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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some rotavirus strains, including vaccine candidates, have been demonstrated to cause hepatitis in immunodeficient and malnourished mice and to grow in human liver cells. To determine whether rotavirus spreads outside the intestine in naturally infected children, we examined tissues from four immunodeficient children affected with severe combined immunodeficiency disease, acquired immunodeficiency disease syndrome, or DiGeorge syndrome. Chronic rotavirus-related diarrhea, which persisted until death, had also developed in each child. Using indirect immunoperoxidase techniques, we identified rotavirus antigen in the liver and kidney with a hyperimmune guinea pig antiserum prepared to double-shelled rotavirus particles. Similar immunostaining with an antiserum to a rotavirus nonstructural protein (NS26) provided evidence of active virus replication. The observed reactivity was eliminated specifically when serial sections were immunostained with the same antiserum that had been absorbed with either double-shelled rotavirus particles or NS26. Immunostaining was not observed in the liver of children with other diseases (alpha 1-antitrypsin deficiency, inspissated bile syndrome, and acute rejection of a transplanted liver). These findings demonstrate that rotavirus infections in children can extend beyond the intestinal tract. Further studies are warranted to determine whether extraintestinal rotavirus replication occurs in children without severe immunodeficiency, such as malnourished children.
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PMID:Extraintestinal rotavirus infections in children with immunodeficiency. 131 19

Adenoviruses are among the many pathogens and opportunistic agents that cause serious infection in the congenitally immunocompromised, in patients undergoing immunosuppressive treatment for organ and tissue transplants and for cancers, and in human immunodeficiency virus-infected patients. Adenovirus infections in these patients tend to become disseminated and severe, and the serotypes involved are clustered according to the age of the patient and the nature of the immunosuppression. Over 300 adenovirus infections in immunocompromised patients, with an overall case fatality rate of 48%, are reviewed in this paper. Children with severe combined immunodeficiency syndrome and other primary immunodeficiencies are exposed to the serotypes of subgroups B and C that commonly infect young children, and thus their infections are due to types 1 to 7 and 31 of subgenus A. Children with bone marrow and liver transplants often have lung and liver adenovirus infections that are due to an expanded set of subgenus A, B, C, and E serotypes. Adults with kidney transplants have viruses of subgenus B, mostly types 11, 34, and 35, which cause cystitis. This review indicates that 11% of transplant recipients become infected with adenoviruses, with case fatality rates from 60% for bone marrow transplant patients to 18% for renal transplant patients. Patients with AIDS become infected with a diversity of serotypes of all subgenera because their adult age and life-style expose them to many adenoviruses, possibly resulting in antigenically intermediate strains that are not found elsewhere. Interestingly, isolates from the urine of AIDS patients are generally of subgenus B and comprise types 11, 21, 34, 35, and intermediate strains of these types, whereas isolates from stool are of subgenus D and comprise many rare, new, and intermediate strains that are untypeable for practical purposes. It has been estimated that adenoviruses cause active infection in 12% of AIDS patients and that 45% of these infections terminate in death within 2 months. In all immunocompromised patients, generalized illness involving the central nervous system, respiratory system, hepatitis, and gastroenteritis usually have a fulminant course and result in death. Treatments for adenovirus infections are of little proven value, although certain purine and pyrimidine analogs have shown beneficial effects in vitro and may be promising drugs.
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PMID:Adenoviruses in the immunocompromised host. 132 83

Male NMRI or BALB/c mice developed severe liver injury as assessed by transaminase release within 8 h when an intravenous dose greater than 1.5 mg/kg concanavalin A (Con A) was given. Histopathologically, only the liver was affected. Electron micrographs revealed leukocyte sticking to endothelial cells and bleb formation of hepatocytes. The hepatotoxicity of the lectin correlated neither with its agglutination activity nor with its sugar specificity. Administration of 0.5 mg/kg dexamethasone or 50 mg/kg cyclosporine A or 50 mg/kg FK 506 (Fujimycin) resulted in protection of the animals whereas indomethacin pretreatment failed to protect. Con A hepatitis was accompanied by the release of IL-2 into the serum of the animals. Mice with severe combined immunodeficiency syndrome lacking B as well as T lymphocytes were resistant against Con A. Athymic nude mice with immature T lymphocytes were also resistant. Pretreatment of mice with an antibody against T lymphocytes fully protected against Con A as did monoclonal anti-mouse CD4. Monoclonal anti-mouse CD8 failed to protect. Pretreatment of mice with silica particles, i.e., deletion of macrophages, prevented the induction of hepatitis. These findings provide evidence that Con A-induced liver injury depends on the activation of T lymphocytes by macrophages in the presence of Con A. The model might allow the study of the pathophysiology of immunologically mediated hepatic disorders such as autoimmune chronic active hepatitis.
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PMID:A T cell-dependent experimental liver injury in mice inducible by concanavalin A. 163 8

