Transfusion-related acute lung injury/transfusion-associated circulatory overload in a child with non-transfusion dependent thalassemia and aplastic crisis due to acute parvovirus B19 infection.

We present a never-transfused girl with thalassemia intermedia who was admitted for febrile aplastic crisis due to human parvovirus B19. After a first transfusion of packed red blood cells, she developed pulmonary oedema. She improved with supportive care including the use of intravenous diuretics. Due to severe anaemia, she received a second blood transfusion, antibiotics for febrile neutropenia and intravenous γ globulin for control of the parvovirus infection. She had an uneventful recovery. The first of her male blood donors had an antibody against a patient's human leukocyte antigens type II antigen with a high mean fluorescent intensity. Our patient had clinical features and supportive laboratory evidence for mild transfusion-related acute lung injury (TRALI). However, she also met the criteria for transfusion-associated circulatory overload (TACO). We conclude that our patient likely suffered from TRALI/TACO, a consensus term proposed in 2019 for patients in whom TRALI cannot be distinguished from TACO or in whom both conditions occur simultaneously.

Erythema nodosum manifestation of Parvovirus B19-associated reactive arthritis.

INTRODUCTION: Parvovirus B19 virus-mediated viral inflammation and immune-complex deposition generate mainly short-term manifestations in the affected individuals. The objective of this study was to determine Parvovirus B19 infection in rheumatoid arthritis (RA) patients. METHODOLOGY: The study employed 50 patients diagnosed with RA and 30 healthy individuals. Blood samples were collected from both groups. The blood samples were screened for Parvovirus B19 infection using polymerase chain reaction to detect B19 DNA and enzyme-linked immunosorbent assay to detect anti-B19 IgM and IgG. RESULTS: 17 (34%) of 50 patients tested positive for parvovirus B19 DNA. In contrast, the mortality rate in the control group was significantly lower (6.7%; p = 0.005). Anti-B19 IgG antibody levels differed significantly with patients and control (p = 0.007), whereas anti-B19 IgM Ab levels did not (p = 0.6). There was a significant correlation between viremia B19 and all measured parameters. Parvovirus-affected patients had significantly higher CRP and ESR, elevated DAS28 scores, and more joint pain compared to parvovirus (-) patients. CONCLUSION: Anti-CCP and RF values were significantly high in parvovirus (+) patients. Joint erosion was also prevalent in patients who tested positive for parvovirus. The findings of this study suggest that infection with parvovirus in patients with RA, and a possible role of this viral infection in the pathogenesis of RA may contribute to the pathogenesis of RA.

Parvovirus B19 Infection Is Associated with the Formation of Neutrophil Extracellular Traps and Thrombosis: A Possible Linkage of the VP1 Unique Region.

Neutrophil extracellular traps (NETs) formation, namely NETosis, is implicated in antiphospholipid syndrome (APS)-related thrombosis in various autoimmune disorders such as systemic lupus erythematosus (SLE) and APS. Human parvovirus B19 (B19V) infection is closely associated with SLE and APS and causes various clinical manifestations such as blood disorders, joint pain, fever, pregnancy complications, and thrombosis. Additionally, B19V may trigger the production of autoantibodies, including those against nuclear and phospholipid components. Thus, exploring the connection between B19V, NETosis, and thrombosis is highly relevant. An in vitro NETosis model using differentiated HL-60 neutrophil-like cells (dHL-60) was employed to investigate the effect of B19V-VP1u IgG on NETs formation. A venous stenosis mouse model was used to test how B19V-VP1u IgG-mediated NETs affect thrombosis in vivo. The NETosis was observed in the dHL-60 cells treated with rabbit anti-B19V-VP1u IgG and was inhibited in the presence of either 8-Br-cAMP or CGS216800 but not GSK484. Significantly elevated reactive oxygen species (ROS), myeloperoxidase (MPO), and citrullinated histone (Cit-H3) levels were detected in the dHL60 treated with phorbol myristate acetate (PMA), human aPLs IgG and rabbit anti-B19V-VP1u IgG, respectively. Accordingly, a significantly larger thrombus was observed in a venous stenosis-induced thrombosis mouse model treated with PMA, human aPLs IgG, rabbit anti-B19V-VP1u IgG, and human anti-B19V-VP1u IgG, respectively, along with significantly increased amounts of Cit-H3-, MPO- and CRAMP-positive infiltrated neutrophils in the thrombin sections. This research highlights that anti-B19V-VP1u antibodies may enhance the formation of NETosis and thrombosis and implies that managing and treating B19V infection could lower the risk of thrombosis.

