Veterinary Pathology

One hundred bovine female reproductive tracts were examined for the presence of Hemophilus somnus, and fifty were examined for gross and microscopic lesions. H. somnus was isolated from eight of 100 tracts. The isolation was made from the vagina in seven cows. Of 24 tracts in which the major vestibular gland was sampled, three were positive at this site, and two of these three also had the organism isolated from the vagina. Further investigations into the role of the major vestibular gland as a source for continuing infections of the reproductive tract of cattle were indicated. In this investigation. H. somnus was as likely to be found in a region without lesions as one with lesions.

Spontaneous lymphocytic thyroiditis was observed at necropsy in 36 BB Wistar diabetic rats (63.2%) and in eight of their nondiabetic siblings (42.1%). The incidence of thyroiditis decreased both with age and with longer duration of diabetes. All rats with pancreatic insulitis (a manifestation of the onset of diabetes) also had thyroiditis. BB Wistar rats with insulitis had more severe lymphocytic thyroiditis, characterized by lymphocytic, plasmacytic, and macrophage infiltration of thyroid interstitium and follicles. A milder, mostly perivascular and interstitial lymphocytic thyroiditis was characteristic of lesions in rats which did not have insulitis. The histological appearance of the thyroiditis suggests that these rats may be subject to autoimmune disease at the onset of diabetes which involves sites other than just the pancreas.

Clinical and postmortem materials from six dogs with a diagnosis of malignant mesothelioma were studied retrospectively. The dogs were urban pets with clinical signs of malignant effusions. Two mesotheliomas were pleural, one pericardial, and one peritoneal. Both pleura and pericardium were involved in one dog, and the pleura and peritoneum in another. On gross examination at necropsy, diffuse granular or velvety plaques covering mesothelial surfaces were found in all dogs; firm discrete pleural nodules also were present in two dogs. Neither distant mestastases nor areas of deep lung invasion were found. The tumors varied histologically, but the most common type was epithelial with a papillary pattern. Ultrastructurally, the neoplastic cells had prominent surface microvilli, numerous desmosomes, and tonofilaments.

Lung tissue from these dogs and from control dogs was evaluated for the presence of ferruginous bodies. Asbestos bodies were found in three of five dogs with mesotheliomas but rarely were found in control dogs. As a group, the mesothelioma cases had significantly more asbestos bodies and total ferruginous bodies than controls. The clinical and morphologic appearance of canine mesothelioma is similar to human mesothelioma and also may be associated with exposure to airborne fibers.

A pituitary mass was found at necropsy of a male Macaca mulatta. Hematoxylin and eosin-stained sections were consistent with a chromophobe adenoma. Ultrastructural examination revealed the tumor to be comprised predominantly of sparsely granulated cells. The tumor cells were negative for prolactin, somatotropin, adrenocorticotropin, luteinizing hormone, and thyrotropin by the peroxidase anti-peroxidase method. Other major lesions were gynecomastia and galactorrhea, testicular atrophy, ankylosing spondylitis, and amyloid deposition in the liver, spleen, adrenal, and intestinal tract.

Erythropoietin concentrations were increased significantly (p < 0.025) in nine cats with natural feline leukemia virus infection and associated erythroid aplasia compared to six clinically normal cats. Adult cats experimentally inoculated with the Kawakami-Theilen isolate of feline leukemia virus developed a progressive simultaneous increase in erythropoietin activity and decrease in packed cell volume. These findings indicate that erythroid aplasia associated with feline leukemia virus infection is not caused by a failure in erythropoietin production.

The cytology of cerebrospinal fluid samples from horses is described. The samples were obtained from 24 normal horses. 35 horses with axonal degeneration and/or spinal cord compression. 29 horses with encephalomyelitis, 14 horses with other lesions of the nervous system, and eight horses with signs of neurologic dysfunction of undetermined origin. (Three of the latter were suspected botulinum intoxications.) Fluid was aspirated from the atlanto-occipital space following general anesthesia or immediately after a lethal dose of barbiturate. In two horses, fluid also was aspirated from the lumbosacral space. Small mononuclear cells were predominant in normal horses, and in most horses with axonal degeneration and encephalomyelitis. Several horses with encephalomyelitis also had neutrophils, eosinophils, and some mitotic figures. Although the cytologic findings were abnormal in many of the horses with disease of the central nervous system, in most horses the cytologic findings were normal.

Direct inoculation of bluetongue virus into 125-day bovine fetuses resulted in development of hydranencephaly. The earliest lesions after virus inoculation were a severe necrotizing encephalitis, which was most prominent in the cerebrum, and an associated nonsuppurative meningitis. At birth, the brains of infected fetuses had thin-walled cerebral hemispheres, dilated lateral ventricles, and cerebral cysts. No gross lesions were observed in the brain stem or cerebellum.

