[Atypical involvement of purpuric syndrome caused by parvovirus B19. Case report in a 12-year-old female]. / Síndrome purpúrico de distribución atípica por parvovirus B19 en una adolescente.

Parvovirus B19 is the cause of a variety of exanthematous diseases during childhood and adolescence, such as erythema infectiosum and papular purpuric gloves and socks syndrome. This is an unusual, benign and acute acrodermatitis. Aphtous stomatitis, fever and other systemic symptoms can be associated with the eruption of the purpuric rash. Uncommon patterns such as asymmetrical distribution or erythematous involvement llave recently been described as additional features of PVB19-associated purpuric petechial eruption. This is a case report of a 12-year-old female with an atypical involvement of a papular-purpuric syndrome caused by human parvovirus B19.

Síndrome purpúrico de distribución atípica por parvovirus B19 en una adolescente / Atypical involvement of purpuric syndrome caused by parvovirus B19: case report in a 12-year-old female

Resumen El parvovirus B19 es causante de una variedad de enfermedades exantemáticas durante la infancia y adolescencia, como el eritema infeccioso y el síndrome papular purpúrico en guante y calcetín. Este último es una acrodermatitis aguda, inusual y benigna, que puede asociarse a aftas orales, fiebre y otros síntomas constitucionales. Existen casos atípicos como la púrpura febril en otras localizaciones, sin cumplir la distribución característica en guante y calcetín de forma simétrica o con un mayor componente de eritrodermia. Presentamos el caso de una adolescente de 12 años con un síndrome papular purpúrico de distribución atípica por parvovirus B19.

Abstract Parvovirus B19 is the cause of a variety of exanthematous diseases during childhood and adolescence, such as erythema infectiosum and papular purpuric gloves and socks syndrome. This is an unusual, benign and acute acrodermatitis. Aphtous stomatitis, fever and other systemic symptoms can be associated with the eruption of the purpuric rash. Uncommon patterns such as asymmetrical distribution or erythematous involvement llave recently been described as additional features of PVB19-associated purpuric petechial eruption. This is a case report of a 12-year-old female with an atypical involvement of a papular-purpuric syndrome caused by human parvovirus B19.

Quantitative real-time PCR for differential diagnostics of parvovirus B19 infection in acute liver failure patients.

BACKGROUND: Human Parvovirus B19 (B19V) is a common pathogen worldwide. After primary infection, B19V-DNA may permanently persist in non-erythroid tissues, including the liver of patients with acute liver failure (ALF). OBJECTIVE: To validate a real-time PCR (qPCR) for the quantification of B19V-DNA, in order to establish a differential diagnosis for B19V infection in ALF patients. METHODS: The qPCR techniques were based on Sybr Green® and TaqMan® methodologies. To evaluate the quality parameters of both methods, samples from patients with or without B19V infection were tested. The diagnostic utility of qPCR in the detection B19V-DNA in patients with ALF was evaluated by testing archived serum and hepatic tissue explants from 10 patients. RESULTS: The Sybr Green® methodology showed 97% efficiency, the limits of detection and quantification were 62.6 and 53,200 copies/mL, respectively. The TaqMan® methodology showed 95% efficiency, the limits of detection and quantification were 4.48 and 310 copies/mL, respectively. A false positive result was found only with the Sybr Green® methodology. Among ALF patients without defined etiology, three (30%) were positive for B19V DNA in serum and liver. CONCLUSION: The qPCR methods validated here were effective in clarifying uncommon cases of B19V-related ALF and are fit for differential diagnosis of ALF causes.

Febrile Neutropenia following Parvovirus B19 Infection and Cross Anti-Kell Reaction to E. Coli in Pregnancy.

