Inoculation of lambs with an ovine isolate of respiratory syncytial virus (RSV) by a combined intranasal and intratracheal route resulted in mild respiratory tract illness, with respiratory tract lesions. Lung lesions were characterized by bronchitis and bronchiolitis, hyperplasia of bronchial and bronchiolar epithelium, peribronchiolar and perivascular accumulations of lymphocytes, alveolar and perivascular accumulations of lymphocytes, alveolar septal thickening, and collapse. Respiratory synctial virus was recovered from the respiratory tract of inoculated lambs, and RSV antigen was demonstrated by immunoperoxidase staining of bronchiolar and alveolar epithelial peroxidase staining of bronchiolar and alveolar epithelia cells in pneumonic lesions of lambs euthanatized on post-inoculation days 5 and 6. Other primary respiratory tract pathogens were not isolated. Clinical signs of respiratory tract illness or respiratory tract lesions did not develop in the in-contact control lamb. Inoculation of the ovine RSV isolate into calves and deer fawns resulted in infection in both species, and at necropsy, pneumonic lesions were present. A mild to moderate respiratory tract illness developed in the calves, but clinical disease was not seen in the fawns. Lung lesions in fawns were similar to those seen in lambs; lesions in calves were characterized by collapse, scattered areas of parenchymal necrosis, and bronchiolitis. Respiratory synctial virus was reisolated from the lower respiratory tract of inoculated calves and fawns, and immunoperoxidase positive epithelial cells were seen in pneumonic lesions Other primary respiratory pathogens were not detected. Respiratory syncytial virus infection was not demonstrable in control animals that were in contact with inoculated animals. We concluded that an ovine RSV isolate, when inoculated in a severe challenge regime, caused mild primary pneumonia in lambs and lesions similar to those described in epizootics of naturally occurring ovine respiratory tract disease. Also, the ovine RSV caused lower respiratory tract lesions in infected calves and deer.

Three Beagles with chronic anemia and reticulocytosis were studied. The dogs originated from a large breeding colony and appeared clinically normal with the exception of splenomegaly. The PCV ranged from 30 to 39% (normal, 46 to 56%), with reticulocyte indices of 2.3 to 9.9. Red blood cells were morphologically normal, and examination of marrow aspirates revealed erythroid hyperplasia. Shortened chromium-51 RBC life-spans (7.2 to 15.4 days in anemic dogs; 22.2 to 25.2 days in control dogs) documented a hemolytic anemia. Acquired causes of hemolytic anemia were ruled out. Red blood cells had normal glycolytic enzyme activities, no evidence of unstable or abnormal hemoglobin, and had altered osmotic fragility curves. The breeding of 2 anemic dogs resulted in off-spring with anemia and reticulocytosis. Polyacrylamide gel electrophoresis revealed no abnormalities in RBC membrane cytoskeletal proteins in all anemic adult dogs and in 3 offspring.

Thirty-three cattle with fatal respiratory tract disease were examined for gross and histologic lesions and for the presence of viral and bacterial agents in the lungs. Fifteen cattle had lesions characteristic of atypical interstitial pneumonia (AIP), and 18 had other respiratory tract diseases, including infectious bovine rhinotracheitis, shipping fever pneumonia, bronchopneumonia, pulmonary abscess, and edema of the trachea. Gross necropsy findings in the cattle with AIP were uncollapsed and emphysematous lungs; histopathologic findings included interstitial edema, thickening of alveolar walls, hyaline membrane formation, and hyperplasia of type-II pneumonocytes. The infective agents found in the lungs of the 33 cattle included bovine respiratory syncytial virus, bovine herpesvirus type 1, Pasteurella sp, mycoplasmas, and Corynebacterium pyogenes. Bovine respiratory syncytial virus was detected by use of immunofluorescence and immunoperoxidase on lung tissue sections; bovine herpesvirus type 1 was detected by these techniques and by isolation of the virus. Bovine respiratory syncytial virus was significantly (P = 0.01) associated with lesions of AIP (11 of 15), compared with those of other respiratory tract diseases (5 of 18).

Morphologic lesions seen in six 8-month-old Labrador Retrievers with hereditary myopathy were predominantly small- and large-group atrophy of muscle cells of all fiber types. The dogs were intolerant of excerise and fatigued rapidly. An isolated gracilis muscle preparation was used to study the hemodynamic features of the microvasculature. Isogravimetric capillary pressure as well as arterial and venous pressures in the isolated gracilis muscle preparation obtained during maximal vasodilatation were within the range reported for healthy, mixed-breed dogs, as were precapillary, postcapillary, and total vascular resistances. Capillary filtration and osmotic reflection coefficients were not different from those reported in other studies on healthy dogs. All measurements and calculations were reported during reperfusion, subsequent to a 4-hour period of global ischemia. Postischemic vascular responses were similar to the pattern previously reported in healthy dogs. These studies did not support the hypothesis of a vascular defect as a cause of hereditary myopathy in Labrador Retrievers.

