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Neonatal Sepsis : A Case Report

dr. Irman Permana, Sp.A1, dr. Ineu Nopita, Sp.A M.Kes1,


dr. Tatan Tandubela, Sp.A1, Ilma Syifannisa2,
Department of Pediatric Waled Hospital Cirebon1Faculty of Medicine
Swadaya Gunung Jati College Cirebon2

Introduction: Neonatal sepsis is a systemic infection occurring in infants at 28 days of life and is
an important cause of morbidity and mortality of newborns. Neonatal sepsis may be categorized
as early-onset or late-onset. Of newborns with early-onset sepsis, present within 48-72 hours.
Onset is most rapid in premature neonates. Early-onset sepsis is associated with acquisition of
microorganisms from the mother. Transplacental infection or an ascending infection from the
cervix. Late-onset sepsis occurs at 4-90 days of life and is acquired from the caregiving
environment
Case report: We present the case of Asian female infant who was born at 34 weeks gestation in
hospital. Born by 26 years old primipara mother at preterm by caesarean section. Mother had
developed impending eclampsia 1 week before birth.
Discussion: Early-onset sepsis remains a common and serious problem for neonates, especially
preterm infants. EOS has been variably defined based on the age at onset, with bacteremia or
bacterial meningitis occurring at 72 hours in infants hospitalized in the neonatal intensive care
unit (NICU). In preterm infants, EOS is most consistently defined as occurring in the first 3 days
of life and is caused by bacterial pathogens transmitted vertically from mother to infant before or
during delivery.
Conclussion: We conclude from our study that preterm infant is on high risk of get the vertical
infection and develop becomes EOS.

keywords: Early onset sepsis (EOS), Late onset sepsis (LOS), Neonatal sepsis, ipreterm nfants.

Introduction

Neonatal sepsis is a systemic infection occurring in infants at 28 days of


life and is an important cause of morbidity and mortality of newborns. Early-onset
neonatal sepsis (EOS) has been variably defined based on the age at onset, with
bacteremia or bacterial meningitis occurring at 72 hours in infants. In preterm
infants, EOS is most consistently defined as occurring in the first 3 days of life
and is caused by bacterial pathogens transmitted vertically from mother to infant
before or during delivery. Late-onset sepsis (LOS) is sepsis occurring after 72 h in
NICU infants and 7 days of life in term infants, has been variably defined as
occurring up to the age of < 90 or 120 days, and may be caused by vertically or
horizontally acquired pathogens. Early-onset neonatal infections of viral or fungal
etiology may also occur at <7 days of life and must be distinguished from
bacterial sepsis.
Organisms causing early-onset neonatal sepsis are typically colonizers of
the maternal genitourinary tract, leading to contamination of the amniotic fluid,
placenta, cervix, or vaginal canal. The pathogen may ascend when the amniotic
membranes rupture or prior to the onset of labor, causing an intra-amniotic
infection. Thus, the infant may acquire the pathogen either in utero or
intrapartum. Risk factors for early-onset neonatal sepsis include both maternal
and infant factors. Maternal risks, such as dietary intake of contaminated foods,
can arise before labor and delivery, with Listeria monocytogenes contamination of
refrigerated foods such as deli meats being the most important example.
Procedures during pregnancy, such as cervical cerclage and amniocentesis, which
disrupt the amniotic cavity, may also increase the rates of intra-amniotic infection
and subsequent neonatal sepsis. During labor, maternal risk factors include
prolonged rupture of membranes, fever, vaginal colonization with group B
streptococcus (GBS), and GBS bacteriuria. A history of a previous infant with
GBS infection is another identified maternal risk factor in subsequent
pregnancies. In addition, adequacy of the maternal immune response is an
important risk factor for neonatal sepsis. Maternal serum IgG antibodies against
specific capsular polysaccharides of GBS have been shown to be protective
against infection with the relevant GBS strain in their infants, and an increased
risk for GBS EOS has been demonstrated in infants de livered to mothers with
low titers. Chorioamnionitis, defined by maternal fever, leukocytosis (>15,000
white blood cells [WBCs]/mm3), maternal tachycardia, uterine tenderness, foul
odor of amniotic fluid, and fetal tachycardia at delivery, is also a major risk factor
for neonatal sepsis. Maternal factors associated with the development of
chorioamnionitis include longer length of labor and membrane rupture, multiple
digital vaginal examinations, placement of internal fetal or uterine monitoring
devices,
spontaneous onset of labor, and meconium-stained amniotic fluid. The risk of
EOS increases to 1% when membranes are ruptured 18 hours prior to delivery,
and the EOS risk of infants delivered to mothers with evidence of
chorioamnionitis is estimated to be between 1 and 4%. In utero inhalation or
swallowing of infected amniotic fluid by the fetus may lead to intrapartum sepsis,
which may partially explain the high sepsis incidence in infants delivered of
mothers with chorioamnionitis; alternatively, colonization of the skin and mucus
membranes by pathogens involved in chorio amnionitis may cause infection
shortly after birth when these barriers lose their integrity.
Infant factors associated with early-onset sepsis in addition to the factors
noted for the mother include prematurity/low birth weight, congenital anomalies,
complicated or instrument-assisted delivery, and low APGAR scores (score of 6
at 5 min). Immaturity of the premature neonatal immune system, including low
immunoglobulin levels related to decreased transplacental transfer of maternal
IgG, also increases the risk of sepsis in preterm infants. Barrier function of the
skin and mucus membranes is diminished in premature infants and is additionally
compromised in ill premature infants by multiple invasive procedures, including
intravenous (i.v.) access and intubation. Poor or late prenatal care, low
socioeconomic status of the mother, poor maternal nutrition, maternal substance
abuse, male sex, and African American mother (higher rate of GBS colonization)
are additional ethnic and social factors associated with neonatal sepsis.
Case Report

