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)

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

The bovine immunodeficiency virus (BIV)/New Zealand (Oryctolagus cuniculus) rabbit model was used to study events that underlie the early and chronic stages of viral replication, routes and time course of viral dissemination and the distribution of the virus in the lymphoid. nonlymphoid and mucosa associated tissues. The results indicated that BIV, a lentivirus with genetic relatedness to the HIV, induced changes of clinical (anorexia, weight loss, muscular wasting, diarrhea, hypoalgesia, torticollis), immunological (recurrent T- and B-cell dysfunctions) and histopathological (lymphadenopathy, splenomegaly) nature that closely parallels those described for cat (Fly), monkey (SIV) and human (HIV) lentiviral diseases. These findings showing that BIV induces both splenomegaly and lymphadenopathy syndromes with associated fatal immune dysfunctions and the ability of the virus to replicate productively at the mucosal surfaces in rabbits, emphasize the importance of the BIV/rabbit system as a good small-animal model for the study of retrovirus-induced AIDS and offers the opportunity to evaluate prophylactic and therapeutic anti-retroviral agents of relevance to HIV-1 as well as the opportunity to study mechanisms of drug resistance phenomena.
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PMID:Bovine immunodeficiency virus in experimentally infected rabbit: tropism for lymphoid and nonlymphoid tissues. 1113 Oct 38

SummaryThe present report describes an outbreak of Pullorum disease in a young layer parent stock in Austria. The flock, which comprised 14,220 Lohmann brown layer chickens, experienced high mortality from the first week of life reaching a total of 1,905 chickens in the fifth week, when the flock was depopulated. Clinical signs included uneven size of the chicks, pasty vents, apathy, diminished water and feed intake, with some birds presenting central nervous system signs such as tremors and torticollis. The post-mortem investigation of 43 birds, ages one to four weeks, revealed retained yolk sacs filled with caseous exudate, purulent airsacculitis, hepatitis with whitish pinpoint coalescing necrotic foci, splenitis with splenomegaly, hemorrhagic-mucoid enteritis in the small intestine, fibrinous typhlitis, nephromegaly and urate deposits in the ureters and cloaca. Inflammation and/or necrosis were identified in liver, spleen, kidney, small intestine and heart by histopathology. However, no histopathological lesions were observed in the brain. Salmonella spp. were isolated from heart, liver, spleen and brain in pure culture. Group specific serotyping determined the presence of group D, with serovar S. Gallinarum being confirmed based on the Kauffmann-White Scheme. A duplex PCR further identified S. Pullorum as the responsible agent for the outbreak. Subsequently, the grandparent flocks, from which the affected flock originated, were tested and found to be negative for S. Pullorum, with no other progenies from the same GPs developing disease. Although the source of the pathogen could not be identified, such findings highlight the importance of "old" pathogens such as S. Pullorum causing sudden high mortality in chicks, even in a highly controlled environment.
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PMID:An outbreak of Pullorum disease in a young layer parent flock in Austria presented with central nervous system signs. 3327 57