Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038002 (splenomegaly)
 9,873 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At 15 days of age and in the presence of measurable levels of maternal antibody against infectious bursal disease virus serotype I (1:170 virus-neutralization geometric mean titer), a recent isolate (U-28) and a prototype virulent isolate (Edgar) of the same virus caused subclinical infections in commercial broiler chickens. Isolate U-28 caused a significant reduction in the size of the bursa of Fabricius, whereas the Edgar isolate produced splenomegaly. Both isolates reduced the serological response to Newcastle disease virus. The experimental immunosuppressive potential and pathogenicity of isolate U-28 in broiler chickens confirms the role of this virus in recent infectious bursal disease outbreaks.
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PMID:Immunosuppressive potential and pathogenicity of a recent isolate of infectious bursal disease virus in commercial broiler chickens. 255 4

Lead acetate was administered continuously in the drinking water to CD-1 male mice beginning at 4 weeks of age. An LD(10-20) of the lytic viruses or 300 plaque-forming units of RLV was inoculated intrapertioneally at 6 weeks of age. Lead increased the response of the mice to all classes of viruses against which it was tested: an RNA picornavirus-encephalomyocarditis (EMCV), a DNA herpesvirus-pseudoribies, an RNA leukemia-virus-Rauscher leukemia (RLV), an RNA arbovirus B-St. Louis encephalitis, and an RNA arbovirus A-western encephalitis. Most studies were performed between lead and EMCV. Increases in EMCV mortality in lead treated mice over controls ranged from 2x at a lead level of 0.004M to 7x (100% mortality) at a 0.1M lead level. Splenomegaly with spleens 800 to 1100 mg in weight containing high titers of RLV occurred in lead (0.03M)-treated mice 3 and 6 weeks after RLV inoculation; spleens or RLV controls were normal in weight (200 mg) and were free of virus. Lead did not reduce the protective effect of mouse interferon (IF) against the lethal action of EMCV, but it did repress the EMCV antiviral effect of poly I/poly C (PIC) and of Newcastle disease virus (NDV) against EMCV mortality. These data indicate several new facts concerning adverse effects lead may have on an animal: (1) lead aggravates viral disease, most likely in part, through reduced IF synthesis; (2) lead represses the anti-EMCV protective effects of both PIC and of NDV, which, in other reports, were shown to induce IF in radioresistant macrophages (PIC) or in radiosensitive lymphocytes (NDV); (3) lead may then be said to repress IF induction in two kinds of cells; (4) however, lead does not inhibit IF action.
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PMID:Lead aggravates viral disease and represses the antiviral activity of interferon inducers. 436 44

Three different mouse strains--BALB/c, C57BL/6J, and CBA/Ca--were compared for their production of viral interferon upon Newcastle disease virus (NDV) inoculation and of interferon gamma upon antigenic stimulation with PPD following BCG sensitization. BALB/c mice were found to be low producers for NDV-induced IFN-alpha, beta as well as for in vivo (serum) and in vitro (spleen cell culture) induced IFN-gamma. C57BL/6 mice were high producers under the three conditions tested and CBA/Ca mice, finally, were high IFN-alpha, beta and in vitro IFN-gamma producers, but low in vivo IFN-gamma producers. Development of splenomegaly following BCG inoculation was not directly related to IFN-gamma responsiveness.
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PMID:Strain variation in interferon gamma production of BCG-sensitized mice challenged with PPD. I. CBA/Ca mice are low producers in vivo, but high producers in vitro. 641 57

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Murine AIDS (MAIDS) is caused by a defective retrovirus present in the LP-BM5 murine leukemia virus mixture. Strains of inbred mice differ in resistance to MAIDS development; some are susceptible (e.g., C57BL/6), while others are resistant (e.g., CBA and B10.BR). As an early block to viral replication in resistant mice has been demonstrated previously by PCR studies, we postulated that alpha/beta interferons (IFN-alpha/beta) may be involved in resistance to MAIDS. Susceptible C57BL/6 mice infected with LP-BM5 were treated with IFN-alpha/beta or Newcastle disease virus. Newcastle disease virus induces high endogenous IFN-alpha/beta production in mice. Both treatments delayed the development of MAIDS, as assessed by splenomegaly and T- and B-cell proliferation. In addition, an IFN-alpha/beta response was detected by reverse transcription-PCR and dot blotting 3, 6, and 9 h after LP-BM5 infection in resistant mice but not in susceptible mice. These results suggest that the ability to produce IFN-alpha/beta in response to LP-BM5 infection may contribute to host resistance to MAIDS.
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PMID:Alpha/beta interferons increase host resistance to murine AIDS. 867 77

Thirty-nine 4- to 5-week-old broiler chickens from an outbreak of Newcastle disease (ND) in Japan were examined pathologically. The causative agent was identified as a mesogenic strain of ND virus. Predominant gross lesions included haemorrhage in the lungs, congestion of the trachea, splenomegaly, atrophy of the thymus and bursa of Fabricius, and whitish discolouration of the brain. Microscopically, there was mild haemorrhagic pneumonia, catarrhal tracheitis, lymphoid necrosis in the spleen, thymus, bursa of Fabricius and caecum and diffuse non-suppurative encephalitis. Lesions associated with encephalitis were characterized by multifocal perivascular cuffing, malacia, demyelination and proliferative vasculitis. Malacic lesions occurred in the hyperstriatum, neostriatum, subleptomeningeal and periventricular regions of the cerebrum, whereas demyelination was seen mainly in the brain stem. The morphological changes that occurred in the brain in these cases were distinctive and the lesions in the lymphoid tissues were related to concurrent infection with infectious bursal disease virus.
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PMID:Brain lesions in young broiler chickens naturally infected with a mesogenic strain of Newcastle disease virus. 1867 Nov 35