2002-01-10-14 Parvovirus infection © Guerrero www.thefetus.net/
Luis D?az Guerrero, MD
Perinatology Unit, Maternidad Privada Las Acacias, Valencia, Venezuela
Definition: fetal parvovirus infection is a congenital disorder, characterized by hydrops, ascites, ventriculomegaly, hypertrophic myocardiopathy, placentomegaly and other findings caused by transplacental transmission of parvovirus to the fetus.
History: Cossart and associates fortuitously discovered Parvovirus B19 in 1975 while essaying sera for hepatitis virus. In 1984 Brown and associates links parvovirus B19 infection to fetal hydrops.
Synonyms: Congenital parvovirus infection. Fifth disease.
Etiology: Parvovirus B19. It is a member of the family Parvoviridae. It can only infect humans. The virus contains a single-stranded DNA. It can be seen on electron microscopy as intranuclear pcases about 20 to 24 nm in size. An icosahedral protein coat and the gene locus codes for two capsid proteins and nonstructural proteins surround the viral genome.
Epidemiology: Congenital infection rates vary depending on the prevalence in the community. Approximately 50 to 75% of adult women are immune. Maternal infection with parvovirus B19 is estimated to occur in 0.25-6% of the susceptible pregnancies. The risk of infection among susceptible adults following household exposure to an infected person is approximately 50%. The risk for congenital infection from an infected mother is between 10% to 20% and is highest in the first and second trimesters. The average time from diagnosis to resolution is about 6 weeks.
Diagnosis: During the first trimester fetuses with parvovirus B19 infection can present with increased nuchal translucency and intrauterine growth restriction. In second and third trimesters fetal infection by parvovirus B19 can be suspected by the use of ultrasound with the presence of fetal hydrops, ascites, pleural or pericardial effusion, skin thickening, cardiomegaly (increased cardiac biventricular outer diameter) and decreased movement in severe cases, hypertrophic myocardiopathy, hyperechoic bowel, hepatomegaly, abdominal wall edema, bilateral hydroceles, hydrocephalus, microcephaly, intracranial calcifications. Placentomegaly may develop and there may be amniotic fluid volume disorders.
These are images from Case of the Week #64. The following images were obtained in a 2nd trimester fetus. They demonstrated a mild hydrops with pleural effusion, minimal ascites but little or no skin edema.
There is also a 2 MB video-clip that demonstrated an essentially normal heart.
Following this examination, a consult was obtained to confirm that the heart was normal. A fetal blood sampling confirmed the anemia and a transfusion done. After the transfusion, the hydrops regressed and the baby had an uneventful course and delivery.
Fetal anemia can be predicted with Doppler measurement of the middle cerebral artery peak systolic velocity in pregnancies complicated by parvovirus B19 infection by increased values of velocities prior to the appearance of sonographically signs of hydrops. Reversed flow in the ductus venosus Doppler have been reported that could be explained by both end-stage heart failure and regurgitation secondary to tricuspid insufficiency.
Specific diagnosis can be made y the following methods
a) Serology: Maternal B19-specific IgG (indicates past infection / immunity); Maternal B19-specific IgM (indicates recent infection), Cordocentesis for B19-specific IgM.
b) Presence of the virus: DNA in amniotic fluid or fetal tissue, Southern blot hybridization, In situ hybridization, Polymerase chain reaction. Virus pcases by electron microscopy.
c) Cytopathic effects: gross examination of tissue (fetus, placenta), histology of erythroid cells
d) Markers of infection: Maternal serum alpha fetoprotein (non specific)
Pathogenesis: the most common route of horizontal transmission is through respiratory secretion, transplacental transmission can occur any time during pregnancy. The primary site of Parvovirus B19 infections is within erythroid precursor cells and it has an affinity for the late normoblast stage and the cardiac myocytes and also causes a decrease in the number of platelets. Hydrops fetalis has been reported with maternal B19 infection and appears to be due primarily to fetal anemia and resulting cardiac failure induced by the anemia and the fetal myocarditis. Parvovirus B19 causes up to 27% cases of non-immune hydrops in anatomically normal fetuses.
Differential diagnosis: other causes of hydrops, heart problems, chromosomal abnormalities, cytomegalovirus, syphilis.
Prognosis: In pregnant woman, the primary infection with Parvovirus B19 may lead to fetal anemia and hydrops fetalis with variable outcomes: fetal death, hydrops fetalis, congenital anemia or spontaneous resolution. There is a 10% risk for fetal death due to hydrops from severe fetal anemia. The risk for fetal death in utero is 17% before 20 weeks and 6% after 20 weeks if the fetus is infected. Increased maternal serum alpha-fetoprotein has been used as a prognostic factor for poor outcome.
Management: because the major fetal manifestation of parvovirus infection is anemia, treatment by in utero transfusion is appropriated when a diagnosis is made in a fetus with hydrops (usually hematocrit of less than 25%). This procedure can lead to resolution of the fetal hydrops. Fetal myocardiopathy treatment by intrauterine digitalization has been attempt as a palliative treatment. Immunoglobulins have been successfully used in postnatal patients. There is even one report of terminal cardiac heart failure in a third trimester fetus, which had a successful transplant postnatally. In view of these therapeutic options, termination of pregnancy is rarely indicated.
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