Two morphologically different lesions were present in the brain of a fetus sacrificed 20 days after virus inoculation. There were discrete foci of hemorrhagic cerebral necrosis that resembled infarcts and widespread microcavitations of the intermediate and subventricular zones. Changes consistent with vascular damage were present in the brains of fetuses sacrificed 12 and 20 days after virus inoculation.

Calves with bluetongue virus-induced hydranencephaly would have poor viability, but they would not be expected to have any significance as virus reservoirs.

The injection of three strains of Hemophilus somnus into the amniotic cavity of pregnant cows produced death of the fetus and abortion followed by retention of the placenta. H. somnus was recovered readily from the placenta but less so from the fetus. Lesions in the placenta were conspicuous in arteries and somewhat resembled vascular lesions observed in septicemic H. somnus. H. somnus was recovered from the maternal circulation in several infected cows. Clinical signs included fever, irritability, lameness, and vulvar discharge, but no cows died. The organism was recovered for prolonged periods in cervicovaginal mucus and urine after remission of clinical signs. This may be a means of spread of infection.

Three strains of Hemophilus somnus were infused into the posterior cervix of six pregnant cows. The organism persisted in the cervicovaginal region for eight to 87 days, and at parturition H. somnus was isolated from chorioallantois in four of six cows; placentitis developed, and fetal membranes were retained. All calves were born alive and no H. somnus was recovered from them. One cow died 14 days after parturition. The death was attributed to severe necrotizing metritis; H. somnus was not isolated from the uterus at death, but was isolated from the placenta at parturition and cervicovaginal mucus two days later.

Monensin toxicosis was induced in lambs by either a single oral dose of 12 mg/kg or six daily doses of 8 mg/kg. Clinical signs of toxicosis consisted of depression, dyspnea, stiffness of gait, reluctance to move, and recumbency. Serum creatine phosphokinase activity was increased. Samples of skeletal and cardiac muscle were obtained over a six-day period and examined by light and electron microscopy. Light microscopic changes in cardiac and skeletal muscles consisted initially of vacuolation and intracellular edema of muscle cells followed by segmental necrosis. Interstitial fibrosis was present on days 5 and 6 postexposure. Muscle fiber necrosis was more severe in skeletal than cardiac muscles and most severe in sheep given 8 mg/kg of monensin daily. Macrophages were seen only in areas of severe necrosis. The earliest ultrastructural change was severe swelling of mitochondria. Secondary changes consisted of lipid accumulation and myofibrillar alterations. Myoblast proliferation was present as early as four days after initial exposure to monensin.

Acute renal papillary necrosis occurred in five horses given normal therapeutic doses of phenylbutazone and deprived of water for 36 to 48 hours prior to euthanasia. Five horses given phenylbutazone alone and four horses subjected to water deprivation alone did not develop papillary necrosis. Urinalyses were normal prior to water deprivation, and also after water deprivation in the horses that did not receive phenylbutazone, but the water-deprived, phenylbutazone-treated horses had many red blood cells, transitional epithelial cells, and large numbers of oxalate crystals in their urine.

Ulceration of the alimentary tract was seen in more than 50% of these horses. Tongue ulceration was present in one of five horses given phenylbutazone and one of five horses which had phenylbutazone and water deprivation. Ulceration of the gastric mucosa was seen in two of the five phenylbutazone-treated horses, four of five horses with phenylbutazone treatment and water deprivation, and one of four horses with water deprivation alone. Severe colonic ulceration with perforation and peritonitis was present in one horse given phenyl-butazone for three months. No other significant changes in the small or large intestine were seen in the other 13 horses.

Diarrhea, dyspnea, tympany, arching of the back, loss of condition, and loss of hair from the back were the prominent signs when Aristolochia bracteata was given orally to goats. The main lesions were hemorrhages in the lungs, heart, and kidneys, fatty change and congestion in the liver, mucoid abomasitis and enteritis and straw-colored fluid in serous cavities. An increase in aspartate aminotransferase activity, ammonia and urea concentrations and a decrease in the concentrations of total protein and magnesium were detected in the serum.

Macrophage numbers increased in the spleen, liver, testes, heart, and kidney of deer mice infected for seven to ten weeks with Trypanosoma brucei EATRO 110. The macrophages were activated as indicated by their increased size and significant increases in numbers of cell organelles including profiles of rough endoplasmic reticulum (which also increased in length), mitochondria, primary and secondary lysosomes, bundles of Golgi's apparatus, and free lysosomes compared to macrophages from control mice. Some macrophages representing epithelioid cells have even greater numbers of organelles than the activated macrophages and had interdigitation in some locations, such as the heart, but with minimal phagocytic activity. These epithelioid cells were present in the kidney, testes, and particularly in the heart of infected mice. Few cardiac macrophages had finely granular deposits on their nuclear membrane. The activated macrophages had enhanced phagocytosis of trypanosomes. red blood cells, neutrophils, eosinophils, lymphocytes, and plasma cells. In addition to phagocytosis, another probable consequence of macrophage activation may be depression of lymphocyte function. Phagocytosis of trypanosomes by neutrophils also was encountered occasionally.