3. Outline
GBS
In Pregnant Women In Newborn
Epidemiology Epidemiology
Guidelines for screening Signs and symptoms of
and prophylaxis GBS (early and late)
Treatment
4.
5. What is Neonatal Sepsis?
Bacteremia with systemic signs and symptoms of
infection in the first 4 weeks of life
SIRS in neonate and pediatric patients (2 or more of the
following):
Temperature instability
Respiratory dysfunction
Cardiac dysfunction
Perfusion abnormalities
Sepsis = SIRS with confirmed infectious process
6. Epidemiology and Etiology
2% of fetuses are infected in utero
10% of infants have infections in the 1st month of
life
Incidence 1-4cases per 1,000 live births in
developed countries
Twofold higher incidence of sepsis in term
males and term females
7. Epidemiology and Etiology
Most common neonatal pathogens:
GBS – group B streptococcus
Escherichia coli
Other common pathogens:
Staphylococcus, Streptococcus
pneumoniae/viridans, Enterococci, Clostridia (in
developing countries)
9. Early Onset
Within 7 days of birth
Most cases occur within 72h
Common with maternal obstetric complications
(mainly vertical transmission)
Intrapartum acquired organisms
10. Early Onset
Risk factors:
Prematurity
PROM occuring ≥ 18h before birth
Maternal bleeding (eg. Placenta previa, abruptio
placentae)
Preeclampsia
Difficult or traumatic delivery
Maternal infection
11. Late Onset
After 7 days of birth
Mainly horizontal transmission (acquired from the
environment)
Newborn nursery, neonatal intensive care unit, or
community
30-60% Staphylococci
Enterobacter cloacae, E. sakazakii suggest
contaminated feedings
12. Late Onset
Risk factors:
Prolonged use of intravascular catheters
Prolonged hospitalization
Preterm infants have prolonged hospitalizations
Contaminated equipment
13. Signs and Symptoms
Common signs:
Diminished spontaneous activity
Feeding intolerance, less vigorous sucking
Apnea, respiratory distress
Tachycardia or bradycardia
Hypotension, poor perfusion with pallor
Temperature instability (hypo or hyperthermia)
14. Signs and Symptoms
Later complications of Sepsis:
Respiratory failure
Pulmonary hypertension
Cardiac failure
Shock
Renal failure
Liver dysfunction
Cerebral edema or thrombosis
Adrenal hemorrhage and/or insufficiency
DIC
15. Signs and Symptoms
Specific signs:
Meningitis, encephalitis, or brain abscess
coma, seizures, opisthotonos
Omphalitis
Periumbilical erythema, discharge, or bleeding without
a hemorrhagic diathesis
Peritonitis or necrotizing enterocolitis
Unexplained abdominal distention, bloody
diarrhea, fecal leukocytes
16. Signs and Symptoms
Specific signs:
Early-onset GBS and L. monocytogenes
Respiratory distress
Osteomyelitis or pyogenic arthritis
Decreased spontaneous movement or
extremity, swelling, warmth, erythema, tenderness
over a joint
17. Diagnostic Tests
CBC/blood culture
Urinalysis and culture
Lumbar puncture
Increased risk of hypoxia
Supplemental O2 is given before
18. Treatment
Antibiotic therapy
Early-onset sepsis:
Initial therapy should include ampicillin or penicillin G
plus an aminoglycoside
Cefotaxime may be added to or substituted for
aminoglycoside if meningitis is suspected
If foul-smelling amniotic fluid is present at birth, therapy
for anaerobes, clindamycin, metronidazole should be
added
19. Treatment
Antibiotic therapy
Late-onset sepsis of a previous well infant:
Ampicillin plus gentamicin or ampicillin plus cefotaxime
If gram –ve meningitis is
suspected, ampicillin, cefotaxime and aminoglycoside
Late-onset sepsis in hospital-acquired:
Vancomycin plus aminoglycoside
If P. aeruginosa is prevalent in nursery, ceftazidime is
used instead of aminoglycoside
20. Treatment
Supportive therapy
Respiratory and hemodynamic management
Other treatments
Exchange transfusion in severely ill (hypotensive and metabolic acidotic
neonates) can be used
Fresh frozen plasma
Can help reverse heat-stable and heat-labile opsonin deficiencies that occur
in low birth weight infants
Granulocyte transfusions have been used but have not improved outcome
significantly
IV immune globulin given at birth may prevent sepsis in high-risk low birth
weight infants
21.
