|Rimler, Richard - Rick|
Submitted to: Avian Diseases
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/29/1996
Publication Date: N/A
Citation: N/A Interpretive Summary: Aspergillosis, caused by infection with Aspergillus fumigatus, is a prevalent and costly respiratory disease of poultry. Productivity losses in turkey flocks are especially significant because aspergillosis tends to occur late in the growing cycle and the air sac lesions caused by the infection result in condemnation at slaughter inspection. The pathogenesis sof aspergillosis is complex and poorly understood. Consequently, there are no vaccines or cost-effective treatments to limit losses in affected flocks. Aspergillosis has long been considered to be a slowly progressive, persistent infection. Significantly, this study demonstrates that pulmonary aspergillosis progresses rapidly to severe disease within 24 hours. Also, we show that the acute lesions have the appearance of chronic inflammatory responses. This is the first study to describe the sequential pathology of aspergillosis in turkeys, and the results clearly refute previous assumptions categorizing the disease as being insidiously progressive. This suggests the possibility of natural resolution of lesions, perhaps leading to acquired immunity. If so, deliberate exposure of young fowl would curtail carcass condemnation losses with enormous benefit to poultry producers. Studies are in progress to test this hypothesis. Consumers are the ultimate beneficiaries of this work through the sustained availability of healthful and economical poultry products.
Technical Abstract: Pathologic changes were characterized by gross examination and light microscopy after intra-air sac inoculation of 9- and 19-week-old turkeys with Aspergillus fumigatus conidia. Turkeys were euthanized and examined at 24, 48, 72, and 96 hours post-inoculation (PI). Lesions were largely confined to air sac membrane and lung tissues and were similar between the two age groups. There was progressive severity of gross lesions in both organs and of microscopic lesions in lung tissue. The character and severity of histologic lesions in air sac membranes were roughly similar at 24 through 96 hr post-inoculation (PI), but there was an increasing amount and consolidation of exudate adherent to the epithelial surface. Lesions in air sac membranes included edema, heterophil and macrophage infiltrates, granulomas, lymphohistiocytic perivasculitis, necrosis, epithelial loss, and surface exudate. Discreet granulomas containing multinucleate giant cells were present at 24 hr PI and thereafter. Lung lesions progressed from mild interstitial pneumonia to extensive effacement by multifocal coalescing granulomas, necrosis, and hemorrhage. Severe pleuritis with local extension into lung parenchyma was seen at all timepoints. Numbers of intralesional fungal elements seen histologically were similar between age groups and appeared to decrease in air sac membranes and increase in lung tissues from 24 to 96 hr PI. Lung tissues of the 19-week-old turkeys contained fewer colony-forming units per gram at timepoints after 24 hr PI.