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Interventions for parvovirus B19 infection need to balance the low risk of infection at a population level with the potential for serious adverse outcome for particular groups, notably the fetus, people with haemoglobinopathies and the immunocompromised. This guidance aims to assist the local decision-making process to be as evidence-based as the available evidence allows.
We present a case of a patient who presented with a febrile illness without obvious source initially, who developed profound cardiac decompensation and left ventricular dysfunction. Viral titers obtained during the course of illness confirmed parvovirus infection. Intravenous aggressive immunoglobulins and medical therapy for heart failure resulted in stabilization and, ultimately, a complete recovery. Recent data from clinical trials are discussed regarding the utility of immunoglobulins in the treatment of myocarditis and heart failure.
We evaluated children with transient synovitis for serologic evidence of infection with parvovirus B-19 (PVB-19) and human herpesvirus-6 (HHV-6) by using a prospective patient series in an urban children's hospital emergency department (ED). There were 20 children enrolled, aged 15 months to 6 years, diagnosed with transient synovitis. Clinical data were collected, and acute PVB-19 and HHV-6 immunoglobulin G (IgG) and IgM serologic titers were measured on all patients. Ten patients returned in 4-6 weeks for convalescent titers. The mean age was 4.1 years. Prodromal symptoms within a week of presentation were noted in 50% of patients, most commonly fever (25%) and upper respiratory infection (20%). Mean sedimentation rate was 11 mm/h (range, 2-22 mm/h), and mean peripheral white blood count was 11,000/microl (range, 6-21,000/ microl). No patient had increased acute or convalescent IgM titers for either PVB-19 or HHV-6, and no patient who returned for follow-up had an increase in serum IgG titers for either virus. A majority of patients (80%) had increased acute HHV-6 IgG titers, reflecting prior immunity to this virus. In conclusion, there is no evidence in this series that acute infection with PVB- 19 or HHV-6 causes or precedes transient synovitis.
Although infection with parvovirus B19 (B19) during pregnancy may cause fetal demise, the true incidence of intrauterine infection is unknown. For 19 women with serologically confirmed B19 infections between 4 and 38 weeks of gestation, we performed follow-up examinations of their infants. Serial sonograms of the 19 fetuses showed that none developed hydrops. All 19 women delivered healthy term infants. Cord sera of four infants were tested for IgM to B19 and three were positive. Between 3 and 21 months of age, all 19 infants had normal physical examinations, developmental evaluations and hematocrits; and 16 lacked IgG to B19. One infant who was IgM-positive to B19 at birth was IgM-positive at age 7 months when he also had an IgG titer to B19 of 1:500,000 (mother's concurrent titer, 1:10,000), and had B19 DNA in serum detected by polymerase chain reaction. The other two infants who were IgM-positive at birth were IgM- and IgG-negative by 11 and 16 months of age. These results suggest that intrauterine B19 infection may be frequent and occasionally cause an asymptomatic postnatal infection.
OBJECTIVE: To define the intrauterine viral transmission rate during primary maternal parvovirus B19 infection and identify factors that may influence this rate. METHODS: Forty-three pregnant women at two medical centers were identified with a primary B19 infection and followed to delivery. At delivery maternal and infant (umbilical cord) blood was obtained for B19 serologic and virologic PCR testing. RESULTS: All of the women delivered healthy infants at term and none was hydropic. Overall 22 (51%) of the 43 infants had some evidence of a congenital B19 infection. B19-specific IgM was detected in 11 infants at delivery, B19 IgA was detected in 10 and B19 DNA was detectable by PCR in 11 infants. One infant was negative at birth but became positive for IgM, IgA and PCR at 6 weeks of age. No association was found between the likelihood of intrauterine infection and: maternal age; symptomatic maternal infection; method of delivery; maternal IgG titer at delivery; maternal IgG avidity at delivery; or maternal viremia at delivery. Intrauterine infection was associated with maternal IgM positivity at delivery; this association may have been a result of maternal infection occurring later in gestation. CONCLUSION: Although the incidence of intrauterine hydrops and fetal demise after maternal infection is low, there is a high rate of intrauterine viral infection that occurs throughout gestation and yields newborns who, although infected in utero, are asymptomatic at birth.
