Abstract
The Great Blue Turaco (Corythaeola cristata) has been raised in captivity for over a hundred years, but their susceptibility to infectious disease is very poorly documented. The macroscopic, histopathologic, and ultrastructural changes in the respiratory tract of nine Great Blue Turacos (Corythaeola cristata) who died in captivity were investigated. Macroscopically diffuse granulomatous lesions were observed in the lung and the associated air sacs, with a grey-greenish mold on their inner surface. Histopathologic examination revealed widespread necrosis in the lungs associated with vasculitis. Microthrombi were observed in the blood vessels suggesting disseminating intravascular coagulation. Intra-alveolar hemorrhage and infiltration with macrophages, plasma cells, epithelioid cells, and multinucleate giant cells were observed. PAS staining showed hyphae and conidia, While, Ziehl-Neelsen stain was negative. Transmission electron microcopy examination revealed the presence of Aspergillus fumigatus conidia invading the pulmonary tissue as semilunar spores within the alveolar macrophages. Lysosomal degranulation was also observed in association with fragmented spores suggesting active phagocyosis. Awareness of this condition might improve the rapid and appropriate treatment of exotic birds kept in captivity.
Highlights
Pulmonary aspergillosis results from a range of factors including bird capture, transportation, overcrowding, high humidity, bad sanitation, inadequate hygiene measures, and contact with other bird species
Resident alveolar macrophages ingest and kill resting conidia, mainly through nonoxidative mechanisms, while neutrophils use oxygen-dependent mechanisms to attack hyphae germinating from conidia that escape macrophage surveillance (Bozza et al, 2002)
The present study describes Aspergillus fumigatus infection and its histopathologic and ultrastructural features in several imported Great Blue Turacos who died in captivity
Summary
Pulmonary aspergillosis results from a range of factors including bird capture, transportation (for instance from tropical to temperate climates), overcrowding, high humidity, bad sanitation, inadequate hygiene measures, and contact with other bird species. Aspergilli are respiratory pathogens and pulmonary infections usually acquired through the inhalation of conidia and able to reach small airways and the alveolar space where the impaired host defense mechanisms allow hyphal germination and subsequent tissue invasion. The invasive pulmonary aspergillosis is the most common manifestation of Aspergillus fumigatus infection in immunocompromised patients and is characterized by hyphal invasion and destruction of pulmonary tissue. Resident alveolar macrophages ingest and kill resting conidia, mainly through nonoxidative mechanisms, while neutrophils use oxygen-dependent mechanisms to attack hyphae germinating from conidia that escape macrophage surveillance (Bozza et al, 2002). Murine pulmonary denderitic cells internalize conidia and hyphae of A. fumigatus both in vitro, and during infection, in vivo. Pulmonary DC, after phagocytosis of conidia or hyphae, migrate to the draining lymph nodes and spleens, undergo functional maturation, and induce selective Th priming of CD4_ T lymphocytes (Bozza et al, 2002)
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