Veterinary Pathology

Wedge biopsy of the liver during episodic clinical illness in three male cats showed chronic lymphocytic cholangitis. Principal clinical findings were increased serum alkaline phosphatase activity and hepatomegaly (two cats) associated with anorexia, pyrexia, and weight loss; these signs of illness were intermittent with asymptomatic periods. The hepatic lesions were characterized by lymphoid aggregate or follicle formation, diffusely dispersed lymphocytes and plasma cells, and abnormal bile ducts and ductules. Lymphoid aggregates and diffusely scattered lymphocytes were seen in the pancreas also. The spectrum of hepatic lesions in three cats seemed to represent a progression in the development of the disease. Similarities and dissimilarities between the findings in the three cats and human primary biliary cirrhosis or chronic nonsuppurative destructive cholangitis are discussed. During a prospective search for cats with this disease, other hepatic lesions were found, and it was concluded that cats may be affected by more than one pathogenic mechanism culminating in chronic cholangitis or cholangiohepatitis.

Gross and light microscopic features of focal nodular hyperplasia of the liver were investigated in beagle dogs used for the study of the long-term effects of low-dose, wholebody, ⁶⁰Co gamma radiation. The nodules were morphologically similar in the irradiated and unirradiated dogs. Microscopically, the normal lobular architecture, although retained, often was distorted. Hepatocytes in the nodules often were vacuolated and the distribution of vacuolated cells varied from focal to diffuse. There were more hepatocytes per unit area within nodules than in the adjacent parenchyma. Nodule hepatocytes were more variable in size. A lower proportion were binucleate and a higher proportion were in mitosis. The cells in the nodules contained less hemosiderin. The incidence of hyperplastic nodules was directly related to age but not to sex, and was higher in irradiated dogs than in controls. Nodular hyperplasia occurred in association with primary hepatocellular neoplasms in only two dogs.

Intestinal carcinoids were diagnosed in three aged dogs. Two of the neoplasms occurred in the rectum and one at the cecocolic junction. Judged by histologic criteria, all three carcinoids were considered to be malignant. Amyloid was present in both rectal tumors. In each tumor the diagnosis was confirmed by the finding of electron-dense intracytoplasmic secretory granules in the neoplastic cells.

Two female rhesus macaques (Macaca mulatta) and one female pigtailed macaque (M. nemestrina) developed acute neurological signs including ataxia, muscular incoordination, and seizures. Light microscopy showed Cowdry Type A intranuclear inclusion bodies in astrocytes and neurons of the cerebral cortex and Purkinje's cells of the cerebellum. Many cells also had intracytoplasmic inclusion bodies. Electron microscopy identified paramyxoviral nucleocapsids in the intranuclear and intracytoplasmic inclusions in two monkeys. We believe these monkeys had measles encephalitis because measles virus is the only paramyxovirus known to cause inclusion bodies in macaques and because the lesions in these monkeys resembled measles encephalitis in man.

In 15 pigs affected with cerebrospinal angiopathy accompanied by demyelination and malacia, the main symptoms were diarrhea and subsequent circling, spasms, sudden forward movements, ataxia, and inability to hold the head straight. Escherichia coli was isolated in a pure culture from the small intestine of pigs with diarrhea. The only gross change was a slight increase in cerebrospinal fluid. Histologic examination showed vascular lesions, demyelination, and malacia, most commonly located in the medulla oblongata, pons, and midbrain. The vascular lesions were degenerative and there were necrotic changes of the vessel walls and formation of periodic acid-Schiff-positive perivascular eosinophilic droplets. Ultrastructurally, the swollen astrocytes around the vessels had many osmiophilic bodies in their cytoplasm with no limiting membrane. Demyelination and malacia, as well as vascular lesions, were considered to be the characteristic changes of cerebrospinal angiopathy. Our study suggests that E. coli may be a cause of cerebrospinal angiopathy.

