Case Files Pediatrics, (LANGE Case Files) 4th Ed.


A 2800-g male is born at 36 weeks’ gestation to a 19-year-old mother through vaginal delivery. Delivery occurred 19 hours after membrane rupture. The mother’s pregnancy was uncomplicated, but her prenatal records are not available at delivery. At 6 hours of age he is “breathing hard” and refusing to breast-feed. His respiratory rate is 60 breaths/min with “grunting.” His temperature is 96.5°F (35.8°C), and his blood pressure is lower than normal. You ask the nurses to obtain a complete blood count (CBC) while you drive to the hospital from home. Upon arrival you confirm that he is in respiratory distress and that his perfusion is poor. The CBC demonstrates a white blood cell (WBC) count of 2500 cells/mm3 with 80% bands. His radiograph is shown in Figure 22-1.


Figure 22-1. Chest radiograph of an infant.

Image What is the most likely diagnosis?

Image What is the best therapy?

ANSWERS TO CASE 22: Group B Streptococcal Infection

Summary: A 2800-g infant born by vaginal delivery at 36 weeks’ gestation is found to have poor feeding, tachypnea, hypothermia, and poor perfusion at 6 hours of age.

• Most likely diagnosis: Group B Streptococcus (GBS) infection.

• Best therapy: Intravenous (IV) antibiotics (after addressing ABCs).



1. Understand the common presentations of neonatal sepsis.

2. Understand the maternal risk factors for neonatal GBS infection.

3. Appreciate the variety of organisms responsible for neonatal infections.

4. Learn treatment options for the common neonatal infections.


The rapid symptom onset, the low WBC count with left shift, and the chest x-ray findings are typical for GBS pneumonia. At this point, management would include rapid application of the ABCs of resuscitation (maintain Airway, control Breathing, and ensure adequate Circulation), followed by rapid institution of appropriate antibiotics once cultures are obtained. Despite these measures, mortality from this infection is high.


Group B Streptococcal Infection


EARLY-ONSET SEPSIS SYNDROME: Neonatal sepsis occurring in the first 6 days of life. The majority of infections (approximately 85%) occur in the first 24 hours of life, an additional 5% by approximately 48 hours, and the remainder throughout the next 4 days. The infection source usually is microorganism acquisition from the mother’s genitourinary tract.

GROUP B STREPTOCOCCUS (GBS) COLONIZATION: Infection with GBS limited to mucous membrane sites in a healthy adult; the gastrointestinal (GI) tract is the most common colonization reservoir.

LATE-ONSET SEPSIS SYNDROME: Neonatal sepsis usually occurring after approximately 7 days but before approximately 90 days of life. The infection source often is the caregiver’s environment.

INTRAPARTUM ANTIBIOTIC PROPHYLAXIS: Intravenous penicillin or ampicillin given during labor to prevent newborn GBS disease.


Signs and Symptoms of Sepsis

The signs and symptoms of neonatal sepsis can be subtle and nonspecific, often overlapping with findings in other conditions, such as respiratory distress syndrome, metabolic disorders, intracranial hemorrhages, and traumatic deliveries. Temperature instability, tachypnea, hypotension, and bradycardia are common findings in sepsis and meningitis. Overwhelming shock is manifested as pallor and poor capillary refill. Neurologic findings of impaired level of consciousness, coma, seizures, bulging anterior fontanelle, focal cranial nerve signs, and nuchal rigidity are unusual, but when present hint at meningitis, a condition more commonly seen in late-onset disease. Examination findings seen frequently with pneumonia (more commonly seen in early-onset disease) include tachypnea, grunting, nasal flaring, retractions (costal or substernal), decreased breath sounds, and cyanosis.

Evaluation of the Potentially Septic Child

Some neonatal sepsis laboratory findings can be nonspecific, including hypoglycemia, metabolic acidosis, and jaundice. The CBC often is used to help guide therapy, although the sensitivity and specificity of this test are low. Evidence of infection on CBC includes the following:

• Markedly elevated or low WBC counts

• Increased neutrophil count

• Increased immature to total neutrophil (I/T) ratios

• Thrombocytopenia with platelet counts less than 100,000/mm3

The C-reactive protein (an acute phase protein increased with tissue injury) can be elevated in septic infants; some use it as an adjunct to assess for neonatal sepsis.

