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Biomedical subjects

L Karstad

Publications and source records attributed to L Karstad.

At least 55 records · Page 3Linked to original sources

Ultrastructural characterization of genome of epizootic hemorrhagic disease virus.

Purified epizootic hemorrhagic disease (EHD) virus preparations were treated with urea and sodium perchlorate. The viral ribonucleic acid (RNA) released when spread on protein monolayers according to the Kleinschmidt technique was examined by rotary shadow-casting electron microscopy. The viral RNA released by urea treatment had filaments which frequently formed three to five loop-shaped figures of varied length. In 80% of the virus particles the lengths of the viral RNA released were 2.5 to 4.5 mum. The sodium perchlorate-released viral nucleic acid also appeared linear, and about 70% had lengths of 0.1 to 2.0 mum, the longest filament measuring 5.8 mum. Evidence was obtained that EHD virus contains double-stranded RNA as its genetic material and the molecular weight of the EHD viral RNA was calculated to be 12.2 x to 10(6) to 15.1 x 10(6) daltons.

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The pathogenesis of epizootic hemorrhagic disease of deer: an electron microscopic study.

Ultrastructural studies on capillaries and arterioles from tongue and heart tissues of 3 deer and from a portion of the cerebral hemisphere of a deer experimentally infected with epizootic hemorrhagic disease (EHD) virus revealed striking changes in the vascular endothelial cells. These changes included the focal development of moderately electron-dense materials (viral matrices), aggregations of virus particles and tubules in the cytoplasm. In addition, enlargement of endothelial cells and degenerative changes in some of the endothelial cells were frequently observed. The lumens of affected capillaries and arterioles were often noted to be occluded by fluffy, moderately electron-dense substances or by aggregates of highly electron-dense fibrin which appeared to be adherent to the surface of endothelial plasma membrane. Platelets were frequently present in the capillaries, intermingled with fibrin materials, and appeared either intact or partially or completely degranulated. These observations suggest that viral injury to endothelial cells resulting from EHD virus replication may initiate intravascular thrombosis, and that the hemorrhagic lesion is a manifestation of virus-cell interaction.

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Pasteurella anatipestifer as a cause of mortality in captive wild waterfowl.

An outbreak of Pasteurella anatipestifer infection in young wild waterfowl at the Niska Waterfowl Research Center resulted in losses of approximately 100 Blue and Snow Geese, one White-fronted Goose, five Mandarin Ducks, one Black Duck and one Wood Duck. Clinical signs included diarrhea, paralysis and tremors. Gross lesions were fibrin deposits on serosal surfaces, hemorrhages on the epicardium, consolidation of the lungs, cloudy or flaky deposits on the air sacs, and dark, swollen spleens. Microscopic lesions included fibrinous meningitis, pneumonitis, air saculitis and serositis. Swollen leg and foot joints were seen in some cases. Chloramphenicol treatment seemed to be of benefit in controlling the outbreak.

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