Nonepisodic angioedema with eosinophilia subsequent to acute parvovirus B19 infection.

Nonepisodic angioedema with eosinophilia (NEAE) is characterised by a single episode of angioedema localised to the extremities and peripheral eosinophilia. While NEAE can develop in response to infection or vaccination, NEAE associated with acute parvovirus B19 (B19V) infection is rare. We describe the case of a young woman with NEAE that developed during acute B19V infection. She presented with 1-week history of pruritus and polyarthralgia in the extremities, followed by the development of peripheral oedema, and was positive for anti-B19V IgM antibody. Her arthralgia improved within 2 weeks without any specific intervention; however, the oedema and pruritic erythema persisted and the peripheral eosinophil count increased. A short course of prednisolone therapy for suspected NEAE alleviated the symptoms, which have not recurred for more than 2 years. Thus, we believe that the patient was affected by NEAE and that NEAE can develop following acute B19 infection.

The emergence of parvovirus B19 as a pathogen in acute encephalitis syndrome.

Despite scarcity of data, in recent years, human parvovirus B19 (PVB19) has been emerging as an important pathogen in acute encephalitis syndrome (AES). But, PVB19 virus is mostly looked for only after the exclusion of other common pathogens implicated in AES. Hence, this study was conducted to correlate clinical, radiological, and sequencing data to establish the crucial role of PVB19 in AES. Cerebrospinal fluid and/or serum samples were collected from AES patients as per WHO criteria and tested by ELISA, real-time PCR and bacterial culture sensitivity for various pathogens. PVB19 positive samples were subjected to sequencing. PVB19 attributed to 5% of total AES cases in the present study with fatalities in two of eight cases. Two isolates of PVB19 belonged to Genotype 1 A whereas one belonged to Genotype 3B. On multivariate analysis of predictive symptoms of PVB19 AES cases, blurring of vision (odds ratio [OR] 20.67; p = 0.001) was found to be significant independent predictor of PVB19 AES. Six of eight patients (two encephalitis specific and four nonspecific) had abnormal radiological findings. Hence, being an emerging viral pathogen, PVB19 should be included in the diagnostic algorithm of AES for prompt diagnosis and definitive management to prevent undesired neurological sequelae.

Viral Myocarditis as a Factor Leading to the Development of Heart Failure Symptoms, Including the Role of Parvovirus B19 Infection-Systematic Review.

Myocarditis (MC) is defined as an immunological inflammatory reaction with various etiologies, clinical presentations and prognoses within the myocardium. Currently, parvovirus B19 (PVB19) has become the main factor leading to this disease, replacing the previously dominant viruses A and B. In the case of chronic heart failure with subsequent dilated cardiomyopathy, approximately 67% have a viral etiology, and most of them are the result of PVB19 infection. However, the analysis showed a correlation between PVB19 infection and the risk of developing inflammatory dilated cardiomyopathy (DCMi). PVB19 is detected in 23% of patients with DCMi. Chronic infection may also contribute to progressive left ventricular failure in patients with a history of MC. The above effect suggests the active replication of PVB19 only in heart biopsies with inflammation due to MC or DCMi. Moreover, the supply of IFN-ß to suppress the active transcription of PVB19 accompanied by DCMi over a period of 6 months results in the normalization of NT-proBNP and an improvement in LVEF along with NYHA performance. The small number of reports on this topic and inaccuracies resulting from constantly conducted research and ongoing changes make it impossible to clearly answer the question of whether PVB19 is a factor inducing de novo MC and DCM or only accompanies the above conditions. However, large clinical cohort studies lead to the perception of PVB19 as a viral etiological agent capable of causing de novo MC together with DCMi.

