Prevention of Early-onset Neonatal Group B Streptococcal Disease |
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Authors: | M. J. Soto Marió I Valenzuela A. E Vásquez S. E Illanes |
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Affiliation: | 1.Department of Obstetrics & Gynaecology and Laboratory of Reproductive Biology, Faculty of Medicine, Universidad de Los Andes,, Santiago, Chile;2.Biotechnology Section, Department of Environmental Health, Instituto de Salud Pública de Chile,, Santiago, Chile |
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Abstract: | Streptococcus agalactiae, also known as Group B Streptococcus (GBS), is an opportunistic pathogen that colonizes the gastrointestinal and genitourinary tracts of up to 50% of healthy adults and newborns; it is responsible for significant morbidity and mortality. Early detection can be used to establish the use of antibiotic prophylaxis to significantly reduce neonatal sepsis. This article reviews methods of detection and prevention of GBS infection in the neonate.Key words: Streptococcus, Neonatal sepsis, PreventionStreptococcus agalactiae, also known as Group B Streptococcus (GBS), is a β-hemolytic Grampositive streptococcus and an opportunistic pathogen that colonizes the gastrointestinal and genitourinary tracts of up to 50% of healthy adults1,2 and newborns; it is responsible for significant morbidity in pregnant women and mortality in the immunocompromised.3–5GBS infection produces two different clinical presentations: early-onset neonatal sepsis (EONS) and late-onset neonatal sepsis (LONS) ( Implementation of different antibiotic prophylactic policies during labor led to a reduction in incidence of 65% by the 1990s, from 1.7 to 0.6 in 1000 live births.7 In recent years this number has continued to decrease, reaching figures of 0.30 and 0.39 per 1000 live births in the United States and United Kingdom, respectively.8,9 It has been suggested, however, that the incidence could be higher than reported, given that the requirements for positive cultures in blood or cerebrospinal fluid can underestimate the real burden of the disease.10 In developing countries, this pathology affects 2 to 4 per 1000 live births, and the incidence in centers without prevention protocols could reach up to 3.5 per 1000 live newborns, with a mortality rate near 15%.11Table 1Clinical Comparison Between Early- and Late-onset Neonatal Sepsis | Early-onset Neonatal Sepsis | Late-onset Neonatal Sepsis |
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Time of presentation | Within 24 hours of birth (range, to day 6 of life) | 4–5 weeks of age (range, 7–89 days) | Clinical manifestations | Generalized sepsis, pneumonia, meningitis | Bacteremia without focus, meningitis, focal infection (septic arthritis, osteomyelitis, pneumonia, cellulitis, adenitis) | Profound shock | Likely | Less likely | Seizures in meningitis | Not likely | Likely | Open in a separate windowColonization during pregnancy is associated with miscarriage, premature labor, chorioamnionitis, and premature prelabor membrane rupture.12 In the newborn, GBS produces EONS in the first week of life with a mortality rate of 10% to 15%7 as a consequence of GBS exposure during labor,4,13 and fetal aspiration of GBS contaminated amniotic fluid due to an ascendant infection from the maternal urogenital tract. By inhaling amniotic fluid the respiratory tract is colonized,14 causing pneumonia and septicemia with the consequential dissemination to different organs.15 When the infection is acquired later (LONS, at 70–90 days of life), the most frequent manifestation is meningitis and sepsis, causing permanent neurologic sequelae in 50% of patients that survive the infection, with an associated mortality rate of 2% to 6%.4,7,14–16 |
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