A blood culture is crucial for patients with suspected sepsis. Some argue that the low meningitis incidence, especially in early-onset disease, does not warrant routine cerebral spinal fluid testing; rather, the test should be reserved for documented (positive cultures) or presumed (patients so sick that a full antibiotic course is to be given regardless of culture results) sepsis. Urine cultures usually are included for late-onset disease evaluation. Chest radiologic findings include segmental, lobar, or diffuse reticulogranular patterns, the latter easily confused with respiratory distress syndrome (lack of surfactant).


The organisms that commonly cause early-onset sepsis colonize in the mother’s genitourinary tract and are acquired transplacentally, from an ascending infection or as the infant passes through the birth canal. Specific organisms include GBS, Escherichia coli, Haemophilus influenzae, and Listeria monocytogenes. Late-onset disease occurs when the infant becomes infected in the postnatal environment, such as from the skin, respiratory tract, conjunctivae, gastrointestinal tract, and umbilicus. For the hospitalized infant, bacteria sources include vascular or urinary catheters or contact with health-care workers. Organisms commonly seen to cause late-onset disease include coagulase-negative staphylococci, Staphylococcus aureus, E coli, Klebsiella sp, Pseudomonas sp, Enterobacter sp, Candida, GBS, Serratia sp, Acinetobacter sp, and anaerobes.

Group B Streptococcus is the most common cause of neonatal sepsis from birth to 3 months. Approximately 80% of cases occur as early-onset disease (septicemia, pneumonia, and meningitis) resulting from vertical transmission from mother to infant during labor and delivery. Respiratory signs (apnea, grunting respirations, tachypnea, or cyanosis) are the initial clinical findings in more than 80% of neonates, regardless of the site of involvement, whereas hypotension is an initial finding in approximately 25% of cases. Other signs are similar to those associated with other bacterial infections described above.

Neonates with GBS meningitis rarely have seizures as a presenting sign, yet 50% develop seizures within 24 hours of infection. The median age at diagnosis of early-onset GBS infection is 13 hours, earlier than for the other bacterial infections described above. Clinical history and findings suggestive of early-onset GBS disease (rather than of a noninfectious etiology for pulmonary findings) include prolonged rupture of membranes, apnea, hypotension in the first 24 hours of life, a 1-minute Apgar score less than 5, and rapid progression of pulmonary disease.

Factors associated with increased risk for early-onset GBS disease are rupture of membranes more than 18 hours before delivery, chorioamnionitis or intrapartum temperature greater than 100.4°F (38°C), previous infant with GBS infection, mother younger than 20 years, and low birth weight or prematurity (<37 weeks’ gestation). Mortality as a result of GBS disease is close to 10%. Major neurologic sequelae (cortical blindness, spasticity, and global mental retardation) occur in 12% to 30% of infants who survive meningitis.

The incidence of early-onset GBS infection decreased from 1.7 per 1000 live births in 1993 to 0.34-0.37 per 1000 live births in 2008. The decline is largely attributed to the widespread use of GBS risk–reduction guidelines. These guidelines recommend screening women at 35 to 37 weeks’ gestation and offering intrapartum antibiotic prophylaxis to those with risk factors or positive GBS cultures at 35 to 37 weeks’ gestation. Infants born at less than 35 weeks’ gestation or born to women who received inadequate intrapartum prophylaxis sometimes undergo a limited evaluation that often includes a CBC and blood culture. The association of early antibiotic use with increased risk of late-onset serious bacterial infections remains under study.


Treatment of suspected early-onset disease includes antibiotics directed at the common pathogens listed earlier, often consisting of a combination of IV aminoglycosides (gentamicin or tobramycin) and penicillin (often ampicillin). For patients with late-onset disease, therapy often consists of β-lactamase–resistant antibiotics (such as vancomycin) and second- or third-generation cephalosporins.

For early- and late-onset disease, antibiotic coverage is adjusted depending on the organism identified and the organism’s specific antibiotic sensitivities.

Antibiotics are continued for at least 48 to 72 hours. If cultures are negative and the patient is well, antibiotics often are stopped. For infants presenting with convincing signs and symptoms of sepsis, antibiotics may be continued even with negative cultures. For infants with positive cultures, therapy continues for 10 to 21 days depending on the organism and the infection site. Close observation for signs of antibiotic toxicity is important for all infants.


