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 unusual features in a 46 year old white woman with mucosal eosinophilic gastroenteritis are described. In addition to involvement of the gastrointestinal tract, she had eosinophilic splenitis and hepatitis. She responded to corticosteroid therapy, but not to an elimination diet or to cromolyn sodium therapy. The possible role of various factors chemotactic for eosinophilia in the patient are reviewed, and the place of the disorder among the hypereosinophilic syndromes is discussed.
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PMID:Mucosal eosinophilic gastroenteritis with systemic involvement. 40 70

Pseudotuberculosis caused by Yersinia enterocolitica was observed as an enzootic disease of the owl monkey (Aotus trivirgatus). A description is given of the natural disease and its successful reproduction in owl monkeys. The disease was characterized by purulent and necrotizing enteritis, hepatitis, and splenitis. Large colonies of the causative organism were consistently associated with the lesions. Although pseudotuberculosis has been reported in other monkeys, the disease in the authors' primate colonies has been restricted to the owl monkey.
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PMID:Pseudotuberculosis (Yersinia enterocolitica) in the owl monkey (Aotus trivirgatus). 82 25

Guinea pigs inoculated with the live M-44 vaccine strain of Coxiella burnetii were examined grossly and microscopically for the presence of Q fever-related lesions. Mild myocarditis was observed in 38% of the infected animals but in none of the control animals. Livers showed significant incidence of hepatitis, necrosis, and granuloma formation, especially during the first eight days of the infection. A much lower incidence of splenitis was also found but was considered to be of borderline significance. Generally, lesions were mild in nature, and none seemed to endanger the life of the animal or to cause observable distress.
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PMID:Lesions in guinea pigs infected with Coxiella burnetii strain M-44. 86 92

Pathogenesis of tularemia in nonimmune rats given (intraperitoneal inoculation) virulent strain (SCHU S4) or vaccinal strain (LVS) of Francisella tularensis and in immune rats given SCHU S4 is described. Both LVS and SCHU S4 caused pyogranulomas in liver and spleen of nonimmune rats. Nonimmune rats given 10(4) SCHU S4 organisms did not survive beyond 72 hours, but immune rats given challenge inoculum of 10(8) SCHU S4 organisms developed lesions and survived. Larger doses of LVS resulted in earlier onset of characteristic hepatitis and splenitis in nonimmune rats. Periportal lymphocytic infiltrates were present in the liver 48 hours after SCHU S4 challenge inoculation of immune rats and 96 hours after inoculation of LVS in nonimmune rats and were associated with intense macrophage aggregation. These changes indicate that the pathogenesis of tularemia is a result of the interdependency of the dose and virulence of the causative agent with the immune status of the host and that cellular immunity has a significant role in the response of the rat to tularemia.
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PMID:Pathogenesis of tularemia in immune and nonimmune rats. 119 May 92

The fetoplacental units and the postgravid uterus of BALB/cJ (H-2d) mice inoculated intraperitoneally with Coxiella burnetii (Nine Mile isolate, phase I) on day 6 of pregnancy were examined histologically and immunocytochemically at 1 to 160 days postinoculation. Clinically, abortions, stillbirths, and perinatal deaths were observed. Histological lesions in the placenta were characterized by severe necrosis of the decidua basalis and the labyrinth, fibrinoid degeneration of decidual vessels, and microthrombosis. Pyometra and endometritis at the sites of previous placental attachment, characterized by ulceration, central necrosis, and moderate cellular infiltration consisting of neutrophils and macrophages, were observed postpartum. Pups sacrificed at the age of 9 days exhibited interstitial pneumonia with few granulomas and granulomatous hepatitis and splenitis. Immunocytochemically, antigen-bearing cells were first detected in the decidua 9 days postconception, and single immunopositive cells were detected in the fetal placenta 4 days later. Thereafter, until abortion or parturition, abundant accumulation of C. burnetii antigen was observed in the maternal and fetal compartments of the placenta. Up to 28 days postinoculation, many immunopositive cells were demonstrated at the sites of previous placental attachment, whereas the adjacent endometrium contained only a few antigen-positive cells. C. burnetii antigen was demonstrated in decidual cells, trophoblasts, and macrophages and extracellularly within the sinuses of the labyrinth and in the uterine lumen but not in granulated metrial gland cells. Fetuses in utero and aborted, stillborn, or perinatally dying offspring were immunocytochemically negative for C. burnetii antigen; however, pups killed 9 days after birth showed lesion-associated positive immunoreaction in the lung, liver, and spleen. The present study shows that infection with C. burnetii during pregnancy results in uncontrolled growth of the organism in the murine uteroplacental unit and that associated lesions are characterized by necrosis of placental tissues, fibrinoid degeneration of decidual vessels, and microthrombosis.
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PMID:Histological and immunocytochemical characterization of Coxiella burnetii-associated lesions in the murine uterus and placenta. 145 56

