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Abstract. Thousands of harbor seals (Phoca vitulina) died in European seas during 1988. Respiratory distress and oculonasal discharge were common clinical signs. We necropsied 76 affected seals. The main necropsy finding was severe pneumonia. Microscopic lung changes were characterized by proliferation of type I1 pneumocytes, filling of alveolar lumina with serofibrinous exudate, leukocytes, and macrophages, and necrosis of bronchial and bronchiolar epithelium. Intracytoplasmic and intranuclear acidophilic inclusion bodies characteristic of morbillivirus infection were seen in bronchial and bronchiolar epithelial cells. Microscopic lesions of non-suppurative demyelinating encephalitis were seen in the brain. There was degeneration and necrosis of neurons, focal gliosis, perivascular cuffing, and patchy demyelination. Many neurons and astrocytes contained intracytoplasmic and intranuclear inclusions. Using an immunoperoxidase technique, we detected morbillivirus antigen in many tissues including lung, brain, spleen, and urinary bladder. The origin of the seal morbillivirus is unknown.A major disease epizootic killed thousands of harbor seals (Phoca vitulina) in European seas during 1988.The first signs were abortion and death in seals along the western coast of Denmark in April 1988. By late June the disease had spread to the coasts of The Netherlands and southern Norway. The most consistent pathologic finding in affected animals was acute pneumonia. A herpesvirus and a picornavirus were initially implicated as primary causes of the disease.*' Subsequently, it was shown that the epizootic was unrelated to these viruses, but serologic examination of convalescent seals indicated rising antibody titers to canine distemper or a closely related morbillivirus.22 In August 1988 seals in the Irish Sea became affected. We found lesions similar to canine distemper in many of these animals." The purpose of this report is to document histopathologic and immunocytochemical changes in affected seals. Materials and MethodsMeasles antiserum from a human with subacute sclerosing panencephalitis was used as primary antibody. Biotinylated goat anti-human immunoglobulin-G (IgG) (Bethesda Research Laboratories, Inc., Gaithersburg, MD) was used as second layer antibody. The other reagents used in this technique were part of a commercially available SAB kit (Histostain-SPO Kit, Zymed Laboratories, Inc., South San Francisco, CA). Reagents included in this kit were normal goat serum and streptavidin-peroxidase conjugate. All steps, unless indicated otherwise, were done at room temperature in a dark humidified chamber. Fresh Tris-saline buffer, pH 7.6, was used for each washing step.Sections were cut at 5 Fm and placed on clean glass slides coated with 3-aminopropyltriethoxysilane as a section adhesive, deparaffinized in xylene, and placed in alcohol. Endogenous peroxidase was inhibited by transferring sections to a freshly prepared solution of 0.5% hydrogen peroxide in methanol for 30 min. After washing in tap water, sections were placed...
Abstract. During 1988 thousands of harbor seals (Phoca vitulina) died in European seas as a result of morbillivirus infection. Six harbor porpoises (Phocoena phocoena) found stranded on the coast of Northern Ireland in late 1988 were submitted to our laboratory for necropsy. Pneumonia was the main necropsy finding in three of these animals. Microscopic lung lesions characterized by necrosis of bronchial and bronchiolar epithelium and infiltration of alveoli with leukocytes, lymphoid cells, macrophages, and multinucleate syncytia were seen in all six porpoises. Cytoplasmic and nuclear acidophilic inclusions characteristic of morbillivirus infection were common in bronchial and bronchiolar epithelial cells and in alveolar macrophages and syncytia. Brain alterations included degeneration and necrosis of neurons, microglial infiltration, and perivascular cuffing. There were cytoplasmic and nuclear acidophilic inclusions in many neurons. Immunoperoxidase staining of morbillivirus antigen was seen in many tissues including lung, brain, spleen, and urinary bladder. Alterations in our porpoises were similar to those seen in distemper in seals and many species of terrestrial mammals. Systemic viral disease has not previously been documented in Cetacea.
Abstract. Twenty pigs were fed a diet containing 187.5 mg kg-' of 3-nitro-4-hydroxyphenylarsonic acid (3-nitro). Ten pigs were euthanized at intervals up to 29 days, 3-nitro was withdrawn from the diet ofthe remaining pigs on day 30, and these animals were subsequently euthanized at intervals up to 49 days after commencement of the experiment. A nervous syndrome characterized by clonic convulsive episodes inducible by exercise, developed at day 11. Paraparesis was apparent at day 22 progressing to paraplegia by day 33 (3 days after cessation of 3-nitro feeding). Histopathologic examination revealed myelin and axonal degeneration in the white matter of the spinal cord coincident with the onset of nervous signs. Marchi-positive degeneration was present in the dorsal funiculus at cervical level at day 22. Lesions intensified with increasing duration of toxicosis and while degenerate fibers were seen in all funiculi, there was preferential involvement of the fasciculi gracilis and cuneatus, the peripheral regions of the ventral and lateral funiculi, and a discrete area of the dorsal region of the lateral funiculus. Peripheral and optic neuropathies were evident from day 32 but were always mild and focal. The experiment establishes 3-nitro as a central-peripheral neurotoxicant of pigs.
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