Characterization of and radioimmunoassay for canine thyroglobulin

Canine thyroglobulin (cTg) has been isolated and purified. It has similar electrophoretic patterns as Tg from other mammalian species. The main fraction had a MW of 660,000, whereas also fractions of a MW of approximately 1,300,000 (dimer) and 330,000 (subunit) were present. The iodine content was 0.8 to 1.0 % (w/w). cTg did not cross-react with antibodies against human Tg to a degree that would allow the use of a radioimmunoassay for human Tg for the determination of cTg in serum or plasma. Therefore a polyclonal antiserum was raised against cTg and a homologous radioimmunoassay was developed, which was sensitive (0.4 μg/l) and specific (cross-reactivity in cTg assay of human Tg, goat Tg, T₄, T₃, and DIT < 0.01 %).

Plasma Tg levels in normal dogs of both sexes and aged 3–15 years amounted to 192 ± 73 μg/l (mean ± SD, n=30). There was no relation between plasma Tg and T₄ levels.     

Some characteristics of a natural infection by parainfluenza-3 virus in a group of calves.

Parainfluenza-3 (Pi3) virus infection in a group of 25 calves is described. The virus was isolated from the lungs of four calve at days 6, 7, 13 and 55 after they were housed together at birth. Intracytoplasmic inclusion bodies were seen by light microscopy in bronchial and bronchiolar epithelial cells of two of these calves. Virus infected cells were detected by electron microscopy in three of the four calves. Haemagglutination inhibition antibodies to Pi3 virus were found in the sera of the calves. Despite the virus being present in the group from one week, a significant increase in antibody titre was found in only two animals although all the calves were in contact with each other during the study period. The pulmonary lesions in the four infected calves consisted of a bronchitis and bronchiolitis with infiltration of the walls and lumena of these structures by neutrophils and an adjacent neutrophil infiltration of alveoli some of which were collapsed.     

Sequential lesions of experimental bovine pneumonic pasteurellosis

A strain of Pasteurella haemolytica biotype A serotype 1, which had been isolated from a pathologically-confirmed outbreak of bovine pneumonic pasteurellosis, was used successfully to reproduce the disease in conventional calves. The development of the various pathological features was studied at regular intervals following infection. The acute inflammatory reaction which had developed by day 2 after initial infection was characterised by flooding of the alveoli by oedema and neutrophils together with a mild degree of bronchiolar epithelial necrosis. This progressed to an acute exudative fibrinous pneumonia with extensive involvement of the interlobular septa and often with pleurisy. Subsequently, these pulmonary lesions became walled off by fibrous tissue which became infiltrated by plasma cells and lymphocytes. At this stage organisms could be demonstrated only within these nodules in the lung tissue.     

Transmission studies with bovine malignant catarrhal fever

The intravenous administration of whole blood from a pathologically confirmed field case of bovine malignant catarrhal fever (MCF) resulted in the appearance of the disease in three of five experimental calves 18 to 28 days later. Infection was maintained by serial calf transmissions, and produced clinical and pathological changes identical to those of the field disease for a total of 10 passages. The sixth passage involved the simultaneous infection of 10 calves from a single donor animal; six of the 10 recipients developed the typical disease after incubation periods ranging from 20 to 36 days and in each of these MCF was confirmed by pathological examination. In addition, clinical and pathological changes in the four other calves which were slaughtered either seven or 14 days post-infection suggested that they too would have developed typical clinical signs had they been allowed to survive for the necessary length of time. The results of a detailed study of the onset, progress and duration of the clinical signs of experimentally induced MCF are presented and the opportunity has been taken to discuss the available information regarding the transmission of MCF under experimental conditions and in the field.