Cases reported "Superinfection"

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1/5. Clearance of HCV rna in a chronic hepatitis c virus-infected patient during acute hepatitis b virus superinfection.

    The routes of hepatitis b virus and hepatitis c virus transmission are quite similar and coexistence of both viruses in one patient is not a rare phenomenon. Until now, the natural course of liver diseases induced by coinfections has not been well documented and the mechanisms of interaction between the two viruses and the human host have not been fully clarified. We report the case of a patient suffering from chronic hepatitis due to hepatitis c virus who developed an acute hepatitis b virus superinfection. serum hepatitis c virus ribonucleic acid became undetectable by reverse transcriptase/polymerase chain reaction at diagnosis of acute hepatitis b virus infection. At the same time, there was a striking increase in the serum concentrations of the antibodies against C22 and C33c hepatitis c virus antigens. Four months after clinical resolution of the acute hepatitis, hepatitis B surface antigen was undetectable in serum and three months later antibodies against hepatitis B surface antigen appeared. Two years after acute hepatitis b virus infection, the patient has had no relapse of markers for viral replication of hepatitis b virus. transaminases are within the reference range and hepatitis c virus ribonucleic acid is undetectable in both serum and liver tissue. We hypothesize that acute hepatitis b virus infection stimulated a specific humoral response against hepatitis c virus as well as triggering non-specific defense mechanisms which finally eliminated both viruses.
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2/5. Ligneous conjunctivitis in a girl with severe type I plasminogen deficiency.

    BACKGROUND: Ligneous conjunctivitis is a rare form of chronic recurrent pseudomembranous disease and may be associated with systemic membranous pathological changes. Recently ligneous conjunctivitis has been linked to severe type I plasminogen deficiency. We report on a patient with plasminogen deficiency and severe bilateral ligneous conjunctivitis. A new treatment approach and its outcome in this patient are described. CASE REPORT: We present the case of a 9-month-old Turkish girl with massive swelling of the eyelids and hard white pseudomembranes on both lids. The conjunctival smear was positive for streptococcus pneumoniae. The clinical diagnosis was: ligneous conjunctivitis with superinfection. Histological investigation showed fibrin as major component of the pseudomembranes. The coagulation analyses revealed decreased plasminogen activity (<5%; normal 80-120%) and decreased plasminogen antigen (<0.4 mg/dl; normal 6-25 mg/dl). The failure of surgical therapy led to the attempt at treatment with intravenous lys-plasminogen. A significant improvement of the ocular symptoms occurred; stabilization with no recurrent pseudomembranes could be achieved for 6 months after treatment. DISCUSSION: The initial amelioration of symptoms in our patient after systemic replacement therapy confirms the etiological importance of plasminogen deficiency in the development of ligneous conjunctivitis. Curative treatment of ligneous conjunctivitis is still not available. However, intravenous application of plasminogen offers new possibilities in therapy, although long-term treatment seems necessary.
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3/5. Reactivation of hepatitis c virus superinfection in a patient seropositive for hepatitis B e antigen.

    During the course of chronic hepatitis b virus (HBV) infection, a patient seropositive for hepatitis B e antigen experienced four episodes of acute hepatic necroinflammation. serum HBV-dna concentration elevated immediately before the first and third exacerbations, whereas serum hepatitis c virus (HCV) rna was detected during the second and fourth exacerbations. The nucleotide sequences of HCV hypervariable region derived from samples of the two exacerbations were identical. Interestingly, "de novo" seroconversion of anti-HCV antibody (Abbott HCV EIA 3.0) followed by reversion occurred in both the second and fourth exacerbations with low sample/cutoff ratios. Immunoblot analysis using a line-immunoassay (Inno-LIA HCV Ab III) revealed a single positive band (C1) developing after the second exacerbation. These data indicate that the second exacerbation in this patient was caused by newly acquired acute HCV superinfection, whereas the fourth exacerbation was likely due to reactivation of the previous HCV infection. Recognition of such a case suggests that the presence of de novo seroconversion of anti-HCV may indicate either reactivation or acute superinfection of HCV in a patient seropositive for hepatitis B e antigen.
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4/5. Late-onset cytomegalovirus reactivation in critically ill renal transplant patients.

    BACKGROUND: cytomegalovirus (CMV) reactivation occurs frequently in the first months after renal transplantation. However, reports concerning long-term kidney transplant recipients are rare and have always pertained to symptomatic CMV disease. methods: We report four cases of late-onset asymptomatic CMV reactivation in critically ill renal transplant patients who suffered from severe bacterial infections and in whom CMV antigenemia was observed. RESULTS AND CONCLUSION: CMV reactivation in these patients might indicate an additional disturbance in the patients' immune defenses at the time of critical illness, possibly even necessitating a temporary reduction in immunosuppressive therapy. Prospective, controlled trials are needed to define the role of CMV antigenemia in critically ill patients, including the role of antiviral therapy for asymptomatic reactivations.
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5/5. hepatitis delta virus super-infection in a co-infected patient with the human immunodeficiency virus type 1 and a surface antigen-negative hepatitis b virus variant.

    Human immunodeficiency virus infection has a major impact on the natural history of chronic hepatitis B and favours the emergence of viral mutants. We describe an acute hepatitis D virus superinfection in an hiv-1-infected patient under HAART treatment who was previously a chronic carrier of a surface negative HBV variant resistant to lamivudine.
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