22. What is GBS?
Group B Streptococcus or Streptococcus agalactiae
Gram +ve
Catalase –ve
Complete hemolysis (Beta) on blood agar
Bacitracin and trimethoprim-sulfamethoxazole
Resistant
Facultative anaerobe
Lancefield group B carbohydrate antigen
23. GBS in Pregnant Women
Epidemiology
30% of women at term have vaginal or rectal
cultures
50% of their infants also become colonized
1-2% develop early-onset disease
24. Early Onset Disease
Same risk factors as sepsis for newborn for early disease
Specific major risk factor for GBS is maternal vaginal or
rectal colonization by GBS
Incidence of early onset GBS infection increases with the
length of rupture of membranes
Screening and intrapartum antibiotic prophylaxis for GBS
have significantly decreased the rate of early-onset disease
Decrease from 1.7 cases per 1,000 live births to 0.6 cases per
1,000
25. Late Onset Disease
GBS acquired later from maternal or non-
maternal sources (eg. Nursery)
Rate of late-onset GBS remained unchanged with
intrapartum screening and antibiotic prophylaxis
(environment)
26. Figure 2 – Incidence of early onset and late onset invasive GBS
disease, 1989 through 2000.
27. CDC Guidelines
Vaginorectal GBS screening cultures should be preformed for all
pregnant women at 35-37weeks gestation
Any woman with positive prenatal screening culture, GBS
bacteriuria during pregnancy, or a previous infant with invasive
GBS should receive intrapartum antibiotics
Any woman with unknown status (culture not done, incomplete, or
results unknown) and who deliver prematurely (<37weeks
gestation) or experience prolonged rupture of membranes (>18hr)
or intrapartum fever (>38oC) should also receive intrapartum
antibiotics
If amnionitis; replace GBS prophylaxis with broad-spectrum
antibiotic therapy that includes an agent active against GBS
Routine intrapartum prophylaxis is not recommended for women
with GBS colonization undergoing planned cesarean delivery who
have not begun labour or had rupture of membranes
29. GBS in Newborn
Epidemiology
Incidence higher in premature and low-birthweight
infants
Density of infant colonization determines the risk of
early-onset invasive disease
40 times higher with heavy colonization
1/100 infants colonized develop invasive disease
30. Clinical Manifestations
Early onset:
Most infants become ill within the first 24hr of birth
Most common manifestation is sepsis
(50%), pneumonia (30%) and meningitis (15%)
Asymptomatic bacteremia is uncommon but can
occur
Case fatality rate 4.7%
31. Clinical Manifestations
Early onset:
Respiratory symptoms are prominent regardless
of the presence of pneumonia and include
Cyanosis, apnea, tachypnea, grunting, flaring, and
retractions
Clinically and radiographically, pneumonia
associated with early onset GBS disease is difficult
to distinguish from hyaline membrane disease
32. Clinical Manifestations
Late onset:
Most commonly manifests as bacteremia (45-
60%), meningitis (25-35%), focal infections (20%)
Infants are often less severely ill on presentation than
infants with early onset disease
No increase risk after obstetric complications
Case fatality rate 2.8%
33. Treatment
Initial treatment should include ampicillin and
aminoglycoside pending organism identification
Penicillin G is treatment of choice of confirmed
GBS infection
In case of meningitis, high dose penicillin
(450,000-500,000U/kg/24hr) and ampicillin (300-
400mg/kg/24hr) are recommended
34. Treatment
Duration of therapy:
Bacteremia without a focus – 10days
Meningitis – 2-4weeks
Ventriculitis – 4weeks
Osteomyelitis – 4weeks
35. References
Caserta, Mary. October 2009. Merck Manual for Health Care Professionals.
