Diagnosis of Peripheral Facial Palsy Associated with Parvovirus B19 Infection by Polymerase Chain Reaction

Human parvovirus B19 (PVB19) infection causes neurological manifestations, including encephalitis, meningitis, and neuropathy, but facial nerve palsy is rare. Moreover, no case of facial nerve palsy related to PVB19 infection that was diagnosed by PCR and serology has been reported. A 19-month-old boy without the medical history developed facial nerve palsy and was treated with prednisolone and valacyclovir. On the 19th day, erythema appeared on his body, and the PVB19-specific IgM and PVB19 DNA were detected in the serum, leading to the diagnosis of infectious erythema associated with PVB19 infection. This case indicates that PVB19 may be one of the causative agents of facial nerve palsy.

Role of Surgical Intervention in Hereditary Spherocytosis with Haemolytic Anaemia, Splenomegaly and Jaundice

haemolytic anaemia, splenomegaly and jaundice, admitted in Chettinad hospital and research institute during one year period from January 2019 to January 2020. Surgical intervention is indicated for selected patients with hereditary spherocytosis with haemolytic anaemia and jaundice to abate the hemolytic process after correction of anaemia with blood transfusion. Pigmented gallstones are seen in more than 50% cases for which incidence increases with severity of hemolysis and with age. Complications include aplastic anemia (most common after parvovirus B19 infection), haemolytic crisis during inter-current infection, megaloblastic crisis – during folic acid deficiency, cardiomyopathy, hematological malignancies.

Symmetrical Polyarthropathy and Hepatosplenomegaly as a Manifestation of Parvovirus B-19: A Case Report

This case was of a 35-years old Egyptian lady, who works as a primary school teacher, who presented to the OPD with complaints of persistent high fever for two days. Along with this fever, she also had severe pain in multiple joints of both hands, wrists, knees, and ankles. In addition, the woman also complained of having developed a rash on both her legs, which was so painful that she was unable to stand without pain. The pain was agonizing and it prevented her from performing her usual jobs as normal. But that was the extent of her symptoms. She did not complain of a cough, shortness of breath, chest pain, back pain, abdominal pain, or any other pain for that matter. In a summary, none of the factors and symptoms that could have pointed towards the patient suffering from a case of COVID19 were present. Moreover, there was no recent history of travel. She also had not contracted any gastrointestinal or genitourinary infections in the preceding few days. The clinical examination of the patient revealed no abnormalities at all. The only thing worth noting was remarkable swelling and tenderness over the metacarpophalangeal and proximal interphalangeal joints. The following series of events are discussed in detail in the subsequent section, and it was concluded that the woman might be suffering from the parvovirus B19 infection. She had several favorable causative factors that pointed toward this diagnosis, with the most important one being her in close contact with primary school children, who are most the likely age group, between five and twenty years, to carry this infection and also contract it. Adults can contract the infection from children, but the range of symptoms varies from person to person. In this case of the woman, further evaluations and investigations were needed to confirm the diagnosis, which was likely due to the obvious risk factors present in this case.

Vitamin A and D Levels Correlate with Outcomes Following Acute Parvovirus B19 Infection in Children with Sickle Cell Disease

