533412

research-article2014

CPJXXX10.1177/0009922814533412Clinical PediatricsHudson et al

Commentary

Congenital Human Parvovirus B19 Infection With Persistent Viremia

Clinical Pediatrics 2015, Vol. 54(5) 409­–413 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/0009922814533412 cpj.sagepub.com

Anthony C. Hudson, MD1,2, Anna E. Montegudo, BS1,2, and Russell W. Steele, MD1,2

Introduction A consequence of parvovirus B19 infection during pregnancy is that the virus may cross the placenta, attacking fetal hematopoetic cells in the bone marrow, liver, and spleen causing anemia and hydrops often leading to death of the fetus. Persistent viremia following congenital infection within the first year of life is an infrequent occurrence and management of such patients is incompletely defined. This case report and review of the literature examines the natural history of congenital parvovirus infection and suggests steps in the prenatal and postnatal management of these children.

Case Presentation The mother of our patient was a healthy 26-year-old G3 P2 woman who was 20 weeks pregnant when her 2 older children developed a pink, raised, pruritic rash on the cheeks that continued as a lacy rash on the arms and legs, diagnosed by the children’s pediatrician as fifth disease. The mother was advised to contact her obstetrician because of her exposure and was seen 2 days later. Blood was drawn for B19 DNA polymerase chain reaction (PCR). However, the sample was mishandled and meaningful results were not obtained. Another appointment was scheduled a week later to repeat the serologic studies, but before this time the mother, now at 22 weeks’ gestation, developed a pruritic, erythematous rash on the ventral surface of her extremities, cheeks, and back. At 24 weeks’ gestation it was reported that both her parvovirus IgM and G serum titers were strongly positive. A fetal echocardiography done at 26 weeks’ gestation demonstrated an enlarged right ventricle, mild tricuspid regurgitation, scalp edema, and a small pericardial effusion all supportive of early fetal hydrops. Doppler studies further indicated fetal anemia presumed due to nonimmune fetal hydrops. Ultrasounds were performed every other day in anticipation of an intrauterine blood transfusion; however placental location obstructed access for the procedure. At 29 weeks’ gestation, the decision for an elective cesarean delivery was made.

At delivery, the infant had weak respiratory effort with Apgars of 3 and 9. Saturations greater than 90% were initially achieved with continuous positive airway pressure and Neopuff. On physical exam, the patient had a weight of 1.5 kg (77.3 percentile for gestational age), length 38.1 cm (34.1 percentile), and a head circumference of 26 cm (22.7 percentile). She had generalized body edema and appeared pink. Micrognathia and glossoptosis were appreciated. There was a grade III/VI systolic murmur and the abdomen was distended with moderate organomegaly, specifically the liver edge was palpated 4 cm below the costal margin. On orogastric tube placement, a small amount of air and secretions were obtained with aspiration. However, the abdomen remained distended. She was intubated on day 1 of life for respiratory failure. Initial complete blood count revealed a hemoglobin level of 6.3 g/dL and hematocrit of 20.5%. A packed red blood cell exchange transfusion was done 4 hours after birth. The patient received 5 more packed red blood cell transfusions on days 2, 7, 11, 31, and 45 of life for hematocrits of 26.5%, 27.9%, 30.5%, 29.7%, and 19.3%, respectively. In addition, the patient received 4 platelet transfusions on days 1, 3, 6, and 7 of life for platelet counts of 29 000, 35 000, 39 000, and 77 000/mm3, respectively. The reticulocyte count was 1.1 on her 45th day of life. The patient’s clinical course gradually improved over 104 days of hospitalization, and she was discharged with a stable hemoglobin but a parvovirus DNA by PCR of >10 000 000 copies/mL on day 74 of life. After discharge from the neonatal intensive care unit, her growth and development from a social, cognitive, and motor standpoint were normal. She was seen by 1

Ochsner Children’s Health Center, Tulane University School of Medicine, New Orleans, LA, USA 2 University of Queensland School of Medicine, Ochsner Clinical Campus, New Orleans, LA, USA Corresponding Author: Anthony C. Hudson, 372 Tudor Avenue, New Orleans, LA 70123, USA. Email: [email protected]

410 ENT secondary to a failed brainstem auditory-evoked response test at the time of discharge from the neonatal intensive care unit but passed an ALGO hearing screen. At 5 months of age the mother brought the patient to her pediatrician because of feeding difficulty and reflux. Exam was normal and the mother was reassured. A few hours after returning from the pediatrician, the mother noticed the patient’s lips were purple and her skin was white prompting her to return to the emergency department that evening. The patient’s physical exam was pertinent for tachycardia, a II/VI systolic murmur over the left sternal border, and a palpable liver edge 2 cm below the right costal margin. A complete blood count was drawn and the hemoglobin was found to be 3.3 g/dL with an absolute reticulocyte count of 0.2. The patient was admitted to the pediatric intensive care unit for severe anemia and was given two 5 cm3/kg transfusions on the day of admission and another two 5 cm3/kg transfusions on the second day. The transfusions were well tolerated and the hemoglobin increased to 13 g/dL, stabilized at this level, and no heart murmur could be appreciated by the date of discharge 7 days later. Parvovirus B 19 DNA was found to be >100 000 000 copies/mL, parvovirus IgG 0.34 (normal

Congenital human parvovirus b19 infection with persistent viremia.

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