Hydrothorax as a Sole Manifestation of Congenital Parvovirus B19 Infection

Abstract

We present a case of congenital parvovirus B19 infection in a term neonate manifested with isolated massive hydrothorax and mild anemia. Parvovirus B19 DNA was detected in maternal and neonatal blood as well as in pleural fluid despite lack of suggestive serology.

Critical cardiac tamponade in newborn, life-saving emergency interventions and possibility of parvovirus B19 congenital infection

“…It is thought, that hydrops fetalis caused by PV-B19 results from destruction of erythroid cells leading to subsequent fetal anemia which causes cardiac failure [5]. To the best of our knowledge there are only few publications reporting the association of isolated pleural or pericardial effusions and PV-B19 congenital infection [4,7,8]. Following the above we have suspected the PV-B19 fetal infection in our patient.…”

“…Except for major cardiac morbidities -an idiopathic pericardial tamponade in newborns is rarely reported in the literature. Alongside previously described isolated pedicardial effusion due to a restrictive cardiomyopathy or dilated and hypertrophic cardiomyopathies in fetal life, we have also considered a possibility of congenital pleural effusions occurring with hydrops fetalis, or congenital chylothorax [1,4]. Congenital PV-B19 infection may present with isolated fluid effusion as a sole manifestation [4].…”

“…PCR should be performed in maternal and neonatal blood whenever clinical suspicion of PV-B19 infection has occured, although the method is not free from limitations [4]. There are some studies that report on the clearance of PV-B19 DNA from peripheral blood after acute infection; in some patients this clearance is registered after one month already, and in 67% of patients in the second month after the onset of illness [14,16].…”

“…There is a considerable possibility of false negative results, because the sensitivity of IgM antibodies detection between 8 and 12 weeks after maternal infection varies between 63 -70% [12,13]. Low sensitivity of the assays, transient low-titer viremia not inducing an immune response and immaturity of the fetal immune system have all been suspected as reasons for the absence of specific PV-B19 IgM antibodies [4,14,15]. In contrast, PV-B19 IgG antibodies increase from 14 days after infection and reach a plateau level after 4 weeks; these antibodies are supposed to be present for a long period [11].…”

“…During pregnancy PV-B19 infection can be asymptomatic or can cause a variety of signs of fetal damage (severe anemia, hydrops fetalis, death) [5]. In hydrops fetalis, nonchylous fluid accumulates in the different serous cavities (ascites, pericarditis, pleura), but widespread edema of subcutaneous fetal tissue is the main clinical manifestation [4]. It is thought, that hydrops fetalis caused by PV-B19 results from destruction of erythroid cells leading to subsequent fetal anemia which causes cardiac failure [5].…”