Cases reported "Erythema Infectiosum"

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1/132. Successful treatment of persistent erythroid aplasia caused by parvovirus B19 infection in a patient with common variable immunodeficiency with low-dose immunoglobulin.

    parvovirus B19 causes persistent erythroid aplasia in immunocompromised hosts. From April through July 1996, we encountered five adult patients presenting with reticulocytopenia and fever caused by parvovirus B19 infection. The reticulocyte count of four patients with normal immunity recovered within two weeks after the onset of fever. However, in the one remaining patient with common variable immunodeficiency (CVI), reticulocytopenia, and other symptoms including fever and the elevation of lactate dehydrogenase (LDH) levels persisted beyond 16 days of onset. Although the dna of parvovirus B19 was detected in the peripheral blood of the CVI patient, neither immunoglobulin Ig-G nor Ig-M antibodies specific to the virus were detectable. We administered 50 mg/kg of Ig to the CVI patient for six days. The reticulocyte count recovered promptly on the sixth day of the treatment and parvovirus B19 dna was not detectable 30 days after therapy. This indicates that although patients with CVI may be susceptible to persistent erythroid aplasia during an endemic of parvovirus B19, the complication can be treated successfully with relatively low-dose Ig. ( info)

2/132. Acute cerebellar ataxia with human parvovirus B19 infection.

    A 2 year old boy developed acute cerebellar ataxia in association with erythema infectiosum. During the disease, genomic dna and antibodies against human parvovirus B19 were detected in serum but not in cerebrospinal fluid. parvovirus B19 associated acute cerebellar ataxia might occur due to transient vascular reaction in the cerebellum during infection. ( info)

3/132. Papular-purpuric "gloves and socks" syndrome: polymerase chain reaction demonstration of parvovirus B19 dna in cutaneous lesions and sera.

    We report a typical case of papular-purpuric "gloves and socks" syndrome (PPGSS) in which primary infection by parvovirus B19 was demonstrated by seroconversion to this virus; parvovirus B19 dna was also identified by polymerase chain reaction (PCR) methods in the sera of the patient and in the cutaneous biopsy specimen, both taken 4 days after the onset of clinical manifestations. To our knowledge, this is the fourth published case in which parvovirus B19 dna has been recovered from the skin by PCR. Serologic studies and PCR investigations in cutaneous biopsy for other viruses including herpes simplex virus types 1 and 2, varicella zoster virus, Epstein-Barr virus, cytomegalovirus, and human herpesvirus 6, 7, and 8 were negative. Clinically, our case presented some additional features, which have not been previously described in cases of PPGSS, namely dysuria with vulvar edema and erythema, and unilateral petechial rash on the breast. The histopathologic findings of our case were nonspecific and consisted of an interface dermatitis with slight vacuolar degeneration at the dermoepidermal junction and a superficial perivascular inflammatory infiltrate mostly composed of lymphocytes, with numerous extravasated erythrocytes. We review the cases of PPGSS published in the literature with respect to the different viruses that have been proposed as etiologic agents and conclude that acute infection by parvovirus B19 is the only one that has been adequately proved. ( info)

4/132. systemic vasculitis and atypical infections: report of two cases.

    Two cases of systemic vasculitis are described; one presenting with adult Henoch-Schonlein purpura secondary to a concomitant chlamydia infection and the other with leucocytoclastic vasculitis and mesangioproliferative glomerulonephritis secondary to a recent parvovirus B19 infection. association of chlamydial infection has not previously been described with Henoch-Schonlein purpura and this infection should, perhaps, be added to the list of aetiologies of this disease. parvovirus B19 causing significant urinary sediment abnormalities associated with mesangioproliferative glomerulonephritis and leucocytoclastic vasculitis has also not been described previously. ( info)

5/132. Raynaud's phenomenon as a manifestation of parvovirus B19 infection: case reports and review of parvovirus B19 rheumatic and vasculitic syndromes.

