Cases reported "Hepatitis B"

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1/64. Three cases of severe subfulminant hepatitis in heart-transplanted patients after nosocomial transmission of a mutant hepatitis b virus.

    Fulminant and severe viral hepatitis are frequently associated with mutant hepatitis b virus (HBV) strains. In this study, the genetic background of a viral strain causing severe subfulminant outcome in heart-transplanted patients was studied and compared with viral hepatitis B strains that were not linked to severe liver disease in the same setting. A total of 46 patients infected nosocomially with HBV genotype A were studied. Five different viral strains were detected, infecting 3, 9, 5, 24, and 5 patients, respectively. Only one viral strain was found to be associated with the subfulminant outcome and 3 patient deaths as a consequence of severe liver disease. The remaining 43 patients with posttransplantation HBV infection did not show this fatal outcome. Instead, symptoms of hepatitis were generally mild or clinically undiagnosed. Comparison of this virus genome with the four other strains showed an accumulation of mutations in the basic core promoter, a region that influences viral replication, but also in hepatitis B X protein (HBX) (7 mutant motifs), core (10 mutant motifs), the preS1 region (5 mutant motifs), and the HBpolymerase open reading frame (17 motifs). Some of these variations, such as those in the core region, were located on the tip of the protruding spike of the viral capsid (codons 60 to 90), also known in part as an important HLA class II-restricted epitope region. These mutations might therefore influence the immune-mediated response. The viral strain causing subfulminant hepatitis was, in addition, the only strain with a preCore stop codon mutation and, thus, hepatitis B e antigen (HBeAg) expression was never observed. The combination of these specific viral factors is thought to be responsible for the fatal outcome in these immune-suppressed heart-transplant recipients.
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2/64. kidney transplantation in a child with posterior urethral valve from a hepatitis B virus-carrier mother. Report of a case with special reference to urinary tract reconstruction for dysfunctionalized uropathies and seroimmunological preparation against viral transmission.

    The case of a 7-year-old boy with posterior urethral valve (PUV) who underwent successful kidney transplantation for progressive renal failure is reported. He required complex reconstructive surgery for PUV-related disorders, and also specific serological preparation for hepatitis B (HB) as his living donor mother was a proven carrier. By carefully executing the principles of reconstructive surgery and with well-planned seroimmunological preparation, we have demonstrated that successful kidney transplantation can be done from an HB Ag-positive mother to an HB Ag- and HB Ab-negative son, even when his urinary tract is severely dysfunctional due to PUV.
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3/64. Quantitative dna analysis of low-level hepatitis B viremia in two patients with serologically negative chronic hepatitis B.

    Low-level viremia due to hepatitis b virus (HBV) was demonstrated in the sera of two patients diagnosed previously as having non-B, non-C chronic hepatitis. Both patients had a "silent" HBV infection, because they were negative for both hepatitis B surface antigen (HBsAg) and anti-hepatitis B core antibody. The TaqMan chemistry polymerase chain reaction (PCR) amplified the HBV dna, enabling quantitation of the virus in their sera. Their serum HBV dna concentrations were low: the amount of each HBV S or X gene amplified showed there were approximately 10(3) copies/ml and HBV dna was detected occasionally during clinical follow-up. Positive HBsAg staining in liver tissues was demonstrated by an immunoperoxidase technique. Vertical transmission of silent HBV from one patient to her daughter was confirmed. Direct nucleotide sequencing of the amplified HBV X region revealed several mutations, suggesting reduced viral replication. One patient had a T-to-C mutation at the extreme 5'-terminus of the direct repeat 2 region and the other exhibited a coexisting X region with a 155-nucleotide deletion. These findings suggest that HBV replication is suppressed considerably in patients with silent hepatitis B.
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4/64. 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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5/64. Nosocomial transmission of hepatitis b virus infection through multiple-dose vials.

    The source of acute hepatitis b virus (HBV) infection in two women (55 and 72 years old) was investigated. They displayed no risk factors for acquiring HBV infection, other than treatment with local anaesthetic injections some months previously. The HBV strains were sequenced and showed distinct homology to strains seen in Swedish intravenous drug users (IVDU). Prior to these patients' acute infection, an outbreak of HBV had occurred among IVDU in the same county. Analysis of the HBV strains from six of these IVDUs showed their core promoter, precore and pre-S sequences (679 nucleotides) to be identical to those from the two patients. Cross-contamination between samples was excluded and the most likely source of infection was thought to be multiple-dose vials of local anaesthetic that had been contaminated with the HBV strain circulating among the IVDU population in the community. We believe that multiple-dose vials have no place in modern healthcare and recommend sequence homology analysis as an alternative or additional way to trace a source of HBV infection.
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6/64. molecular epidemiology of a large outbreak of hepatitis B linked to autohaemotherapy.

