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Ultrastructural studies were carried out on liver obtained after the appear- ance of clinical signs of bunostomosis from a group of experimentally infested lambs. In the hepatocytes of the liver severe changes affecting the endoplasmic reticulum, especially the rough one, and the nucleic chromatin were determined. The formation of lipid drops into the injured hepatocytes followed the way of a fat degeneration rather than of a lipid infiltration. Both the liver parenchyma and mesenchyma compounds were affected. This is an evidence of a direct toxic pathogenic action of the etiology agent. These data add to the knowledge of the bunostomosis pathogenesis more information about the leading role of the toxic factor.

The authors have followed up experimentally the migration of the larvae of Bunostomum trigonocephalum through uninjured skin of an ovine host.  Studies were conducted on the duration of the prepatent and patent period of B. trigonocephalum infection. The larvae are comparatively quick in penetrating the uninjured skin of the host. Five minutes after their infestation they were present under the epidermis and caused significant traumatic changes in the skin. Ten minutes later the larvae were present in the derma layer. After two days the larvae were situated in the host lungs and caused damage of the alveoli. The mature stages of B. trigonocephalum are localized primarily in the jejunum, where nematodes attach themselves to the intestinal mucosa and damage it during blood feeding.

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