Chronic rotavirus infection of an infant with severe combined immunodeficiency (SCID) was studied by virological examinations in association with long-term observation of his symptoms and immune status. During eleven months of hospitalization, the patient was suffering from incurable severe diarrhea with persisting excretion of rotaviruses detected by electron microscopy and the reversed-passive hemagglutination (R-PHA) test and had transient hepatitis symptom despite multiple administrations of human gammaglobulin and high calorie fluids. The detected viruses were morphologically recognized as rotavirus with double capsid structure. Polyacrylamide gel electrophoretic (PAGE) analysis of their genomic RNAs showed the long electropherotype of group A virus with abnormal migration profiles changing considerably from the early to the late phase of illness: (1) The 11th segment became undetectable; (2) the molecular weight of the 6th segment slightly increased; (3) seven to fourteen extra segments appeared; and (4) PAGE patterns of viral genomic RNAs changed every three or four months. These findings suggest that chronic infection with rotavirus accompanied the generation of extra viral genomic segments and their unusual assortments in an immunodeficient host.
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PMID:Serial observations of chronic rotavirus infection in an immunodeficient child. 166 75

Adenovirus type 31 (Ad31) was isolated from 15 immunocompromised patients in 12 of whom seroconversion was also recorded. Ad31 infection has a substantial clinical relevance since 8 of 10 with lower respiratory tract infection and 4 of 4 with hepatitis died. Therefore, Ad31 isolates from immunocompetent and immunodeficient hosts were compared by restriction endonuclease analysis. Nine genome types were identified among the 79 Ad31 isolates. Pairwise comparison of comigrating restriction fragments indicated that the genome types could be divided into three genomic clusters. Several Ad31 genome types were isolated from immunocompromised patients, but no highly virulent genome type could be found. A genome type was identified in a child with severe combined immunodeficiency who originally was infected with another genome type. This observation is suggested to have evolutionary implications.
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PMID:Genome analysis of adenovirus type 31 strains from immunocompromised and immunocompetent patients. 198 11

Viable Borrelia burgdorferi (B. burgdorferi) organisms induce a chronic infection associated with arthritis, carditis and hepatitis in severe combined immunodeficiency (scid) mice but not in most of the adult mice from the various immunocompetent inbred strains tested. Furthermore, we have found that experimental inoculation of normal mice with B. burgdorferi organisms leads to the generation of antibodies and T cells specific for various spirochetal antigens including the outer surface proteins A and B (OspA, OspB) as well as flagellin. The assumption of a protective role of the immune response during B. burgdorferi infection in mice is supported by our recent findings that passively transferred B. burgdorferi-specific immune mouse sera as well as monoclonal antibodies to OspA are able to prevent the development of the disease in scid mice. We show now that purified OspA protein both in its native and recombinant form is immunogenic and that the antibodies generated are able to confer protection to scid mice against B. burgdorferi infection.
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PMID:A mouse model for Borrelia burgdorferi infection: pathogenesis, immune response and protection. 204 47

The pathogenic profiles of two heterologous animal rotaviruses, rhesus rotavirus strain MMU 18006 and bovine rotavirus strain WC3, were evaluated in mice with severe combined immunodeficiency (SCID mice) and normal BALB/c mice. Control animals were inoculated with homologous murine strain EDIM 5099 or a tissue culture-adapted murine rotavirus. Heterologous infection with rhesus rotavirus resulted in hepatitis in 84% of SCID and 21% of BALB/c mice, with mortality rates of 27 and 0%, respectively. Surviving SCID animals developed chronic liver disease, while symptoms in BALB/c mice resolved in 2 to 4 weeks after onset. Histopathologic examination revealed a diffuse hepatitis with focal areas of parenchymal necrosis. Rotavirus was detected in liver tissue from 100% of 29 SCID and 85% (11 of 13) BALB/c animals tested by cell culture infectivity, immunofluorescence, or electron microscopy. No extramucosal spread of virus or hepatitis was observed after infection with heterologous bovine strain WC3 or homologous murine rotaviruses. This finding of a novel rotavirus-induced disease manifestation suggests altered tissue tropism in a heterologous host for a group of viruses previously shown to replicate exclusively in the gut mucosa. The implications of our observations suggest that in human vaccine trials utilizing heterologous rotavirus strains, special attention should be paid to children with immunodeficiency disorders, and screening for hepatic function should be included in vaccine protocols.
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PMID:Extramucosal spread and development of hepatitis in immunodeficient and normal mice infected with rhesus rotavirus. 215 22

