal titers, and physical exam findings and other laboratory studies.12 The approach to diagnosis, evaluation, and treatment of infants with potential congenital syphilis is summarized in Figure 128-2.
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Treatment for the remaining intrauterine infections, including CMV, rubella, varicella, parvovirus, and enterovirus, is primarily supportive. Infants in congestive heart failure require careful fluid management and treatment with inotropic agents and/or diuretics. Bleeding and coagulopathy due to hepatic failure may necessitate frequent replacement therapy with packed red blood cells, platelets, fresh-frozen plasma, and vitamin K. Intravenous immunoglobulin (IVIG) has been used for neonates with life-threatening enterovirus infections, although proof of efficacy is lacking. The use of antiviral drug pleconaril in neonatal enteroviral sepsis syndrome is currently being studied. For congenital CMV, antiviral therapy is not recommended routinely for neonates due to potential toxicity. However, parenteral ganciclovir or oral valganciclovir can be used in symptomatic infants with CNS involvement and may be helpful in protecting against hearing deterioration and developmental impairment. Finally, newborns with severe varicella infection should be treated with acyclovir, as it may reduce mortality risk. Treatment should begin as soon as possible after onset of symptoms.
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ADMISSION AND DISCHARGE CRITERIA
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Admission to a neonatal intensive care unit should be considered for newborns with
++
Severe IUGR
Preterm birth (between 35 and 36 weeks gestation, this may depend upon clinical assessment and whether the postnatal ward can provide an appropriate level of care)
Respiratory compromise, including apnea, cyanosis, or requirement for supplemental oxygen or ventilator support
Hemodynamic instability
CNS involvement
Gastrointestinal symptoms, including feeding difficulty or concern for intestinal anomalies
Requirement for an exchange transfusion
Physical exam or laboratory findings concerning for disseminated infection
++
Discharge home is appropriate when
++
Infant is clinically stable
Any necessary diagnostic and hospital-based treatment regimens are complete
Appropriate primary care and specialty follow-up appointments have been arranged
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With suspected congenital infections, consultation with a pediatric infectious disease specialist may be warranted to help guide diagnostic workup, interpretation of laboratory results, and treatment. Consultation with an expert in pediatric HIV infection is recommended in the care of HIV-exposed neonates. Treatment of herpes simplex virus ocular infection should involve an ophthalmologist.
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SPECIAL CONSIDERATIONS
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Risk of TTN may be lowered by limiting cesarean sections whenever possible, and planning elective cesarean deliveries, when deemed necessary, at 39 weeks’ gestation or later. All women should be screened serologically for syphilis early in pregnancy with a nontreponemal test (e.g. RPR or VDRL) and preferably again at delivery. HIV screening is also recommended as part of standard prenatal care. Routine serological screening for herpes simplex virus (HSV) in asymptomatic pregnant women is not recommended, as it has not been shown to reduce transmission of HSV to newborns. Pregnant women identified as rubella nonimmune should be immunized in the immediate postpartum period to protect future pregnancies, however, immunization is contraindicated during pregnancy and in the 3 months before conception.
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Awareness of congenital viral infections, their potential risks, and appropriate hand hygiene measures to minimize acquired infection are important for pregnant women and women of childbearing age. Current research of an investigational CMV vaccine for use in pregnancy appears promising. Serologic testing for varicella should be considered only for pregnant women who do not have evidence of immunity (reliable history of chickenpox or documented vaccination). There is no single recommendation for monitoring for parvovirus B19 in pregnancy, but serological testing may be indicated when there are potential exposures. Pregnant women whose serostatus for T. gondii is negative or unknown should avoid activities that potentially expose them to cat feces (such as changing litter boxes, gardening, and landscaping), or they should wear gloves and wash their hands if such activities are unavoidable.