    infection with human parvovirus B19 is manifested as erythema infectiosum, transient aplastic crisis, or hydrops fetalis. Rheumatic manifestations include arthropathy and various vasculitic syndromes. Isolated Raynaud's phenomenon due to parvovirus B19 has never been described. We report on 2 previously healthy sisters with new-onset Raynaud's phenomenon accompanied by severe generalized polyarthralgia. A full workup was negative, except serology for parvovirus B19, which was positive. All symptoms gradually subsided within 3-5 months, and no recurrence has been noted during the 3 years since onset. We review all the studies in the English-language literature on parvovirus B19-induced rheumatic and vasculitic syndromes. We hypothesize that the pathogenesis of Raynaud's phenomenon in our patients involved immune-mediated endothelial damage leading to platelet activation and vasoconstriction. We recommend that in cases of unexplained Raynaud's phenomenon, serology for parvovirus B19 be included in the evaluation. ( info)

6/132. immunoglobulin m and G immunoblots in the diagnosis of parvovirus B19 infection.

    BACKGROUND AND PURPOSE: To identify parvovirus B19 infection by means of immunoglobulin (Ig) G and IgM immunoblots among immunocompetent patients who tested negative or had low-titer B19 IgM antibodies in enzyme-linked immunosorbent assays (ELISA). methods: serum samples were obtained from 20 patients with parvovirus B19 infection. Another 130 study subjects presumed to be without B19 infection (40 medical personnel and 90 prisoners) were also included. All sera from the patient and study groups tested positive for IgG or IgM with ELISA and were further evaluated using the immunoblot method. Detection of B19 dna by nested polymerase chain reaction (PCR) was also performed on IgG and IgM positive sera. RESULTS: IgM immunoblots disclosed one false positive IgM ELISA result in the patient group and three false positive results in the study group. In the patient group, four patients were in the latter stage of antibody response to B19 infection as suggested by the low titer of anti-B19 IgM, incomplete IgM immunoblots, with only a weak viral capsid protein VP-N reaction band, and fading but still strong reaction bands on IgG immunoblots. Strong reaction bands on IgG immunoblots comparable to these four patients were found in three of the 130 study group sera. Furthermore, B19 dna was detected in three of the four patients and one of the three study subjects by means of nested-PCR. A serum sample from one study subject showed strong IgG but no IgM reactivity to viral capsid protein VP2; nested PCR identified B19 dna in this serum sample. CONCLUSIONS: Immunoblots and nested PCR should be applied in the diagnosis of B19 infection for patients with low-titer anti-B19 IgM tested by means of ELISA. For diagnosis of B19 infections in certain clinical entities such as chronic arthritis of recent onset and hydrops fetalis, B19 IgM antibodies may have disappeared but B19 infection can still be recognized by the intensity of the reaction bands on IgG immunoblots. The correlation between chronic B19 infection and persistence of antilinear VP2 epitopes requires further study. ( info)

7/132. parvovirus B19 infection in a human immunodeficiency virus-infected patient with anemia.

    anemia is generally attributed to zidovudine therapy in human immunodeficiency virus (hiv)-infected patients, although parvovirus B19 infection has been reported as a rare cause. We report on a 24-year-old homosexual man infected with hiv who presented with anemia. He had received aggressive daily antiretroviral therapy (zidovudine 600 mg, lamivudine 300 mg, and saquinavir 1,800 mg) for 2 years. At the time of admission, his CD4 count was 10 x 10(6) cells/L. A bone marrow aspirate smear showed a marked decrease in erythropoiesis and immunocytochemical staining for parvovirus B19 was positive. parvovirus B19 viral dna was detected in the peripheral blood using a polymerase chain reaction-based assay. Serologic studies were positive for parvovirus B19 immunoglobulin (Ig)M antibodies, but negative for IgG antibodies. The patient was treated with packed red blood cell transfusion. zidovudine was stopped and replaced with zalcitibine 2.25 mg daily after anemia occurred. He did not receive intravenous Ig therapy because of its cost. After discontinuation of zidovudine for 1 year, anemia persisted and the patient depended on regular blood transfusions to control the anemia. This case emphasizes that, in addition to drug-related causes, parvovirus B19 infection should be included in the differential diagnosis of chronic anemia in hiv-infected individuals. ( info)

8/132. Presumed parvovirus B19-associated retinal pigment epitheliopathy.

