Our objectives were to describe the ultrastructural morphogenesis of pulmonary lesions induced by 3-methylindole in 30- to 45-day-old Holstein calves and to determine whether toxic exposure to 3-methylindole exacerbates pulmonary lesions induced by bovine respiratory syncytial virus. Administration of 3-methylindole (0.25 g/kg) to calves resulted in interstitial edema and ultrastructural swelling of type-I alveolar epithelial cells and nonciliated bronchiolar epithelial cells as early as 4 to 6 hours after intraruminal administration. More severe alveolar edema containing protein was associated with swelling of capillary endothelial cells at 2 days after administration. Proliferation of type-II alveolar epithelial cells was first observed at 2 days after 3-methylindole administration, and marked hyperplasia of type-II epithelial cells and nonciliated bronchiolar epithelial cells was evident by 4 days after administration. Pulmonary cytochrome P-450 monooxygenase concentrations decreased significantly (P < 0.001) by 12 hours after administration and did not increase significantly again by 8 days after administration. Calves were inoculated with bovine respiratory syncytial virus 3 days after administration of 3-methylindole, and pulmonary lesions were assessed 5 days after viral inoculation. Viral replication was demonstrated by fluorescence microscopy for viral antigen or by transmission electron microscopy in ciliated and nonciliated airway epithelial cells. Viral antigen was identified infrequently in alveolar macrophages and in type-II alveolar epithelial cells. 3-Methylindole exposure in calves did not result in more widespread distribution of viral antigen in alveolar tissue of respiratory syncytial virus-inoculated calves or in significant enhancement of viral pneumonia. The results indicated that young calves are susceptible to 3-methylindole-induced pulmonary injury and that nonciliated bronchiolar epithelial cells, type-I alveolar epithelial cells, and pulmonary endothelial cells are most susceptible to injury. The results failed to indicate that 3-methylindole pulmonary toxicosis significantly enhances respiratory disease induced by bovine respiratory syncytial virus.

A sublethal dose of ethylene glycol was administered orally to 3 groups of dogs; dogs of a control group were given distilled water instead. Renal cortical biopsy samples were obtained from dogs of experimental and control groups at various times after treatment. Tissue was examined by use of light microscopy and transmission electron microscopy. In dogs of the control group, the light and electron microscopic appearances of tissue were within normal limits at all sample collection hours. In dogs of the experimental groups, renal corpuscular structure remained within normal limits by use of light and electron microscopy throughout the study, though morphologic change was seen in other structures of the cortex. Light microscopic lesions first appeared at 12 hours, and were similar to those reported in the literature. Ultrastructural lesions were first observed in the 5-hour samples, and similar to the light microscopic lesions, were most common in the proximal convoluted tubules (PCT). Initial PCT cellular changes included vacuolization of cells and distention of the parabasal extracellular spaces; PCT cellular lesions seen in later-hour samples included formation of apical buds and cellular rupture. Internalization or sloughing of the PCT brush border was not observed. Distal convoluted tubules (DCT) were frequently dilated and/or packed with cellular debris. A few DCT cells had degenerative or necrotic changes. In PCT and DCT, abnormal cells were frequently flanked by normal or nearly normal cells. During later hours, a few cells with types of changes first observed in early hours continued to be observed, implying ongoing response of cells to the toxin.

An immunoperoxidase technique was used to study the relationship between the necrotic lesions and causative bacteria found in lungs of 53 calves that had naturally acquired pneumonia. Four types of necrotic lesions were identified on the basis of morphologic characteristics as follows: type 1 had coagulation necrosis surrounded by a dense zone of numerous degenerated leukocytes; type 2 was similar to type 1, but the central area of the lesions was severely affected, had no alveolar architecture remaining, and was surrounded by a thin, sparse layer of degenerated leukocytes; type 3 had small swirling accumulation of degenerated leukocytes; and type 4 had necropurulent lesions resembling abscesses. By use of the immunoperoxidase technique, Pasteurella haemolytica serovar 1 antigen was confirmed to be associated with the necrotic lesions in many cases of type 1 and in some cases of types 2 and 3. Although some lesions were induced by other bacteria (Haemophilus somnus or Actinomyces pyogenes), the pneumonic lesions associated with P haemolytica could be differentiated from other pneumonic lesions in calves by use of the immunoperoxidase technique.

