Cases reported "Roseolovirus Infections"

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11/52. Human herpesvirus-6 encephalitis after unrelated umbilical cord blood transplant in children.

    Three children developed human herpesvirus-6 (HHV-6), variant B encephalitis after unrelated umbilical cord blood transplant, in a single center. They developed clinical manifestations of encephalitis around day 17 post transplant. Impairment of consciousness, incoherent speech, episodic focal pruritis, motor weakness, convulsions and severe hyponatremia were features at presentation. Radiological investigation of brain ranged from unremarkable to extensive white matter and meningeal lesions. Diagnosis was established by the presence of HHV-6 dna in cerebrospinal fluid (CSF). Retrospective analyses of plasma revealed the presence of viral DNAemia prior to the onset of disease in two subjects. Treatment with ganciclovir or foscarnet was given. Two subjects did not achieve engraftment and died of other transplant-related complications on day 38 and 56 post-transplant, respectively. One subject achieved disease-free survival for more than 1 year with a satisfactory neurological outcome. In conclusion, HHV-6 encephalitis is not uncommon among patients undergoing umbilical cord blood transplantation. It is worth conducting further studies on early diagnosis and optimal management of this potentially fatal disease. ( info)

12/52. Human herpesvirus 6 encephalitis associated with hypersensitivity syndrome.

    Hypersensitivity syndrome, a serious systematic reaction to a limited number of drugs, is associated with the reactivation of human herpesvirus 6. A 56-year-old man developed acute limbic encephalitis followed by multiple organ failure during the course of toxic dermatitis induced by aromatic anticonvulsants. The clinical features of skin eruptions, high fever, eosinophilia, and atypical lymphocytosis were compatible with drug hypersensitivity syndrome. The patient showed seroconversion for human herpesvirus 6, and polymerase chain reaction detected human herpesvirus 6 dna in the cerebrospinal fluid. To our knowledge, this is the first report of human herpesvirus 6 encephalitis associated with hypersensitivity syndrome. ( info)

13/52. A computational analysis of Canale-Smith syndrome: chronic lymphadenopathy simulating malignant lymphoma.

    OBJECTIVE: The objective of this study was to simulate changes in the human T cell system representing Canale-Smith syndrome using a dynamic computer model of T cell development and comparing with available human data. STUDY DESIGN: Physiological stepwise maturation and function of T lymphocytes in the computer model is altered by introducing functional disturbances following lymphotropic virus infection. In the present model, acute and chronic persistent infection with the human herpesvirus-6 (HHV-6) was simulated, and ensuing changes in T cell populations were compared with those measured in human patients. RESULTS: Using our computer model we previously found that simulated acute HHV-6 infection produced T cell computer data, which resembled an infectious mononucleosis-like disease in patients. Simulated chronic persistent infection, instead, resulted in variable cell changes comparing well to patients with chronic fatigue syndrome. In one setting, however, persistent immature lymphocytosis was observed similar to what initial has been described in this journal as Canale-Smith syndrome. CONCLUSION: Using a computer model developed by us we were able to produce simulations that resemble the immune system features of Canale-Smith syndrome. Further understanding of these simulation results may possibly guide future investigations into this disorder. ( info)

14/52. guillain-barre syndrome after exanthem subitum.

    A female infant developed guillain-barre syndrome 20 days after having exanthem subitum confirmed serologically as human herpesvirus 6 infection. dna of human herpesvirus 6 was detected in peripheral blood mononuclear cells collected on admission. ( info)

15/52. Severe encephalopathy associated with reactivated human herpesvirus 6 in a six year-old immunocompetent child.

    When a six year-old immunocompetent child affected by encephalitis was subjected to virological studies, human herpesvirus 6 variant B2 resulted to be the cause of illness. Laboratory diagnosis based on the finding of human herpesvirus 6 genome in the cerebrospinal fluid of the patient both at the beginning of the disease and on the occasion of a relapse which occurred forty days after the patient's hospital discharge. The presence of high-avidity IgG to human herpesvirus 6 detected in the patient's serum at the time of the first hospital admission proved that he had suffered from a past infection by human herpesvirus 6. In the consequence of this, the human herpesvirus 6 dna finding in the patient's cerebrospinal fluid was to ascribed to virus reactivation. In the light of virological and serological results, the clinical case described underlines the ability of human herpesvirus 6 to cause neurological disorders not only during primary infections but also during infections supported by rescued virus. ( info)

16/52. Large vessel arteritis associated with human herpesvirus 6 infections.