Background: Human parvovirus B19, a common childhood infection that typically causes mild disease in healthy individuals, causes life-threatening anemia due to transient red cell aplasia (aplastic crisis) in individuals with sickle cell disease (SCD). This complication often leads to hospitalization and red blood cell transfusions. Limiting the amount of transfusions is imperative to avoid alloimmunization. Strategies to mitigate complications from parvovirus B19 or reduce disease severity in SCD patients are needed. In this prospective observational study, we aim to describe the relationship between vitamin A and D levels and severity of symptoms during parvovirus B19 infection in pediatric patients with SCD. Methods: Twenty pediatric patients with SCD admitted to St. Jude Children's Research Hospital experiencing aplastic crisis and identified as having an active parvovirus B19 infection were under an IRB approved protocol (NCT02261480) and followed prospectively for 120 days post-infection. Acute parvovirus B19 infection was diagnosed by fever and a positive virus-specific IgM ELISA or PCR. Aplastic crisis was defined by worsened anemia without sufficient compensatory reticulocytosis in the setting of an acute parvovirus B19 infection. Virus-specific antibody responses were measured from sera or nasal washes (NW) by ELISA using parvovirus B19 virus-like particles (VLP) as target antigens. Peak serum antibody titers were defined (among measurements from Days 0, 7, 30, and 120). Total erythrocyte transfusion volumes required during the admission were quantified. Hematologic indices and vitamin A and D levels were obtained on Day 0. Vitamin A (retinol) was measured using UPLC and vitamin D (25[OH]D) was measured using a Roche Elecsys Vitamin D ELISA. Statistical analyses were performed with Spearman's rank correlation coefficient or Mann Whitney tests. We scored significance as p<0.05. Results: Twenty patients with different genotypes of SCD requiring hospital admission due to acute parvovirus B19 infection were sequentially enrolled (15 HbSS, 3 HbSC, 1 HbSD, 1 HbSβeta +thalassemia). Thirty-five percent (7/20) of patients were vitamin D deficient (VDD, defined here as <20 ng/mL) while 89% (17/19, one sample was not measured) of patients were marginally or severely vitamin A deficient (defined here as <20 μg/dL) on Day 0. Correlative analyses between vitamin levels and markers of disease severity are shown in figure 1. Lower vitamin D levels trended with lower hemoglobin (r=0.399, p=0.082) and there was a significant inverse correlation between transfused volume and vitamin D levels (r=-0.626, p=0.003, Figure 1B). There was a significant positive correlation of vitamin A levels on Day 0 with hemoglobin concentration (r=0.549, p=0.015, Figure 1D), and an inverse correlation between vitamin A levels and lactate dehydrogenase (r=-0.505, p=0.027, Figure 1F). Children with replete vitamin D levels exhibited significantly better peak virus-specific serum IgG (p=0.037) and IgA (p=0.011) responses (Figure 2A-B). Additionally, vitamin A, which plays an important role in mucosal immunity, correlated positively with virus-specific IgG (r=0.574, p=0.013) and IgA (r=0.480, p=0.044) in nasal passages on Day 30 (Figure 2C-D). Conclusions: In pediatric patients admitted to the hospital for acute parvovirus B19 infection, low vitamin A and D levels were associated with greater disease severity (greater hemolysis, lower hemoglobin concentration, and greater transfusion volumes). Higher vitamin levels were associated with better virus-specific antibody responses. While cause-effect relationships were not discerned in this study, we hypothesize that poor nutritional status contributed to poor outcomes and that efforts to improve nutrition may reduce the severity of parvovirus B19 disease in patients with SCD. Figure 1 Figure 1. Disclosures Hankins: UpToDate: Consultancy; Vindico Medical Education: Consultancy; Global Blood Therapeutics: Consultancy; Bluebird Bio: Consultancy.

Hemophagocytic lymphohistiocytosis and thrombotic microangiopathy after parvovirus B19 infection and renal transplantation: a case report

Background Hemophagocytic lymphohistiocytosis (HLH) is a rare and life-threatening disease characterized by hyperactivation of the immune system that causes hypercytokinemia and potentially multi organ failure. HLH can occur in patients with underlying rheumatic or autoinflammatory disorders. Additionally, HLH can develop in patients during infections or malignancies without a known genetic predisposition. Case presentation We herein report a patient, who presented with fever, both acute kidney and liver injury, anemia, thrombocytopenia and HSV stomatitis. HLH was diagnosed based on clinical criteria and qPCR revealed an acute parvovirus B19 infection as potential underlying infectious trigger. Treatment was started with both IVIG and dexamethasone. Subsequently, kidney biopsy demonstrated TMA. Conclusions In rare cases both HLH and aHUS can occur simultaneously in a patient as a consequence of viral infections. Insights from this unusual case might help physicians understand this complex symptom constellation.

Echogenic Intestine: a Case of Intrauterine Fetal Demise at Term

Introduction/Objective Parvovirus B19 is a non-enveloped, single-stranded DNA virus that preferentially infects early erythroids, and is commonly associated with second trimester hydrops fetalis. Third trimester non-hydropic intrauterine fetal demise due to parvovirus B19 infection with associated pathologic changes has rarely been described, particularly in the context of IgG seroconverted mother. Methods/Case Report We present a case of a 37 weeks’ gestation stillborn female fetus born to a 29 year-old mother who presented with lack of fetal movement for one day. Fetal ultrasound demonstrated diffuse intestinal echogenicity. Maternal parvovirus B19 IgG level was high (5.48, reference: <=0.90 Index). Postmortem examination revealed a non-dysmorphic fetus. Gross examination was unremarkable. Microscopic examination of small intestine revealed mucosal inflammation and multifocal calcifications. Prominent extramedullary hematopoiesis was present in the liver. Viral cytopathic effect was noted microscopically within nucleated red blood cells present intravascularly within chorionic villi, small intestine, liver, and spleen. Parvovirus B19 infection was confirmed by immunohistochemistry. Results (if a Case Study enter NA) NA Conclusion The cause of clinically puzzling intrauterine fetal demise at term with prominent intestinal echogenicity on ultrasound was determined to be parvovirus B19 infection on postmortem examination. We emphasize the possibility of this diagnostic differential in non-hydropic, third trimester fetal demise in presence of maternal IgG seroconversion and lack of signs of active infection.