    PURPOSE: To describe a patient with a white dot syndrome associated with acute erythema infectiosum. methods: A patient with a clinical history of erythema infectiosum and multifocal punctate white lesions at the level of the retinal pigment epithelium was followed up for an 8-month interval. serum was tested for immunoglobulin m (IgM) and IgG antibodies to parvovirus B19 at the time of the initial evaluation and during convalescence using an indirect immunofluorescence antibody technique. Serial photographs and fluorescein angiograms were obtained. RESULTS: IgM and IgG antibodies to parvovirus were detected in the serum at the time of initial evaluation; IgM antibodies had disappeared but IgG antibodies persisted in serum obtained at 1-month follow-up. Fundus evaluation revealed clinical disappearance of some lesions, with increased pigmentation of others over the course of follow-up. CONCLUSION: The authors have identified an adult patient who presented with a white dot syndrome associated with acute erythema infectiosum documented by serologically proved parvovirus B19 infection. ( info)

9/132. Acute glomerulonephritis after human parvovirus B19 infection.

    We evaluated clinical and histological characteristics of four adult patients who presented with acute glomerulonephritic syndrome with serological confirmation of recent HPB19 infection. All patients had generalized edema with urinary abnormalities. body weight gain ranged from 3 to 10 kg. Three of the patients had contact with erythema infectiosum simultaneously with or within 10 days before development of flu-like symptoms. Two patients had an erythematous rash, and one patient had lower-extremity purpura. Joint pain was present in three of the patients. All patients had proteinuria and hematuria. Renal functions were normal except in one patient who had a serum creatinine of 3.2 mg/dL. Three of the patients had hypocomplementemia. All renal biopsy specimens were characterized by glomerular leukocyte infiltration and endothelial cell swelling. Mesangiolysis was seen in three of the patients. C3 was deposited in a coarse granular pattern along the capillary walls in all cases. Electron microscopic examination showed marked expansion of the subendothelial space of glomerular capillaries in all patients. Subendothelial electron-dense deposits were present in all patients. Immunohistochemical analysis using monoclonal anti-HPB19 antibody showed that one of the four patients had positive staining in the glomeruli. dna extracted from renal biopsy specimens contained HPB19 dna, as shown by polymerase chain reaction (PCR) analysis in all patients. PCR amplification of the renal dna generated a 104-bp product, which hybridized to an HPB19-specific probe. No control group subjects contained HPB19 dna as determined by PCR. This circumstantial evidence indicates that HPB19 infection may be one of the causes of acute glomerulonephritis in normal individuals. ( info)

10/132. Endocapillary proliferative glomerulonephritis in a patient with parvovirus B19 infection.

    A 45-year-old woman developed acute nephritic syndrome after erythema infectiosum. Laboratory data on admission showed decreased serum C3, C4, and CH50 levels and the presence of both immunoglobulin (Ig) M and IgG antibodies to human parvovirus B19 (HPV). A renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. Immunofluorescence microscopy indicated 2 granular staining for IgG, IgM, and C3 over the mesangial area and along glomerular capillary walls. HPV antigen was also detected in glomeruli by immunohistochemistry. Electron microscopy showed electron-dense deposits in the subendothelial space and the paramesangial area. These findings suggest that immune complex-type glomerulonephritis is caused by glomerular deposition of HPV antigen-antibody complexes in some patients with HPV infection. ( info)
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