Parasite-free, 4-month-old-calves were inoculated with Ostertagia ostertagi and/or Trichostrongylus axei, followed 6 weeks later by inoculation with increasing doses of O ostertagi for 8 weeks in the 2 groups (n = 9) of calves that had been given O ostertagi. Gastrin immunoreactivity concentration in serum was measured before and after infection and was correlated with changes in mucosal thickness. Gastrin immunoreactivity concentration in preinoculation control sera ranged from 95.2 to 287.1 pg/ml, and increased values were measured in all parasitized calves after 15 weeks. Significantly (P < 0.05) increased serum gastrin immunoreactivity concentration compared with the preinfection value, was found in calves infected with O ostertagi or T axei, and highly significant (P < 0.01) values were observed in calves infected with both parasites. Abomasal mucosal hyperplasia was observed in all parasitized calves; increased mucosal thickness and mucosal cross-sectional area were most prominent in calves infected with O ostertagi and T axei.

A percutaneous biopsy technique for the study of endochondral bone formation in the dog was developed. With the dogs under general anesthesia or sedated with a combination of a tranquilizer and a local anesthetic, biopsy specimens were obtained from the proximal growth plate of the humerus with the use of a Jamshidi bone biopsy needle. Biopsy specimens were structurally intact, and contained epiphysis, growth plate, and metaphysis. The procedure proved to be a simple, safe technique, which caused minimal discomfort for the patient and did not affect the growth of the proximal end of the humerus, even after multiple biopsies.

Nine 7-month-old Beagle dogs were inoculated with 200 third-stage larvae of Dirofilaria immitis. The development of cardiac disease secondary to heartworm infection was confirmed by thoracic radiography, echocardiography, and angiography with blood pressure measurements. The only indication of renal disease was mild-to-moderate proteinuria. The dogs were euthanatized approximately 18 months after inoculation. The mean microfilarial count in blood at the time of euthanasia was 88,700/ml, with a mean of 89 adult heartworms in the vena cavae, heart, and pulmonary arteries. The kidneys were perfused for microangiographic and correlative histologic examination of the intrarenal microvasculature and associated renal morphologic features. Angiograms of whole kidneys from 6 dogs revealed attenuation or truncation of the major renal vessels. Microangiograms of all kidney slices revealed attenuation in the microangiographic appearance of the glomerular capillaries. Histologic examination of all kidney slices revealed mild-to-intense, diffuse, chronic interstitial nephritis and generalized membranoproliferative glomerulonephritis. Microfilariae were observed within the glomerular capillaries and the medullary vessels. The microangiographic changes correlated with and were explained in part by the histologic changes in the renal parenchyma.

Ten-day-old chicken embryos were inoculated with isolates of myeloblastosis-associated virus that induced osteopetrosis of slow or rapid onset. Bursa of Fabricius, thymus, spleen, bone marrow, kidney, liver, and lung were examined at 15, 17, and 19 days in ovo and at 7 and 25 days after hatching by histologic and immunoperoxidase techniques. Tissues from 19-day-old in ovo embryos also were examined by electron microscopy. The lymphoid organs of embryos inoculated with all isolates manifested changes suggesting inhibited development. Virus was most often associated with macrophages, heterophils, and non-lymphoid stromal cells in these organs. Viral particles and antigen were abundant in tissues from embryos inoculated with slow-onset isolates, but cell necrosis was infrequent. The kidney and bursa had especially abundant viral particles and antigen. Conversely, viral particles and antigen were minimal in tissues from embryos inoculated with the rapid-onset isolate, yet intravascular cellular thrombi, substantial cell necrosis, and increased heterophils and hemocytoblasts were found.

Strangulation obstruction was induced in anesthetized ponies for periods of 2 and 3 hours by clamping 45-cm segments of jejunum and associated veins (venous strangulation obstruction) and arteries and veins (arterial and venous strangulation obstruction). Four segments were studied in each of 7 ponies allowed to survive 12 hours, 2 segments in a pony that was allowed to survive 1 hour, and 1 segment in each of 10 ponies allowed to survive 42 days after the strangulation periods ended. Fifteen minutes after the periods of strangulation obstruction ended, the viability of test segments was assessed by clinical judgment (40 segments), fluorescein fluorescence (40 segments), and Doppler ultrasound (32 segments). Because thetest segments were normal at necropsy in long-term survivors, all segments were designated as viable. The overall accuracy of the methods used to predict viability was 88% for Doppler ultrasound and 53% each for clinical judgment and fluorescein fluorescence (P less than 0.005). Failures in the last 2 techniques could be attributed to their tendency to score venous strangulation obstruction segments as nonviable (90% for each). Doppler ultrasound was 94% accurate in these segments.