Distinct clinical characteristics of bocavirus and Mycoplasma pneumoniae infection in children plastic bronchitis.

BACKGROUND: This study investigated clinical and laboratory characteristics of human bocavirus type 1 (HBoV1)-plastic bronchiolitis (PB), Mycoplasma pneumoniae (MP)-associated plastic bronchitis (PB) and MP-NPB in children, highlighting inflammation, coagulation, and bronchoscopic needs. METHODS: Data on preschool children with PB during HBoV1 or MP infection were collected, comparing MP-PB to severe Mycoplasma pneumoniae pneumonia. RESULT: Compared with the MP-PB group, the HBoV1-PB group, with younger children, had significantly milder clinical symptoms but higher WBC counts (p = .028). The MP-PB group exhibited notably elevated Fibrinogen (p = .045) and d-dimer levels (p < .001). When contrasting the MP-PB with the MP-NPB group, children in MP-PB group still had higher levels of d-dimer and increased inflammatory indicators such as C-reactive protein, procalcitonin, lactate dehydrogenase, and interleukin-6, which were significantly elevated compared with the MP-NPB group. MP-PB showed a higher prevalence of plastic bronchial casts in lower lobes (p = .016) and a dominance of neutrophils in BALF cytology. Additionally, children in the MP-PB group tended to undergo a greater number of bronchoscopies. CONCLUSION: This study identifies key differences in plastic bronchitis in children due to HBoV1 and MP, highlighting HBoV1's milder inflammation in younger kids and MP's link to severe inflammatory and coagulation responses, guiding clinical diagnosis and treatment.

[The 507th case: hemolytic anemia, parvovirus B19, and multiple organ dysfunction].

A 19-year-old male patient with high-risk acute B-cell lymphoblastic leukemia received haploidentical stem cell transplantation. He developed anemia repeatedly and parvovirus B19 nucleic acid was positive in blood plasma. The patient was diagnosed with cold agglutinin syndrome and multiple organ dysfunction including respiratory failure and hepatitis. In the conflict between viral infection and the treatment of cold agglutinin syndrome, we provided supportive treatment, complement inhibitors to control hemolysis, and antiviral therapy. After timely glucocorticoid and immunosuppressant therapy, the patient had achieved a good response.

Plastic bronchitis associated with human bocavirus 1 infection in children.

BACKGROUND: Plastic bronchitis (PB) is a clinical-pathological syndrome characterized by the abnormal accumulation of endogenous substances in the bronchial airways, causing partial or complete obstruction and resulting in impaired lung ventilation. METHODS: In this retrospective analysis, we aim to summarize the clinical manifestations, imaging characteristics, diagnostic methods, and treatment approaches to enhance clinicians' ability to detect children who are infected with human bocavirus 1 (hBoV 1) and develop PB. RESULTS: In the period from January 2021 to January 2024, a total of six hBoV 1 infection children were diagnosed with PB through bronchoscopy. The onset of the condition was mainly concentrated between June and December. The detection methods used included metagenomic next-generation sequencing for pathogen identification (three cases) and respiratory pathogen nucleic acid 13-plex detection (oropharyngeal swab) (three cases), both of which confirmed the presence of hBoV 1. Out of the six children with PB, two were girls and four were boys. Their ages ranged from 10 months to 4 years old. Common symptoms reported by all patients included fever, cough, and wheezing. Chest high-resolution computed tomography scans revealed atelectasis in six cases, in addition to pneumonia. After the removal of the plastic bronchi via bronchoscopy, the airway obstruction symptoms in the children were relieved, and no recurrence was observed during the follow-up period. Pathological findings indicated cellulose exudation and inflammatory cell infiltration, consistent with nonlymphatic PB. CONCLUSION: When children infected with hBoV 1 exhibit persistent or worsening symptoms such as cough, fever, and wheezing despite treatment, clinicians should remain highly vigilant for the potential occurrence of PB. Bronchoscopy plays a crucial role not only in diagnosing the presence of a plastic bronchus but also in effectively treating PB.

