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)

Myositis and septicemia caused by Acinetobacter calcoaceticus were diagnosed in a mare. The infection was characterized clinically by ventral swelling and edema, diarrhea, listlessness, and rectal temperature of 39.4 C. The mare was treated symptomatically for 2 days but died on the 3rd day. Conditions seen at necropsy were myositis, enteritis, typhlitis, colitis, and hepatitis. Lymph nodes were moderately enlarged throughout the body. Gross lesions in musculature were edema, scarring, petechiae, and an occasional exxhymosis. The enteritis was catarrhal, with excessive mucus and moderate hyperemia. The typhlitis and colitis were hemorrhagic. The swollen liver had a diffuse mottled pale and red pattern. Microscopic lesions in skeletal muscle consisted of petechiation, necrosis, scarring, and edema. Cardiac muscle was also scarred and necrotic, but edema was not prominent. Periacinal necrosis was found in the liver. Acinetobacter calcoaceticus was isolated from myocardium and liver.
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PMID:Equine myositis and septicemia caused by Acinetobacter calcoaceticus infection. 62 Nov 83

The objective of this study was to characterize the hemostatic defect in dogs with infectious canine hepatitis (ICH), a naturally occurring viral disease of dogs. Five littermate dogs were inoculated with 10(3) TCID50 of ICH virus intravenously. Two littermates were controls. The clinicopathologic manifestations of ICH were fever, depression, anorexia, hematemesis, melena, widespread mucocutaneous petechiae, prolonged bleeding from venipunctures, faceial edema, leukopenia, and proteinuria. The hemostatic defect of ICH was characterized by thrombocytopenia, abnormal platelet function, prolonged one-stage prothrombin time and activated partial thromboplastin time, normal thrombin times, depressed factor VIII activity, and increased fibrin-fibrinogen degradation products. These findings suggested that the central pathologic mechanism of the abnormal hemostasis in ICH was disseminated intravascular coagulation (DIC). ICH is an example of DIC induced by viral infection. This disease is a suitable model for investigation of the detection, pathogenesis, and therapy of DIC.
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PMID:Infectious canine hepatitis: animal model for viral-induced disseminated intravascular coagulation. 124 23

A 7-year-old girl was admitted to our hospital because of fever and multiple petechiae following non-A non-B hepatitis. Peripheral blood on admission showed pancytopenia, and she was diagnosed to have hepatitis-associated severe aplastic anemia. She was treated with oxymetholone, prednisolone, 2 courses of bolus methylprednisolone, 2 courses of high dose gamma-globulin therapy and ALG (Pressimmun) without success. Nineteen months after diagnosis. ALG (Lymphoser) and bolus methylprednisolone followed by oxymetholone and prednisolone were tried. Hematologic conditions improved gradually, and have become normal except mild thrombocytopenia over a year. This case suggests that there is a difference in clinical efficacy between ALG preparations, and this observation gives the basis of repeating ALG therapy using a different preparation even if the preceding one has failed.
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PMID:[Successful treatment of a case of hepatitis-associated severe aplastic anemia by anti-lymphocyte globulin (ALG)]. 212 23

Richardson's ground squirrels were infected with 1500 or 9000 sporocysts of Sarcocystis campestris from badgers. No lesions were found in animals killed one to three days postinfection (pi). Hepatitis and phlebitis of hepatic veins were present in animals killed between four and eight days pi. No meronts were detected in these animals, but the lesions suggested that a generation of merogony occurred in the hepatic veins. Meronts were found in endothelial cells in many tissues beginning on day 9 pi. They were most numerous on day 10 pi, and less so on day 11, and subsequently. Meronts were most numerous in the lung; none was found in liver or spleen. Four of ten squirrels infected with 1500 sporocysts in one trial died between days 11 and 13 pi. There were petechial hemorrhages in skeletal muscle, lung, serosal membranes, and brain in these animals, with microscopic evidence of pulmonary, myocardial, and brain injury. One animal infected with 9000 sporocysts had petechiae in the liver at six days pi. Foci of inflammation were visible in the myocardium and brain of animals killed to 64 days pi. This species may serve as an experimental model for sarcocystosis in domestic animals.
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PMID:Pathology of Sarcocystis campestris infection in Richardson's ground squirrels (Spermophilus richardsoni). 641 6

