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Pathologic Manifestations in a Case of Intrauterine Fetal Demise due to Parvovirus B19 Infection

Pathologic Manifestations in a Case of Intrauterine Fetal Demise due to Parvovirus B19 Infection
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Author: Elnaz Panah, M.D; Brandon Zelman, D.O.; Kristina Gvozdjan, M.D.
Category: Red Cell: Hemolytic Anemia (HA) > Autoimmune Hemolytic Anemias > Cold-active antibodies > Cold agglutinin disease (CAD) > Secondary CAD > Infectious > Other viruses
Published Date: 03/22/2022

A 37 weeks' gestation stillborn female fetus was born to an asymptomatic mother who presented with lack of fetal movement for one day. Fetal ultrasound demonstrated diffuse intestinal echogenicity. 

The postmortem examination revealed a non-dysmorphic fetus. The gross examination was unremarkable.  The microscopic examination revealed prominent extramedullary hematopoiesis in the liver (Fig. 1a). Small intestinal multifocal calcifications and mucosal inflammation were seen (Fig. 1b-c). Parvovirus cytopathic effect was noted microscopically within the nucleated red blood cells present intravascularly within the small intestine, liver, spleen, and chorionic villi (Fig. 1c-f, respectively).

Parvovirus B19, discovered by Yvonne Cossart in 1975, is known to cause a wide range of pathologic conditions, including anemia and hydrops fetalis, particularly in the second trimester [1-2].  Although parvovirus B19 infection has also been associated with non-hydropic intrauterine fetal demise in late gestation, very limited pathologic manifestations were observed in such cases [2].

The postmortem examination in our case revealed the presence of abundant extramedullary erythropoiesis and multifocal viral cytopathic effect, associated with inflammatory response and calcifications, particularly in the gastrointestinal tract. Abundant extramedullary hematopoiesis may explain the non-hydropic and delayed presentation in this case.  The inflammatory manifestations and calcifications may be explained by a direct attack of parvovirus on endothelial cells of fetal bowel and stimulation of cytotoxic cytokine release [3]. Parvovirus is also known to induce apoptosis, one of the principal mechanisms of physiologic and pathologic calcifications [3]. 

References

1. Qiu J, Söderlund-Venermo M, Young NS. Human Parvoviruses. Clin Microbiol Rev. 2017;30(1):43-113. doi:10.1128/CMR.00040-16

2. Norbeck O, Papadogiannakis N, Petersson K, Hirbod T, Broliden K, Tolfvenstam T. Revised clinical presentation of parvovirus B19-associated intrauterine fetal death. Clin Infect Dis. 2002;35(9):1032-1038. doi:10.1086/342575

3. Gabrielli L, Bonasoni MP, Chiereghin A, et al. Pathophysiology of Hyperechogenic Bowel in Congenitally Human Cytomegalovirus Infected Fetuses. Microorganisms. 2020;8(5):779. doi:10.3390/microorganisms8050779