    A 9-month-old boy presented with chronic arteritis of the aorta and its major branches. The clinical manifestations at onset of his illness were compatible with those of Kawasaki syndrome. However, the febrile period lasted for 2 months despite various immunosuppressive therapies, and the levels of c-reactive protein remain high 18 months after onset. Elevated circulating immune complexes, decreased serum complement levels, hypergammaglobulinaemia and monoclonal gammopathy were observed. Active HHV-6 infection was shown by increased serum levels of antihuman herpesvirus-6 (HHV-6) IgG and IgM antibodies, and positive HHV-6 dna in sera, peripheral blood mononuclear cells (PBMNC) and lymph nodes. HHV-6 was actively replicating in PBMNC and lymph nodes, as shown by the detection of transcripts for the virus structural antigen. These results suggest that large vessel arteritis can be associated with HHV-6 infection. ( info)

17/52. Human herpesvirus-7 infection of the CNS with acute myelitis in an adult bone marrow recipient.

    The beta-herpesviruses, human herpesviruses-6 and -7 (HHV-6 and HHV-7), are closely related and have very similar biological behaviour. While HHV-6 is associated with encephalitis in immunosuppressed adults, HHV-7 is not recognised as a cause of neurological disease in such patients. This report describes the identification of a reactivated HHV-7 infection in the cerebrospinal fluid of an adult who presented with an acute myelitis 11 months after unrelated donor bone marrow transplant. ( info)

18/52. Human herpesvirus 6B infection of the large intestine of patients with diarrhea.

    Four patients had severe diarrhea after undergoing stem cell transplantation. Human herpesvirus 6B (HHV-6B) dna was detected in large intestine tissue specimens and in peripheral blood mononuclear cells. in situ hybridization was positive for HHV-6B dna in the nuclei of goblet cells and, sometimes, in the histiocytes in the submucous region of the large intestine, which suggests that HHV-6B may infect and reactivate in these cells. ( info)

19/52. Human herpesvirus 6 genome and antigen in acute multiple sclerosis lesions.

    Evidence for a candidate multiple sclerosis (MS) virus, human herpesvirus 6 (HHV-6), was sought in biopsy specimens of acute lesions that presented clinically as cerebral tumors obtained from 5 patients. Histopathology, magnetic resonance imaging, and clinical course confirmed the diagnosis of MS in each case. A sensitive in situ polymerase chain reaction (ISPCR) method was used to detect HHV-6 genome, in conjunction with immunocytochemical staining (ICC) to detect viral and cellular antigens. ISPCR revealed numerous oligodendrocytes, lymphocytes, and microglia containing HHV-6 genome within all lesions, whereas ICC showed only the HHV-6 glycoprotein 116 antigen in some reactive astrocytes and microglia. High frequencies of neuroglial and inflammatory cells containing HHV-6 genome were present in acute-phase lesion tissue from patients who were free of the effects of chronic MS and had not been received immunomodulatory therapy for MS. The prevalence of HHV-6 genome-containing cells, including oligodendrocytes, in each lesion suggests that HHV-6 plays a role in the demyelinative pathogenesis of MS; the significance of the discrepant expression of viral antigens remains uncertain. ( info)

20/52. Drug-induced hypersensitivity syndrome associated with Epstein-Barr virus infection.

    association of drug-induced hypersensitivity syndrome with viral infection is debated. Human herpesvirus 6 (HHV-6) reactivation has been the most frequently reported infection associated with this syndrome. However, a case of cytomegalovirus (CMV) infection was recently described associated with anticonvulsant-induced hypersensitivity syndrome. We report a case of severe allopurinol-induced hypersensitivity syndrome with pancreatitis associated with Epstein-Barr virus (EBV) infection. Active EBV infection was demonstrated in two consecutive serum samples by the presence of anti-EBV early antigen (EA) IgM antibodies and an increase in anti-EBV EA IgG antibodies, whereas no anti-EBV nuclear antigen IgG antibodies were detected. EBV dna was detected by polymerase chain reaction (PCR) in peripheral blood mononuclear cells. Reactivation of HHV-6 was suggested only by the presence of anti-HHV-6 IgM antibodies, but HHV-6 dna was not detected by PCR in the serum. Other viral investigations showed previous infection (CMV, rubella, measles, parvovirus B19), immunization after vaccination (hepatitis b virus), or absence of previous infection (hepatitis c virus, human immunodeficiency virus). We suggest that EBV infection may participate in some cases, as do the other herpesviruses HHV-6 or CMV, in the development of drug-induced hypersensitivity syndrome. ( info)
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