22.1 A newborn infant was born at home. At 2 days of life he has puffy, tense eyelids, red conjunctivae, a copious purulent ocular discharge, and chemosis. Which of the following is the most likely diagnosis?

A. Chemical conjunctivitis

B. Chlamydial conjunctivitis

C. Dacryocystitis

D. Gonococcal ophthalmia

E. Pneumococcal ophthalmia

22.2 A term 3500-g female delivered by cesarean section develops a respiratory rate of 70 breaths/min and expiratory grunting at 1 hour of life. She has good tone, good color, and a strong suck. Which of the following is the most appropriate next intervention?

A. Intubation and suctioning below the vocal cords

B. Administration of surfactant

C. Initiation of antibiotic therapy

D. Swallow study and upper GI series

E. Observation for a period of several hours

22.3 A term infant is born to a 23-year-old known HIV-positive mother. The mother has been followed closely during the pregnancy, and she has been taking antiretroviral medications for the weeks prior to the delivery. Routine management of the healthy infant should include which of the following?

A. Administration of intravenous immunoglobulin to the baby to decrease the risk of perinatal HIV infection

B. Admission to the neonatal intensive care unit for close cardiovascular monitoring

C. Beginning a course of zidovudine for the infant

D. Chest radiographs to evaluate for congenital Pneumocystis carinii E. HIV enzyme-linked immunosorbent assay (ELISA) on the infant to determine if congenital infection has occurred

22.4 A 2150-g infant is delivered at 34 weeks’ gestation. The mother had prenatal care in Mexico and says she had no problems. Her highest temperature during labor was 100.8°F (38.2°C). The amniotic fluid had a brown-stained appearance. At birth the infant had a diffuse erythematous pustular rash, pallor, poor feeding, tachypnea, and cyanosis. His CBC indicates marked monocytosis. He dies at 4 hours of age, soon after initiation of antibiotics. He most likely had which of the following?

A. Congenital syphilis

B. Congenital varicella

C. Disseminated herpes

D. GBS disease

E. Listeriosis


22.1 D. The time of symptom onset in a neonate with conjunctivitis can be helpful. Chemical conjunctivitis that is self-limited and presents within 6 to 12 hours of birth is the result of ocular prophylaxis irritation. Gonococcal conjunctivitis usually occurs within 2 to 5 days of birth and is the most serious of the bacterial infections; prompt and aggressive topical treatment and systemic antibiotics can prevent serious complications such as corneal ulceration, perforation, and resulting blindness. Parents are treated for gonococcal disease to prevent a child’s reinfection. Chlamydial conjunctivitis often presents 5 to 14 days after birth and often is treated with systemic erythromycin (in part to reduce the infant’s risk of chlamydial pneumonia at 2-3 months of age). The risks of oral erythromycin treatment must be weighed against the increased risk of hypertrophic pyloric stenosis, a condition associated with oral erythromycin use in children. Both parents of a child with chlamydial conjunctivitis also are treated.

22.2 E. Transient tachypnea of the newborn is a respiratory condition resulting from incomplete evacuation of fetal lung fluid in full-term infants. It occurs more commonly with cesarean deliveries and usually disappears within 24 to 48 hours of life. Often no treatment is indicated unless the infant requires low amounts of supplemental oxygen. Antibiotics would be indicated for a child for whom pneumonia would be suspected; these children usually do not have a vigorous suck as outlined in the question. Intubation and suctioning below the vocal folds hints at meconium aspiration; the intubation would appropriately be accomplished in the delivery room and not hours later. The barium swallow and upper GI series might be helpful to identify a tracheoesophageal fistula. Exogenous surfactant is used for premature infants for whom surfactant deficiency is suspected.

22.3 C. HIV transmission from mother to infant has decreased dramatically over the last 20 years, probably as a result of perinatal antiretroviral administration to the mother and a zidovudine course to the exposed infant. Transplacentally transmitted maternal HIV antibodies will result in a positive neonatal ELISA; it is not a useful test for determining newborn infection. Intravenous immunoglobulin has not been shown to have a role in decreasing perinatal transmission. Healthy infants born to HIV-infected mothers require neither special monitoring nor routine radiographs.