Parvovirus B19 has tropism for red line blood cells, causing immune hydrops during pregnancy. A positive anti-Kell Coombs reaction usually happens during pregnancy when there is production of antibodies that target Kell antigens, but cross reactions to other antigens may occur. A 24-year-old Gypsy primigravida, 0 Rhesus positive, presented with persistent isolated hyperthermia for 2 weeks and a positive indirect Coombs test result with anti-Kell antibodies at routine tests. She had a 19-week live fetus. The blood tests revealed bicytopenia with iron deficiency anemia, leucopoenia with neutropenia, and elevated C-reactive protein. She was medicated with imipenem, and had a slow clinical recovery. Blood, urine and sputum samples were taken to perform cultures and to exclude other systemic infections. Escherichia coli was isolated in the urine, which most probably caused a transient cross anti-Kell reaction. Haemophilus influenza in the sputum and seroconversion to parvovirus B19 was confirmed, causing unusual deficits in the white cells, culminating in febrile neutropenia. Despite the patient's lack of compliance to the medical care, both maternal and fetal/neonatal outcomes were good. This a rare case report of 2 rare phenomena, a cross anti-Kell reaction to E. coli and parvovirus B19 infection with tropism for white cells causing febrile neutropenia, both events occurring simultaneously during pregnancy.

O parvovírus B19 tem tropismo para as células sanguíneas da linha vermelha, causando hidropsia imune durante a gravidez. O teste Coombs anti-Kell positivo ocorre durante a gravidez quando há produção de anticorpos contra os antígenos de Kell, mas pode haver reações cruzadas para outros antígenos. Uma grávida primigesta de etnia cigana, de 24 anos, 0 Rhesus positivo, recorreu ao hospital às 19 semanas de gestação por hipertermia isolada persistente por 2 semanas e um teste Coombs indireto positivo por anticorpos anti-Kell em testes de rotina da gravidez. O estudo analítico revelou bicitopenia com anemia ferropênica, leucopenia com neutropenia, e elevação da proteína C-reativa. A paciente foi medicada com imipenem, e teve uma recuperação clínica lenta. Foram colhidas amostras de sangue, urina e expectoração para culturas bacterianas. Na urina, foi isolada Escherichia coli, o que provavelmente causou a reação anti-Kell cruzada transitória. Na expectoração, foi isolada Haemophilus influenza, e foi confirmada seroconversão para o parvovírus B19, que causou um déficit incomum na linhagem sanguínea branca, culminando com neutropenia febril. Apesar da má adesão aos cuidados médicos, os desfechos materno e fetal/neonatal foram bons. Este é um caso de 2 fenômenos raros, uma reação cruzada anti-Kell à infecção por E. coli, e parvovírus B19 com tropismo para células brancas causando neutropenia febril, ambos ocorrendo simultaneamente durante a gravidez.

Febrile neutropenia following parvovirus B19 infection and cross anti-kell reaction to E. coli in pregnancy / Infeção por parvovírus B19 causando neutropenia febril e reação cruzada anti-Kell com E. coli na gravidez

Abstract Parvovirus B19 has tropism for red line blood cells, causing immune hydrops during pregnancy. A positive anti-Kell Coombs reaction usually happens during pregnancy when there is production of antibodies that target Kell antigens, but cross reactions to other antigens may occur. A 24-year-old Gypsy primigravida, 0 Rhesus positive, presented with persistent isolated hyperthermia for 2 weeks and a positive indirect Coombs test result with anti-Kell antibodies at routine tests. She had a 19-week live fetus. The blood tests revealed bicytopenia with iron deficiency anemia, leucopoenia with neutropenia, and elevated C-reactive protein. She was medicated with imipenem, and had a slow clinical recovery. Blood, urine and sputum samples were taken to perform cultures and to exclude other systemic infections. Escherichia coli was isolated in the urine, which most probably caused a transient cross anti-Kell reaction. Haemophilus influenza in the sputum and seroconversion to parvovirus B19 was confirmed, causing unusual deficits in the white cells, culminating in febrile neutropenia. Despite the patient's lack of compliance to the medical care, both maternal and fetal/neonatal outcomes were good. This a rare case report of 2 rare phenomena, a cross anti-Kell reaction to E. coli and parvovirus B19 infection with tropism for white cells causing febrile neutropenia, both events occurring simultaneously during pregnancy.