The authors describe the histopathologic evolution of Lyme disease in severe combined immunodeficiency (scid) and normal C.B-17 and C57BL/6 mice inoculated with Borrelia burgdorferi. Starting on day 7 after inoculation, all scid mice infected subcutaneously in the tail with a low-passage European tick isolate of B. burgdorferi had clinical evidence of arthritis characterized by reddening and swelling of tibiotarsal joints. Later on, other joints, ie, metatarsal and ulnacarpal joints were also affected. The infection of scid mice resulted in a persistent spirochetemia and the development of a multisystem disease with chronic progressive inflammation of joints, heart, and liver. Major histopathologic alterations included 1) severe joint lesions, characterized by the presence of hyperplastic inflamed synovial lining cells associated with the erosion and destruction of cartilage and/or bone; 2) pancarditis with infiltrations of mononuclear cells in the endocardium, myocardium, and pericardium; and 3) hepatitis with mononuclear cell infiltrations confined to the portal field and central vein, granulomatous reactions, and eventually the development of liver fibrosis. In addition, smaller more confined lesions were found in kidneys, lung, brain, and striated muscle. The inflammatory infiltrates in the various organs were associated mostly with Mac-1+ cells, largely monocytes and macrophages, as well as some polymorphonuclear leukocytes, but not B and T lymphocytes. Infective spirochetes could be readily isolated from blood and joints and were found at the site of inoculum and the myocardium. In contrast, subcutaneous inoculation of normal C.B-17 or C57BL/6 mice with spirochetes in general did not result in clinical signs of arthritis. Only 10% to 20% of the C57BL/6 mice, but none of the C.B-17 mice, showed clinical evidence of oligoarthritis, which appeared not before day 36 after inoculation. In general, the infection of normal mice resulted in minimal lesions in various organs, and no spirochetes could be visualized or reisolated from their tissues. The data demonstrate that Lyme borreliosis may develop in mice in the absence of detectable specific B and T cells and thus suggest an immunologic control of the disease in this species. The scid mouse model therefore can be used to define the components of the immune system responsible for the suppression and/or the progression of the disease.
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PMID:Lyme borreliosis in the severe combined immunodeficiency (scid) mouse manifests predominantly in the joints, heart, and liver. 222 Oct 14

An autopsy case of adenovirus hepatitis with severe combined immunodeficiency (SCID) is presented. A 7-month-old female was admitted to the Kitasato University Hospital with chief complaint of persistent fever. A diagnosis of severe combined immunodeficiency (SCID) was made because of defective function in both T and B lymphocytes. Respiratory disturbance and severe hepatic dysfunction were manifested after admission. She died of respiratory failure on the 40th hospital day. Autopsy findings revealed many focal necroses scattered irregularly throughout the liver. Degenerating hepatocytes around the focal necrosis contained nuclear inclusion bodies, and crystalline arrays of adenovirus virions were recognized in these cells by electron microscopy. Adenovirus antigens were brilliantly detected in the nuclear inclusion bodies by indirect immunofluorescence.
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PMID:Adenovirus hepatitis in a patient with severe combined immunodeficiency. 303 94

Adenoviruses are ubiquitous organisms but only infrequently have been implicated as a cause of hepatitis and rarely as a cause of fatal disease. A fatal case of disseminated adenovirus serotype 31 infection is described. It occurred in a patient with severe combined immunodeficiency who received a fetal liver transplant and subsequently developed massive hepatic necrosis. To the best knowledge of the authors, this is the first reported case of disseminated disease due to serotype 31.
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PMID:Disseminated adenovirus serotype 31 infection in an immunocompromised host. 609 98


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