History

A twenty-two year old female sea lion was housed in a mixed exhibit with several other sea lions arid harbor seals. She was euthanized after a two-year history of vague neurologic signs. Initial signs occurred in November, 1992, and included swimming in circles to the left, depression and apparent loss of vision. The circling was frequent initially, but became more sporadic, and lasted for one week. By early December, the sea lion seemed to have regained some vision and was no longer circling or depressed. The trainers felt the sea lion remained weak on her right side, and used her right front flipper weakly to move on land or in the water. Other than the right-sided weakness and poor vision, the sea lion had no further clinical problems until June, 1994, when it was noticed that the left pupil was dilated. The trainers felt she may have had limited vision in the right eye. During this time her appetite had been normal, and she was cognizant of her surroundings. She ate well, but only when fish was thrown in the water just in front of her as she swam in small circles to the left. In December, 1994, the sea lion became inactive, and at times seemed unaware of her surroundings. Her appetite was depressed, and she would float most of the day around the exhibit, occasionally bumping into walls. These signs progressed, and she was euthanized at the end of December.

Gross lesions

When the brain was removed during the post mortem examination, approximately 50 cc of clear fluid was released from tile right and left lateral ventricles. The lungs were atalectic and fibrotic, and there were numerous pax lesions on the face and neck of the sea lion. examination of the brain after formalin fixation revealed moderate-to dilatation of the left lateral ventricle, with less prominent dilatation of the right lateral ventricle. The intertalallic adhesion was effaced by a finely nodular, pale grey-white mass approximately 2.0 cm in diameter. Similar finely nodular masses, 3.0-10.0 mm diameter, were present in the ependymal lining of the lateral ventricles, and extended into the adjacent white matter. There was mild compression of the cerebral cortex, with atrophy of the gray matter and narrowing of the cortical sulci.

Histopathology

The masses seen grossly consisted of densely cellular aggregates of pleomorphic individualized cells. Cells had scant, granular-to-foamy eosinophilic cytoplasm. Nuclei had clumped to reticular chromatin, with indistinct nucleoli, and ranged from 5-25 microns in greatest dimension. Many areas contained prominent gliosis, fibrosis and vascular proliferation, as well as foci of acute necrosis. Adjacent neuropil frequently contained nests and perivascular cuffs of small lymphocytes. Special stains for fungi (P.A.S.), bacteria (Brown and Brenn), and protozoa (Giemsa) failed to reveal an etiologic agent. Immuno-histochernical staining of formalin-fixed tissue for cytokeratins, neuron specific enolase, myelin basic protein, glial fibrillary acidic protein, pan-T cell marker (CD3), and histiocyte markers (3ClO) stained normal cell types adjacent to the mass, hut failed to stain the tumor cells themselves. Additionally, there was mild, chronic interstitial pneumonia, marked splenic hemosiderosis, and focally extensive hyperkeratotic dermatitis. Based on the cellular morphology and immuno-histochemical staining results, and undifferentiated sarcoma, possibly of macrophage origin, was diagnosed. This tumor apparently occluded the interventricular foramina and mesencephalic aqueduct, resulting in bilateral hydrocephalus.