In this study, we compared hepatic ultrastructure in healthy cats, in cats with severe hepatic lipidosis, and in cats with experimentally induced, chronic, extrahepatic bile duct occlusion. Ultrastructural features unique to the lipidosis syndrome included an apparent reduction in number of peroxisomes and alteration in their morphologic features. The quantity of endoplasmic reticulum, Golgi complexes, and lysosomes was subjectively reduced, and paucity of cytosolic glycogen was observed. Bile canaliculi appeared collapsed because of cytosolic distention with lipid. Mitochondria were reduced in number and were markedly pleomorphic. Cristae assumed a variety of shapes, lengths, and orientations. Ultrastructural features of bile duct occlusion were similar to those described in other species and differed from those in cats with hepatic lipidosis.

Ultrastructures of knobbed spermatozoa in a boar were observed. The knobs, found at the apex of the spermatozoa, were spherical swellings of the acrosome; vacuoles were found in the swellings. According to the contents, 2 types of the vacuoles were recognized: a vacuole containing cell debris that was surrounded by 2 or 3 layers of membranes, and a vacuole containing an amorphous material that was surrounded by a single membrane. Several vacuoles might be observed in a knob. Observations of both testes indicated that the cell debris in the vacuole of the knob was derived from the cytoplasm of the Sertoli cell, which evaginated into the spermatid. Origin of the amorphous material in the other type of knob is not known.