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Group B streptococci has been a common cause of invasive infection
in neonates and young infants for several decades.1 In
recent years, it has been understood that group B streptococci also
is an important cause of maternal obstetrical morbidity and of fetal
loss. Within the past decade, a significant decline in the incidence
of early-onset group B streptococcal neonatal infections has been
observed in association with universal culture-based screening of
pregnant women and administration of intrapartum antibiotic prophylaxis
to women colonized with group B streptococci.
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Rates of maternal rectal and vaginal colonization with group
B streptococci during pregnancy range from 20% to 30%.
Without interruption of transmission, approximately 50% of
infants delivered of a colonized mother acquire mucous membrane
colonization. The risk for invasive infection among colonized infants
is approximately 1%. This risk is increased when there
is premature onset of labor, maternal chorioamnionitis, a prolonged
interval between rupture of membranes and delivery, twin pregnancy,
or maternal postpartum bacteremia, among other factors. Heavy maternal
colonization also increases the risk for neonatal infection. Fetal
aspiration of infected amniotic fluid can result in the development
of congenital pneumonia with symptoms at or shortly after birth.
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Group B streptococci are gram-positive cocci that grow readily
as white to gray white colony-forming units with a narrow zone of β-hemolysis
when inoculated on blood agar. Group B streptococci have been classified, based
on capsular polysaccharide antigens, into 8 types. Contemporary
data indicate that types Ia, III, and V predominate in early-onset disease,
accounting for more than three quarters of isolates from infants
with invasive infection.2,3 Together with types
Ib and II, these 5 types account for 99% of isolates from
infant invasive early-onset disease. Among late-onset cases of group
B streptococcal infection, type III strains predominate, accounting
for approximately two thirds of infections. Serotype III strains
also account for approximately 90% of isolates from infants
with meningitis.
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Clinical Manifestations
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The clinical features of early-onset and later-onset group B
streptococcal infections are shown in Table 286-1.
Risk for early-onset infection is increased in the setting of maternal
obstetric complications but term infants usually present with no risk
factors other than maternal colonization. The three common clinical
presentations for early-onset disease are septicemia without a focus,
pneumonia, and meningitis. In excess of 75% of infants
present with respiratory signs, including tachypnea, grunting, or
cyanosis. Radiographic findings can be suggestive of surfactant
deficiency, transient tachypnea, or congenital pneumonia. Other
signs of early-onset infection are those common to neonatal sepsis,
including temperature or vascular instability, poor feeding, and lethargy.
Clinical signs suggesting meningeal involvement can be unapparent
at the initial presentation, but seizures develop within 24 hours
of presentation in 50% of infants with meningitis.
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