OBJECTIVE: To clarify the relation between the time of parvovirus B19 (B19) infection in pregnancy and fetal outcome, including the viral persistence in the fetus. METHODS: Among 57 pairs showing serologic and/or virologic evidence of maternal and fetal B19 infection between 1986 and 1999 in Japan, 13 maternal-fetal pairs with the time of maternal B19 infection documented were retrospectively evaluated for fetal outcome and viral persistence. RESULTS: Nonimmune hydrops occurred at 23, 21 and 26 gestational weeks (gw) in three fetuses as a result of their mothers' symptomatic infection (erythema infectiosum) at 3, 16 and 19 gw, respectively. Spontaneous abortion without hydrops and intrauterine growth retardation resulting in small-for-gestational age (SGA) classification occurred in two fetuses whose mothers had developed erythema infectiosum at 5 and 16 gw, respectively. Eight fetuses were asymptomatic as a result of their mothers' infection at 6, 9, 12, 15, 18, 23, 23 and 33 gw, respectively. B19 DNA was detected in neonatal serum in all nine cases tested. CONCLUSION: Maternal B19 infection throughout gestation including the early stage after fertilization caused fetal infection that persisted until intrauterine fetal death with or without nonimmune hydrops or until the neonatal period after birth.
BACKGROUND: Chronic red cell aplasia can develop in immunocompromised patients including transplant recipients infected with parvovirus B19 (PV B19). Renal involvement with PV B19 infection is not well-recognized. METHODS: We diagnosed erythroid hypoplasia associated with PV B19 infection in three renal transplant recipients; one of them developed de novo collapsing glomerulopathy. These patients were treated with intravenous immunoglobulin (IVIG). RESULTS: In two patients, anemia responded promptly to IVIG therapy. One of them had recurrence of anemia that responded to a second course of IVIG. Despite IVIG treatment, persistent infection with PV B19, recurrent anemia, and de novo collapsing glomerulopathy leading to allograft failure developed in the third patient, who had received the most intense immunosuppression. CONCLUSIONS: These findings indicate that PV B19 infection in transplant recipients can cause chronic red cell aplasia that generally responds to IVIG therapy. In some patients, particularly those who are heavily immunosuppressed, infection may persist despite treatment. As the cellular receptor for PV B19 is expressed in the kidney, persistent infection may result in development of glomerulopathies in these patients.
Renal transplant patients were screened for the presence of parvovirus B19, before transplantation and monthly for 4 months after transplantation, by means of a sensitive nested PCR assay. Upon screening plasma from 110 patients, we found that two asymptomatic patients were B19 DNA positive. One of these patients was PCR positive in the plasma sample taken 2 months after transplantation; the plasma contained anti-B19 IgG antibodies before transplant and throughout the follow-up period, with an increase in the IgG level in the second posttransplant sample coinciding with the detection of B19 DNA. IgM antibodies to B19 were not detected in this patient. Because, for this patient, the donor's spleen DNA was also B19 DNA positive, we suspect B19 transmission from the donor and limited B19 replication, inasmuch as this patient already had a primed immune response to B19. The other patient was PCR positive in the pretransplant and in the plasma sample taken 1 month after transplant and contained a strong anti-B19 IgG response in the pretransplant sample and throughout the follow-up period-and anti-B19 IgM antibodies were not detected before or after transplantation. By testing samples taken from this patient at 2 weeks, 2 months, and 3 months before transplantation, we were able to determine that the infection occurred shortly before transplantation. Unexpectedly, this graft failed and was removed 2 days after transplantation despite a negative cross-match. A pathological examination of the kidney indicated acute vascular rejection, suggesting a possible role for B19 in this complication.
BACKGROUND: Parvovirus B19 (B19) infection is known to cause chronic infection leading to anemia in immunocompromised patients. Although nosocomial B19 infections in immunocompetent patients have been documented, no outbreaks in immunocompromised patients have been previously reported. Whether transmission can occur from a patient with chronic infection is also unknown. METHODS: An outbreak of B19 infection in a renal transplant unit was investigated by molecular analysis of the virus strains and a case-control study. RESULTS: Three patients had genetically identical virus strains suggesting the occurrence of nosocomial transmission. The index case transmitted infection many weeks after the onset of her clinical symptoms. Other patients at risk of acquiring infection were those most intensively immunosuppressed. Viral load in the serum correlated with the hematological response. A rebound in the viral load was associated with clinical relapse and the failure of i.v. immunoglobulin therapy. CONCLUSION: Nosocomial transmission of B19 can occur from immunocompromised patients even when they are in the chronic stage of the infection. The clinical and virological response to i.v. immunoglobulin therapy is variable and depends on the overall level of immunosuppression of the patient.