Viral myocarditis in combination with genetic cardiomyopathy as a cause of sudden death. An autopsy series.

Sudden cardiac death (SCD) is a major public health issue worldwide. In the young (< 40 years of age), genetic cardiomyopathies and viral myocarditis, sometimes in combination, are the most frequent, but underestimated, causes of SCD. Molecular autopsy is essential for prevention. Several studies have shown an association between genetic cardiomyopathies and viral myocarditis, which is probably underestimated due to insufficient post-mortem investigations. We report on four autopsy cases illustrating the pathogenesis of these combined pathologies. In two cases, a genetic hypertrophic cardiomyopathy was diagnosed in combination with Herpes Virus Type 6 (HHV6) and/or Parvovirus-B19 (PVB19) in the heart. In the third case, autopsy revealed a dilated cardiomyopathy and virological analyses revealed acute myocarditis caused by three viruses: PVB19, HHV6 and Epstein-Barr virus. Genetic analyses revealed a mutation in the gene coding for desmin. The fourth case illustrated a channelopathy and a PVB19/HHV6 coinfection. Our four cases illustrate the highly probable deleterious role of cardiotropic viruses in the occurrence of SCD in subjects with genetic cardiomyopathies. We discuss the pathogenetic link between viral myocarditis and genetic cardiomyopathy. Molecular autopsy is essential in prevention of these SCD, and a close collaboration between cardiologists, pathologists, microbiologists and geneticians is mandatory.

Managing recurrent parvovirus B19-associated anemia after a pediatric kidney transplant.

A 13-year-old girl who had a kidney transplant four weeks prior presented with a 10-day history of fatigue, paleness, and headache. On physical examination, tachycardia and paleness were noted. Laboratory testing was notable for severe anemia and mild leukopenia and thrombocytopenia. Polymerase chain reaction (PCR) test for Epstein-Barr virus (EBV) and cytomegalovirus (CMV) were negative and for parvovirus B19 (PVB19) was positive. Despite lower immunosuppression and administration of intravenous immunoglobulin (IVIG) it persisted for 15 months, and frequent red blood cell transfusions were needed. PVB19 is a less common but significant complication. The patient's clinical course demonstrates the importance of this complication and the challenges in its management. A notable void exists in the literature regarding standardized treatment protocols for PVB19-induced recurrent anemia after kidney transplant. This case indicates the need for further research and consensus to guide effective clinical interventions in similar cases.

Pure Red Cell Aplasia Secondary to Parvovirus B19 Infection as a Rare Cause of Anemia in a Dialysis Patient.

Parvovirus B19 infection can cause chronic pure red cell aplasia in immunosuppressed hosts or acute and transient aplastic crisis in immunocompetent hosts. In dialysis patients, only transient aplastic crisis induced by parvovirus B19 infection has been reported. We herein report the first case of an adult dialysis patient who developed chronic pure red cell aplasia associated with parvovirus B19 infection. Repeated pneumonia and heart failure may contribute to an immunocompromised status, making the patient more vulnerable to parvovirus B19 infection. This case expands on the differential diagnosis of chronic anemia in patients undergoing dialysis.

Effect of the Functional VP1 Unique Region of Human Parvovirus B19 in Causing Skin Fibrosis of Systemic Sclerosis.

Human parvovirus B19 (B19V) is a single-stranded non-enveloped DNA virus of the family Parvoviridae that has been associated with various autoimmune disorders. Systemic sclerosis (SSc) is an autoimmune connective tissue disorder with high mortality and has been linked to B19V infection. However, the precise mechanism underlying the B19V contribution to the development of SSc remains uncertain. This study investigated the impacts of the functional B19V-VP1 unique region (VP1u) in macrophages and bleomycin (BLE)-induced SSc mice. Cell experimental data showed that significantly decreased viability and migration of both B19V-VP1u-treated U937 and THP-1 macrophages are detected in the presence of celastrol. Significantly increased MMP9 activity and elevated NF-kB, MMP9, IL-6, TNF-α, and IL-1ß expressions were detected in both B19V-VP1u-treated U937 and THP-1 macrophages. Conversely, celastrol revealed an inhibitory effect on these molecules. Notably, celastrol intervened in this pathogenic process by suppressing the sPLA2 activity of B19V-VP1u and subsequently reducing the inflammatory response. Notably, the administration of B19V-VP1u exacerbated BLE-induced skin fibrosis in mice, with augmented expressions of TGF-ß, IL-6, IL-17A, IL-18, and TNF-α, ultimately leading to α-SMA and collagen I deposits in the dermal regions of BLE-induced SSc mice. Altogether, this study sheds light on parvovirus B19 VP1u linked to scleroderma and aggravated dermal fibrosis.

