Hindawi

Case Reports in Pediatrics

Volume 2020, Article ID 8841607, 3 pages
https://doi.org/10.1155/2020/8841607

Case Report
Leukoerythroblastosis as an Unusual Presentation of Parvovirus
B19 Infection in a Sickle Cell Patient

Pratik A. Patel,1 Elizabeth P. Weinzierl,2 and Daniel S. Wechsler 1,3

1
Aflac Cancer & Blood Disorders Center, Children’s Healthcare of Atlanta, Atlanta, GA, USA
2
Department of Pathology, Children’s Healthcare of Atlanta, Emory University School of Medicine, Atlanta, GA, USA
3
Department of Pediatrics, Emory University School of Medicine, Atlanta, GA, USA

Correspondence should be addressed to Daniel S. Wechsler; dan.wechsler@emory.edu

Received 16 April 2020; Revised 9 September 2020; Accepted 10 September 2020; Published 22 September 2020

Academic Editor: Marie Louise von Linstow

Copyright © 2020 Pratik A. Patel et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Parvovirus B19 infection in pediatrics most commonly causes fifth disease, a mild viral illness. Hematologic manifestations
include severe anemia, especially in patients with chronic hemolytic anemias or who are immunocompromised. Because of the
shortened life span of erythrocytes in patients with sickle cell disease, parvovirus infection can cause transient aplastic crisis which
can be life-threatening. However, leukocytosis and thrombocytosis are rarely seen. We report leukoerythroblastosis as an unusual
presentation of acute parvovirus B19 infection in a previously splenectomized 12-year-old boy with sickle cell disease.

1. Introduction count was 1.2%. Morphologic examination of the pe-

ripheral blood showed a marked leukoerythroblastosis, rare
Parvovirus B19 infection is frequently diagnosed in the myeloblasts (∼1%), markedly abundant nucleated RBCs,
pediatric population and can be severe in patients with and thrombocytosis with many large and giant platelets
chronic hemolytic anemias such as sickle cell disease. Pa- (Figure 1). Lactate dehydrogenase was 772 U/L (normal
tients typically present with severe anemia and/or pancy- 157–272 U/L), and uric acid was 5.6 mg/dL (normal
topenia. Here, we describe an unusual presentation of acute 2.6–6.8 mg/dL). Coagulation studies were within normal
parvovirus B19 infection in a patient with sickle cell disease. limits. Of note, ten days earlier, the patient was evaluated at
an outside hospital for fever and had a normal CBC : WBC
2. Case Presentation of 12 × 109/L, hemoglobin 9.2 g/dL, and PLT 550 × 109/L.
Based on the presenting CBC, there was concern for a
A 12-year-old boy with sickle cell disease (HbSS) with a myeloproliferative neoplasm (MPN) such as chronic mye-
history of splenectomy presented to the emergency room for loid leukemia (CML). Peripheral blood flow cytometry
fatigue, headaches, and near syncope. On examination, the showed a myeloid left shift but no abnormal hema-
patient was tachycardic with a grade 3/6 systolic ejection tolymphoid cell population. Fluorescence in situ hybrid-
murmur, marked pallor, and shotty cervical and inguinal ization (FISH) testing for the BCR-ABL1 translocation was
lymphadenopathy. negative. CMV and EBV were undetectable by PCR. Because
Complete blood count (CBC) showed a white blood cell of the severe sudden drop in hemoglobin combined with
(WBC) count of 72.2 × 109/L (65.4% neutrophils, 10.3% reticulocytopenia, parvovirus studies were also sent. Par-
band forms, 2.7% metamyelocytes, 0.3% myelocytes, vovirus B19 IgM was positive, and IgG was negative; the
12.3% lymphocytes, 6.7% monocytes, 0.3% eosinophils, parvovirus B19 PCR titer was 6.6 × 107 IU/ml (negative
and 2% blasts), hemoglobin 3.9 g/dL (baseline hemoglobin <199 IU/ml) with 1 IU equal to 0.79 copies of parvovirus
9 g/dL), platelets (PLT) 1533 × 109/L, and 15.3 nucleated B19. The patient was transfused with packed red blood cells
red blood cells (RBCs) per 100 WBCs. The reticulocyte and received intravenous hydration. Within 48 hours, his
2 Case Reports in Pediatrics

(a) (b)

Figure 1: Peripheral blood smear (Wright–Giemsa stain, 50x magnification) showing nucleated red blood cells (open arrows), sickle cells
(S), myelocytes (arrows), platelets (asterisks), and a blast (arrowhead). Numerous target cells are also present.

WBC count had fallen to 20.7 × 109/L and he was discharged cases of parvovirus B19-associated leukoerythroblastosis
with close outpatient follow-up. Six days later in clinic, his have been reported [13–17], but all of these patients were
WBC had normalized to 9.35 × 109/L and his PLT count was neonates and infants (age range preterm neonates to
1143 × 109/L. 11 months) and none had thrombocytosis (range
63–250 109/L); in addition, none of them had sickle cell
3. Discussion disease. The 12-year-old sickle cell patient described here
had an unusual presentation of leukoerythroblastosis in
This child with sickle cell disease presented with blood conjunction with transient aplastic crisis secondary to
counts concerning for a MPN but was ultimately diag- parvovirus B19 infection. The profound thrombocytosis was
nosed with transient leukoerythroblastosis in the setting likely due to a hyperactive marrow, given the degree of
of acute parvovirus B19 infection. The diagnosis of acute anemia on presentation. Patients with splenectomies also
parvovirus B19 is typically made with serology being tend to have higher platelet counts, including those with
positive for IgM and negative for IgG and parvovirus B19 chronic hemolytic anemias such as sickle cell disease and
DNA PCR positive [1–3]. While parvovirus B19 viral hyposplenism [18]. Although Jen and Jackups noted similar
DNA can be detectable for many months, the titer is findings in a 3-year-old patient with sickle cell disease [19],
usually highest during the acute presentation [4]. Par- our patient is the oldest reported patient with leukoery-
vovirus B19 infection can span from asymptomatic to life- throblastic reaction in response to parvovirus B19 infection.
threatening, depending on the status of the infected host. Disorders such as myelodysplastic syndrome and CML have
Patients with sickle cell disease and other chronic he- been temporally associated with concurrent viral infections
molytic anemias often develop transient aplastic crisis as a such as EBV and parvovirus B19 [20–23]. Our patient’s
result of acute parvovirus B19 infection [5, 6], which presentation suggests that viral serologies and parvovirus
primarily affects erythroid progenitor cells. Other com- B19 DNA PCR should be considered in the workup of older
mon hematologic manifestations of acute infection in this children who present with leukoerythroblastosis.
patient population include reticulocytopenia and leuco-
penia [1]. Similarly, immunocompromised patients (e.g.,
those undergoing treatment of leukemia) with parvovirus Disclosure
infection may develop cytopenias as well [7]. Other causes
of severe anemia in patients with sickle cell disease include This work was performed as part of the authors’ employment
splenic sequestration, acute chest syndrome, hyper- by Children’s Healthcare of Atlanta, Atlanta, GA
hemolysis, and sepsis [8, 9]. Along with severe anemia,
parvovirus infection in patients with sickle cell disease
classically presents with reticulocytopenia which was seen
Conflicts of Interest
in this patient. However, the patient also had marked The authors have no conflicts of interest to disclose relevant
leukocytosis and thrombocytosis, unusual in the setting of to this article.
parvovirus infection [1, 10, 11]. Leukocytosis >50 × 109/L
can be an indication of hematologic malignancy, but is not
always associated with a diagnosis of leukemia [12].
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