In immunocompromised patients, clinical manifestations of human parvovirus B19 (PVB19) infection are mostly reported as acute or chronic hematological disorders. Recently, PVB19 infection has been associated with nonhematological symptoms. Four years after lung transplantation, a 9-year-old girl developed a severe anemia with reticulocytopenia requiring blood transfusion. PVB19 DNA was found by polymerase chain reaction in blood. Blood marrow aspiration revealed typical features of PVB19 infection. She was successfully treated with high dose of i.v. Ig. Then, she exhibited recurrent nonregenerative anemia requiring another course of i.v. Ig. PVB19 DNA has been persisted in blood with no specific immune response. At the same time, she suffered from several lung infection syndromes with no microorganism found except PVB19 DNA. Recurrent mild renal dysfunction was noticed with no other explanation than PVB19 infection. This report indicates that pediatric transplanted patients are at risk of chronic PVB19 infection, which can be associated with lung and/or renal disorders.
BACKGROUND: Clinically, liver dysfunction in renal transplant recipients is related to hepatitis B virus (HBV) or hepatitis C virus (HCV) infection. The contribution of parvovirus B19 (B19) to liver disease in renal transplant recipients has not been studied. Here we present the association of liver dysfunction with or without the coinfection of B19, HBV, and HCV after renal transplantation. METHODS: We used enzyme-linked immunosorbent assay to identify B19, HBV, and HCV infections in serum samples taken from 144 renal transplant recipients before transplantation and at 12 and 24 months after transplantation. After each patient had fasted for 12 hr, blood was taken for measurement of aspartate aminotransferase and alanine aminotransferase monthly for at least 6 months. RESULTS: Liver dysfunction developed at the significantly higher incidence of 47% in the anti-HCV(+) patients compared with 6% in the noninfected group (P<0.0001). HBV infection had no impact on the incidence of liver dysfunction in renal transplant recipients. A higher incidence of liver dysfunction was found in 42% of B19 IgG(+)IgM(-) group patients compared with 13% of the B19 IgG(+)IgM(+) group (P=0.0051) and 9.5% of the B19 IgG(-)IgM(-) group (P=0.0003). A B19 polymerase chain reaction (PCR) assay revealed significantly higher liver dysfunction in 29% of B19 PCR(+) group patients compared with 13.6% of B19 PCR(-) patients (P=0.0419). Patients who were anti-HCV(+) and B19 PCR(+) had a significantly higher incidence of liver dysfunction than B19 PCR(-) patients (P=0.002). CONCLUSIONS: Chronic B19 infection and HCV infection, both separately and in combination, increase the incidence of liver dysfunction in renal transplant recipients. HBV infection does not seem to be independently or synergistically associated with liver dysfunction.
PURPOSE: To present a first descriptive serologic study on the clinical and hematologic implications of parvovirus B19 (B19) infection in children with acute lymphoblastic leukemia from the time of initial admission until discontinuation of chemotherapy. PATIENTS AND METHODS: Seventy-five patients were studied by polymerase chain reaction, enzyme-linked immunosorbent assay, sequencing, and immunodiffusion. RESULTS: During the period of observation, 8% (4/48) of B19-seronegative patients seroconverted and infection triggered profound anemia and thrombocytopenia. B19-specific IgG disappeared in 26% (8/31) of B19-seropositive patients, and these patients were significantly younger and the B19 IgG titers were lower on admission compared with patients who continuously displayed B19 IgG. B19 DNA was detected in the seroconverting patients, and this helped in determining the time of infection, which coincided with a B19 epidemic in 75% (3/4) of patients. Patients typically presented with fever and myalgia; a rash, indicative of B19 infection, was observed in only one patient. CONCLUSIONS: B19 infection was able to mimic a leukemic relapse or therapy-induced cytopenia and led to hospital admission, frequent blood sampling, renewed bone marrow aspirates, multiple transfusions of red blood cells or platelets, and cessation of maintenance chemotherapy for up to 3 weeks. The peculiar disappearance of B19-specific IgG, which could not be ascribed to a generalized low level of serum immunoglobulins, has not been previously reported. The results indicate that B19 should be assayed at diagnosis of leukemia to avoid subsequent diagnostic uncertainty, and during treatment in B19-seronegative patients exhibiting unexplained cytopenia.
The Brugada syndrome is characterized by a distinct ECG pattern consisting of ST segment elevation in the right precordial leads and right bundle branch block, a propensity for life-threatening arrhythmias, and an apparently structurally normal heart. The authors describe the case of a patient with an aborted sudden cardiac death and the typical ECG signs of Brugada syndrome. Nevertheless, magnetic resonance imaging displayed signal enhancement in the left ventricular myocardium. Additionally, histologic examination, in-situ hybridization, and PCR revealed evidence of a locally restricted inflammation due to parvovirus B19. Brugada syndrome is regarded as a primary electrical disease due to dysfunction of distinctive ion channels, but focal myocarditis may serve as a trigger for ventricular arrhythmias in this patient. Further morphologic studies will be helpful to establish the possible role of structural changes in the pathophysiology of this syndrome.
