ArticleParasitology research1991
Morphological investigations on the pathology of Dictyocaulus viviparus infections in cattle.
Article in Parasitology research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 22 citations in OpenAlex.
- Large lungworms (Nematoda: Dictyocaulidae) recovered from the European bison may represent a new nematode subspecies.International journal for parasitology. Parasites and wildlife · 2020Article
- Pathogenesis and pathology of bovine pneumonia.The Veterinary clinics of North America. Food animal practice · 2010Review
- Deep insights into Dictyocaulus viviparus transcriptomes provides unique prospects for new drug targets and disease intervention.Biotechnology advancesReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Morphological investigations of lungs obtained from cattle that had been experimentally infected with Dictyocaulus viviparus were carried out using a new fixation technique that excludes post-mortem changes in the samples. Light and electron microscopical investigation showed a substantial loss of ciliated epithelial cells in the bronchi, severely affecting the mucociliary clearance. Bronchiolitis, peribronchiolitis and cell-rich mucus caused bronchial atelectasis and consolidation of the related alveoli. Interlobular septa completely separated diseased from normal tissue. Clara cells contained abundant intraplasmatic glycogen. Alveolary walls were thickened and showed cellular infiltration, loss of functional epithelial cells and hyperplasia of alveolar type II cells. Increased connective tissue indicated an irreversible chronic decline in lung performance. Lung eosinophilia and the cytotoxic abilities of eosinophils are discussed as a cause of the changes in lung tissue after infection with D. viviparus.
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Registered trials
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