SEPSIS AND MENINGITIS

 Systemic and local infections (lung, cutaneous,

ocular, umbilical, kidney, bone-joint, and
meningeal) are common in the newborn period.

 Infection may be acquired in utero through the

transplacental or trans-cervical routes and during or
after birth.
 Ascending infection through the cervix, with or
without rupture of the amniotic fluid membranes,
may result in amnionitis, funisitis (infection of the
umbilical cord), congenital pneumonia, and sepsis.
 The bacteria responsible for ascending infection of the
fetus are common bacterial organisms of the maternal
geni-tourinary tract, such as group B streptococci, E.
coli, Haemophilus influenzae, and Klebsiella.

 Herpes simplex virus (HSV)-1 or more often HSV-2 also

causes ascending infection that at times may be
indistinguishable from bacterial sepsis.

 Syphilis and Listeria monocytogenes are acquired by

transplacental infection.
 Maternal humoral immunity may protect the fetus
against some neonatal pathogens, such as group B
streptococci and HSV.

 Nonetheless, various deficiencies of the neonatal

antimicrobial defense mechanism probably are more
important than maternal immune status as a contributing
factor for neonatal infection, especially in the LBW
infant.
 Preterm infants before 32 weeks of gestational age
have not received the full complement of maternal
antibodies (IgG), which cross the placenta by active
transport predominantly in the latter half of the
third trimester.

 In addition, although LBW infants may generate

IgM antibodies, their own IgG response to infection
is reduced.
 These infants also have deficiencies of the alternate and,
to a smaller degree, the classic complement activation
pathways, which results in diminished complement-
mediated opsonization.

 Newborn infants also show a deficit in phagocytic

migration to the site of infection (to the lung) and in the
bone marrow reserve pool of leukocytes.
 In addition, in the presence of suboptimal activation of
complement, neonatal neutrophils ingest and kill bacteria
less effectively than adult neutrophils do.
 Bacterial sepsis and meningitis often are linked closely
in neonates.

 Despite this association, the incidence of meningitis

relative to neonatal sepsis has been on a steady
decline. The incidence of meningitis is approximately 1
in 20 cases of sepsis.

 The causative organisms isolated most frequently are

the same as for neonatal sepsis: group B streptococci,
E. coli, and L. monocytogenes. Gram-negative
organisms, such as Klebsiella and Serratia marcescens,
 are more common in less developed countries, and
coagulase-negative staphylococci need to be
considered in VLBW infants. Male infants seem to
be more susceptible to neonatal infection than
female infants. Severely premature infants are at
even greater risk secondary to less effective
defense mechanisms and deficient transfer of
antibodies from the mother to the fetus (which
occurs mostly after 32 weeks' gestation).
 Neonatal sepsis presents during three periods.
 Early-onset sepsis:

 often begins in utero and usually is a result of infection

caused by the bacteria in the mother's genitourinary tract.
Organisms related to this sepsis include group B
streptococci, E. coli, Klebsiella, L. monocytogenes, and
nontypable H. influenzae. Most infected infants are
premature and show nonspecific cardiorespiratory signs,
such as grunting, tachypnea, and cyanosis at birth.
 Risk factors for early-onset sepsis include vaginal
colonization with group B streptococci, prolonged
rupture of the membranes (>24 hours), amnionitis,
maternal fever or leukocytosis, fetal tachycardia, and
preterm birth.

 African American race and male sex are unexplained

additional risk factors for neonatal sepsis
 Early-onset sepsis (birth to 7 days) is an overwhelming
multiorgan system disease frequently manifested as
respiratory failure, shock, meningitis (in 30% of cases),
DIC, acute tubular necrosis, and symmetric peripheral
gangrene.

 Early manifestations-grunting, poor feeding, pallor,

apnea, lethargy, hypothermia, or an abnormal cry-may be
nonspecific.

 Profound neutropenia, hypoxia, and hypotension may be

refractory to treatment with broad-spectrum antibiotics,
 The clinical manifestations of sepsis are difficult
to separate from the manifestations of meningitis in
the neonate.

 Infants with early-onset sepsis should be evaluated

by blood and CSF cultures, CSF Gram stain, cell
count, and protein and glucose levels.

 Normal newborns generally have an elevated CSF

protein content (100 to 150 mg/dL) and may have 25
to 30/mm3 white blood cells (mean 9/mm3), which
are 75% lymphocytes in the absence of infection.
 The initial clinical manifestations of nosocomial
infection in a premature infant may be subtle and
include apnea and bradycardia, temperature
instability, abdominal distention, and poor feeding.

 In the later stages, signs of infection are shock,

DIC, worsening respiratory status, and local
reactions, such as omphalitis, eye discharge,
diarrhea, and bullous impetigo.
 The treatment of nosocomially acquired sepsis
depends on the indigenous microbiologic flora of
the particular hospital and the antibiotic
sensitivities.

 Because S. aureus (occasionally methicillin-

resistant), Staphylococcus epidermidis (methicillin-
resistant), and gram-negative pathogens are
common nosocomial bacterial agents in many
nurseries, a combination of vancomycin or
oxacillin/nafcillin (some use ampicillin) with an
aminoglycoside (gentamicin or tobramycin) is
appropriate.