Resumo O parvovírus B19 tem tropismo para as células sanguíneas da linha vermelha, causando hidropsia imune durante a gravidez. O teste Coombs anti-Kell positivo ocorre durante a gravidez quando há produção de anticorpos contra os antígenos de Kell, mas pode haver reações cruzadas para outros antígenos. Uma grávida primigesta de etnia cigana, de 24 anos, 0 Rhesus positivo, recorreu ao hospital às 19 semanas de gestação por hipertermia isolada persistente por 2 semanas e umteste Coombs indireto positivo por anticorpos anti-Kell em testes de rotina da gravidez. O estudo analítico revelou bicitopenia com anemia ferropênica, leucopenia com neutropenia, e elevação da proteína C-reativa. A paciente foi medicada com imipenem, e teve uma recuperação clínica lenta. Foram colhidas amostras de sangue, urina e expectoração para culturas bacterianas. Na urina, foi isolada Escherichia coli, o que provavelmente causou a reação anti-Kell cruzada transitória. Na expectoração, foi isolada Haemophilus influenza, e foi confirmada seroconversão para o parvovírus B19, que causou um déficit incomum na linhagem sanguínea branca, culminando com neutropenia febril. Apesar da má adesão aos cuidados médicos, os desfechos materno e fetal/neonatal foram bons. Este é um caso de 2 fenômenos raros, uma reação cruzada anti-Kell à infecção por E. coli, e parvovírus B19 comtropismo para células brancas causando neutropenia febril, ambos ocorrendo simultaneamente durante a gravidez.

Clinical presentation of parvovirus B19 infection in HIV-infected patients with and without AIDS.

Human parvovirus B19 replicates in erythrocyte precursors. Usually, there are no apparent hematological manifestations. However, in individuals with high erythrocyte turnover, as in patients with sickle-cell disease and in the fetus, the infection may lead to severe transient aplasia and hydrops fetalis, respectively. In AIDS patients, persistent infection may result in chronic anemia. By contrast, in HIV-positive patients without AIDS the infection evolves as a mild exanthematous disease. Two clinical descriptions exemplify these forms of presentation. In the first, an AIDS patient presented with bone marrow failure that responded to immunoglobulin. In the second, an HIV-positive patient without AIDS had a morbilliform rash, and needed no treatment. Knowing that an AIDS patient has chronic B19 anemia lessens concern about drug anemia; protects the patient from invasive diagnostic maneuvers; and prevents the patient from disseminating the infection. In AIDS patients with pure red cell aplasia, a search for parvovirus B19 DNA in the serum or in the bone marrow is warranted.

Clinical presentation of parvovirus B19 infection in HIV-infected patients with and without AIDS

Human parvovirus B19 replicates in erythrocyte precursors. Usually, there are no apparent hematological manifestations. However, in individuals with high erythrocyte turnover, as in patients with sickle-cell disease and in the fetus, the infection may lead to severe transient aplasia and hydrops fetalis, respectively. In AIDS patients, persistent infection may result in chronic anemia. By contrast, in HIV-positive patients without AIDS the infection evolves as a mild exanthematous disease. Two clinical descriptions exemplify these forms of presentation. In the first, an AIDS patient presented with bone marrow failure that responded to immunoglobulin. In the second, an HIV-positive patient without AIDS had a morbilliform rash, and needed no treatment. Knowing that an AIDS patient has chronic B19 anemia lessens concern about drug anemia; protects the patient from invasive diagnostic maneuvers; and prevents the patient from disseminating the infection. In AIDS patients with pure red cell aplasia, a search for parvovirus B19 DNA in the serum or in the bone marrow is warranted

Survey of parvovirus B19 infection in a cohort of pregnant women in Belém, Brazil

A total of 300 pregnant women were screened for the presence of human parvovirus B19 IgG and IgM antibodies by an enzyme-linked immunosorbent assay (ELISA). Overall, 253 (84.3 percent) were found to be IgG-positive and IgM-negative (IgG+IgM-), 42 (14 percent) had neither IgG nor IgM antibodies (IgG-/IgM-) and 5 (1.7 percent) were both IgM- and IgG-positive (IgG+/IgM+). Maternal serology was performed routinely for cytomegalovirus, rubella, toxoplasmosis and syphilis. All IgG-/IgM- and IgG+/IgM+ women were followed until the time delivery, with venous blood samples taken monthly from each, one IgG-/IgM- mother seroconverted to IgG+/IgM- and B19 DNA was detected by nested polymerase chain reaction technique (PCR) in her serum. All babies born to IgG+/IgM+ mothers (and from the one who seroconverted) were IgG+IgM-, but no B19 DNA could be detected in their sera and no adverse effects were documented either by ultrasonographic examination or by detection of maternal serum alpha-fetoprotein. While 5 of the mothers delivered normal children at term, one gave birth to a premature (low-weight) baby who developed severe anemia and had convulsions. However, this mother was found to have toxoplasma-specif IgM. Our data indicate a low frequency of B19 infection in pregnancy in our region, at least during interepidemic periods. This appears to be partly due to high prevalence of prior infection among pregnant women. Recent B19 infection in 6 women did not lead to adverse fetal outcomes. This observation, however, in a small number of serologically positive patients, does not contradict the observations by others that recent infection does converg a risk for the fetus.

