Congenital and acquired melanocytomas (benign melanomas) in eighteen young horses.

In a retrospective study, cutaneous melanocytic tumors from 18 horses, less than 2 years old, were examined histopathologically and clinical follow-up requested. Melanocytomas (benign melanomas) occurred in a variety of breeds and in horses of varied coat color. The age of the horses at the time of biopsy ranged from 3 weeks old to 2 years old. Four melanocytomas were congenital, 11 melanocytomas were acquired by 1 year of age, and three were acquired prior to 2 years of age. Of the 18 horses, five were male, and 13 were female. All tumors were solitary and located on the legs or trunk; none were in the perineal region. Ulceration of the overlying epidermis was common. Tumors were generally localized and were not encapsulated. The tumors had a variety of cell patterns ranging from sheets, to streams, or nests of melanocytes. Cellular morphologic findings also ranged from epithelioid, to a mixture of epithelioid and spindle cells or to a spindle pattern. The nuclei were large and euchromatic, especially in the epithelioid cells. Several tumors had moderate cellular pleomorphism and binucleate cells. Mitotic activity was generally low (less than 1/high-powered field), but was readily detected (1-2/high-powered field) in bleached sections of four cases. Melanin pigmentation varied from mild to heavy. Melanophages were admixed with the tumor cells or in the adjacent tissue. Follow-up information was obtained on 15/18 horses and revealed that 14/15 horses were free of recurrence following excision. One neoplasm, that was poorly demarcated and had a spindle cell pattern, was not completely resected and continued to grow. These melanocytic tumors in young horses are distinct from melanomas in aged horses in their location, epithelial involvement, and age of horses affected. The majority of these tumors appear to be benign and share features of melanocytic nevi of human beings.

Acute sarcocystosis-like disease in a dog.

Two of 8 littermate Rottweiler dogs developed persistent diarrhea at 6.5 weeks of age. Dog 1 was euthanatized at 14 weeks of age and had hepatitis characterized by necrosis and mixed leukocyte infiltrations in association with a previously unrecognized Sarcocystis-like protozoon. The organism was free in the hepatocyte cytoplasm without a parasitophorous vacuole, had divided by schizogony, and stained with anti-Sarcocystis serum, but did not stain with anti-Toxoplasma gondii or anti-Neospora caninum serum in an immunohistochemical test. Dog 2 was euthanatized at 10 weeks of age. This dog had large necrotic, hemorrhagic mesenteric lymph nodes. Numerous T gondii tachyzoites were observed in association with these lesions. The organism divided by endodyogeny and stained specifically with anti-T gondii serum.

Herpesvirus-like infection in black-footed penguins (Spheniscus demersus).

A herpesvirus-like infection is described in the black-footed penguin (Spheniscus demersus). Clinically, the infection was characterized by debilitation and respiratory distress. Histopathological lesions were confined to the respiratory tract and consisted of inflammation and syncytial cell formation with Type A intranuclear inclusions in sinuses, trachea, and mainstem bronchi. Electron microscopy demonstrated polyhedral viral particles 80-140 nm in size consistent with Herpetoviridae. The lesions resembled those seen in infectious laryngotracheitis.

Pathogenesis of Borna disease in rats: evidence that intra-axonal spread is the major route for virus dissemination and the determinant for disease incubation.

Borna disease virus is an uncharacterized agent that causes sporadic but fatal neurological disease in horses and sheep in Europe. Studies of the infection in rats have shown that the agent has a strict tropism for neural tissues, in which it persists indefinitely. Inoculated rats developed encephalitis after an incubation period of 17 to 90 days. This report shows that the incubation period is the time required for transport of the agent in dendritic-axonal processes from the site of inoculation to the hippocampus. The immune responses to the agent had no effect on replication or transport of the virus. The neural conduit to the brain was proven by intranasal inoculation of virus that resulted in rapid transport of the agent via olfactory nerves to the hippocampus and in development of disease in 20 days. Virus inoculation into the feet resulted in spread along nerve fibers from neuron to neuron. There was sequential replication in neurons of the dorsal root ganglia adjacent to the lumbar spinal cord, the gracilis nucleus in the medulla, and pyramidal cells in the cerebral cortex, followed by infection of the hippocampal neurons and onset of disease. This progression required 50 to 60 days. The exclusiveness of the neural conduit was proven by failure to cause infection after injection of the virus intravenously or into the feet of neurectomized rats.