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High mortality rates have been reported in budgerigars between one and 15 days of age in 19 aviaries in the Province of Quebec. The most consistent signs of disease were abdominal distention, lack of down feathers on the back and abdomen, lack of filoplumes on the head and neck, and retarded growth of the tail and contour feathers in birds that either survived or died later. Internal gross lesions were hydropericardium, enlarged heart and liver with multiple pinpoint white spots or large, yellow foci, pale or congested kidneys, congested lungs, and ascites. Histologic examination revealed large, slightly basophilic inclusion bodies in the enlarged nuclei of many different cells. These inclusion bodies were composed of viral particles. Multiple foci of coagulation necrosis were scattered in the myocardium and liver parenchyma, and granulovacuolar degeneration was common in renal tubular epithelial cells. Ballooning degeneration was multifocal in the epidermis and very extensive in the epithelial cells of developing feather follicles, and this led to their partial or complete destruction. Viral particles 50 to 55 nm in diameter were observed in negatively stained preparations from different organs of affected birds. These particles had the size and morphology of a papovavirus. In experimentally infected 25-day-old budgerigars, histologic examinations revealed the presence of intranuclear inclusions in hepatocytes, epithelial cells of the kidney tubules, and reticular cells of the spleen, despite the absence of clinical signs. We feel that this disease is caused by a papovavirus-like agent that can replicate in many tissues of the body, causing widespread lesions responsible for the high mortality rate of very young budgerigars and for the absence and/or incomplete development of feathers.

A retrospective study on pig lung tissues from 60 cases of proliferative and necrotizing pneumonia (PNP) was performed to determine the presence of porcine reproductive and respiratory syndrome virus (PRRSV), swine influenza virus (SIV), and porcine circovirus type 2 (PCV2) in these lesions. Cases selected included 30 cases diagnosed between 1988 and 1992 and 30 cases diagnosed between 1997 and 2001. In each group of 30 cases, 10 were from suckling piglets, whereas the other 20 were from postweaned animals representing either nursery or grower-finisher pigs. Immunohistochemistry using a monoclonal antibody to influenza virus type A was used to determine the presence of SIV, and in situ hybridization was used for the detection of PRRSV and PCV2 nucleic acids. PRRSV was detected in 55 of the 60 cases examined (92%), PCV2 in 25 cases (42%), and SIV in only 1 case (2%). In 30 cases (50%), PRRSV was the only virus detected, whereas in 25 other cases (42%), a combination of PRRSV and PCV2 could be detected in the lungs with PNP lesions. PCV2 could not be detected in the lungs of suckling pigs with PNP. All PCV2-positive cases were found in postweaned pigs and were always in combination with PRRSV. In this latter age group, PCV2 was detected in 63% of the cases (25/40). Data from our study indicate that SIV is rarely identified in PNP and that PCV2 infection is not essential for the development of PNP lesions. The results of the present study demonstrate that PRRSV is consistently and predominantly associated with PNP and should be considered the key etiologic agent for the condition.

The ability of a nonenterotoxigenic, K88-negative porcine Escherichia coli strain of serogroup O45:K"E65" to induce attaching-effacing lesions was investigated in newborn pigs. Typical attaching-effacing lesions, characterized by intimate adherence of bacteria to mature enterocyte brush borders with effacement of the microvilli, were observed on light and electron microscopy. Bacteria were also seen in intracytoplasmic vacuoles of mature enterocytes and, in areas of heavier colonization, in the lamina propria of the intestinal mucosa. A moderate inflammatory response with mild focal ulceration of the intestinal mucosa was observed. In a sequential study, we observed that the attaching-effacing lesions were well established in the duodenum, jejunum, and ileum at 12 h postinoculation but did not develop in the cecum and colon until 24 to 48 h postinoculation, although bacteria had colonized the latter areas as early as 12 h postinoculation. Initially, bacteria were very intimately attached, with an irregular arrangement on the enterocyte apical cell membrane, and subsequently reoriented to form a typical palisade arrangement with a narrow regular gap between the bacterial cell wall and the enterocyte apical cell membrane. This phenomenon of early intimate attachment of irregularly disposed bacteria has not been reported for human enteropathogenic attaching and effacing E. coli and could represent a new and different mechanism of attachment and effacement to intestinal epithelial cells.