[Hemophagocytic Syndrome Secondary to Human Parvovirus B19 Infection in an Acquired Immunodeficiency Syndrome Patient:Report of One Case].

The acquired immunodeficiency syndrome patients with compromised immunity are prone to hemophagocytic syndrome secondary to opportunistic infections.This paper reports a rare case of hemophagocytic syndrome secondary to human parvovirus B19 infection in an acquired immunodeficiency syndrome patient,and analyzes the clinical characteristics,aiming to improve the diagnosis and treatment of the disease and prevent missed diagnosis and misdiagnosis.

Hematologic Manifestations of Parvovirus B19 Infection.

Parvovirus B19 virus infection is widespread among humans because of its highly infectious and obstinate nature, with up to 80% of the population testing positive for IgG antibodies against the virus. Pronormoblasts observed in biopsy are the hallmarks of PVB19 infection. In addition, PVB19 affects the skin, heart, brain, joints, and liver and can be diagnosed through antibody detection or DNA detection via PCR. Due to its capsid proteins' high affinity for bone marrow receptors, its main presentation is the suppression of bone marrow functions. It has been shown to affect patients with hemolytic anemia and patients with hematological malignancies, presenting with pure red cell aplasia. The main available effective treatment option is IV immunoglobulins; however, the risk of recurrence remains high after treatment.

Clinical Presentation of Parvovirus B19 Infection in Adults Living with HIV/AIDS: A Case Series.

Parvovirus B19 (B19V) infection varies clinically depending on the host's immune status. Due to red blood cell precursors tropism, B19V can cause chronic anemia and transient aplastic crisis in patients with immunosuppression or chronic hemolysis. We report three rare cases of Brazilian adults living with human immunodeficiency virus (HIV) with B19V infection. All cases presented severe anemia and required red blood cell transfusions. The first patient had low CD4+ counts and was treated with intravenous immunoglobulin (IVIG). As he remained poorly adherent to antiretroviral therapy (ART), B19V detection persisted. The second patient had sudden pancytopenia despite being on ART with an undetectable HIV viral load. He had historically low CD4+ counts, fully responded to IVIG, and had undiagnosed hereditary spherocytosis. The third individual was recently diagnosed with HIV and tuberculosis (TB). One month after ART initiation, he was hospitalized with anemia aggravation and cholestatic hepatitis. An analysis of his serum revealed B19V DNA and anti-B19V IgG, corroborating bone marrow findings and a persistent B19V infection. The symptoms resolved and B19V became undetectable. In all cases, real time PCR was essential for diagnosing B19V. Our findings showed that adherence to ART was crucial to B19V clearance in HIV-patients and highlighted the importance of the early recognition of B19V disease in unexplained cytopenias.

Case Report: Parvovirus B19 infection complicated by hemophagocytic lymphohistiocytosis in a heart-lung transplant patient.

Immunosuppressed patients can contract parvovirus B19, and some may experience hemophagocytic lymphohistiocytosis (HLH). Herein, we describe the first report of hemophagocytic lymphohistiocytosis in a heart-lung transplant patient with concomitant parvovirus B19 infection. The patient was treated with intravenous immune globulin (IVIG) and the features of HLH were remission. This instance emphasizes the significance of parvovirus B19 monitoring in transplant patients with anemia; if HLH complicates the situation, IVIG may be an adequate remedy. Finally, a summary of the development in diagnosing and managing parvovirus B19 infection complicated by HLH is provided.