During 1986 and 1987, electroencephalographic examinations were done on 8 dogs with intracranial mass lesions confirmed by computerized tomography, biopsy, necropsy, or a combination of these techniques. Tumor types included 1 astrocytoma, 1 undifferentiated glioma, 2 mixed gliomas, 2 meningiomas, 1 choroid plexus papilloma, and 1 cholesterol granuloma. It was found that no EEG pattern was pathognomonic for tumor type or location. Slow-wave activity was observed in the EEG of most of the dogs; asymmetry in amplitude or frequency was observed in approximately half the cases.

Twenty-two Hereford heifers were injected IM with prostaglandin F2 alpha(a), 11 days apart to synchronize estrous cycles. Twelve of 14 heifers that had signs of estrus were inoculated IV with 1 of 3 modified-live infectious bovine rhinotracheitis virus vaccines, and 2 were assigned to a nonvaccinated control group. Also, 6 of the 8 anestrous heifers were inoculated IV with 1 of the 3 vaccines on the fourth day after the last prostaglandin injection and the other 2 were assigned to the nonvaccinated group. Vaccine virus was isolated from the blood and nasal and vaginal secretions from the vaccinated heifers on postvaccination days 4, 7, and 9. On postvaccination day 9, all heifers were ovariectomized and ovarian tissues were processed for virus isolation and histologic examination. Vaccine virus was isolated from ovarian tissues of some heifers in each of the vaccine groups. Necrotic oophoritis characterized by multifocal areas of ovarian tissue necrosis, hemorrhage, and mononuclear lymphocytic infiltration was observed. The corpora lutea and surrounding ovarian tissues taken from vaccinated heifers in each group had varying amounts of necrotic and inflammatory change, but the changes appeared to be more severe in 1 group than in the other 2. Virus also was isolated from 2 of the controls; these heifers apparently became infected with vaccine virus that had been excreted from the vaccinated animals.

Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there was multifocal congestion and small thrombocyte aggregates within small blood vessels by PIH 0.5, with a few vessels containing small numbers of marginating heterophils. By PIH 1.5, thrombocyte aggregates were larger and more numerous, and moderate numbers of heterophils were located perivascularly. Erythrocytes and proteinaceous fluid were in air sac interstitium. By PIH 3 and 6, hemorrhage and exudation of proteinaceous fluid had increased, in some instances severely distending the air sac. Ultrastructurally, changes resulting from PMA-induced injury were thrombocyte aggregation and degeneration, air sac epithelial cell vacuolation with separation of interdigitating cell processes, and endothelial cell vacuolar degeneration with loss of vascular integrity. Air sac lavage fluids had mildly increased total cell counts by PIH 1.5, but values returned to baseline by the end of the experiment, indicating lack of cell exudation into the air sac lumen. Circulating leukocyte changes included transient lymphopenia at PIH 3 and marked heterophilia at PIH 6. These results indicate that thrombocytes and/or heterophils are central to the pathogenesis of injury induced in air sacs by PMA and that the air sac responds differently to PMA than to pathogenic bacteria.

Five dogs with mucopolysaccharidosis I, 3 of which had been treated with bone marrow transplantation (BMT), were evaluated for 20 months with electrocardiography, thoracic radiography, and M-mode and 2-dimensional echocardiography. Treated and untreated (control) dogs had widened P waves on ECG. Thoracic radiographs remained normal for all dogs throughout the study. Thickening of the mitral valve was observed on echocardiograms of dogs in both groups, but the untreated dogs appeared to have thicker valves. Concentrations of glycosaminoglycans in the mitral valves and myocardium were higher in control dogs than in treated dogs. Markedly large aortic root diameters were observed on echocardiograms in both untreated dogs, but aortic root diameters remained normal in treated dogs. Echocardiography, but notelectrocardiography, was useful in monitoring heart enlargement in each dog. Dogs treated with BMT generally had less-severe cardiac changes and slower disease progression than control dogs.

Genital tracts from 15 cows with catarrhal and purulent inflammation of the uterus and uterine tubes, cystic hyperplasia of the endometrium, or hydrosalpinx were evaluated by use of scanning electron microscopy to determine epithelial changes associated with these conditions. Uterine epithelium was revealed to be easily damaged, even in the course of mild inflammation, whereas epithelium of the uterine tube was more resistant.