Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Cardiac involvement in patients with acquired immunodeficiency syndrome (AIDS) is being reported with increasing frequency, although the factors responsible for the cardiac abnormalities are rarely identified. We report a case of sudden and unexpected death of an infant with AIDS in whom histologic and virologic studies documented generalized infection with cytomegalovirus (CMV), including pancarditis, sialitis, nephritis, colitis, hepatitis, prostatitis, orchitis, myositis, pneumonitis, and meningoencephalitis. CMV was isolated from four of five tissues cultured. Lymphocytic infiltration in the region of the sinoatrial node could have been responsible for the development of a fatal cardiac arrhythmia, and the autopsy failed to reveal any other cause of death in this infant. Children infected with the human immunodeficiency virus (HIV) need to be closely monitored for cardiac complications bearing in mind that opportunistic infections in AIDS patients may cause cardiac involvement that is atypical or that is overshadowed by the primary manifestations of the infection.
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PMID:Unexpected death in an infant with AIDS: disseminated cytomegalovirus infection with pancarditis. 284 41

Lyme disease typically begins with a unique skin lesion, erythema chronicum migrans (ECM) (stage 1). Patients with this lesion may also have headache, meningeal irritation, mild encephalopathy, multiple annular secondary lesions, malar or urticarial rash, generalized lymphadenopathy and splenomegaly, migratory musculoskeletal pain, hepatitis, sore throat, non-productive cough, conjunctivitis, periorbital edema, or testicular swelling. After a few weeks to months (stage 2), about 15% of patients develop frank neurologic abnormalities, including meningitis, encephalitis, cranial neuritis (including bilateral facial palsy), motor or sensory radiculoneuritis, mononeuritis multiplex, or myelitis. At this time, about 8% of patients develop cardiac involvement--AV block, acute myopericarditis, cardiomegaly, or pancarditis. Throughout this stage, many patients continue to experience migratory musculoskeletal pain in joints, tendons, bursae, muscle, or bone. Months to years after disease onset (stage 3), about 60% of patients develop frank arthritis, which may be intermittent or chronic. Recently evidence suggests that Lyme disease may also be associated with chronic neurologic or skin involvement. Thus, Lyme disease occurs in stages with different clinical manifestations at each stage, but the course of the illness in each patient is highly variable.
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PMID:Clinical manifestations of Lyme disease. 355 39

The presence of serum autoantibodies directed against single-stranded DNA (ssDNA), RNA, histones, nuclear antigen SS-A, mitochondria and cardiolipin were investigated in 30 HIV-negative drug addicts (from years 1986-87), 30 addicts actually infected with HIV and 31 AIDS patients presenting with clinical symptoms indicating autoimmune disorders. Positive results were found in 12 (40%) drug addicts from years 1986-87, 5 (16.7%) actually infected and 16 (51.6%) AIDS patients. Autoantibodies were more often detectable in patients with thrombocytopenia 8/12 (66.7%) than in remaining 8 out of 19 subjects (42.1%) who presented dermatitis, hepatitis, pancarditis, ulcerative colitis and polyneuropathy. The prevalence of autoantibodies in all investigated groups were significantly higher than in controls-1/20 (3.3%).
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PMID:[Presence of autoantibodies in patients infected with HIV]. 915 38

Since 2016, annually occurring species-specific die-offs of brown trout (Salmo trutta fario) occurred in the Thur River, situated in the Eastern part of Switzerland. These events lead to drastically reduced population densities in the impacted river regions. Clinical signs in brown trout and mortality were restricted to few weeks in August/September. To characterize the syndrome and to find possible causes, from end of March to November 2018, one-year-old brown trout (Salmo trutta fario) and rainbow trout (Oncorhynchus mykiss) were exposed to water from Thur River, fish were sampled regularly and screened for infectious agents, including viral metagenomics, and pathology was described. Starting approximately four months post-exposure, brown trout showed severe lymphohistiocytic pancarditis and necrotizing and haemorrhagic hepatitis. These lesions were recorded until the end of the experiment in November. Rainbow trout were not affected at any point in time. No infectious agents could be identified so far as cause of disease, especially no viral aetiology. Even if pathogenesis and pathology point in the direction of an infectious agent, a causative relationship could not be confirmed and aetiology remains unclear.
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PMID:Mysterious syndrome causing high mortality in wild brown trout in Eastern Switzerland, pathology and search for a possible cause. 3283 Mar 24

While the health effects of trypanosomes in Australian mammals in their native range are not fully understood, there is evidence of an impact in those species introduced to other geographical regions. Here we report the pathological and molecular features of concurrent fatal trypanosomiasis and toxoplasmosis in an adult female captive red-necked wallaby (syn. Bennett's wallaby; Macropus rufogriseus) from Bee County, Texas, USA. The animal exhibited no clinical signs prior to sudden death. On necropsy, the main findings were generalized organ congestion and bilateral renal petechiation. Microscopically, the main finding was lymphohistiocytic and necrotizing pancarditis with intrasarcoplasmic protozoal pseudocysts containing amastigotes and occasional intrahistiocytic amastigotes, morphologically compatible with Trypanosoma cruzi, as well as rare intrasarcoplasmic protozoal tissue cysts with zoites morphologically compatible with Toxoplasma gondii. Other lesions included acute centrilobular to panlobular necrotizing hepatitis with intrahepatocellular T. gondii cysts, necrotizing splenitis, pulmonary oedema with fibrin, histiocytosis and rare fibrin microthrombi, and acute renal tubular degeneration with proteinosis and pigmented casts suggestive of haemoglobinuria or myoglobinuria. Immunohistochemical labelling confirmed intralesional T. gondii cysts and molecular analyses identified T. cruzi genotype I and T. gondii. This is a unique case that, to the best of our knowledge, represents the first description of T. cruzi and T. gondii co-infection, as well as the first record of naturally occurring infection T. cruzi genotype I infection in macropodids. This case adds to the epidemiological knowledge on Chagas disease in the USA, particularly in Texas where there is a high prevalence of human and canine trypanosomiasis.
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PMID:Trypanosoma cruzi Genotype I and Toxoplasma gondii Co-infection in a Red-Necked Wallaby. 3295 48