Cholangiohepatitis was diagnosed in a dog with a 4-day history of anorexia, vomiting, fever, and icterus. Additional findings included signs of depression, dehydration, hepatosplenomegaly, and abdominal discomfort. Exploratory laparotomy was performed, and specimens of liver, spleen, and bile were obtained. Histologic evaluation of liver and spleen revealed acute, suppurative cholangio-hepatitis and splenitis, respectively. Cultures of liver and bile yielded Klebsiella sp. The dog responded to rehydration and intravenous administration of chloramphenicol. Although uncommon, cholangiohepatitis should be suspected in dogs with anorexia, fever, vomiting, icterus, and signs of abdominal discomfort. Definitive diagnosis requires bacterial cultures of liver and bile. Administration of an appropriate antibiotic should resolve clinical signs.
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PMID:Cholangiohepatitis in a dog. 162 52

Three cases of atypical, clinically unsuspected cat-scratch disease (CSD), diagnosed by demonstration of the CSD bacillus in an abdominal visceral organ, are presented. In two cases CSD bacilli were demonstrated for the first time in splenic granulomas in a child and in an adult with acquired immunodeficiency syndrome (AIDS)-related complex. In both cases, there was granulomatous hepatitis as well as splenitis. In the third case, the CSD bacillus was present in hepatic granulomas in an adult with granulomatous hepatitis. In all cases, granulomatous inflammation with suppuration in the viscera was identical to that previously described for lymph nodes in CSD. All patients eventually recovered completely. Clinical awareness of the broad spectrum of CSD should avoid the cost and morbidity of prolonged hospitalization, medications, and invasive surgery for a disease that is self-limited and not clearly responsive to antibiotics and that can usually be diagnosed by noninvasive means.
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PMID:Cat-scratch disease presenting as abdominal visceral granulomas. 168 2

Previously bis(5-amidino-2-benzimidazolyl)methane (BABIM) was identified as a strong inhibitor of the multisystem inflammatory disease induced in Lewis rats by injection of streptococcus group A cell wall-derived peptidoglycan polysaccharide (PG-APS). A BABIM derivative, trans-bis(5-amidino-2-benzimidazolyl)ethene (BBE), has attracted attention because of striking qualitative and quantitative differences in its activities when compared with the parent compound. BBE could control destructive tibial osteitis and necrotizing granulomatous splenitis and hepatitis, regardless if given in a preventive or curative mode. The compound had little effect on synovitis, however. BABIM, on the other hand, was active against synovitis and osteitis, but not against splenic granuloma formation. To be effective, it needed to be applied in a preventive mode. BBE caused a characteristic enlargement of PG-APS-laden splenic and hepatic macrophages suggesting that those cells represent targets of the inhibitor. BBE may be a powerful tool for the study of granulomatous lesions.
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PMID:Streptococcal cell wall-induced systemic disease. Beneficial effects of trans-bis(5-amidino-2-benzimidazolyl)ethene, a novel, macrophage-directed anti-inflammatory agent. 192 7

Bobwhite quails (Colinus virginianus) were inoculated with 10(6) mean tissue-culture infective dose of quail bronchitis virus at 1, 3, 6, or 9 weeks of age by intratracheal, intraperitoneal, or subcutaneous routes. Quails developed necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia; multifocal necrotizing hepatitis; necrotizing splenitis, with or without hyperplasia of splenic mononuclear phagocytes; bursal lymphoid necrosis; and bursal atrophy. Lesions were more extensive and severe in quails inoculated at 1 or 3 weeks of age than in older quails. Large intranuclear inclusions, characteristic of adenovirus infection, were identified in trachea, lung, liver, and bursa of Fabricius. This is the first report of the histopathology of experimentally induced quail bronchitis.
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PMID:Pathology of experimentally induced quail bronchitis. 215 96

An adenovirus (isolate 1452) associated with inclusion body hepatitis of bobwhite quails (Colinus virginianus) was characterized as a group I, serotype 1 avian adenovirus and was indistinguishable from quail bronchitis virus. Bobwhite quails were inoculated via the intratracheal or intraperitoneal route with 10(6) mean tissue-culture infective dose of isolate 1452 at 1, 3, 6, or 9 weeks of age. Lesions produced by either route of inoculation were similar to those of quail bronchitis and included necrotizing tracheitis, proliferative and necrotizing bronchitis and pneumonia, and multifocal necrotizing hepatitis, necrotizing splenitis with or without hyperplasia of splenic macrophages, and lymphoid necrosis and atrophy of the bursa of Fabricius. Basophilic intranuclear viral inclusions were present in respiratory mucosal epithelium, hepatocytes and occasionally bile duct epithelium, and the mucosal epithelium overlying follicles of the bursa. Results indicate that isolate 1452 is a field isolate of quail bronchitis virus and that inclusion body hepatitis of bobwhite quails is a manifestation of quail bronchitis.
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PMID:Further characterization of an avian adenovirus associated with inclusion body hepatitis in bobwhite quails. 217 32


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