[Pathomorphology of fetal parvovirus B19 infection].
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For hepatitis B, universal screening of pregnant women for HBsAg along with the combined use of hepatitis B vaccine and HBIG in infants of infected mothers appears to be the best way to detect and prevent vertically transmitted infection. Cytomegalovirus is the most common congenital viral infection, but the lack of a good screening test precludes its accurate and rapid diagnosis. For HPV-B19, larger and more controlled studies are needed to confirm the safety and effectiveness of fetal blood transfusions in the management of hydrops fetalis caused by this infection. Finally, the fact that most mothers of HSV- and toxoplasma-infected neonates have no history of infection, and are asymptomatic at the time of delivery, underscores the need for a high index of clinical suspicion in sick neonates.
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We recently observed that more than one third of pediatric patients who presented with non-A, non-B fulminant liver failure (FLF) also developed aplastic anemia (AA) either before or shortly after liver transplantation. Factors involved in the suppression of bone marrow could be the same as those causing hepatic failure. We considered parvovirus B19 a candidate etiologic agent because of the known tropism of B19 for erythroid precursors. Archived liver and serum from six patients undergoing liver transplantation for non-A, non-B, non-C FLF with associated AA were analyzed for the presence of B19 DNA and anti-B19 serology. An age- and gender-matched control group (N = 44) was analyzed in parallel. B19 DNA studies and anti-B19 serology were performed in a blinded fashion. B19 serologies were performed by antibody capture enzyme-linked immunosorbent assay (ELISA). B19 DNA was detected after polymerase chain reaction (PCR) amplification of target B19 DNA sequences in liver and serum. Liver tissue showed evidence of B19 DNA in four of six (66%) patients with FLF and associated AA. Two of 4 patients with cryptogenic FLF but without AA had B19 DNA detected in the liver tissue. Of the 34 remaining controls, only 5 (15%) showed evidence of B19 DNA in liver tissue (66% vs. 15%, P = .016). B19 DNA was not detected in any of the test or control sera. This study provides evidence to support the role of parvovirus B19 in the development of FLF and associated AA.
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In four patients, all girls, aged 2, 3.5, 4 and 5 years, transient erythroblastopenia was diagnosed. The children were presented because of acute pallor. The haemoglobin levels were 2.8 to 5.0 mmol/l. After 3 weeks all patients had recovered or were recovering with increasing haemoglobin values. Three of the four patients needed one blood transfusion. In two patients there was evidence of a parvovirus B19 infection. Transient erythroblastopenia is mostly seen in patients aged 1-4 years. Most cases are postinfectious and there is evidence that human parvovirus B19 is responsible for many cases. In the very young child the differential diagnosis from Blackfan-Diamond anaemia may be very difficult.
Infection with parvovirus B19 is an important cause of late fetal mortality in the second trimester, and many infections in pregnancy remain undiagnosed. A serological survey stratified by age has been used to estimate the incidence of maternal infection with parvovirus B19 in pregnancy. Serum remaining from specimens submitted for diagnosis from 6864 people of all ages to seven public health laboratories in England was tested for antibody to parvovirus B19. The antibody prevalence rose with age to 45% at 10 years and 60% to 70% in adults. The age specific force of infection was highest in children aged less than 10 years and lowest in adults. Maternal infection with parvovirus B19 is estimated to occur in approximately one pregnancy in 400. It has been estimated that fetal death occurs in 9% of these cases, which suggests that parvovirus B19 may cause more than 150 fetal deaths in England and Wales each year. Testing for evidence of recent infection with parvovirus B19 should be considered for unexplained cases of fetal hydrops in the second trimester, especially in years of parvovirus B19 epidemics.
A 30-year-old postpartum woman was admitted to our hospital because of progressive anemia, malaise, night sweating, headache and low grade fever which began 9 days after delivery (day 0). She had normocytic hypochromic anemia accompanied with marked decrease in reticulocytes. In addition, a temporary decrease in platelets and white blood cells especially neutrophils were observed. Bone marrow smears showed an apparent decrease in erythroid cells and the presence of giant proerythroblasts (1.2%) as well as hemophagocytes (1.2%). IgM and IgG antibody against human parvovirus B19 (HPV) was detected on day 22 of the disease although negative results were obtained on day 3. The presence of the virus in the blood on admission was confirmed by dot-blot analysis. Thus, this case was diagnosed as acute pure red cell aplasia and hemophagocytic syndrome caused by HPV infection. This patient had been given iron for iron deficiency anemia before delivery and the iron deficiency was still present after the episode of the present disease although the iron metabolism data was perturbed during the disease. These findings suggest that HPV could cause acute pure red cell aplasia not only in patients with hemolytic anemia but also in patients with iron deficiency anemia or after acute bleeding. Furthermore it is suggested that pancytopenia often observed on HPV infection could be at least partly caused by hemophagocytic syndrome.
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The infectious erythema is usually childhood disease associated with rash and caused by parvovirus B19. At the beginning of 1993., at the Clinic for infectious and tropical diseases of the Military Medical Academy 36 patients were treated for this disease, the average age 21 years. The prodromal phase of illness lasted approximately 2.9 days, the elevated temperature 5.2 days, and 17 patients had temperature above 39 degrees C. The rash was usually maculo-papullous and lasted about 6 days. Four patients had the recurrence of rash. The polyarthralgia appeared for short in six patients and in one patient lasted longer than 4 months. The mild anemia during infectious erythema was observed in 18 patients. IgM antiparvo B19 antibodies were proven in serum in 91.7%, and IgG antibodies in 58.3% of patients.
BACKGROUND: Parvovirus B19 is the etiologic agent of transient aplastic crisis, an acute episode of bone marrow failure in persons with underlying hemolysis. Successful administration of gammaglobulin in some chronic cases and immunocompromised patients infected with parvovirus B-19, resulting in the elimination of this virus has been reported. However little is known about the evolution of acute aplastic crisis in treated patients with chronic hemolysis nor about the minimal effective dose of immunoglobulin. METHODS: We report a family infected by Parvovirus B 19, discovered when a pure red blood-cell aplasia broke out in one family member who was suffering from a chronic haemolytic disease. The diagnosis was considered by presence of giant proerythroblasts in bone marrow and later confirmed by DNA viral detection using PCR technique. RESULTS: The patient was treated with a small dose of polivalent intravenous gammaglobulin, with a temporary disappearance of the virus from his serum during treatment. CONCLUSION: The usefulness, doses and length of immunoglobulin treatment in patients with transient aplastic crisis is discussed. Our results show that treatment with low doses of I.V. gammaglobulin able to control viremia and probably shorten the episode of anemia and acute aplastic crisis in this patient with chronic hemolytic anemia and parvovirus B-19 infection. This observation could be useful and cost saving also in chronic cases and in immunocompromised.
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