Human parvovirus B19 shows remarkable tropism for human erythroid progenitor cells. The pathogenesis of disease resulting from infection is a dynamic between the viral suppression of erythropoiesis and the host's ability to mount an effective immune response. Understanding this process has led to strategies for treating chronic anemia in persistently infected patients and may result in the development of a vaccine to prevent infection.
BACKGROUND: The extent and clinical manifestations of acute human parvovirus B19 (B19) infection were assessed in previously healthy hospitalized children admitted with clinical syndromes potentially associated the virus. PATIENTS AND METHODS: The study was prospective and was conducted between October 2002 and August 2004 in the pediatric departments of 3 hospitals in Israel. The survey included previously healthy children who were hospitalized with 1 or more of the following acute diseases: acute nonallergic exanthema, fever for >1 week, aplastic anemia or pancytopenia, acute nonbacterial arthropathy, immune thrombocytopenic purpura (ITP), Henoch-Schönlein purpura (HSP) and aseptic meningitis. A control group of children with a proven, non-B19 infection was also studied. Serum samples obtained from each child on admission were tested for B19 DNA by real-time PCR and B19 IgM by ELISA. Acute B19 infection was defined by the following criteria: positive serum B19-DNA and/or B19 IgM, negative serum B19 IgG, and no other proven infection. RESULTS: Overall, 167 children were included in the study. The mean age was 5.5 +/- 4.6 years (range, 0.5-17), males and females equally divided. Acute B19 infection was demonstrated in 12.6% (n = 21) of the children. Both tests were performed in 19 children and were positive in 10 (53%). In 7 and 2 children, only B19-DNA or B19 IgM, respectively, was positive. Acute B19 infection was documented in 27% (10/39) of children who presented with a variety of acute exanthema diseases; 9% (5/57) of children with acute arthropathy (all 5 had transient synovitis); 10% (2/21) of children with fever >1 week, both presented as mononucleosis syndrome; and in 44% (4/9) of children with transient pancytopenia or aplastic anemia. No acute B19 infection was demonstrated in 15 children with ITP, 9 with HSP, and 6 with aseptic meningitis and among 70 children in the control group. By logistic regression analysis, manifestations significantly associated with acute B19 infection were exanthema (OR 2.9; 95% CI = 1.1-7.5), anemia (OR 6.35; 95% CI = 2.2-18.2) and leucopenia (OR 4.14; 95% CI =1.2-14.2). CONCLUSIONS: Acute B19 infection was documented among 12.6% of children hospitalized with clinical syndrome potentially associated with the virus. Clinical and laboratory features associated with acute B19 infection were exanthema, anemia and leucopenia. Determination of both serum B19-DNA and serum B19 IgM should be performed for the accurate diagnosis of acute B19 infection.
The etiology of transient erythroblastopenia of childhood (TEC) remains unknown, although an association with viral infections has been proposed. The authors describe a 3.5-year-old girl with classic TEC concomitantly with human parvovirus B19 (HPV) infection. The infection was evident by detection of HPV genome in the blood and the bone marrow by polymerase chain reaction. Viral genome was no longer detected when the TEC resolved clinically. The patient was immunocompetent and the anemia has not recurred. To the authors' knowledge, this is one of the few documented cases of classic TEC attributable to HPV infection.
The authors report an unusual presentation of a Philadelphia chromosome-positive acute lymphoblastic leukemia with two unusual features: a bcr-abl fusion mRNA coding for p210 protein and a T-cell immunophenotype. The patient was a 16-year-old boy who presented with septic shock and pancytopenia, likely precipitated by an acute parvovirus B19 infection. Management consisted of supportive therapy, followed by chemotherapy for T-cell acute lymphoblastic leukemia and stem cell transplantation. He died 8 months after transplant due to idiopathic pneumonia syndrome, but without evidence of relapsed disease.
Thermosensitive mutants were isolated from nitrous acid-treated Kilham rat virus (KRV). At a restrictive temperature (39.5 degrees C), the mutants tested did not produce appreciable amounts of infectious particles, haemagglutinin or progeny single-stranded DNA. Virus antigen accumulation as detected by immunoperoxidase was reduced. Complementation tests revealed two distinct groups. The three members of complementation group 1 synthesized normal amounts of replicative forms but were restricted in single-stranded DNA production and capsid protein expression, exhibiting phenotypes compatible with cap mutations. The sole representative of group 2, KRV ts6, failed to accumulate replicative forms, displaying a rep- phenotype. These mutants provide new tools to test the role of viral products in the biology of autonomous parvoviruses.