Ependymal tumors are reported rarely in domestic animals. The aims of this study were to examine the clinical and pathologic features of ventricular and extraventricular ependymomas and subependymomas in 18 domestic cats examined between 1978 and 2011. Parameters examined included age, sex, breed, clinical signs, and macroscopic and histopathologic features. The mean age of affected cats was 9 years, 4 months; median age, 8.5 years. There were 8 female and 4 male cats, and 6 cats for which sex was not recorded. Breeds included 10 domestic shorthaired, 2 domestic longhaired, 1 Persian, and 1 Siamese. Clinical signs included altered mentation or behavior, seizures, circling, propulsive gait, generalized discomfort, and loss of condition. The tumors often formed intraventricular masses and usually arose from the lining of the lateral or third ventricles, followed by the fourth ventricle, mesencephalic aqueduct, and spinal cord central canal. Three tumors were extraventricular, forming masses within the cerebrum and adjacent subarachnoid space. Histologically, 15 tumors were classified as variants of ependymomas (classic, papillary, tanycytic, or clear cell) and 3 as subependymomas. Tumors were generally well demarcated; however, 6 ependymomas focally or extensively infiltrated the adjacent neural parenchyma. Characteristic perivascular pseudorosettes were observed in all ependymomas; true rosettes were less common. Some tumors had areas of necrosis, mineralization, cholesterol clefts, and/or hemorrhage. This cohort study of feline ependymal tumors includes subependymoma and primary extraventricular ependymoma, variants not previously described in the veterinary literature but well recognized in humans.

Abstract. Canine vascular tumors (47 hemangiomas, 36 hemangiosarcomas) were investigated for the endothelial cell marker factor VIII-related antigen (F VIII RAg). The primary antibody was a commercial rabbit anti-human (r/h) F VIII RAg antiserum. All (100%) hemangiomas and 32 (89%) of 36 hemangiosarcomas stained for F VIII RAg. One hemangiosarcoma (3%) was negative, and three tumors (8%) were equivocal in staining. Rarely, the interpretation of stained immature endothelial cells was difficult. The r/h F VIII RAg antibody was a positive marker of normal, reactive, and neoplastic endothelial cells in the dog.

Abstract. Intoxication by pods of Prosopis juliflora (mesquite beans) causes an impairment of cranial nerve function in cattle and goats. In goats, vacuolation of neurons in the trigeminal motor nuclei has been reported. To study the lesions in cattle caused by consumption of P. juliflora pods and dry ground pods, eight 6-to 12-month-old male cattle were divided into 4 groups: group 1 was fed a ration containing 50% of pods; groups 2 and 3 received a ration containing 50 and 75% of dry ground pods, respectively; group 4 was the control. After 200 days, all cattle were killed and sampled for histologic evaluation. Samples of the trigeminal motor nucleus were examined by electron microscopy. All cattle from groups 1, 2, and 3 showed clinical signs resulting from impaired function of cranial nerves V, IX, X, and XII, starting 45-75 days after consumption of the plant. The main histologic lesions were vacuolation and loss of neurons in trigeminal motor nuclei and other motor cranial nerve nuclei with Wallerian-like degeneration in the cranial nerves. Mild denervation atrophy was observed in the masseter and other masticatory muscles. On electron microscopy, neurons of the trigeminal nuclei had markedly swollen mitochondria, with the mitochondrial cristae displaced peripherally, disoriented and disintegrating. Intoxication by P. juliflora seems to have a novel pathogenesis, characterized by a selective, primary, chronic, and progressive injury to mitochondria of neurons of the trigeminal and other cranial nerve nuclei. Cranial nerve degeneration and denervation atrophy of the muscles occurs as a consequence of the neuronal lesion.

Over the past 10 years, 10 cats with primary central nervous system infection by larvae of Cuterebra flies have been documented at Cornell University. Clinical abnormalities noted in all cats were progressive and most commonly consisted of depression (6/10), blindness (6/10), and behavior changes (2/10). Affected cats presented most commonly in July (2/10) and August (7/10); one cat was presented in September. The diverse histopathologic changes are unique to this aberrant migration and consist of a combination of five characteristic features: 1) parasitic track lesion (7/10), 2) superficial laminar cerebrocortical necrosis (10/10), 3) cerebral infarction (8/10), 4) subependymal rarefaction and astrogliosis with or without ependymal cell loss (7/10), and 5) subpial astrogliosis (7/10). Changes 2-5 occurred throughout the parenchyma unassociated with the track lesion or the parasite in the affected tissue. The larvae have been recovered most commonly in the region of the olfactory bulbs and peduncles, optic nerves, and cribriform plate, suggesting entry from the nasal cavity. Many of the changes noted are suggestive of a toxic factor elaborated by the parasite and borne within the cerebrospinal fluid, as well as vascular compromise as a component in those cats with brain infarction. Because of the prevalence of infarction associated with this syndrome and the lack of reported cases of such lesions in regions of the world devoid of the fly, we propose that aberrant cuterebral larval migration in the brain is the cause of feline ischemic encephalopathy.