A 26-year-old primigravid woman delivers preterm (34 weeks gestational


age) female infant weighing 1990 grams through caesarean section delivery. Her
height was 42 cm, and the head circumference was 31 cm. The infant's first vital
signs and physical examinations were normal. The mother had history of
impending eclampsia, but had no history of DM and rupture of membranes. Apgar
scores of the infants were 9 and 10 at 1 and 5 minutes, respectively. She had weak
reflexes. No nasal flaring, grunting, and retraction sign were presented. Poor
feeding appeared two hours after the delivery. An empiric treatment with
intravenous (IV) ampicillin and gentamicin initiated.
Patient was bought to the perinatology room with low birth weight and
preterm birth. The vital sign in the first and second day were normal. Complete
blood count showed normal hemoglobin, hematocrit, and thrombocyte.
Leukocytes number was high 24.000/mm3 showed leukocytosis. Considering the
high level of leukocytes and preterm birth as the risk factor of early-onset
neonatal sepsis, the baby was given a plan of antibiotic with intravenous
ampicillin and gentamicin. Supportive therapy was given and to resolve the
feeding problem, the baby was not given enteral nutrition for the first and second
day. An orogasric tube was applied to see the retention and also to give test
feeding for the baby.
Discussion
Neonatal sepsis may be categorized as early-onset or late-onset. Of
newborns with early-onset sepsis, 85% present within 24 hours, 5% present at 24-
48 hours, and a smaller percentage present within 48-72 hours. Onset is most
rapid in premature neonates. Early-onset sepsis is associated with acquisition of
microorganisms from the mother. Transplacental infection or an ascending
infection from the cervix may be caused by organisms that colonize the mothers
genitourinary (GU) tract; the neonate acquires the microorganisms as it passes
through the colonized birth canal at delivery. The microorganisms most
commonly associated with early-onset infection include the following Group B
Streptococcus (GBS), Escherichia coli, Coagulase-negative Staphylococcus,
Haemophilus influenzae, Listeria monocytogenes. Trends in the epidemiology of
early-onset sepsis show a decreasing incidence of GBS disease. This can be
attributed to the implementation of a prenatal screening and treatment protocol for
GBS.
Late-onset sepsis occurs at 4-90 days of life and is acquired from the
caregiving environment. Organisms that have been implicated in causing late-
onset sepsis include the following Coagulase-negative Staphylococcus,
Staphylococcus aureus, E coli, Klebsiella, Pseudomonas, Enterobacter, Candida,
GBS, Serratia, Acinetobacter, Anaerobes. Trends in late-onset sepsis show an
increase in coagulase-negative streptococcal sepsis; most of these isolates are
susceptible to first-generation cephalosporins. The infants skin, respiratory tract,
conjunctivae, gastrointestinal (GI) tract, and umbilicus may become colonized
from the environment, and such colonization to the possibility of late-onset sepsis
from invasive microorganisms. Vectors for such colonization may include
vascular or urinary catheters, other indwelling lines, or contact with caregivers
who have bacterial colonization.
Conclusion