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PERINATALLY ACQUIRED INFECTION
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In addition to congenital infections acquired in utero, infections acquired during birth from the maternal genital tract can present as systemic infection in the neonate. An estimated 10% to 30% of pregnant women are rectally or vaginally colonized with group B streptococcal (GBS), the leading cause of neonatal early-onset sepsis and meningitis in the United States. As a result of prevention efforts, including improved antenatal screening and antibiotic prophylaxis, the incidence of GBS early-onset disease has declined dramatically over the past 15 years, from 1.7 cases per 1000 live births in the early 1990s to 0.34–0.37 cases per 1000 live births recently.13 However, available GBS prevention strategies will not prevent all cases of early-onset disease and any cases of late-onset disease, and rapid neonatal detection and treatment is necessary to minimize morbidity and mortality for those cases that do occur.
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GBS is a gram-positive bacterium that primarily infects infants, pregnant women, and older adults, with the highest incidence among young infants. Neonatal infections within the first week of life are designated early-onset disease, while late-onset infections occur in infants greater than 1 week, with most infections evident during the first 3 months. Early-onset infections are acquired vertically through exposure from the colonized vagina; infection occurs primarily when the bacterium ascends to the amniotic fluid after onset of labor or rupture of membranes, although it also can invade through intact membranes. GBS can then be aspirated into the fetal lungs, leading to bacteremia. Infants also can become infected during passage through the birth canal.
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Maternal colonization with GBS is the primary risk factor for early-onset GBS disease. Additional factors that increase the risk include preterm birth, longer duration of membrane rupture, intra-amniotic infection, young maternal age, black race, low maternal levels of GBS-specific antibody, and previous delivery of an infant with invasive GBS disease.13
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The incidence of late-onset disease, at <0.5 per 1000, has not been reduced with implementation of antenatal screening and maternal antibiotic prophylaxis. The pathogenesis of late-onset GBS disease remains obscure, but it is likely that even when vertical transmission at birth does not occur, exposure to either the mother or other colonized family members and caregivers can serve as a source for colonization and subsequent infection.1
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CLINICAL PRESENTATION
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Infants with early-onset GBS disease generally present with respiratory distress, apnea, or other signs of sepsis (including temperature instability, tachycardia, lethargy, irritability, abdominal distention, and poor feeding) within the first 24 to 48 hours of life. The most common clinical syndromes of early-onset disease are sepsis and pneumonia; less frequently, early-onset infections can lead to meningitis. Case fatality ratio for early-onset disease ranges between 4% and 6% in recent years, with highest mortality risk in infants born preterm.
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DIFFERENTIAL DIAGNOSIS
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The differential diagnosis for symptoms of early-onset neonatal sepsis is broad. Critical congenital heart disease should be considered, as many duct-dependent anatomic lesions and tachyarrhythmias manifest early with features that can overlap with sepsis (i.e. tachypnea, tachycardia, and poor perfusion). Hypovolemia resulting from acute perinatal blood loss may also present with nonspecific signs including tachycardia, pallor, and hypotension. Additional conditions include transient tachypnea of the newborn, pneumothorax, pulmonary hypertension, respiratory distress syndrome, congenital anatomic lesions (e.g. congenital diaphragmatic hernia, choanal atresia), neonatal abstinence syndrome, polycythemia, and endocrine and metabolic abnormalities.
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DIAGNOSTIC EVALUATION AND MANAGEMENT
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Detection of early-onset GBS infection can be challenging, as neonatal providers must consider multiple factors, including the infant’s clinical appearance, presence of maternal risk factors (i.e. presence of chorioamnionitis, duration of rupture membranes), and exposure to intrapartum antibiotic prophylaxis. In 2010, a revised algorithm for secondary prevention of neonatal early-onset GBS disease was put forth by the Centers for Disease Control and Prevention (CDC) and endorsed by the American Academy of Pediatrics (AAP) (see Figure 128-3). This algorithm guides evaluation and management for all newborns, who can be categorized into one of five groups: (1) neonates with any signs of sepsis, (2) well-appearing neonates whose mothers had suspected chorioamnionitis, (3) well-appearing neonates without suspected chorioamnionitis and without indication for GBS prophylaxis, (4) well-appearing neonates with adequate GBS prophylaxis, and (5) well-appearing neonates with inadequate GBS prophylaxis. Adequate intrapartum antibiotic prophylaxis is defined as ≥4 hours of IV penicillin, ampicillin, or cefazolin prior to delivery.