“Infections in Neonates”.
Figure 1. “Bacterial Causes of Systemic Neonatal Infections”. Nelson Textbook of
Pediatrics. 19th ed. pp 267.
Figure 2. Schrag SJ, Zywicki S, Farley MM, et al: Group B streptococcal disease in
the era of intrapartum antibiotic prophylaxis. N Engl J Med 2000;342:15-20.
Figure 3. Schrag SJ, Gorwitz et.al,. “Prevention of Perinatal Group B
Streptococcal Disease”. Morbidity and Mortality Weekly Report 51(RR-11): 1-
22, 2002.
Lachenauer, C.S., Wessels, M.R.“Group B Streptococcus”. Nelson Textbook of
Pediatrics.19th ed. pp879-883.
Notes de l'éditeur
The differences between gender is less clear in preterm low-birthweight infants
Symptoms within 6h of birthMainly vertical transmission – neonate is exposed to potentially pathogenic bacteria until the membranes rupture and the infant passes through the birth canal and/or enters the extrauterine environment
The most important factor predisposing to infection is prematurity or Low Birth WeightThey have 3-10 fold higher incidence of infection than full-term, normal birth weight infantsPossible explanations: 1. maternal genital tract infection (cause of preterm labour) with increased risk of vertical transmission 2. premature infants have documented immune dysfunction 3. premature infants often require prolonged IV access, endotracheal intubation, or other invasive procedures
Staph: frequently due to intravascular devices (umbilical artery or vein catheters)
Gram +ve = environment and patient’s skinGram –ve = mainly from personnel ie. Crowding, handwashingCandida sepsis = prolonged (>10 days of central IV catheters, previous surgery, necrotizing enterocolitis, or abdominal pathology>
Fever is present in only 10-15% of cases, but when sustained (>1hr) it generally indicated infection.
Neurologic findings = seizures/jitterinessJaundice especially occurring within the first 24h without Rh or ABO blood group incompatibility and with a higher than expected direct bilirubin concentration
Omphalitis infection prevents obliteration of the umbilical vessels
Omphalitis infection prevents obliteration of the umbilical vessels
Other CBC: absolute band count is not sensitive enough to predict sepsis, but a ratio of immature:totalpolymorphonuclear leukocytes of <0.2 has high negative predictive valuePLT: may fall hours to days before the onset of clinical sepsis but more often remains elevated until a day or so after the neonate becomes ill.Urinalysis and culture: should be obtained by catheterization or suprapubic aspiration NOT by urine collection bags. If you see >5 WBCs/high power field is presumptive evidence of a UTILP: risk of increasing hypoxia during an LP in already hypoxemic neonates; thus supplement O2 is given before LP to prevent hypoxia.
Start empiric therapy, and then adjust drug according to sensitivities and site of infection. If no growth by 48h and neonate appears well, antibiotics are stopped
Start empiric therapy, and then adjust drug according to sensitivities and site of infection. If no growth by 48h and neonate appears well, antibiotics are stopped
Note: for penicillin-intolerant women, cefazolin should be usedErythromycin has shown up to 25% resistance in GBSClindamycin has shown up to 15% resistance in GBSFor penicillin-allergic women at high risk for anaphylaxi, clindamycin or erythromycin should be used if isolates are susceptible. If resistant, then Vancomycin should be used.
Incidence is higher in premies and LBW infants; however most cases occur in full-term infants
Incidence is higher in premies and LBW infants; however most cases occur in full-term infantsNote: other neonatal pathogens, such as E.coli or Listeria monocytogenes may produce illness that is clinically indistinguishable from that due to GBS
Note: RDS secondary to surfactant deficiency can coexist with bacterial pneumonia. Distinguishing between hyaline membrane disease and invasive neonatal GBS infection -severe apnea, early onset of shock, abnormalities in the peripheral leukocyte count, and greater lung compliance may be more likely in infants with GBS disease.
Focal infections involving bone and joints, skin and soft tissues, urinary tract, or lungs. Cellulitis and adenitis are often localized to the submandibular or parotid regions