Naturally occurring, oval opacities at the junction of the middle and inferior thirds of the cornea were found in an experimental beagle dog colony and were examined by light and electron microscopy. Abnormalities were limited to the anterior stroma and consisted of extracellular rhomboid crystalline spaces. Spherical or elliptical vacuolar spaces, sometimes containing electron-dense amorphous debris, distorted stromal lamellae. Stromal keratocytes in affected areas revealed a range of changes from hyperplasia of organelles to degeneration and necrosis.

Three Arabian male foals were presented with cyanosis, heart murmur, and exercise intolerance. Results of clinical evaluation suggested a tentative diagnosis of ventricular septal defect in conjunction with malformations of the great arteries. Each foal had a poor prognosis and was killed at the owners' requests. At necropsy, the malformed hearts of the three foals were virtually identical. Each heart had a large defect in the upper interventricular septum. The aorta originated from the hypertrophied right ventricle and partially overrode the ventricular septal defect. The aortic ostium was guarded by three semilunar valvules. The position of the valvules and the ostia of the coronary arteries was abnormal. The pulmonary arteries arose from the persistent ductus arteriosus. The pulmonary trunk was reduced to a thin, fibrous cord extending from a short and narrow persistent ductus arteriosus to the level of the semilunar valve, where it fused with the wall of the aorta. No communication of the atretic pulmonary trunk with the cavity of the right ventricle was seen.

Histological and ultrastructural changes in the nasal mucosa of normal and leukopenic mice exposed to Pseudomonas aeruginosa were compared and correlated with changes in the distribution of pseudomonads by use of immunoperoxidase labeling. Pseudomonas was limited to the surface of the nasal mucosa of normal mice and was cleared rapidly. Concurrently, granulocytes were recruited across unaltered nasal epithelium and contained phagocytosed bacilli within two hours. Pseudomonas was limited to the surface of the nasal mucosa of most leukopenic mice at two hours. By four hours, pseudomonads had penetrated interepithelial junctions of all leukopenic mice. Granulocytes were not recruited and nasal epithelium underwent necrosis at points of invasion. These results show that neutrophils participate in the clearance of P. aeruginosa from the surface of the nasal mucosa and that the failure to recruit granulocytes may be important in the breakdown of epithelial barriers. Possible mechanisms of mucosal invasion are discussed.

The sequential enteric lesions of experimental porcine adenovirus strain 6618 infection were studied in 18 hysterotomy-derived, colostrum-deprived piglets, by histology, transmission electron microscopy, and an immunoperoxidase technique.

Viral particles could be seen in altered epithelial cells of the lower small intestine from 24 hours until 16 days after inoculation. With the immunoperoxidase technique, viral antigen could be found in epithelial cells at 45 days after challenge.

Destruction of epithelial cells and shortening of villi could be related directly to the presence of the virus.

Histology of the lower jejunum and ileum, which demonstrates intranuclear inclusion bodies, is proposed as a useful diagnostic technique.

The small intestines of calves inoculated orally with the enteropathogenic strain of Escherichia coli 0101:K'B41′, K99 were examined by electron microscopy at 3, 6, 12, 16, 21, 36, 69, 70 and 72 hours after inoculation. The challenge organism adhered to the mucosa of the distal small intestine from six hours post-inoculation. Bacteria were separated from the microvillous brush border by a gap of 200 to 300 nm in which bacterial fimbriae and the microvillous glycocalyx were seen. Bacteria never were found in epithelial cells but were present in macrophages in the lamina propria from 12 hours. At three and six hours, cytopathic changes were not seen in the small intestine, but from 12 hours epithelial cells on affected villi had blunt and thick microvilli and contained cytoplasmic inclusions. Epithelial cells were seen frequently in the process of extrusion from the villi, either singly, in small groups, or as ribbons of cells. Intervillous bridges, characteristic of villous fusion, were seen frequently from 69 hours.