Glomerulonephritis after human parvovirus infection in homozygous sickle-cell disease.

Glomerulonephritis with proteinuria of sufficient degree to manifest the nephrotic syndrome followed aplastic crises induced by human parvovirus (B19) in seven patients with homozygous sickle-cell disease, within 7 days in five patients and 6-7 weeks in two. Segmental proliferative glomerulonephritis was found in all four patients who underwent acute renal biopsies and focal segmental glomerulosclerosis was found in the fifth patient who had a biopsy 4 months later. One patient recovered completely, one died in chronic renal failure after 3 months, and the others had impaired creatinine clearance, four with continuing proteinuria.

Glomerulonephritis after human parvovirus infection in homozygous sickle-cell disease

Glomerulonephritis with proteinuria of sufficient degree to manifest the nephrotic syndrome followed aplastic crises induced by human parvovirus (B19) in seven patients with homozygous sickle-cell disease, within 7 days in five patients and 6-7 weeks in two. Segmental proliferative glomerulonephritis was found in all four patients who underwent acute renal biopsies and focal segmental glomerulosclerosis was found in the fifth patient who had a biopsy 4 months later. One patient recovered completely, one died in chronic renal failure after 3 months, and the others had impaired creatinine clearance, four with continuing proteinuria (AU)

Human parvovirus infection in homozygous sickle cell disease.

We studied the epidemiology of human parvovirus B19 infection in 308 children with homozygous sickle cell (SS) disease and 239 controls with a normal haemoglobin (AA) genotype followed from birth in a cohort study. Annual serum samples identified the time and frequency of B19 infection, which did not differ between SS and AA children, about 40% of each group developing specific IgG by age 15. B19 infection followed an epidemic pattern similar to that observed for aplastic crises; accounted for all 91 aplastic crises that occurred; and was found in an additional 23 SS patients, of whom 10 showed mild haematological changes and 13 no changes. The magnitude or duration of IgG response did not differ between these groups. No patient had 2 attacks of aplasia and no patient nor control had 2 attacks of B19 infection. Following B19 infection, serial specific IgG concentrations remained high after 5 years in only 45% of SS patients, although the rarity of recurrent aplasia suggests lifelong immunity. B19 infection accounts for most if not all aplastic crises in SS disease, but at least 20% of infections do not result in aplasia. An effective vaccine against B19 might make an important contribution to the management of sickle cell disease.

Acute splenic sequestration together with aplastic crisis caused by human parvovirus B19 in patients with sickle cell disease.

Three children with homozygous sickle cell disease, 22 months and 8 and 10 years of age, had clinical and hematologic manifestations of aplastic and splenic sequestration crisis simultaneously. They had an acute drop in hemoglobin level (16, 20, and 45 gm/L), reticulocytopenia (0.1%, 0.6%, and 0.3%), and sudden splenic enlargement. Evidence of recent parvovirus infection was demonstrated.

Aplastic crisis due to human parvovirus B19 infection in hereditary hemolytic anaemia

Specific anti-B19 IgM was demonstrated in sera from three children showing transient aplastic crisis. A two years-old boy living in Rio de Janeiro suffering from sickle-cell anaemia showed the crisis during August, 1990. Two siblings living in Santa Maria, RS, developed aplastic crisis during May, 1991, when they were also diagnosed for hereditary spherocytosis. For a third child from this same family, who first developed aplastic crisis no IgM anti-B19 was detected in her sera

Aplastic crisis due to human parvovirus B19 infection in hereditary hemolytic anaemia.

Specific anti-B19 IgM was demonstrated in sera from three children showing transient aplastic crisis. A two years-old boy living in Rio de Janeiro suffering from sickle-cell anaemia showed the crisis during August, 1990. Two siblings living in Santa Maria, RS, developed aplastic crisis during May, 1991, when they were also diagnosed for hereditary spherocytosis. For a third child from this same family, who first developed aplastic crisis no IgM anti-B19 was detected in her sera.