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Neonates with Signs of Sepsis
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As shown in Figure 128-3, all symptomatic infants should receive a full diagnostic evaluation, including blood culture, CBC with differential, chest radiograph if respiratory signs are present, and lumbar puncture if stable enough to tolerate the procedure. Antibiotic therapy should be promptly initiated pending laboratory results, and should include IV ampicillin as well as coverage for Escherichia coli and other gram-negative organisms.
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Suspected Chorioamnionitis
++
It is recommended that for infants with suspected chorioamnionitis, a blood culture and CBC should be obtained, and antibiotics initiated pending laboratory results.
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ADMISSION AND DISCHARGE CRITERIA
++
Admission to a neonatal intensive care unit is indicated for any newborn with signs of sepsis. Well-appearing infants undergoing limited evaluation and empiric antibiotic treatment pending results may be appropriate for care in the routine postnatal ward, depending on institution policies and procedures. As shown in Figure 128-3, discharge home of the well-appearing neonate with adequate intrapartum prophylaxis may occur as early as 24 hours, if sufficient follow-up and observation are available. For well-appearing newborns with inadequate intrapartum prophylaxis, observation in the hospital for at least 48 hours is recommended.
++
Consultation with a neonatologist should be considered for infants with symptoms of sepsis, including temperature instability, feeding difficulty, lethargy, abdominal distension, poor tone, respiratory distress, and hemodynamic instability.
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SPECIAL CONSIDERATIONS
++
Prevention strategies have substantially reduced the burden of early-onset GBS disease. The 2010 CDC guidelines recommend universal screening of all pregnant women for vaginal and rectal colonization between 35 and 37 weeks gestation. Any woman with a positive screen, a history of GBS bacteriuria during pregnancy, or previous delivery of an infant with invasive GBS disease requires antibiotic prophylaxis at the time of labor onset or membrane rupture; a planned cesarean delivery obviates the need for antibiotics if labor has not begun and membranes have not ruptured. For women with an unknown GBS status, amniotic membrane rupture ≥18 hours, intrapartum temperature ≥100.4° Fahrenheit, preterm delivery (<37 weeks), or intrapartum testing positive for GBS are indications for intrapartum antibiotic prophylaxis.
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Neonatal providers should be aware of current recommendations for appropriate intrapartum prophylaxis regimens. As penicillin is the first-line agent for antibiotic prophylaxis, with ampicillin as an acceptable alternative. Penicillin-allergic women without a history of anaphylaxis or other severe allergic reactions should receive cefazolin. For penicillin-allergic women at high risk for anaphylaxis, susceptibility testing should be performed on antenatal GBS cultures. In such cases, clindamycin should be used if the GBS isolate is susceptible. If the isolate is resistant to clindamycin or demonstrates inducible resistance, penicillin-allergic women should receive vancomycin. Erythromycin should not be used as an alternative for GBS prophylaxis.
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KEY POINTS
Current conceptualization of TORCH infections has expanded to include HIV, enterovirus, parvovirus B19, and varicella.
Clinical presentation for intrauterine infections is dependent on several factors, including gestational age at infection, organism virulence, and maternal disease severity.
Maternal history, prenatal laboratory results, physical exam findings, and initial laboratory studies should guide the approach to further diagnostic evaluation and management of congenital infections.
May infants with congenital infections are asymptomatic at birth, necessitating a thorough review of antenatal laboratory screening results and maternal exposure history.
Despite prevention efforts, group B streptococcal (GBS) remains the leading cause of neonatal early-onset sepsis and meningitis.
Neonatal providers should be aware of maternal GBS status and recommendations for appropriate intrapartum prophylaxis in order to guide approaches to evaluation and management of the newborn.
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