Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a retrospective study, a negative-sense digoxigenin-labeled RNA probe, corresponding to the gene encoding nonstructural protein-1 of African horse sickness virus (AHSV) serotype 4, was applied to formalin-fixed, paraffin-embedded tissue taken from horses in the terminal stages of infection with AHSV. Fifteen infected ponies and one noninfected control were studied. Ponies exhibited a range of clinical signs and lesions. Thirteen ponies were infected with serotype 4, one with serotype 1, and one with serotype 2. Ponies were monitored clinically and euthanatized when severely clinically ill. The following tissues were available for study by in situ hybridization and histopathology: lung, heart, spleen, neck muscle, and supraorbital fat. Histologically, the most striking changes were pulmonary edema and, in some, acute myocardial necrosis. In situ hybridization revealed virus distributed widely in sections of lung and heart examined, with relatively less in spleen, neck muscle, or supraorbital fat. Virus was localized to target cells with morphologic features compatible with endothelium in all organs except spleen, where it was found in both endotheliumlike cells and large mononuclear cells.
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PMID:Presence of African horse sickness virus in equine tissues, as determined by in situ hybridization. 786 85

African horse sickness (AHS) is a disease of equids, characterized by severe pulmonary oedema and caused by an orbivirus. To determine the role of pulmonary intravascular macrophages (PIMs) in the development of pulmonary microvascular changes in this disease, five horses were given an intravenous inoculation of 10(6)TCID50of serotype 4 of AHS virus. Viral replication was detected in endothelial cells, PIMs, interstitial macrophages and fibroblasts. Alveolar and interstitial oedema, and changes in pulmonary microvasculature, consisting mainly of the sequestration of neutrophils and the formation of platelet aggregates and fibrinous microthrombi, were related to endothelial changes and to a high degree of PIM activation. This suggested that the PIMs, once activated, contributed to these vascular changes by releasing chemical inflammatory mediators.
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PMID:The role of pulmonary intravascular macrophages in the pathogenesis of African horse sickness. 1037 91

Sheep inoculated with a virulent South African strain of bluetongue (BT) virus serotype 4 developed severe clinical signs and lesions characteristic of fulminant BT, including coronitis, hemorrhage and ulceration of the mucosal lining of the oral cavity and forestomaches, hemorrhage in the wall of the pulmonary artery, and focally extensive necrosis of skeletal muscle, especially of the neck. At necropsy, up to 14 days after infection, the infected sheep exhibited striking pulmonary edema, edema of the subcutaneous tissues and fascial planes of the head and neck, and pleural and pericardial effusion of varying severity. A reliable model for experimental reproduction of fulminant BT in sheep will facilitate future studies to better characterize the pathogenesis of this disease, particularly as it regards the mechanisms responsible for the increased vascular permeability that characterizes BT and related orbiviral diseases such as African horse sickness.
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PMID:Experimental reproduction of severe bluetongue in sheep. 1848 87