    BACKGROUND: Unregulated skin-piercing procedures potentially facilitate the transmission of bloodborne pathogens. In February, 1998, a patient who had recently received autohaemotherapy at an alternative medicine clinic in the UK was diagnosed with acute hepatitis B. The autohaemotherapy procedure involved the drawing of 1 mL of the patient's blood, mixing with saline, and reinjection of the autologous blood mixture. We investigated the extent of hepatitis b virus (HBV) infection in patients and staff of the clinic. methods: patients who had attended the clinic between January, 1997, and February, 1998, were tested for serological markers of HBV, and for HBV dna by PCR. HBV dna was sequenced to assess the relatedness of the virus identified in the cases. We analysed the number and dates of visits with regard to HBV status. FINDINGS: serum samples were received from 352 patients and four staff members. Serological evidence of exposure to HBV was found in 57 (16%). Of the 33 patients and staff who were positive for hepatitis B surface antigen, 30 (91%) showed complete nucleotide identity in the dna segments derived from the surface and core genes. Five patients with linked infection had markers of chronic hepatitis B, and one of these was regarded as the likely source of the outbreak. The attack rate was associated with the number of visits (p<0.0001) and the week of visit (p=0.011). Contaminated saline in a repeatedly used bottle was the probable vehicle of transmission. INTERPRETATION: We have described a large community-based outbreak of hepatitis B due to transmission by a single HBV variant. Our findings emphasise the continuing risk of transmission of bloodborne viruses in all health-care settings where skin-piercing procedures are used.
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7/64. Molecular evolutionary analysis of the complete nucleotide sequence of hepatitis B virus (HBV) in a case of HBV infection acquired through a needlestick accident.

    To elucidate needlestick transmission of hepatitis b virus (HBV), strains isolated from 1 physician who acquired HBV infection through a needlestick accident and 3 patients with chronic hepatitis B (donor patients A, B, and C) were tested using molecular evolutionary analysis based on full-length HBV genomic sequences. Nucleotide sequences of these isolates were aligned with 55 previously reported full-length genomic sequences. Genetic distances were estimated using the 6-parameter method, and phylogenetic trees were constructed using the neighbor-joining method. Strains isolated from patient A and the recipient pair were clustered within a closer range of evolutionary distances than were strains recovered from the recipient pair and patients B and C. Furthermore, strains from patient A and the recipient were also clustered on the S gene sequences of HBV. These results demonstrated that patient A alone was the source of direct transmission to the recipient. This approach can be used to investigate the transmission route of HBV.
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8/64. Acute hepatitis B in two patients transmitted from an e antigen negative cardiothoracic surgeon.

    hepatitis b virus (HBV) infection was transmitted by a locum cardiothoracic surgeon to two patients during coronary artery bypass surgery. Both patients presented 12 weeks after surgery and developed serious clinical illness. The surgeon was known to be hepatitis B surface antigen (HBsAg) positive, hepatitis B e antigen (HBeAg) negative, and to have antibodies to HBeAg (anti-HBe). Sequences of regions of the HBV surface and core genes from the patients and surgeon were indistinguishable. An exercise was undertaken to notify all patients on whom the surgeon had operated while employed at the hospital where the transmissions occurred. One hundred and twenty-three out of 126 patients were tested. No evidence of transmission to any other patient was found. Revised recommendations by the UK health Departments as to which health care workers should be permitted to perform exposure prone procedures have recently been published.
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9/64. blood donors infected with the hepatitis b virus but persistently lacking antibodies to the hepatitis B core antigen.

    BACKGROUND AND OBJECTIVES: antibodies to the core of hepatitis b virus (anti-HBc) are considered to be the best serologically reliable markers of hepatitis b virus (HBV) infection. Through a national epidemiological survey, two young and first-time blood donors, originating from HBV-endemic areas, were identified as HBV carriers with an absence of anti-HBc reactivity. MATERIALS AND methods: We followed up these two subjects in order to investigate the evolution of their HBV serological profiles. Nucleotide sequencing was performed of the entire pre-C/C region of the strains infecting these donors. RESULTS: The same serological profile of active viral replication with an apparent persistent lack of anti-HBc and normal alanine aminotransferase (ALT) levels was found for both subjects throughout a follow-up of 19 months and 4 months, respectively. Neither donor was immunocompromised. Nucleotide sequence analysis of the pre-C/C region did not show mutations or deletions in encoded proteins. CONCLUSION: The hypothesis of an in utero HBV infection responsible for an immune tolerance to HBV seems to be the most probable explanation for this particular immunological situation. Such occurrences in the blood donor population are probably rare as less than 0.1% of hepatitis B surface antigen (HBsAg)-positive donors exhibit such a profile, in our experience. Moreover, this phenomenon does not impose a risk of HBV transmission by blood donation, as the exclusion of HBV-infected blood donation is based on HBsAg detection. However, such a risk might be encountered with the hepatitis c virus (HCV) for which at present only antibodies to HCV are screened.
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10/64. Acute self-limiting hepatitis B after immunoprophylaxis failure in an infant.

    The occurrence of acute hepatitis after failure of immunoprophylaxis in cases of mother-to-infant transmission of hepatitis b virus (HBV) is uncommon. Because immunoprophylaxis failure is caused by the emergence of an "a" determinant escape mutant, the infants usually become HBV carriers. To evaluate whether mutations in the S gene coding for the surface protein that contains the "a" determinant are associated with acute hepatitis after immunoprophylaxis failure, HBV dna of an infant in with acute hepatitis developed with seroconversion to anti-HBs antibodies at 12 months of age despite administration of anti-hepatitis B immunoglobulin and hepatitis B vaccine was analyzed. The S gene from HBV dna isolated from the serum of the infant at 12, 19, and 27 months of age was cloned and sequenced. Mutations affecting amino acid residues in the first loop within the "a" determinant (codons 124-147) were found at 12 months of age. Moreover, a novel deletion mutant, with a 1-bp deletion at nucleotide 449 of the S gene, was found at 19 and 27 months of age. This deletion resulted in a frame shift and it introduced a stop codon (TAG) at codon 176. Because the open reading frame of the S gene is completely overlapped by the polymerase gene, mutations in the S gene may affect the polymerase gene. Based on this case, this study suggests that the observed frame-shift mutation in the S gene might affect the polymerase protein and induce prompt suppression of viral replication.
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