Veterinary Pathology

Equine viral rhinopneumonitis type I virus was isolated from spinal cord and brain of a paraparetic horse with disseminated necrotizing myeloencephalitis. Necrotic arteriolitis, nonsuppurative necrotizing myeloencephalitis and Gasserian ganglioneuritis were present. On record were 12 more cases of horses with similar lesions. The horses had been ataxic or paretic for up to several weeks. A field survey indicated that 14 of 24 horses with acute myelitic signs developed them after recent exposure to respiratory disease.

Chronic hypertrophic gastritis in a 7-year-old Boxer dog is described. This gastritis resembles Menetrier's disease in man. The dog was emaciated, lethargic, vomiting and had a poor appetite over a 4-month period. There was anaemia, and the blood smear was characterized by hypochromasia, strong anisoplania and striking poikilocytosis. There was a protein loss and at a later stage of the disease, a hypoalbuminaemia. On gastroscopic examination the plicae gastricae were numerous and strongly marked; moreover, they were granulated with numerous small haemorrhages. Radiographically, the stomach had a marked folding, primarily at the greater curvature. The passage of contrast medium from the stomach into the duodenum was strongly retarded. The pathological findings included macroscopical folding caused by local gland cell hyperplasia in the body as well as the pylorus, foveolar hyperplasia and, in the fundus and in the corpus near the greater curvature, folding of the muscularis mucosae and the submucosa. A superficial gastritis was found particularly in the fundus and corpus, whereas the pyloric antrum showed a more diffuse inflammation.

Twenty-four minimal disease pigs were inoculated intracerebrally, intravenously or intradermally with an English strain of swine vesicular disease virus. In the skin, snout, tongue and tonsil the main lesion was a full-thickness coagulative necrosis of the stratified squamous epithelium. In the renal pelvis, bladder, tonsillar crypts and the collecting ducts of salivary glands and pancreas, epithelial degeneration with the formation of periodic acid-Schiff-positive material were consistent features of this disease. Histopathological examination alone could not be relied upon to differentiate between well-established skin lesions caused by swine vesicular disease and foot and mouth disease. The relationship between vesicular disease and Coxsackie B5 is discussed briefly.

Gnotobiotic piglets were infected with a strain of rotavirus that had been isolated from a calf and passaged four times in piglets. The resulting disease was studied by light and electron microscopy at 21, 44 and 68h after inoculation. In the small intestine infection caused desquamation of the epithelial cells of the villi resulting in severe stunting. There was severe damage to microvilli and accumulation of lipid within the cytoplasm. Virus particles were seen in epithelial cells covering the stunted villi. Infection also caused desquamation of the superficial epithelial cells of the stomach mucosa and of the epithelial cells of the bronchi, bronchioles, and alveoli of the lungs.

Each of two Desert Sheep was infected with 1500 cercariae of Schistosoma mansoni of Northern Sudan. Signs of infection were anorexia, soft faeces, progressive weakness and loss of wool. The sheep were killed 254 and 269 days after infection. The findings were heavy infiltration of the lamina propria with inflammatory cells, numerous ova in the submucosa, hyperplasia of lymphoid tissue, oedema of the mesenteric lymph nodes, and focal pulmonary oedema and congestion. There were egg granulomas, focal necrosis, schistosomal pigment, fatty change, depletion of glycogen and reduction in the activity of adenosine triphosphatase, succinic tetrazolium reductase and glucose-6-phosphatase in the liver. In one sheep 1330 cercariae penetrated and 700 matured to produce males and females in a 5:2 ratio. In the other sheep, about one third of the cercariae penetrated and matured. The ratio of males to females was 3:1.

Conventional kittens, 12–27 weeks old, were inoculated with cell-cultured feline panleucopenia virus and killed sequentially between day 3 and day 24 after inoculation. All developed a non-fatal mild disease between days 2 and 9, characterized by lymphopenia, neutropenia, listlessness, depression and the development of neutralizing antibodies to the virus. Small intestinal bacterial counts were reduced during the period of maximal clinical disease, presumably a result of decreased food intake. There was involution of the thymus with marked depletion of lymphocytes between days 3 and 12. Depletion of lymphocytes also characterized the lesions in the lymph nodes between days 3 and 8. At the same time crypt lesions with spotty distribution were in the small intestinal and colonic mucosa. The changes were loss of crypt epithelial cells with compensatory attenuation of the remaining epithelium. Electron microscopically, the number and size of microvilli and secretory granules were reduced but there was no change indicating lethal cell injury. There were no virus particles. The findings point to an early and transient cellular damage by the virus. Intestinal alkaline phosphatase activity disappeared from the luminal surface of the attenuated crypt epithelial cells. Otherwise, intestinal alkaline and acid phosphatase activity were not altered in inoculated cats.