We conclude from our study that preterm infants have higher risk to suffer
early onset neonatal sepsis that can be caused by the vertical transmission from
mother to child or ascending transmission during intranatal from mothers
genitourinary tract to the amniotic fluid.

Reference

1. American Academy of Pediatrics. In: Pickering LK, Baker CJ, Kimberlin


DW, Long SS, eds. Red Book: 2012 Report of the Committee on Infectious
Diseases. 29th ed. Elk Grove Village, IL: American Academy of
Pediatrics; 2012:774789.
2. Remington J, Klein J. Infections Diseases of the Fetus and Newborn
Infant. 25th ed. Philadelphia: Saunders; 2000.
3. Gotoff SP. Chemoprophylaxis of early-onset group B streptococcal
disease in 1999. Curr Opin Pediatr 2000;12(2):105-10.
4. Schimmel MS, Samueloff A, Eidelman AI. Prevention of neonatal group
B streptococcal infections. Is there a rational prevention strategy? Clin
Perinatol 1998;25(3):687-97.
5. Desantis SM, Baker NL, Back SE, Spratt E, Ciolino JD, Moran-Santa
MM, et al. Gender differences in the effect of early life trauma on
hypothalamic-pituitary-adrenal axis functioning. Depress Anxiety
2011;10.
6. Decreasing incidence of perinatal Group B streptococcal disease--United
States, 1993-1995. MMWR Morb Mortal Wkly Rep 1997; 46(21):473-7.
7. Peralta-Carcelen M, Fargason CA, Jr., Cliver SP, Cutter GR, Gigante J,
Goldenberg RL. Impact of maternal group B streptococcal screening on
pediatric management in full-term newborns. Arch Pediatr Adolesc Med
1996;150(8):802-8.
8. Spitzer A. Intensive Care of the Fetus and Newborn. St Louis: Mosby;
1996.
9. Schrag SJ, Zywicki S, Farley MM, Reingold AL, Harrison LH, Lefkowitz
LB, et al. Group B streptococcal disease in the era of intrapartum
antibiotic prophylaxis. N Engl J Med 2000;342(1):15-20.
10. Tumbaga P, Philip A. Perinatal Group B Streptococcal Infections: Past,
Present, and Future. NeoReviews 2003;(4):65-72.
11. Kaufman D, Fairchild KD. Clinical microbiology of bacterial and fungal
sepsis in very-low-birth-weight infants.Clin Microbiol Rev 2004;
17(3):638-80.
12. Rench MA, Baker CJ. Neonatal sepsis caused by a new group B
streptococcal serotype. J Pediatr 1993;122(4):638-40.
13. Sabnis H, Sood BG, Zilberman M, Becker C. Visual diagnosis: sepsis,
respiratory distress, and a persistent right lung opacification in a newborn.
Pediatr Rev 2009;30(11):453-6.
14. Nandyal RR. Update on group B streptococcal infections: perinatal and
neonatal periods. J Perinat Neonatal Nurs 2008; 22(3):230-7.
15. Puopolo.KM,.Madoff.LC,Eichenwald EC. Early-onset group B
streptococcal disease in the era of maternal screening. Pediatrics 2005;
115(5):1240-6.

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