Fatal hepatic sarcocystosis was diagnosed in 2 polar bears from a zoo in Anchorage, Alaska. Gross lesions were icterus and systemic petechiae. Marked microscopic lesions were detected only in the liver and included severe random necrotizing hepatitis with hemorrhage. Only asexual stages of an apicomplexan parasite were detected within hepatocytes, and rare extracellular zoites were seen in foci of necrosis. The parasite divided by endopolygeny, and occasionally merozoites formed rosettes around a central residual body. Ultrastructural features of the merozoites included a conoid and low numbers of micronemes at the apical pole, centrally located nuclei, and absence of rhoptries. The parasites failed to react with anti-Neospora sp., anti-Toxoplasma gondii, or anti-Sarcocystis neurona sera. The microscopic and ultrastructural morphology of the parasite are most compatible with an apicomplexan protozoan of the genus Sarcocystis. The life cycle of this parasite in bears is not known.
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PMID:Fatal hepatic sarcocystosis in two polar bears (Ursus maritimus). 919 39

Minocycline hydrochloride, a synthetic tetracycline, is a systemic antibiotic that has received much attention over the past several years. Currently, minocycline is considered the most widely prescribed oral antibiotic in the management of acne. Minocycline has been associated with autoimmune events, hepatitis, lupus-like syndromes, serum sickness, vasculitis, Sweet's syndrome, and hyperpigmentation. We report a case of a patient who developed drug-induced immune thrombocytopenic purpura (DITP) after taking minocycline. The initial clinical presentation of nonpalpable, discrete nonblanching petechiae and cayenne pepper-like macules on his lower legs was diagnosed as pigmented purpuric dermatosis (Schamberg's disease). We report the first case of DITP with the clinical picture of Schamberg's disease associated with minocycline therapy.
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PMID:Minocycline-induced immune thrombocytopenia presenting as Schamberg's disease. 1284 17

In Bucaramanga, Colombia, dengue haemorrhagic fever (DHF) has become endemo-epidemic since 1992. A cross-sectional study covering a period of 10 years (February, 1992 to February, 2002) was undertaken in children under 13 years of age hospitalized at the University Hospital. Observations were recorded on the clinical features, laboratory tests and the natural development of the disease. A total of 763 patients were examined, of whom 617 were classified as having DHF according to the WHO criteria (9.1% Grade I, 61.5% Grade II, 21.7% Grade III and 7.5% Grade IV). One hundred forty six patients could not be classified. The highest incidence took place in 1997, 1998 and 2001. Seventy four per cent of patients came from the metropolitan area of Bucaramanga; 48% were males; 0.3%, newborns; 11.8%, infants; 23%, pre-school children, and 64.9%, school children. The most important clinical features were fever and haemorrhagic manifestations (100%); vomiting (60%); abdominal pain (57%); headache (50%); osteomyalgia (40.8%); hepatomegaly (33%), and macular rash (29%). Among the haemorrhagic manifestations we found petechiae (56%); positive tourniquet test (35%); gastrointestinal bleeding (34%), and epistaxis (32%). Serous effusion was found in 17.7% of cases. Alarm signs of shock were found in 29%. Fifty two per cent had leucopenia and 37.3% atypic lymphocytes. Among other unusual manifestations were hepatitis, encephalopathy, alithiasic cholecystitis, acute renal failure, haemophagocytic syndrome and coinfections. Of the 617 cases, 12 died (1.5%).
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PMID:[Dengue haemorrhagic fever in children: ten years of clinical experience]. 1287 57

Antigenic mimicry has been proposed as a major mechanism by which viruses could trigger the development of immune thrombocytopenic purpura (ITP). However, because antigenic mimicry implies epitope similarities between viral and self antigens, it is difficult to understand how widely different viruses can be involved by this sole mechanism in the pathogenesis of ITP. Here, we report that in mice treated with antiplatelet antibodies at a dose insufficient to induce clinical disease by themselves, infection with lactate dehydrogenase-elevating virus (LDV) was followed by severe thrombocytopenia and by the appearance of petechiae similar to those observed in patients with ITP. A similar exacerbation of antiplatelet-mediated thrombocytopenia was induced by mouse hepatitis virus. This enhancement of antiplatelet antibody pathogenicity by LDV was not observed with F(ab')2 fragments, suggesting that phagocytosis was involved in platelet destruction. Treatment of mice with clodronate-containing liposomes and with total immunoglobulin G (IgG) indicated that platelets were cleared by macrophages. The increase of thrombocytopenia triggered by LDV after administration of antiplatelet antibodies was largely suppressed in animals deficient for gamma-interferon receptor. Together, these results suggest that viruses may exacerbate autoantibody-mediated ITP by activating macrophages through gamma-interferon production, a mechanism that may account for the pathogenic similarities of multiple infectious agents.
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PMID:Exacerbation of autoantibody-mediated thrombocytopenic purpura by infection with mouse viruses. 1520 64