22.4 E. Listeria is a gram-positive rod isolated from soil, streams, sewage, certain foods, silage, dust, and slaughterhouses. The foodborne transmission of disease is related to soft-ripened cheese, whole and 2% milk, undercooked chicken and hot dogs, raw vegetables, and shellfish. The newborn infant acquires the organism transplacentally or by aspiration or ingestion at delivery. The mortality rate of early-onset disease is approximately 30%.


Image Sepsis in the neonate can present with nonspecific findings of temperature instability, tachypnea, poor feeding, bradycardia, hypotension, and hypoglycemia.

Image Early-onset neonatal infection (occurring in the first 6 days of life) usually is caused by organisms of the maternal genitourinary system, including group B Streptococcus (GBS),E coli,H influenzae, and L monocytogenes. Pneumonia and sepsis are common presentations; GBS is the leading cause.

Image Late-onset neonatal infection (occurring between 7 and 90 days of life) is often caused by organisms found in the infant’s environment, including coagulase-negative staphylococci, S aureus, E coli, Klebsiella sp, Pseudomonassp,Enterobacter sp,Candida, GBS,Serratia sp,Acinetobacter sp, and anaerobic bacteria.

Image Treatment of early-onset neonatal infection usually includes penicillin and an aminoglycoside, whereas treatment of late-onset disease consists of a β-lactamase–resistant antibiotic (such as vancomycin) and often a third-generation cephalosporin.

Image The incidence of early-onset GBS infection is decreasing, likely as a result of the widespread implementation of GBS risk–reduction guidelines.


Brady MT. Human immunodeficiency virus type 1 infection. In: Rudolph CD, Rudolph AM, Lister G, First LR, Gershon AA, eds. Rudolph’s Pediatrics. 22nd ed. New York, NY: McGraw-Hill; 2011:1164-1170.

Braverman RS. Ophthalmia neonatorum. In: Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Current Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011:418-419.

Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal disease. Revised guidelines from CDC. MMWR Recomm Rep. 2010;59 (RR-10): 1-32.

Edwards MS. Group B streptococcal infections. In: Rudolph CD, Rudolph AM, Lister G, First LR, Gershon AA, eds. Rudolph’s Pediatrics. 22nd ed. New York, NY: McGraw-Hill; 2011:1097-1099.

Gallagher PG, Baltimore RS. Sepsis neonatorum. In: McMillan JA, Feigin RD, DeAngelis CD, Jones MD, eds. Oski’s Pediatrics: Principles and Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:482-492.

Guinn AG. Red eye. In: Rudolph CD, Rudolph AM, Lister G, First LR, Gershon AA, eds. Rudolph’s Pediatrics. 22nd ed. New York, NY: McGraw-Hill; 2011:2300-2304.

Lachenauer CS, Wessels MR. Group B Streptococcus. In: Kleigman RM, Stanton BF, St. Geme JW, Schor NF, Behrman RE, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: WB Saunders; 2011:925-928.

McFarland EJ. Human immunodeficiency virus infection. In: Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Current Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011:1148-1158.

Moylett EH, Shearer WT. Pediatric human immunodeficiency virus infection. In: McMillan JA, Feigin RD, DeAngelis CD, Jones MD, eds. Oski’s Pediatrics: Principles and Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:942-952.

Ogle JW, Anderson MS. Group B streptococcal infections. In: Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Current Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011:1163-1166.

Olitsky SE, Hug D, Plummer LS, Stass-Isern M. Disorders of the conjunctiva. In: Kleigman RM, Stanton BF, St. Geme JW, Schor NF, Behrman RE, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: WB Saunders; 2011:2166-2169.

Thilo EH, Rosenberg AA. Infections in the newborn infant. In: Hay WW, Levin MJ, Sondheimer JM, Deterding RR. Current Diagnosis & Treatment: Pediatrics. 20th ed. New York, NY: McGraw-Hill; 2011:48-56.

Traboulsi EI. Ophthalmia neonatorum. In: McMillan JA, Feigin RD, DeAngelis CD, Jones MD, eds. Oski’s Pediatrics: Principles and Practice. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:811-812.

Yogev R, Chadwick E. Acquired immunodeficiency syndrome (human immunodeficiency virus). In: Kleigman RM, Stanton BF, St. Geme JW, Schor NF, Behrman RE, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: WB Saunders; 2011:1157-1177.