Four female and 3 male Taita falcons (Falco fasciinucha) out of a breeding colony of 14 Taita falcons (7 pairs) died during the breeding season after showing lethargy and anorexia for 1 to 2 days. All animals were submitted for necropsy. Gross lesions in the female falcons were characterized by anemia secondary to marked hemorrhage into the ovary and oviduct, serofibrinous effusion into the cardioabdominal cavity and serosal petechiae. In addition, marked necrotizing splenitis and pulmonary hemorrhage were present. Histologically, the female falcons had mild necrotizing hepatitis with numerous intranuclear inclusion bodies and necrotizing splenitis with rare inclusion bodies. There were no gross lesions in the male falcons, and the histological lesions were characterized by urate deposition and rare intranuclear inclusion bodies in the renal tubular epithelial cells. Adenoviral particles were found by electron microscopy in the cloacal contents of the female Taita falcons but not in the male falcons. DNA in situ hybridization revealed widespread aviadenoviral nucleic acid within the nuclei of hepatocytes, renal tubular epithelial cells, and adrenal cells in the female falcons but no aviadenoviral nucleic acid in 1 male falcon and only a low quantity of adenoviral nucleic acid in the liver and kidney of another male Taita falcon. PCR amplified aviadenoviral DNA in the liver and intestine of all Taita falcons. The amplicons were sequenced, and the virus was identified as falcon adenovirus. The deaths of the female and male birds were attributed to the aviadenovirus infection.
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PMID:Falcon adenovirus infection in breeding Taita falcons (Falco fasciinucha). 1678 19

Here we report a familial cluster of 3 cases of coxsackievirus B3 infection: a recent history of illness in a woman's 3-year-old son with a coxsackievirus B3-positive stool culture indicated that he probably infected his mother at home during her last week of pregnancy. Consequently, she delivered an infected neonate who developed severe hepatitis, disseminated intravascular coagulation, and bilateral intracranial hemorrhage. The neonate remained well for the first 2 days of life. On the third day, he developed fever (39 degrees C) and poor peripheral circulation. On the fourth day, he developed petechiae and bruises over his chest wall and extremities, and prolonged bleeding was observed over venipuncture sites. Investigations revealed severe thrombocytopenia (platelets: 41 x 10(9)/L) and a markedly deranged coagulation profile (prothrombin time: 19 seconds [reference: < 10 seconds]; activated partial thromboplastin time: > 120 seconds [reference: 24.2-37.0 seconds], serum D-dimers: 6722 ng/mL [reference: < 500 ng/mL]), suggestive of disseminated intravascular coagulopathy. Clinical examination revealed yellow sclera, hepatomegaly (5 cm), and splenomegaly (2 cm), consistent with hepatitis. Serial chest radiographs showed bilateral pleural effusions, and an ultrasound of the abdomen demonstrated ascites. An echocardiogram showed normal cardiac structure and good contractility of both ventricles. However, a cranial ultrasound revealed bilateral grade 2 intraventricular hemorrhages. Serum C-reactive protein increased to 33.9 mg/L. Liver-function tests were also markedly deranged at this time, with maximum values for serum alanine transferase, bilirubin, alkaline phosphatase, and ammonia concentration of 1354 IU/L, 258 micromol/L, 189 IU/L, and 147 micromol/L, respectively. Serum glucose levels were normal. Over the next 3 days, his fever subsided, and his liver function and clotting profile normalized by day 13 after onset of illness. A stool sample from the older brother, collected 14 days after his onset of illness at home, was positive for coxsackievirus B3 by both virus culture and enterovirus reverse-transcription polymerase chain reaction. He had neutralizing coxsackievirus B3 antibody titers of 1:2560 and 1:1280 on days 14 and 28 after his onset of illness, respectively. No virus was cultured from the mother's stool sample, collected 5 days after her onset of illness, but the enterovirus polymerase chain reaction was positive and maternal sera neutralized the coxsackievirus B3 isolated from the neonate. The maternal sera also showed a more than fourfold rise in antibody titer from 1:80 to 1:640 on days 5 and 16 after her onset of illness, respectively. Neonatal antibody titers also showed a more than fourfold rise from < 1:80 to 1:2560 on days 1 and 21 after his onset of illness, respectively. This demonstrates that both the mother and the neonate had had recent coxsackievirus B3 infections. Serially collected neonatal throat swab and stool samples were culture negative for enterovirus by 4 and 8 days after his onset of illness, respectively. However, enterovirus RNA remained detectable by reverse-transcription polymerase chain reaction in these samples for considerably longer, only becoming undetectable by 16, 23, and 41 days after his onset of illness. We show that even mild household infections may have potentially serious consequences for pregnant women and their infants.
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PMID:Probable intrafamilial transmission of coxsackievirus b3 with vertical transmission, severe early-onset neonatal hepatitis, and prolonged viral RNA shedding. 1690 22


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